F

S
F

H
N
N O

2025 O
N

Nelson’s Pediatric
O O
H

Antimicrobial Therapy
31st Edition
Debra L. Palazzi, MD, MEd
Editor in Chief
John S. Bradley, MD
Past Editor
John D. Nelson, MD
Emeritus, Founding Editor

John C. Arnold, MD
Elizabeth D. Barnett, MD
Joseph B. Cantey, MD, MPH
David W. Kimberlin, MD
Paul E. Palumbo, MD
Jason Sauberan, PharmD
J. Howard Smart, MD
William J. Steinbach, MD
Contributing Editors
 Make the best possible treatment
decisions for neonates.

Completely updated and revised, the second edition provides the

most current, practical, and evidence-based recommendations.
Get expert advice on
• Dosing for neonates, including
low-birth-weight newborns
• Updated drugs, dosing, and
guidance for treatment of
bacterial, viral, fungal, and
parasitic infections
• Antimicrobial stewardship
in the nursery
• Drug monographs for commonly
prescribed drugs, with new
monographs for
• Ceftazidime
• Micafungin
• Nafcillin or oxacillin
• Piperacillin/tazobactam
Paperback, April 2024—92 pages
MA1121
Book ISBN 978-1-61002-698-7
eBook ISBN 978-1-61002-699-4
Price: $28.95 Member Price: $23.95

Visit aap.org/shopaap-books.
 2025 Nelson’s Pediatric Antimicrobial Therapy
1. Antimicrobial Therapy According to Clinical Syndromes

2. Antimicrobial Therapy for Neonates

3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

4. Choosing Among Antibiotics Within a Class

5. Preferred Therapy for Fungal Pathogens

6. Choosing Among Antifungal Agents

7. Preferred Therapy for Viral Pathogens

8. Choosing Among Antiviral Agents

9. Preferred Therapy for Parasitic Pathogens

10. Choosing Among Antiparasitic Agents

11. How Antibiotic Dosages Are Determined

12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

13. Antibiotic Therapy for Children With Obesity

14. Sequential Parenteral-Oral Antibiotic Therapy for Serious Infections

15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

16. Approach to Antibiotic Allergies

17. Antibiotic Stewardship

18. Systemic & Topical Antimicrobial Dosing & Dose Forms

Appendix: Nomogram for Determining Body Surface Area

References

Index
 F
S
F

H
N
O

2025
N

N
O

Nelson’s Pediatric
O O
H

Antimicrobial Therapy
31st Edition
Debra L. Palazzi, MD, MEd
Editor in Chief
John S. Bradley, MD
Past Editor
John D. Nelson, MD
Emeritus, Founding Editor
John C. Arnold, MD
Elizabeth D. Barnett, MD
Joseph B. Cantey, MD, MPH
David W. Kimberlin, MD
Paul E. Palumbo, MD
Jason Sauberan, PharmD
J. Howard Smart, MD
William J. Steinbach, MD
Contributing Editors
 American Academy of Pediatrics Publishing Staff
Mark Grimes, Vice President, Publishing
Jeff Mahony, Senior Director, Professional and Consumer Publishing
Cheryl Firestone, Senior Manager, Digital Publishing
Soraya Alem, Digital Production Specialist
Barrett Winston, Senior Manager, Publishing Acquisitions and Business Development
Grace Klooster, Editor, Professional/Clinical Publishing
Shannan Martin, Production Manager, Consumer Publications
Amanda Helmholz, Medical Copy Editor
Mary Louise Carr, MBA, Marketing Manager, Professional Resources
Published by the American Academy of Pediatrics
345 Park Blvd
Itasca, IL 60143
Telephone: 630/626-6000
Facsimile: 847/434-8000
www.aap.org
The American Academy of Pediatrics is an organization of 67,000 primary care pediatricians, pediatric medical
subspecialists, and pediatric surgical specialists dedicated to the health, safety, and well-being of all infants,
children, adolescents, and young adults.
While every effort has been made to ensure the accuracy of this publication, the American Academy of
Pediatrics does not guarantee that it is accurate, complete, or without error.
The recommendations in this publication do not indicate an exclusive course of treatment or serve as a
standard of medical care. Variations, taking into account individual circumstances, may be appropriate.
Statements and opinions expressed are those of the authors and not necessarily those of the
American Academy of Pediatrics.
Any websites, brand names, products, or manufacturers are mentioned for informational and identification
purposes only and do not imply an endorsement by the American Academy of Pediatrics (AAP). The AAP is not
responsible for the content of external resources. Information was current at the time of publication.
The publishers have made every effort to trace the copyright holders for borrowed materials. If they have
inadvertently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity.
This publication has been developed by the American Academy of Pediatrics. The contributors are expert
authorities in the field of pediatrics. No commercial involvement of any kind has been solicited or accepted
in the development of the content of this publication. Disclosures: Dr Elizabeth Barnett has not disclosed any
relationships relevant to the content area she contributed to in this publication. Dr Paul Palumbo has disclosed
a data safety monitoring financial relationships with Gilead and Janssen. Any relevant disclosures have been
mitigated through a process approved by the AAP Board of Directors.
Every effort has been made to ensure that the drug selection and dosages set forth in this publication are in
accordance with current recommendations and practice at the time of publication. We encourage the health
care professional to check the package insert of each drug for any change in indications or dosage and for added
warnings and precautions as well as to review data published in the medical literature since our current review, for
updated data on safety and efficacy.
Please visit www.aap.org/errata for an up-to-date list of any applicable errata for this publication.
Special discounts are available for bulk purchases of this publication. Email Special Sales at nationalaccounts@aap.
org for more information.
© 2025 Debra L. Palazzi, MD, MEd, and John D. Nelson, MD
Publishing rights, American Academy of Pediatrics. All rights reserved. No part of this publication may be
reproduced, stored in a retrieval system, used for the purpose of training artificial intelligence technologies
or systems, or transmitted in any form or by any means—electronic, mechanical, photocopying, recording, or
otherwise—without prior permission from the authors. First edition published 1975; 31st edition, 2025.
Printed in the United States of America
9-505/0224 9-520/0225   1 2 3 4 5 6 7 8 9 10
MA1185
ISSN: 2164-9278 (print)
ISSN: 2164-9286 (electronic)
ISBN: 978-1-61002-824-0
eBook: 978-1-61002-825-7
 iii

Editor in Chief Emeritus, Founding Editor

Debra L. Palazzi, MD, MEd, FAAP John D. Nelson, MD
Professor of Pediatrics Professor Emeritus of Pediatrics
Baylor College of Medicine The University of Texas
Division Chief, Pediatric Infectious Diseases Southwestern Medical Center at Dallas
Texas Children’s Hospital Southwestern Medical School
Houston, TX Dallas, TX

Past Editor
John S. Bradley, MD, FAAP
Distinguished Professor of Pediatrics
Division of Infectious Diseases, Department of
Pediatrics
University of California, San Diego, School of
Medicine
Medical Director, Infectious Diseases, Rady Children’s
Hospital San Diego
San Diego, CA
Lead editor: Chapters 1, 3, 4, 11, 12, 14, and 15

Contributing Editors

John C. Arnold, MD, FAAP Joseph B. Cantey, MD, MPH, FAAP

Rady Children’s Hospital San Diego Associate Professor of Pediatrics
Associate Professor of Pediatrics Divisions of Allergy, Immunology, and Infectious
University of California, San Diego, School of Diseases
Medicine Division of Neonatology
Lead editor: Chapters 1 and 3 University of Texas Health Science Center at San
Antonio
Elizabeth D. Barnett, MD, FAAP San Antonio, TX
Professor of Pediatrics
Lead editor: Chapters 2 and 17
Boston University Chobanian & Avedisian School of
Medicine David W. Kimberlin, MD, FAAP
Chief of the Division of Pediatric Infectious Diseases Professor of Pediatrics
Boston Medical Center Codirector, Division of Pediatric Infectious Diseases
Boston, MA University of Alabama at Birmingham
Lead editor: Chapters 9 and 10 Birmingham, AL
Lead editor: Chapters 7 and 8
iv

Contributing Editors (continued)

Paul E. Palumbo, MD J. Howard Smart, MD, FAAP

Professor of Pediatrics and Medicine Chairman, Department of Pediatrics
Geisel School of Medicine at Dartmouth Sharp Rees-Stealy Medical Group
Director, International Pediatric HIV Program Assistant Clinical Professor of Pediatrics
Dartmouth-Hitchcock Medical Center University of California, San Diego, School of
Lebanon, NH Medicine
Lead editor: Chapters 2, 7, and 8 San Diego, CA
Lead editor: app development
Jason Sauberan, PharmD
Neonatal Research Institute William J. Steinbach, MD, FAAP
Sharp Mary Birch Hospital for Women & Newborns Robert H. Fiser, Jr, MD, Endowed Chair in Pediatrics
Rady Children’s Hospital San Diego Chair, Department of Pediatrics
San Diego, CA Associate Dean for Child Health
Lead editor: Chapters 2, 3, 13, and 18 University of Arkansas for Medical Sciences
Pediatrician in Chief, Arkansas Children’s
Little Rock, AR
Lead editor: Chapters 5 and 6

Additional Contributor
Margaret Taylor Danner, MD, FAAP
Assistant Professor of Pediatrics
Division of Pediatric Infectious Diseases
Baylor College of Medicine
Associate Medical Director, Antimicrobial
Stewardship
Texas Children’s Hospital
Houston, TX
Lead editor: Chapter 16
Equity, Diversity, and Inclusion Statement
The American Academy of Pediatrics is committed to principles of equity, diversity, and
inclusion in its publishing program. Editorial boards, author selections, and author transi-
tions (publication succession plans) are designed to include diverse voices that reflect
society as a whole. Editor and author teams are encouraged to actively seek out diverse
authors and reviewers at all stages of the editorial process. Publishing staff are committed
to promoting equity, diversity, and inclusion in all aspects of publication writing, review,
and production.
 vii

Contents
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Abbreviations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiii
Notable Changes to 2025 Nelson’s Pediatric Antimicrobial Therapy, 31st Edition. . . . xvii
1. Antimicrobial Therapy According to Clinical Syndromes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
A. Skin and Soft Tissue Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
B. Skeletal Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
C. Eye Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
D. Ear and Sinus Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
E. Oropharyngeal Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
F. Lower Respiratory Tract Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
G. Cardiovascular Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
H. Gastrointestinal Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
I. Genital and Sexually Transmitted Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
J. Central Nervous System Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
K. Urinary Tract Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64
L. Miscellaneous Systemic Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66
2. Antimicrobial Therapy for Neonates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
A. Recommended Therapy for Select Neonatal Conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . 77
B. Antimicrobial Dosages for Neonates. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100
C. Aminoglycosides. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104
D. Vancomycin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
E. Use of Antimicrobials During Pregnancy or Breastfeeding. . . . . . . . . . . . . . . . . . . . . . . 105
3. Preferred Therapy for Specific Bacterial and Mycobacterial Pathogens. . . . . . . . .107
A. Common Bacterial Pathogens and Usual Pattern of Susceptibility
to Antibiotics (Gram Positive) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108
B. Common Bacterial Pathogens and Usual Pattern of Susceptibility
to Antibiotics (Gram Negative). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
C. Common Bacterial Pathogens and Usual Pattern of Susceptibility
to Antibiotics (Anaerobes). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
D. Preferred Therapy for Specific Bacterial and Mycobacterial Pathogens. . . . . . . . 114
4. Choosing Among Antibiotics Within a Class: β-Lactams and β-Lactamase
Inhibitors, Macrolides, Aminoglycosides, and Fluoroquinolones . . . . . . . . . . . . . . . . 141
5. Preferred Therapy for Specific Fungal Pathogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
A. Overview of More Common Fungal Pathogens and Their Usual Pattern of
Antifungal Susceptibilities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
B. Systemic Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152
C. Localized Mucocutaneous Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168
viii — Contents

6. Choosing Among Antifungal Agents: Polyenes, Azoles, and Echinocandins . . . 171

7. Preferred Therapy for Specific Viral Pathogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
A. Overview of Non-HIV, Non–Hepatitis B or C Viral Pathogens and Usual
Pattern of Susceptibility to Antivirals. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
B. Overview of Hepatitis B or C Viral Pathogens and Usual Pattern of
Susceptibility to Antivirals. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183
C. Preferred Therapy for Specific Viral Pathogens. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
8. Choosing Among Antiviral Agents. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .201
9. Preferred Therapy for Specific Parasitic Pathogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
A. Select Common Pathogenic Parasites and Suggested Agents
for Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
B. Preferred Therapy for Specific Parasitic Pathogens. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208
10. Choosing Among Antiparasitic Agents: Antimalarial Drugs,
Nitroimidazoles, Benzimidazoles, and Neglected Tropical Diseases. . . . . . . . . . . . .231
11. How Antibiotic Dosages Are Determined by Susceptibility Data,
Pharmacodynamics, and Treatment Outcomes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative
Bacilli and Methicillin-Resistant Staphylococcus aureus . . . . . . . . . . . . . . . . . . . . . . . . . . . .237
13. Antibiotic Therapy for Children With Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
14. Sequential Parenteral-Oral Antibiotic Therapy (Oral Step-Down Therapy)
for Serious Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .251
15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection. . . . . . . . . . . . . . . .253
A. Postexposure Antimicrobial Prophylaxis to Prevent Infection. . . . . . . . . . . . . . . . . . . 255
B. Long-Term Antimicrobial Prophylaxis to Prevent Symptomatic
New Infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262
C. Prophylaxis of Symptomatic Disease in Children Who Have Asymptomatic
Infection/Latent Infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265
D. Surgical/Procedure Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266
16. Approach to Antibiotic Allergies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
17. Antibiotic Stewardship. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .283
18. Systemic and Topical Antimicrobial Dosing and Dose Forms . . . . . . . . . . . . . . . . . . . . . .289
A. Systemic Antimicrobials With Dosage Forms and Usual Dosages . . . . . . . . . . . . . . . 290
B. Topical Antimicrobials (Skin, Eye, Ear, Mucosa) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315
Appendix: Nomogram for Determining Body Surface Area . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .325
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351
 ix

Introduction
It is with great pleasure I share the news that the title and responsibility of the editor in
chief for this 31st edition, and subsequent editions, is now in the very capable hands of
Debra Palazzi, MD, MEd, a professor of pediatric infectious diseases and the division
chief of Pediatric Infectious Diseases at the Baylor College of Medicine in Houston, TX.
She not only takes regular calls as a pediatric infectious disease doctor at Texas Children’s
Hospital (973 beds) but also has directed their antimicrobial stewardship program (knows
when to use, and when not to use, antibiotics). She has been an editor and a course direc-
tor of the American Academy of Pediatrics (AAP) PREP Infectious Diseases program as
well as an associate editor for JAMA Pediatrics and is the incoming president of the Pedi-
atric Infectious Diseases Society! Dr Palazzi is an outstanding clinician and teacher (from
personal observation), with many awards to her credit…and she is a really nice person.
It has been my honor and privilege to work with all of you and the AAP for the past 25
years (my first edition with John Nelson was the 2000–2001 edition). Readers are likely
to see some new (and improved) approaches to infectious diseases in this edition, similar
to some that occurred as I started sharing writing responsibility with John Nelson. Our
field keeps evolving rapidly, with new antibiotics, new data on antibiotic efficacy and
safety from clinical trials, and now molecular diagnostics that can give us the name of a
pathogen, but without antimicrobial susceptibilities to guide therapy. Dr Palazzi and our
distinguished editors will continue to translate these data into practical suggestions for
clinical care and will keep the AAP book Nelson’s an invaluable print/online/app resource
for clinicians for decades to come!
John Bradley
December 10, 2024
Welcome to the 31st edition of Nelson’s Pediatric Antimicrobial Therapy! It is an incred-
ible honor for me to assume the role of editor in chief of this renowned resource and
to work with and learn from such amazing contributors. We are thankful that Dr John
Bradley—after serving as editor in chief of Nelson’s for more than 20 years!—has agreed
to continue to share his expertise as a contributing editor for many of the chapters in this
edition. We are so fortunate to learn from his extensive knowledge of anti-infective phar-
macokinetic and pharmacodynamic principles and his many years of experience treating
children with simple and complex infectious diseases.
For the 31st edition of Nelson’s, we have thoroughly reviewed and updated the chapters by
not only referencing the most recent medical literature but also sharing our opinions as
practicing clinicians. More than ever, the field of clinical infectious diseases is moving at a
tremendous pace, and we have tried to share with you salient updates from clinical trials
while filling in evidence gaps with advice about how we would treat.
We are extremely fortunate to have nationally/internationally recognized editors, who are
experts in each field, contribute to the Nelson’s chapters, both the clinical chapters and
x — Introduction

the mini-educational chapters on why they picked specific agents within a class to use
for therapy. We are grateful to Dr Maggie Danner, who updated the chapter on antibiotic
allergies.
We continue to work closely with the American Academy of Pediatrics (AAP), and many
of us have close connections with the AAP Committee on Infectious Diseases, particu-
larly Dr David Kimberlin, the editor of the Red Book. Although Nelson’s is published by
the AAP, it is not actually AAP policy (in contrast to the Red Book), so we are able to
share personal observations that may not be possible in an AAP publication that requires
approval by the AAP Board of Directors.
The Nelson’s app is a critical part of the success of the Nelson’s book. We continue to
update the searchability of the app, making it an excellent reference for the busy clini-
cian. We welcome comments and feedback to improve this resource; please contact us at
[email protected].
We provide grading of our recommendations—our assessment of how strongly we
feel about a recommendation and the strength of the evidence to support our recom-
mendation (noted in the Table). This is not the GRADE (Grading of Recommendations
Assessment, Development, and Evaluation) method but certainly uses the concepts on
which GRADE is based: the strength of recommendation and level of evidence. As with
GRADE, we review the literature (and the most important manuscripts are referenced),
but importantly, we work within the context of professional society recommendations
(eg, the AAP) and our experience.

Strength of Recommendation Description

A Strongly recommended
B Recommended as a good choice
C One option for therapy that is adequate, perhaps among
many other adequate therapies
Level of Evidence Description
I Based on well-designed, prospective, randomized, and
controlled studies in an appropriate population of
children
II Based on data derived from prospectively collected, small
comparative trials, or noncomparative prospective trials,
or reasonable retrospective data from clinical trials in chil-
dren, or data from other populations (eg, adults)
III Based on case reports, case series, consensus statements,
or expert opinion for situations in which sound data do
not exist
 Introduction — xi

As we state each year, many of the recommendations by the editors for specific situations
have not been systematically evaluated in controlled, prospective, comparative clinical
trials.
We thank Barrett Winston, senior manager, publishing acquisitions and business develop-
ment, for doing an impressive job of organizing the editors and being an outstanding
advocate for us and the clinician-users of the book. Thank you, Barrett, for working with
the Nelson’s editors to meet our deadlines!
It continues to be a privilege to work with all our friends at AAP Publishing. AAP Pub-
lishing shares the book at pediatric meetings as well as personally meets with clinicians
and answers questions (or sends them to one of the editors!). Thanks to Mark Grimes,
vice president, publishing; to Jeff Mahony, senior director, professional and consumer
publishing; and to Mary Louise Carr, marketing manager, professional resources. We are
all truly honored that providing better care to children remains our focus in the evolving
book and app. We are also very pleased that the AAP is supporting the third edition of
Nelson’s Neonatal Antimicrobial Therapy.
Our molecule of the year is baloxavir, an antiviral approved in 2018 for use in adults and
children aged 5 years and older to treat influenza A and B. It is given as a single dose and
is most effective if started within 48 hours of symptom onset. Baloxavir can also be used
for prophylaxis against influenza.
Thank you for your interest in the Nelson’s book. The editors love to hear from you about
your thoughts on improving this resource. Please contact us at [email protected].
Warmly,
Deb Palazzi, MD, MEd
November 2024
 xiii

Abbreviations
3TC, lamivudine BAL, bronchoalveolar lavage
AAAAI, American Academy of Allergy, bid, twice daily
Asthma and Immunology BL, β-lactamase
AAP, American Academy of Pediatrics BLI, β-lactamase inhibitor
AASLD, American Association for the BMI, body mass index
Study of Liver Diseases BPD, bronchopulmonary dysplasia
ABLC, amphotericin B lipid complex BSA, body surface area
(Abelcet) CABP, community-acquired bacterial
ABPA, allergic bronchopulmonary pneumonia
aspergillosis CA-MRSA, community-associated
ABR, auditory brainstem response methicillin-resistant Staphylococcus
ACOG, American College of Obstetri- aureus
cians and Gynecologists cap, capsule
ADH, antidiuretic hormone CAP, community-acquired pneumonia
AFB, acid-fast bacilli CAZ/AVI, ceftazidime/avibactam
AGEP, acute generalized exanthematous CBC, complete blood cell count
pustulosis CDC, Centers for Disease Control and
AHA, American Heart Association Prevention
ALT, alanine aminotransferase cephalosporin-R, cephalosporin-resistant
AmB, amphotericin B CF, cystic fibrosis
AmB-D, amphotericin B deoxycholate Ch(s), chapter(s)
amox/clav, amoxicillin/clavulanate CLD, chronic lung disease
(Augmentin) Cmax, maximal concentration of drug
amp/sul, ampicillin/sulbactam achieved in serum and at the tissue site
AOM, acute otitis media CMV, cytomegalovirus
A/P, atovaquone/proguanil CNS, central nervous system
ARC, augmented renal clearance CPB, cardiopulmonary bypass
ARF, acute rheumatic fever CrCl, creatinine clearance
ART, antiretroviral therapy CRGNB, carbapenem-resistant gram-
ARV, antiretroviral negative bacilli
ASPR, Administration for Strategic Pre- CRO, carbapenem-resistant organism
paredness & Response CRP, C-reactive protein
AST, aspartate aminotransferase CSD, cat-scratch disease
ASTMH, American Society of Tropical CSF, cerebrospinal fluid
Medicine and Hygiene CT, computed tomography
ATM/AVI, aztreonam/avibactam cUTI, complicated urinary tract infection
AUC, area under the curve (the math- DAA, direct-acting antiviral
ematically calculated area under the DAT, diphtheria antitoxin
serum concentration-versus-time DEC, diethylcarbamazine
curve) div, divided
xiv — Abbreviations

DOT, directly observed therapy HCV, hepatitis C virus

DR, delayed-release HHS, US Department of Health and
DRESS, drug rash with eosinophilia and Human Services
systemic symptoms HHV, human herpesvirus
DS, double-strength HRSA, Health Resources and Services
EBV, Epstein-Barr virus Administration
EBW, expected body weight hs, bedtime
ECMO, extracorporeal membrane HSV, herpes simplex virus
oxygenation HUS, hemolytic uremic syndrome
EM, erythema multiforme I&D, incision and drainage
EMR, electronic medical record IAI, intra-abdominal infection
EPEC, enteropathogen-producing Esch- IBS-D, irritable bowel syndrome with
erichia coli diarrhea
ER, extended-release ID, infectious disease
ESBL, extended-spectrum β-lactamase IDSA, Infectious Diseases Society of
ESR, erythrocyte sedimentation rate America
ETEC, enterotoxin-producing Escherichia IFN, interferon
coli IGRA, interferon-γ release assay
EUA, Emergency Use Authorization IM, intramuscular(ly)
FDA, US Food and Drug Administration IMI/REL, imipenem/relebactam
FQ, fluoroquinolone IMP, imipenemase
G6PD, glucose-6-phosphate IND, investigational new drug
dehydrogenase INH, isoniazid
GA, gestational age IUGR, intrauterine growth restriction
GBS, group B streptococcus IV, intravenous(ly)
GC, Neisseria gonorrhoeae IVesic, intravesical
G-CSF, granulocyte colony-stimulating IVIG, intravenous immune globulin
factor IVPB, intravenous piggyback (premixed
gentamicin-S, gentamicin-susceptible bag)
GI, gastrointestinal KPC, Klebsiella pneumoniae
GNB, gram-negative bacilli carbapenemase
GNR, gram-negative rod (bacilli) L-AmB, liposomal amphotericin B
HAART, highly active antiretroviral LD, loading dose
therapy LFT, liver function test
HACEK, Haemophilus aphrophilus, LP, lumbar puncture
Aggregatibacter (formerly Actino- LRTI, lower respiratory tract infection
bacillus) actinomycetemcomitans, MAC, Mycobacterium avium complex
Cardiobacterium hominis, Eikenella max, maximum
corrodens, Kingella species MBL, metallo–β-lactamase
HAP, hospital-acquired pneumonia MDR, multidrug resistance/
HAT, human African trypanosomiasis multidrug-resistant
HBeAg, hepatitis B e antigen mero/vabor, meropenem/vaborbactam
HBV, hepatitis B virus MF, microfilariae/microfilarial
 Abbreviations — xv

MIC, minimum inhibitory concentration PEP, postexposure prophylaxis

MIS-C, multisystem inflammatory syn- PHMB, polyhexamethylene biguanide
drome in children PICU, pediatric intensive care unit
MRI, magnetic resonance image/imaging PIDS, Pediatric Infectious Diseases
MRSA, methicillin-resistant Staphylococ- Society
cus aureus PIMS-TS, pediatric inflammatory multi-
MRSE, methicillin-resistant Staphylococ- system syndrome temporally associated
cus epidermidis with SARS-CoV-2
MSM, men who have sex with men PIP, piperacillin
MSSA, methicillin-susceptible Staphylo- PK, pharmacokinetic(s)
coccus aureus PMA, postmenstrual age (weeks of ges-
MSSE, methicillin-sensitive Staphylococ- tation since most recent menstrual
cus epidermidis period PLUS weeks of chronologic age
NA, not applicable since birth)
NARMS, National Antimicrobial Resis- PNA, postnatal age
tance Monitoring System for Enteric PO, oral(ly)
Bacteria PPD, purified protein derivative
NDM, New Delhi metallo–β-lactamase PrEP, preexposure prophylaxis
NEC, necrotizing enterocolitis PTLD, posttransplant lymphoproliferative
NICU, neonatal intensive care unit disorder
NNRTI, non-nucleoside reverse transcrip- pwd, powder
tase inhibitor PZA, pyrazinamide
NRTI, nucleoside reverse transcriptase q, every
inhibitor qd, once daily
NS, normal saline (physiologic saline qhs, every bedtime
solution) qid, 4 times daily
NVP, nevirapine qod, every other day
oint, ointment RAE, retinol activity equivalent
OPC, oropharyngeal candidiasis RAL, raltegravir
ophth, ophthalmic RIG, rabies immune globulin
PAIR, puncture, aspiration, injection, RIVUR, Randomized Intervention for
re-aspiration Children with Vesicoureteral Reflux
PBPK, physiologic-based pharmacokinetic RSV, respiratory syncytial virus
PCP, Pneumocystis pneumonia RTI, respiratory tract infection
PCR, polymerase chain reaction RT-PCR, real-time polymerase chain
PCV13/20, pneumococcal 13-valent/20- reaction
valent conjugate vaccine SBL, serine β-lactamase
PCT, procalcitonin SCr, serum creatinine
PD, pharmacodynamic(s) SIADH, syndrome of inappropriate antidi-
ped, pediatric uretic hormone
PEG, pegylated SJS, Stevens-Johnson syndrome
pen-R, penicillin-resistant SMX, sulfamethoxazole
pen-S, penicillin-susceptible soln, solution
xvi — Abbreviations

SPAG-2, small particle aerosol generator-2 TIG, tetanus immune globulin

spp, species TMP, trimethoprim
SSLR, serum sickness–like reaction TOL/TAZ, ceftolozane/tazobactam
SSSI, skin and skin-structure infection top, topical
staph, staphylococcal UCSF, University of California, San
STEC, Shiga toxin–producing Escherichia Francisco
coli ULN, upper limit of normal
STI, sexually transmitted infection URTI, upper respiratory tract infection
strep, streptococcal UTI, urinary tract infection
SUBQ, subcutaneous vag, vaginal
susp, suspension VCUG, voiding cystourethrogram
tab, tablet VDRL, Venereal Disease Research
TAF, tenofovir alafenamide Laboratories
TAZO, tazobactam VIGIV, vaccinia immune globulin
TB, tuberculosis intravenous
TBW, total body weight VIM, Verona integron-encoded
Td, tetanus, diphtheria metallo–β-lactamase
TD, travelers diarrhea VSIG, varicella-zoster immune globulin
Tdap, tetanus, diphtheria, acellular VZV, varicella-zoster virus
pertussis WBC, white blood cell
TDM, therapeutic drug monitoring WHO, World Health Organization
TEN, toxic epidermal necrolysis ZDV, zidovudine
tid, 3 times daily
 xvii

Notable Changes to 2025 Nelson’s Pediatric Antimicrobial Therapy, 31st Edition

We are quite grateful to Dr Howard Smart for the continual upgrading of the Nelson’s app
search function. We have linked “similar” terms for each disease entity, based on National
Library of Medicine search libraries, so the different terminology used by clinicians better
matches the terminology used by an editor (eg, “suppurative lymphadenitis” vs “cervical
lymph node abscess”).
Bacterial/Mycobacterial Infections and Antibiotics
New Infectious Diseases Society of America/Pediatric Infectious Diseases Society guide-
lines for treatment of pediatric acute bacterial arthritis were published in 2023 and now
recommend as short as 10 to 14 days of total therapy (intravenous [IV] + oral [PO]) for
uncomplicated infections without adjacent osteomyelitis.
While pediatric guidance for the treatment of Clostridioides difficile infection continues
to recommend metronidazole and vancomycin as first-line therapy, adult guidelines
recommend fidaxomicin as first-line therapy of initial and recurrent infections. Fidax-
omicin can be considered when treating C difficile disease in pediatric patients. Addition-
ally, bezlotoxumab (monoclonal antibody directed against the C difficile toxin) has been
approved for patients who are 1 year or older and should be considered for patients at
high risk for recurrence.
Once again, a number of new antibiotics for the treatment of multidrug-resistant gram-
negative bacilli are available for adult patients, although only one is approved for children
(ceftazidime/avibactam). Some of the new β-lactam/β-lactamase inhibitors for metallo–β-
lactamases are now in clinical trials.
Children with an immediate hypersensitivity reaction to penicillin or amoxicillin or a
positive skin test result should be offered repeat skin testing in 5 to 10 years; up to 80% of
children will outgrow penicillin allergies in 10 years. Antibiotics causing Stevens-Johnson
syndrome, toxic epidermal necrolysis, drug rash with eosinophilia and systemic symp-
toms, or acute generalized exanthematous pustulosis should be avoided permanently.
Some allergists will consider PO amoxicillin challenge for children with a history of
erythema multiforme minor or serum sickness–like reaction out of concern for infection-
mediated reaction (eg, viral, Mycoplasma).
Fungal Infections and Antifungal Agents
Revised international clinical practice guidelines for allergic bronchopulmonary aspergil-
losis reaffirm itraconazole preference.
Viral Infections and Antiviral Agents
Over this past year, developments relating to antiviral agents have centered less on intro-
ducing new drugs or new indications for use and more on improving implementation of
relatively recent recommendations that were noted in last year’s edition of Nelson’s. Per-
haps the most significant of these is the use of nirsevimab for passive immunoprophylaxis
to prevent severe respiratory syncytial virus (RSV) disease. Nirsevimab is a long-acting
xviii — Notable Changes to 2025 Nelson’s Pediatric Antimicrobial Therapy, 31st Edition

monoclonal antibody that prevents 80% to 90% of the severe outcomes of RSV infec-
tion in young infants. It is recommended for universal use as a single dose in all infants
younger than 8 months. A second dose is recommended for infants 8 through 19 months
with certain risk criteria. Approved just before the 2023–2024 RSV season, nirsevimab
was in short supply in much of the country last year. That has been resolved, and now
pediatricians and health systems are working on their processes for administering this
remarkable drug to every baby in the United States. This is no small task!
Another example is the treatment of infants with congenital cytomegalovirus (CMV) dis-
ease. An increasing number of states and localities are implementing universal or targeted
testing for CMV in babies, so an increasing number of babies are being identified. With
that comes inevitable questions of what to do once a baby is confirmed to have congenital
CMV. Recommendations for treatment of congenital CMV infection were liberalized
somewhat last year, with 6 months of PO valganciclovir continuing to be recommended
for infants with moderate to severe symptomatic congenital CMV disease and now 6 weeks
of PO valganciclovir being recommended for infants with isolated sensorineural hearing
loss secondary to congenital CMV infection. Age of initiation of antiviral therapy for
the treatment of congenital CMV infection can be up to 13 weeks, whereas previously it
needed to be started within the first month after birth.
So, overall, 2025 is likely going to be a year where we catch our breath with antiviral
drugs. That said, there are many exciting candidate drugs in differing companies’ pipe-
lines, so we anticipate that this pause will be short-lived!
Parasitic Infections and Antiparasitic Agents
We continue to encourage readers faced with diagnosing and treating children with
malaria, leishmaniasis, and other uncommon parasitic infections to contact the Centers
for Disease Control and Prevention (CDC) for consultation about management and
antiparasitic drug availability (770-488-7100). We have not provided detailed treatment
recommendations for human African trypanosomiasis and instead encourage readers to
check current guidelines and seek expert advice if treating patients with these condi-
tions, as management options are evolving quickly. Availability and sources of drugs to
treat parasitic infections change frequently (sodium stibogluconate is no longer available,
IV artesunate is no longer provided by the CDC, and fexinidazole has been approved
by the US Food and Drug Administration but is unavailable at this time), so clinicians
are encouraged to check recent sources of information for the most up-to-date recom-
mendations. Shortages of drugs occur sporadically and unpredictably (mefloquine is one
example); checking local availability of drugs and making changes if the drug is unavail-
able will reduce patient and provider frustration.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 1

1. Antimicrobial Therapy According to Clinical Syndromes 1

NOTES

Antimicrobial Therapy According to Clinical Syndromes

• A list of table abbreviations and acronyms can be found at the start of this publication.
• This chapter should be considered guidance for a typical patient. Dosage recom-
mendations (the dose amount, the number of doses per day, and the number of days
of treatment) are primarily provided for patients with normal hydration, renal, and
hepatic function. Because the dose required is based on the exposure of the antibiotic
to the pathogen at the site of infection, higher doses may be necessary if the antibiotic
does not penetrate well into the infected tissue (eg, meningitis) or if the child’s body
eliminates the antibiotic more quickly than average. Higher doses/longer courses may
also be needed if the child is immunocompromised, and the immune system can-
not help resolve the infection. It is becoming more apparent that the host contributes
significantly to microbiologic and clinical cure above and beyond the antimicrobial-
attributable effect. Most of the dosages reviewed and approved by the US Food and
Drug Administration (FDA) are from the original clinical trials for drug registration,
unless a safety issue becomes apparent when the label is modified or in cases in which
the original industry sponsor of an antibiotic wishes to pursue approval for additional
infection sites (“indications”) and conducts new prospective clinical trials to share
with the FDA. The original sponsor of the drug may not have studied all pathogens at
all sites of infection in neonates, infants, and children. The FDA carefully reviews data
presented to it but is not required to review the entire literature on each antibiotic and
update the package labels. If the FDA has not reviewed data for a specific indication
(eg, ampicillin for group A streptococcal cellulitis), there is usually no opinion about
whether the drug may or may not be effective and safe. Ampicillin is not “approved”
for skin and soft tissue infections caused by any bacteria. That does not mean that the
drug does not work or is unsafe; rather, data on safety and efficacy have not been pre-
sented to the FDA to expand the package label. The editors will provide suggestions for
clinical situations that may not have been reviewed and approved by the FDA. These
recommendations are considered off-label, signifying that safety and efficacy data have
not been reviewed by the FDA at its high level of rigor.
• Duration of treatment should be individualized. Durations recommended are based
on the literature, common practice, and general experience. Critical evaluations of the
duration of therapy have been carried out in very few infectious diseases. In general, a
more extended period of treatment should be used (1) for tissues in which antibiotic
concentrations may be relatively low (eg, undrained abscess, central nervous system
[CNS] infection); (2) for tissues in which repair following infection-mediated damage
is slow (eg, bone); (3) when the organisms are less susceptible; (4) when a relapse of
infection is unacceptable (eg, CNS infections); or (5) when the host is immunocom-
promised in some way. An assessment after therapy will ensure that your selection
of antibiotic, dose, and duration of treatment was appropriate. Until prospective,
comparative studies are performed for different durations, we cannot assign a specific
 2 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

1 increased risk of failure for shorter courses. We support the need for these studies in an
outpatient or inpatient controlled clinical research setting.
Antimicrobial Therapy According to Clinical Syndromes

• Our approach to therapy is continuing to move away from the concept that “one dose
fits all.” In addition to the dose that provides antibiotic exposure and host immuno-
competence, the concept of target attainment is being better defined. The severity of
illness and the willingness of the practitioner to accept a certain rate of failure need
to be considered; hence, broad-spectrum, high-dose treatment is used for a child in
florid septic shock (where you need to be right virtually 100% of the time), compared
with the child with impetigo (where a treatment that is approximately 70% effective is
acceptable, as you can see the child back in the office in a few days and alter the therapy
as necessary).
• Combination therapy (eg, adding an aminoglycoside or rifamycin to the primary
antimicrobial agent) to improve clinical or microbiologic outcomes in children with
serious or disseminated infection caused by enteric bacilli, Pseudomonas aeruginosa,
or Staphylococcus aureus has not been prospectively studied in pediatrics. Retrospec-
tive adult data support the use of combination therapy based on outcomes, but data
(primarily in adults) also support that the addition of aminoglycosides adds to toxic-
ity. Although a clinical trial to adequately assess the benefits and risks of combination
therapy in critically ill children would be difficult to conduct, it is necessary to provide
evidence to support recommendations. In this 31st edition of Nelson’s, combination
therapy continues to be recommended for critical illness, but only initially, until antibi-
otic susceptibility data are known, except for certain infections, like endocarditis, that
follow national guidelines or other recommendations for combination therapy.
• Diseases in this chapter are arranged by body systems. Consult Chapter 3 for an alpha-
betized listing of bacterial and mycobacterial pathogens and uncommon organisms
not included in this chapter.
• A more detailed description of treatment options for methicillin-resistant Staphylococ-
cus aureus (MRSA) infections and multidrug-resistant gram-negative bacilli (GNB)
infections, including a stepwise approach to increasingly broad-spectrum agents for
increasingly antibiotic-resistant GNB, is provided in Chapter 12. Although, in the past,
vancomycin has been the mainstay of therapy for invasive MRSA, it is nephrotoxic and
ototoxic, and it requires monitoring renal function and serum drug concentrations. Its
use against organisms with a minimal inhibitory concentration of 2 or greater may not
provide adequate exposure for a cure with safe, realistic pediatric doses. Ceftaroline,
the first MRSA-active β-lactam antibiotic approved by the FDA for adults in 2010,
children in 2016, and neonates in 2019, is as effective for most staphylococcal tissue site
infections (no controlled data on CNS infections) as vancomycin, but safer, and may be
considered preferred therapy over vancomycin for MRSA.
A. SKIN AND SOFT TISSUE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
NOTE: CA-MRSA (see Ch 12) is prevalent in most areas of the world. Recommendations for staph infections are given for these scenarios: stan-
1,2

dard MSSA and CA-MRSA. Antibiotic recommendations “for CA-MRSA” should be used for (1) empiric therapy in regions with >5%–10% of inva-
sive staph caused by MRSA; (2) clinical suspicion of CA-MRSA; and (3) documented CA-MRSA infections. “Standard recommendations” refers to
treatment of MSSA. Oxacillin/nafcillin are considered equivalent agents. For MSSA causing most skin and soft tissue infections and bone/joint
infections, 1st-generation cephalosporins (ie, cephalothin, cefazolin, cephalexin) are considered equivalent to oxacillin/methicillin, but for MSSA
infections in other tissues (eg, endocarditis), cephalosporins other than 1st generation may not be equivalent (need more high-quality data to
know with better certainty). Before using clindamycin for empiric therapy, check your local susceptibility data for S aureus (MSSA and MRSA), as
resistance can be as high as 40% in some locations. For MRSA skin infections caused by susceptible organisms, clindamycin and TMP/SMX pro-
vide similar clinical cure rates.
Adenitis, acute bacterial3–7 Empiric therapy May need surgical drainage for staph/strep infection;
(S aureus, including CA-MRSA, and Standard: oxacillin/nafcillin 150 mg/kg/day IV div not usually needed for CSD.
group A streptococcus; consider q6h OR cefazolin 100 mg/kg/day IV div q8h (AI), Additional antibiotics may not be required after drain-
Bartonella [CSD] for subacute OR cephalexin 50–75 mg/kg/day PO div tid age of mild to moderate suppurative adenitis caused
adenitis.)8 CA-MRSA: clindamycin 30 mg/kg/day IV or PO (AI) by staph/strep.

2025 Nelson’s Pediatric Antimicrobial Therapy —

Also called “suppurative adenitis” div q8h OR ceftaroline: 2 mo–<2 y, 24 mg/kg/day For PO therapy for MSSA: cephalexin or amox/clav. For
or “lymph node abscess” IV div q8h; ≥2 y, 36 mg/kg/day IV div q8h (max CA-MRSA: clindamycin, TMP/SMX, or linezolid.
single dose 400 mg); >33 kg, either 400 mg/dose For PO therapy for group A streptococcus: amoxicillin
IV q8h or 600 mg/dose IV q12h (BI), OR vancomy- or penicillin V.
cin 40 mg/kg/day IV q8h (BII), OR daptomycin: Daptomycin is generally avoided in infants until age
<6 y, 12 mg/kg IV qd; 7 to ≤11 y, 9 mg/kg IV qd; 1 y due to potential neurotoxicity.
≥12 and ≤17 y, 7 mg/kg IV qd; ≥18 y, 6 mg/kg IV Total therapy (IV + PO) for 7–10 days.
qd For CSD: this is the same high dose of azithromycin
CSD: azithromycin 10 mg/kg qd (max 500 mg) on that is recommended routinely and FDA approved
day 1, then 5 mg/kg (max 250 mg) for for strep pharyngitis.
4 additional days (BIII)
 Antimicrobial Therapy According to Clinical Syndromes

4 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

A. SKIN AND SOFT TISSUE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Adenitis, nontuberculous Excision is usually curative (BII); azithromycin PO Antibiotic susceptibility patterns are quite variable;
(atypical) mycobacterial9–14 OR clarithromycin PO for 6–12 wk (with or cultures should guide therapy: excision >97%
Also called “subacute without rifampin or ethambutol) if susceptible effective; medical treatment 60%–70% effective. No
lymphadenitis” (BII). well-controlled trials are available. With surgical and
medical therapy, children usually achieve symptom-
atic cure within 6 mo.12
For more resistant organisms, other antibiotics may be
active, including TMP/SMX, FQs, doxycycline, or, for
parenteral therapy, amikacin, meropenem, or
cefoxitin. See Ch 3 for specific mycobacterial
pathogens.
Adenitis, tuberculous15,16 INH 10–15 mg/kg/day (max 300 mg) PO, IV qd for Surgical excision is not usually indicated because
(Mycobacterium tuberculosis and 6 mo AND rifampin 15–20 mg/kg/day (max organisms are treatable.
Mycobacterium bovis) 600 mg) PO, IV qd for 6 mo AND PZA 30–40 mg/ Adenitis caused by M bovis (unpasteurized dairy prod-
kg/day PO qd AND ethambutol 15–25 mg/kg/ uct ingestion) is uniformly resistant to PZA. Treat
day PO for first 2 mo of therapy (BI); then INH 9–12 mo with INH and rifampin if susceptible (BII).
and rifampin daily for drug-susceptible TB No contraindication to fine-needle aspirate of the node
INH 20–30 mg/kg/day (max 900 mg) PO AND for diagnosis.
rifampin 15–20 mg/kg/day (max 600 mg) PO
AND PZA 50 mg/kg/day PO qd (max 2 g) (AII)
Anthrax, cutaneous17 Empiric therapy: ciprofloxacin 20–30 mg/kg/day If susceptible, amoxicillin or clindamycin (BIII).
PO div bid OR doxycycline 4.4 mg/kg/day (max Ciprofloxacin and levofloxacin are FDA approved for
200 mg) PO div bid (regardless of age) (AIII) inhalational anthrax for children >6 mo and should
be effective for skin infection (BIII).
Bites, dog and cat3,18–24 Amox/clav 45 mg/kg/day PO div tid (amox/clav 7:1; Amox/clav and amp/sul have good Pasteurella, MSSA,
(Pasteurella multocida; S aureus, see Aminopenicillins in Ch 4) for 5–10 days (AII). and anaerobic coverage but lack MRSA coverage.
including CA-MRSA; For hospitalized children, amp/sul OR, if MRSA Ceftriaxone plus clindamycin or vancomycin has good
Streptococcus spp, anaerobes; suspected, ceftriaxone AND clindamycin or Pasteurella, MSSA, MRSA, and anaerobic coverage.
Capnocytophaga canimorsus, vancomycin (BII). For IV therapy options: ceftaroline has good Pasteurella,
particularly in asplenic hosts) MSSA, and MRSA coverage but lacks Bacteroides
fragilis anaerobic coverage.23
Amp/sul, meropenem, and PIP/TAZO lack MRSA
coverage.
Consider rabies prophylaxis24 for bites from at-risk ani-
mals that were not provoked (observe animal for
10 days, if possible) (AI); state and local public health
departments and the CDC can provide advice on risk
and management (www.cdc.gov/rabies/hcp/
prevention-recommendations/pre-exposure-
prophylaxis.html; accessed June 3, 2024); consider
tetanus prophylaxis.
For penicillin allergy, ciprofloxacin (for Pasteurella) plus

2025 Nelson’s Pediatric Antimicrobial Therapy —

clindamycin (BIII). Tigecycline or doxycycline may be
considered for Pasteurella coverage.
Bites, human3,20,21,25 (Eikenella Amox/clav 45 mg/kg/day PO div tid (amox/clav 7:1; Human bites have a very high infection rate (do not
corrodens; S aureus, including see Aminopenicillins in Ch 4) for 5–10 days (AII). routinely close open wounds).
CA-MRSA; Streptococcus spp, For hospitalized children, amp/sul OR, if MRSA Amox/clav and amp/sul have good Eikenella, MSSA,
anaerobes) suspected, ceftriaxone AND clindamycin or and anaerobic coverage but lack MRSA coverage.
vancomycin (BII). Meropenem lacks MRSA coverage.
For penicillin allergy, moxifloxacin can be used.25
Bullous impetigo3,4,6,26 (usually Standard: cephalexin 50–75 mg/kg/day PO div tid For topical therapy if mild infection: mupirocin or
S aureus, including CA-MRSA) OR amox/clav 45 mg/kg/day PO div tid (CII) retapamulin oint
CA-MRSA: clindamycin 30 mg/kg/day PO div tid OR
TMP/SMX 8 mg/kg/day of TMP PO div bid; for
5–7 days (CI)
 Antimicrobial Therapy According to Clinical Syndromes

6 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

A. SKIN AND SOFT TISSUE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Cellulitis of unknown IV empiric therapy for non-facial cellulitis For periorbital or buccal cellulitis, also consider
etiology (usually S aureus, Standard: oxacillin/nafcillin 150 mg/kg/day IV div Streptococcus pneumoniae or Haemophilus influenzae
including CA-MRSA, or group A q6h OR cefazolin 100 mg/kg/day IV div q8h (BII) type b in unimmunized infants. Periorbital swelling
streptococcus)3,4,26–29 CA-MRSA: clindamycin 30 mg/kg/day IV div q8h OR that looks like cellulitis may occur with severe sinus-
ceftaroline: 2 mo–<2 y, 24 mg/kg/day IV div q8h; itis in older children.
≥2 y, 36 mg/kg/day IV div q8h (max single dose Total IV + PO therapy for 7–10 days.
400 mg); >33 kg, either 400 mg/dose IV q8h or Because nonsuppurative cellulitis is most often caused
600 mg/dose IV q12h (BI) OR vancomycin 40 mg/ by group A streptococcus, cephalexin alone is usually
kg/day IV q8h (BII) OR daptomycin: 1–<2 y, effective. In adults, a prospective, randomized study
10 mg/kg IV qd; 2–6 y, 9 mg/kg IV qd; 7–11 y, of non-purulent cellulitis did not show that the addi-
7 mg/kg qd; 12–17 y, 5 mg/kg qd (BI) tion of TMP/SMX improved outcomes over cephalex-
For PO therapy for MSSA: cephalexin (AII) OR in alone.28
amox/clav 45 mg/kg/day PO div tid (BII); for
CA-MRSA: clindamycin (BII), TMP/SMX (AII),
doxycycline (age >7 y), or linezolid (BII)
Cellulitis, buccal (for Ceftriaxone 50 mg/kg/day (AI) IV, IM q24h, for Rule out meningitis (larger doses may then be
unimmunized infants and 2–7 days parenteral therapy before switch to PO needed).
preschool children, H influenzae (BII) For penicillin allergy, levofloxacin IV/PO covers patho-
type b)30 gens, but no clinical data available.
PO therapy: amoxicillin if BL negative; amox/clav or PO
2nd- or 3rd-generation cephalosporin if BL positive.
Cellulitis, erysipelas Penicillin G 100,000–200,000 U/kg/day IV div Clindamycin is also effective for most strains of group A
(Streptococcus pyogenes)3,4,7,31 q4–6h (BII) initially, then penicillin V 100 mg/kg/ streptococcus. Few well-designed prospective stud-
day PO div qid (BIII) OR amoxicillin 50 mg/kg/day ies exist to provide evidence for recommendations
PO div tid (BIII) for 10 days for cellulitis and erysipelas.31
Gas gangrene (See Necrotizing fasciitis later in this table.)
Impetigo (S aureus, including Mupirocin OR retapamulin topically (BII) to lesions A meta-analysis suggests that topical therapy is as
CA-MRSA; occasionally group A tid; OR, for more extensive lesions, PO therapy effective as PO therapy for mild infection, but many
streptococcus)3–7,32 Standard: cephalexin 50–75 mg/kg/day PO div tid studies did not specify outcomes based on pathogen
OR amox/clav 45 mg/kg/day PO div tid (AII) susceptibilities, and more extensive infection, partic-
CA-MRSA: clindamycin 30 mg/kg/day (CII) PO div ularly caused by MRSA, may respond better to PO
tid OR TMP/SMX 8 mg/kg/day of TMP PO div bid antibiotic therapy.32 Controlled data are needed.
(AI); for 5–7 days
Ludwig angina33 (mixed oral Ceftriaxone 50 mg/kg/day IV PLUS clindamycin Alternatives: amp/sul; meropenem, imipenem or PIP/
aerobes/anaerobes) 40 mg/kg/day IV div q8h or metronidazole TAZO if aerobic GNB also suspected (CIII); high risk of
30–40 mg/kg/day IV div q8h (AIII) respiratory tract obstruction from inflammatory
edema
Lymphadenitis (See Adenitis, acute bacterial, earlier in this table.)
Lymphangitis (usually group A Penicillin G 200,000 U/kg/day IV div q6h (BII) ini- Cefazolin IV (for group A strep or MSSA infection) or
streptococcus, rarely S tially, then penicillin V 100 mg/kg/day PO div qid clindamycin IV (for group A strep, most MSSA and
aureus)3,4,7 OR amoxicillin 50 mg/kg/day PO div tid for MRSA) or vancomycin
10 days For mild disease, penicillin V 50 mg/kg/day PO div qid

2025 Nelson’s Pediatric Antimicrobial Therapy —

for 10 days
Myositis, suppurative34 (S aure- Standard: oxacillin/nafcillin 150 mg/kg/day IV div Surgical debridement is usually necessary.
us, including CA-MRSA; syn- q6h OR cefazolin 100 mg/kg/day IV div q8h (CII) For disseminated MRSA infection, may require
onyms: “tropical myositis,” CA-MRSA: clindamycin 40 mg/kg/day IV div q8h aggressive, emergent debridement; consider
“pyomyositis,” “muscle abscess”) OR ceftaroline: 2 mo–<2 y, 24 mg/kg/day IV div use of clindamycin to help decrease toxin production
q8h; ≥2 y, 36 mg/kg/day IV div q8h (max single (BIII); consider IVIG to bind bacterial toxins for life-
dose 400 mg); >33 kg, either 400 mg/dose IV threatening disease (CIII); abscesses may develop
q8h or 600 mg/dose IV q12h (BI) OR vancomycin during therapy.
40 mg/kg/day IV q8h (CIII) OR daptomycin:
1–<2 y, 10 mg/kg IV qd; 2–6 y, 9 mg/kg IV qd;
7–11 y, 7 mg/kg qd; 12–17 y, 5 mg/kg qd (BIII)
 Antimicrobial Therapy According to Clinical Syndromes

8 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

A. SKIN AND SOFT TISSUE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Necrotizing fasciitis (Pathogens Empiric therapy: ceftazidime 150 mg/kg/day IV div Aggressive emergent wound debridement (AII).
vary depending on the age of q8h, or cefepime 150 mg/kg/day IV div q8h AND ADD clindamycin to inhibit synthesis of toxins during
the child and location of clindamycin 40 mg/kg/day IV div q8h (BIII); OR the first few days of therapy (AIII).
infection. Single pathogen: meropenem 60 mg/kg/day IV div q8h; OR PIP/ Consider IVIG to bind bacterial toxins for life-
group A streptococcus; Clostridia TAZO 400 mg/kg/day PIP component IV div q6h threatening disease (BIII).
spp, S aureus [including (AIII). Value of hyperbaric oxygen is not well established
CA-MRSA], P aeruginosa, Vibrio ADD vancomycin OR ceftaroline for suspected (CIII).35,39,40
spp, Aeromonas spp. Multiple CA-MRSA, pending culture results (AIII). Focus definitive antimicrobial therapy based on culture
pathogen, mixed aerobic/ Mixed aerobic/anaerobic/gram-negative: results.
anaerobic fasciitis: any meropenem or PIP/TAZO (AIII).
organism[s]: above, plus GNB,
plus Bacteroides spp, and other
anaerobes.)3,35–38
Pyoderma, cutaneous Standard: cephalexin 50–75 mg/kg/day PO div tid I&D when indicated; IV for serious infections.
abscesses (S aureus, including OR amox/clav 45 mg/kg/day PO div tid (BII) Approaches to prevention of recurrent MRSA infection
CA-MRSA; group A CA-MRSA: clindamycin 30 mg/kg/day PO div tid include the use of baths with chlorhexidine soap daily
streptococcus)4,6,7,26,27,41 (BII) OR TMP/SMX 8 mg/kg/day of TMP PO div bid or qod (BIII) OR the use of bleach baths twice weekly
(AI) (½ cup of bleach per full bathtub) (BII). Decolonization
with nasal mupirocin in a specific child may also be
helpful; decolonization of the entire family may be
important in certain situations.42
Rat-bite fever (Streptobacillus Penicillin G 100,000–200,000 U/kg/day IV div q6h Organisms are normal oral flora for rodents. One does
moniliformis, Spirillum minus)43,44 (BII) for 7–10 days; for endocarditis, ADD genta- not require a bite for infection to develop.
micin for 4–6 wk (CIII). High rate of associated endocarditis.
For mild disease, PO therapy with amox/clav (CIII). Alternatives: doxycycline; 2nd- and 3rd-generation
cephalosporins (CIII).
Staphylococcal scalded skin Standard: oxacillin 150 mg/kg/day IV div q6h OR Burow or Zephiran compresses for oozing skin and
syndrome (S aureus [MSSA, cefazolin 100 mg/kg/day IV div q8h (CII) intertriginous areas.
occasionally CA-MRSA])45,46 CA-MRSA: clindamycin 30 mg/kg/day IV div q8h Corticosteroids are contraindicated.
B. SKELETAL INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
NOTE: Recommendations are given for CA-MRSA and MSSA. Antibiotic recommendations for empiric therapy should include CA-MRSA when
suspected or documented, while treatment of MSSA with β-lactam antibiotics is preferred over clindamycin. During the past few years,
clindamycin resistance in both MSSA and MRSA has remained stable at 10%–20%, with higher resistance reported by laboratories that report
clindamycin-susceptible but D-test–positive strains (methylase-inducible) as resistant. Check your local susceptibility data for S aureus before
using clindamycin for empiric therapy. For MSSA skeletal infections, oxacillin/nafcillin and cefazolin are considered equivalent.
The first PIDS-IDSA guidelines for bacterial osteomyelitis were published in the Journal of the Pediatric Infectious Diseases Society, September 2021,47
and the PIDS-IDSA acute bacterial arthritis guidelines were published in the Journal of the Pediatric Infectious Diseases Society, 2023.48
Arthritis, bacterial47–52 Switch to appropriate high-dose PO therapy when clinically improved, CRP decreasing (see Ch 14).50,53,54
– Newborns See Ch 2.
– Infants (Kingella kingae, now Empiric therapy: cefazolin 100 mg/kg/day IV div q8h (in Dexamethasone adjunctive therapy (0.15 mg/kg/
recognized as the most com- locations where MRSA causes <10% of infections); dose q6h for 4 days in one study) demonstrated
mon pathogen; S aureus, ADD clindamycin 30 mg/kg/day IV div q8h (to cover significant benefit in decreasing symptoms and
including CA-MRSA; group A CA-MRSA unless clindamycin resistance locally is earlier hospital discharge (but with some

2025 Nelson’s Pediatric Antimicrobial Therapy —

streptococcus) >10%, then use vancomycin). Ceftaroline can be “rebound” symptoms).55,56 Until additional
– Children (S aureus, including used for MSSA, MRSA, and Kingella. controlled data are available, dexamethasone is
CA-MRSA; group A streptococ- Dexamethasone adjunctive therapy is not routinely not recommended. NOTE: Children with rheu-
cus; K kingae) recommended48 (see Comments). matologic, postinfectious, fungal/mycobacterial
– Unimmunized or immunocom- For documented CA-MRSA: clindamycin 30 mg/kg/day infections or malignancy are also likely to
promised children (pneumococ- IV div q8h (AI) OR ceftaroline: 2 mo–<2 y, 24 mg/kg/ improve with steroid therapy.
cus, H influenzae type b) day IV div q8h; ≥2 y, 36 mg/kg/day IV div q8h (max PO step-down therapy options48:
For Lyme disease and brucellosis, single dose 400 mg); >33 kg, either 400 mg/dose IV For CA-MRSA: clindamycin OR linezolid. Little data
see Table 1L. q8h or 600 mg/dose IV q12h (BI) OR vancomycin published on TMP/SMX for invasive MRSA
40 mg/kg/day IV q8h (BI). infection, although some experts routinely use
For MSSA: oxacillin/nafcillin 150 mg/kg/day IV div q6h TMP/SMX for osteoarticular infections.57,58
OR cefazolin 100 mg/kg/day IV div q8h (AI). For MSSA: cephalexin OR dicloxacillin caps for older
For Kingella, BL-negative: cefazolin 100 mg/kg/day IV div children.
q8h OR ampicillin 150 mg/kg/day IV div q6h; OR, for For Kingella: most penicillins or cephalosporins
BL-positive, ceftriaxone 50 mg/kg/day IV, IM q24h (AII). (but not clindamycin or linezolid).
 Antimicrobial Therapy According to Clinical Syndromes

10 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

B. SKELETAL INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Infants (Kingella kingae, now For pen-S pneumococci or group A streptococcus:
recognized as the most com- penicillin G 200,000 U/kg/day IV div q6h (BII).
mon pathogen; S aureus, For pen-R pneumococci or Haemophilus: ceftriaxone
including CA-MRSA; group A 50–75 mg/kg/day IV, IM q24h (BII).
streptococcus) Total therapy (IV + PO) for 14–21 days (AII).47,48,52
– Children (S aureus, including
CA-MRSA; group A streptococ-
cus; K kingae)
– Unimmunized or immunocom-
promised children (pneumococ-
cus, H influenzae type b)
For Lyme disease and brucellosis,
see Table 1L. (continued)
– Gonococcal arthritis or Ceftriaxone 50 mg/kg IV, IM (max 1 g) q24h (BII) for Per 2021 CDC guidance, “[w]hen treating for the
tenosynovitis56,59,60 7 days. Consider empiric therapy for Chlamydia arthritis-dermatitis syndrome, the provider can
trachomatis. switch to an oral agent guided by antimicrobial
susceptibility testing 24–48 hours after substan-
tial clinical improvement, for a total treatment
course of at least 7 days.”
Alternative parenteral regimens include cefotaxime
(50 mg/kg q8h). www.cdc.gov/std/
treatment-guidelines/gonorrhea-adults.htm.
– Other bacteria See Ch 3 for preferred antibiotics.
Osteomyelitis47–59,61–65 Step down to appropriate high-dose PO therapy when clinically improved (see Ch 14).47,50,52,53,64
– Newborns See Ch 2.
– Acute osteomyelitis: usually Empiric therapy: cefazolin 100 mg/kg/day IV div q8h In children with open fractures secondary to trau-
S aureus, including CA-MRSA; (in locations where MRSA causes <10% of bone ma, consider adding ceftazidime or cefepime for
group A streptococcus; infections), OR clindamycin 30 mg/kg/day IV div q8h extended aerobic GNB activity.
K kingae47 (to cover CA-MRSA unless clindamycin resistance is Kingella is resistant to clindamycin, vancomycin,
locally >10%; then use ceftaroline or vancomycin). and linezolid.
For CA-MRSA: clindamycin 30 mg/kg/day IV div q8h OR For MSSA (BI) and Kingella (BIII), PO step-down
ceftaroline: 2 mo–<2 y, 24 mg/kg/day IV div q8h; therapy with cephalexin 100 mg/kg/day PO div
≥2 y, 36 mg/kg/day IV div q8h (max single dose tid. Kingella is usually susceptible to amoxicillin.
400 mg); >33 kg, either 400 mg/dose IV q8h or PO step-down therapy options for CA-MRSA
600 mg/dose IV q12h (BI), OR vancomycin 40 mg/kg/ include clindamycin and linezolid66; some
day IV q8h (BII). experts routinely use TMP/SMX for osteoarticular
For MSSA: oxacillin/nafcillin 150 mg/kg/day IV div q6h infections.53,58
OR cefazolin 100 mg/kg/day IV div q8h (AII). For prosthetic devices, biofilms may impair micro-
For Kingella, BL-negative: cefazolin 100 mg/kg/day IV bial eradication, requiring the addition of
div q8h OR ampicillin 150 mg/kg/day IV div q6h; OR, rifampin or other agents.65
for BL-positive, ceftriaxone 50 mg/kg/day IV, IM q24h No prospective, controlled data on the use of
(AII), or ceftaroline. antibiotic-containing beads/cement placed at

2025 Nelson’s Pediatric Antimicrobial Therapy —

Total therapy (IV + PO) usually 3–4 wk for surgery in the site of infection.47
uncomplicated MSSA, but may need >4–6 wk
for CA-MRSA (BII).
Follow closely for clinical response to empiric therapy.
– Acute: other organisms See Ch 3 for preferred antibiotics.
 Antimicrobial Therapy According to Clinical Syndromes

12 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

B. SKELETAL INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Chronic osteomyelitis (may be a Initial IV therapy, often with cefazolin unless pathogens Surgery to debride sequestrum is usually required
complication of poorly treated other than S aureus are suspected, as chronically for cure. For prosthetic joint infection caused by
acute staph osteomyelitis or the infected bone is surgically debrided (often with staphylococci, add rifampin (CIII).65
result of trauma-associated multiple procedures). Then prolonged PO step-down Osteomyelitis associated with foreign material
infection with multiple potential therapy may be required for 6–12 mo depending on (spinal rods, prostheses, implanted catheters)
pathogens), not to be confused the success of debridement. may be difficult to cure without removal of the
with chronic nonbacterial For MSSA: cephalexin 100 mg/kg/day PO div qid or tid material, but long-term suppression may be
osteomyelitis and chronic recur- OR dicloxacillin caps 75–100 mg/kg/day PO div qid undertaken if risks of surgery are high, until
rent multifocal osteomyelitis, for ≥3–6 mo (CIII). some stabilization of the healing infected bone
which are autoinflammatory For CA-MRSA: clindamycin, linezolid, or TMP/SMX (CIII). occurs.
diseases Watch for β-lactam–associated neutropenia with
high-dose, long-term therapy and for linezolid-
associated neutropenia/thrombocytopenia with
long-term (>2 wk) therapy.66
PO dicloxacillin is poorly tolerated.
Osteomyelitis of the foot67 Cefepime 150 mg/kg/day IV div q8h (BIII); ADD Surgical debridement with cultures to focus
(secondary to penetrating injury vancomycin (enhanced gram-positive coverage) OR antibiotic therapy. Treatment course is based on
to the plantar surface; S aureus, gentamicin (enhanced gram-negative coverage), pathogen and extent of infection and
including CA-MRSA, with other pending culture results. debridement.
organisms colonizing foreign
bodies)
Osteochondritis after a puncture
wound through a shoe;
P aeruginosa
C. EYE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Cellulitis, orbital 68–71
(cellulitis Ceftriaxone 50 mg/kg/day q24h AND clindamycin Surgical drainage of significant orbital or
of the contents of the orbit; may 30 mg/kg/day IV div q8h (for S aureus, including subperiosteal abscess present by CT scan or MRI.
be associated with orbital CA-MRSA) or vancomycin 40 mg/kg/day IV div q8h or Try medical therapy alone for cellulitis without
abscess; usually secondary to ceftaroline single-drug therapy: 2 mo–<2 y, abscess or with small abscesses (BIII).72,73
sinus infection; caused by 24 mg/kg/day IV div q8h; ≥2 y, 36 mg/kg/day IV div Amp/sul for respiratory flora/anaerobic coverage.73
respiratory tract flora and q8h (max single dose 400 mg); >33 kg, either Treatment course for 10–14 days after surgical
S aureus, including CA-MRSA) 400 mg/dose IV q8h or 600 mg/dose IV q12h (BIII). drainage, up to 21 days. CT scan or MRI can
If MSSA isolated, use oxacillin/nafcillin IV OR confirm cure (BIII).
cefazolin IV. Insufficient evidence about the concurrent use of
steroids.68
Cellulitis, periorbital74,75 Periorbital tissues are TENDER with cellulitis.
(preseptal cellulitis) Periorbital edema with sinusitis can look
identical but is NOT tender. A multidisciplinary
approach with an otolaryngologic,

2025 Nelson’s Pediatric Antimicrobial Therapy —

ophthalmologic, and pediatric focus is helpful.74
– Cellulitis associated with entry Standard: oxacillin/nafcillin 150 mg/kg/day IV div q6h PO antistaphylococcal antibiotic (eg, cephalexin or
site lesion on skin (S aureus, OR cefazolin 100 mg/kg/day IV div q8h (BII) clindamycin) for empiric therapy for less severe
including CA-MRSA; group A CA-MRSA: clindamycin 30 mg/kg/day IV div q8h or infection; treatment course for 7–10 days
streptococcus) in the fully vancomycin 40 mg/kg/day IV div q8h or ceftaroline:
immunized child 2 mo–<2 y, 24 mg/kg/day IV div q8h; ≥2 y,
36 mg/kg/day IV div q8h (max single dose 400 mg);
>33 kg, either 400 mg/dose IV q8h or 600 mg/dose
IV q12h (BII)
– True cellulitis with no associated Ceftriaxone 50 mg/kg/day q24h OR cefuroxime Treatment course for 7–10 days; rule out
entry site (in febrile, 150 mg/kg/day IV div q8h (AII) meningitis if bacteremic with H influenzae.
unimmunized infants): Alternative agents for BL-positive strains of
pneumococcal or H influenzae H influenzae: other 2nd-, 3rd-, 4th-, or
type b 5th-generation cephalosporins, amp/
sul IV or amox/clav PO.
 Antimicrobial Therapy According to Clinical Syndromes

14 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

C. EYE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Periorbital edema, not true Ceftriaxone 50 mg/kg/day q24h OR cefuroxime For PO convalescent antibiotic therapy, see
cellulitis; non-tender 150 mg/kg/day IV div q8h (BIII). Sinusitis, acute, in Table 1D; total treatment
erythematous swelling. Usually For suspected S aureus, can use ceftaroline instead of course of 14–21 days or 7 days after resolution of
associated with sinusitis; sinus ceftriaxone to cover both sinus pathogens and symptoms.
pathogens may rarely erode MSSA/MRSA.
anteriorly, causing cellulitis. For chronic sinusitis, ADD clindamycin (covers
anaerobes) to either ceftriaxone or ceftaroline (AIII).

Conjunctivitis, acute (Most Polymyxin/TMP ophth soln OR polymyxin/bacitracin Other topical antibiotics (gentamicin, tobramycin,
conjunctivitis is caused by a ophth oint OR ciprofloxacin ophth soln (BII), for erythromycin, besifloxacin, moxifloxacin,
virus and does not require 7–10 days. norfloxacin, ofloxacin, levofloxacin) may offer
antibiotic treatment; purulent For neonatal infection, see Ch 2. advantages for particular pathogens (CII).
conjunctivitis is primarily caused Steroid-containing therapy only if HSV ruled out.
by Haemophilus and
pneumococcus.)76,77
Conjunctivitis, herpetic78–80 1% trifluridine or 0.15% ganciclovir ophth gel (AII) AND Consultation with ophthalmologist recommended
(may be associated with keratitis) acyclovir PO (80 mg/kg/day div qid; max daily dose: for assessment and management (eg, concomi-
For neonatal, see Ch 2. 3,200 mg/day) has been effective in limited studies tant use of topical steroids in certain situations).
(BIII). PO valacyclovir (60 mg/kg/day div tid) has Recurrences common; corneal scars may form.
superior PK to PO acyclovir and can be considered for Long-term suppression (≥1 y) of recurrent infection
systemic treatment. Parenteral (IV) acyclovir if extent with PO acyclovir 80 mg/kg/day in 3 div doses
of disease is severe (CIII). (max dose 800 mg) or PO valacyclovir 40 mg/kg/
day in 2 div doses (max dose 1,000 mg);
decisions to continue suppressive therapy should
be revisited annually. The frequency of dosing
may need to be increased to qid, or the drug
may need to be changed to valacyclovir, if
breakthrough ocular infection occurs. Potential
risks must balance potential benefits to vision
(BIII)
Dacryocystitis81 (S aureus most No antibiotic usually needed; PO antibiotic therapy for Warm compresses; may require surgical probing of
often, and other skin flora) more symptomatic infection, based on Gram stain nasolacrimal duct
and culture of pus; topical therapy as for
conjunctivitis may be helpful.
Endophthalmitis82,83
NOTE: This is a medical emergency. Subconjunctival/sub-tenon antibiotics are likely to be Refer to ophthalmologist; vitrectomy may be
required (vancomycin/ceftazidime or clindamycin/gentamicin); steroids commonly used necessary for advanced endophthalmitis. No
(except for fungal infection); requires anterior chamber or vitreous tap for microbiologic prospective, controlled studies.
diagnosis. Listed systemic antibiotics to be used in addition to ocular injections.
– Empiric therapy following open Vancomycin 40 mg/kg/day IV div q8h AND cefepime Consider ceftaroline for empiric MRSA treatment,
globe injury 150 mg/kg/day IV div q8h (AIII) as it may penetrate the vitreous better than
vancomycin (BIII).
– Staphylococcal Vancomycin 40 mg/kg/day IV div q8h pending Consider ceftaroline for definitive MRSA treatment,
susceptibility testing; oxacillin/nafcillin 150 mg/kg/ as it may penetrate the vitreous better than
day IV div q6h if susceptible (AIII) vancomycin.

2025 Nelson’s Pediatric Antimicrobial Therapy —

– Pneumococcal, meningococcal, Ceftriaxone 100 mg/kg/day IV q24h; penicillin G Treatment course for 10–14 days
Haemophilus 250,000 U/kg/day IV div q4h if susceptible (AIII)
– Gonococcal Ceftriaxone 50 mg/kg q24h IV, IM AND azithromycin Treatment course ≥7 days
(AIII)
– Pseudomonas Cefepime 150 mg/kg/day IV div q8h for 10–14 days Cefepime is preferred over ceftazidime for
(AIII) or, if susceptible, levofloxacin84 (See Ch 3 for Pseudomonas based on decreased risk of
dosing.) development of resistance during therapy;
meropenem IV and imipenem IV are alternatives
(no clinical data). Very poor outcomes. PO
convalescent therapy with FQs in the adherent
child.
 Antimicrobial Therapy According to Clinical Syndromes

16 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

C. EYE INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Candida 85
Fluconazole (25 mg/kg LD, then 12 mg/kg/day IV), OR Echinocandins given IV may not be able to achieve
voriconazole (9 mg/kg LD, then 8 mg/kg/day IV); adequate antifungal activity in the eye.
for resistant strains, L-AmB (5 mg/kg/day IV). For
chorioretinitis, systemic antifungals PLUS intravitreal
amphotericin 5–10 mcg/0.1-mL sterile water OR
voriconazole 100 mcg/0.1-mL sterile water or
physiologic (normal) saline soln (AIII). Duration of
therapy is at least 4–6 wk (AIII).
Hordeolum (sty) or None usually needed. Topical erythromycin-containing Warm compresses; I&D when necessary
chalazion86 eye oint often used (CIII). If cellulitis develops, may
– Staphylococcus spp need systemic therapy.
Retinitis
– Cytomegalovirus86,87 See Ch 7. Consultation with an ophthalmologist is
For congenital, see Ch 2. Ganciclovir 10 mg/kg/day IV div q12h for 2 wk (BIII); if recommended for assessment and management.
Predominantly in immunocom- needed, continue at 5 mg/kg/day q24h to complete Neutropenia risk increases with duration of
promised and transplant 6 wk total (BIII). therapy.
patients. Foscarnet IV and cidofovir IV are alternatives but
For HIV-infected children, demonstrate significant toxicities. Letermovir has
see https://clinicalinfo.hiv.gov/ been approved for prophylaxis of CMV in adult
en/guidelines/pediatric- stem cell transplant patients but has not been
opportunistic-infection/ studied as treatment of CMV retinitis.
cytomegalovirus (accessed PO valganciclovir has not been evaluated in
September 12, 2024). HIV-infected children with CMV retinitis but
is an option primarily for older children who
weigh enough to receive the adult dose of
valganciclovir (CIII).
 Maribavir is approved for the treatment of adults
and pediatric patients (aged ≥12 y and
weighing at least 35 kg) with posttransplant
CMV infection/disease that is refractory to
treatment (with or without genotypic resistance)
with ganciclovir, valganciclovir, cidofovir, or
foscarnet. However, it should not be used for
CMV retinitis, as this was an exclusion criterion in
its licensure study.
Intravitreal ganciclovir and combination therapy
for non-responding, immunocompromised hosts;
however, intravitreal injections may not be
practical for most children.

2025 Nelson’s Pediatric Antimicrobial Therapy —

D. EAR AND SINUS INFECTIONS
https://clinicalinfo.hiv.gov/en/guidelines/ped
cytomegalovirus
opportunistic-infection/

Clinical Diagnosis Therapy (evidence grade) Comments

Bullous myringitis (See Otitis Believed to be a clinical manifestation of acute
media, acute, later in this table.) bacterial otitis media
Mastoiditis, acute (pneumococcus Ceftriaxone 50 mg/kg/day q24h AND clindamycin Consider CNS extension (meningitis); surgery as
[less since introduction of conjugate 40 mg/kg/day IV div q8h (BIII), OR ceftaroline IV needed for mastoid and middle ear drainage.
pneumococcal vaccines]; S aureus, For adolescents: cefepime 150 mg/kg/day IV div Step down to appropriate PO therapy after clinical
including CA-MRSA; group A q8h AND clindamycin 40 mg/kg/day IV div q8h improvement, guided by culture results. Duration
streptococcus; Pseudomonas in (BIII) of therapy not well-defined; look for evidence of
adolescents, Haemophilus rare)88–90 mastoid osteomyelitis or subperiosteal abscess.
Based on severity of disease and success of
surgical debridement, may need 3–4 wk of
therapy.
 Antimicrobial Therapy According to Clinical Syndromes

18 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

D. EAR AND SINUS INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Mastoiditis, chronic (See also Otitis, Antibiotics only for acute superinfections Daily cleansing of ear important; if no response to
chronic suppurative, below.) (according to culture of drainage); for antibiotics, surgery.
(anaerobes; Pseudomonas; S aureus, Pseudomonas: cefepime 150 mg/kg/day IV div Be alert for CA-MRSA.
including CA-MRSA)91 q8h
Alternatives to enhance anaerobic coverage:
meropenem 60 mg/kg/day IV div q8h, OR PIP/
TAZO 240 mg/kg/day IV div q4–6h (BIII)
Otitis, chronic suppurative Topical antibiotics: FQ (ciprofloxacin, ofloxacin, Presumed middle ear drainage through open
(P aeruginosa; S aureus, including besifloxacin) with or without steroid (BIII) tympanic membrane. Avoid aminoglycoside-
CA-MRSA; and other respiratory Cleaning of canal, view of tympanic membrane, for containing therapy given risk of ototoxicity.92
tract/skin flora)91 patency; cultures important Other topical FQs with/without steroids available.
Otitis externa
– Bacterial, malignant otitis externa Cefepime 150 mg/kg/day IV div q8h (AIII) Other antipseudomonal antibiotics should also be
(P aeruginosa)93,94 effective: ceftazidime IV AND tobramycin IV, OR
meropenem IV or imipenem IV or PIP/TAZO IV.
For more mild infection, ciprofloxacin PO.
– Bacterial, acute otitis externa Topical antibiotics: FQ (ciprofloxacin or ofloxacin) Wick moistened with Burow (aluminum acetate
(P aeruginosa; S aureus, including with steroid, OR neomycin/polymyxin B/ topical) soln, used for marked swelling of canal;
CA-MRSA)93,94 hydrocortisone (BII) to prevent swimmer’s ear, 2% acetic acid to canal
Also called “swimmer’s ear” Irrigating and cleaning canal of detritus important after water exposure will restore acid pH.
– Bacterial furuncle of canal (S aureus, Standard: oxacillin/nafcillin 150 mg/kg/day IV div I&D; antibiotics for cellulitis.
including CA-MRSA) q6h OR cefazolin 100 mg/kg/day IV div q8h (BIII) PO therapy for mild disease, convalescent therapy.
CA-MRSA: clindamycin, ceftaroline, or vancomycin For MSSA: cephalexin. For CA-MRSA:
(BIII) clindamycin, TMP/SMX, OR linezolid (BIII).
– Candida Fluconazole 6–12 mg/kg/day PO qd for 5–7 days May occur following antibiotic therapy for bacterial
(CIII) external otitis; debride canal.
Otitis media, acute
NOTE: The incidence of AOM and subsequent complications have decreased substantially in the era of conjugate pneumococcal vaccines.95 With a
decrease in disease caused by pen-R pneumococci requiring alternatives to first-line therapy, very few new antibiotics have entered clinical trials
within the past few years. Although the risk of antibiotic-resistant pneumococcal otitis has decreased,96 the percentage of Haemophilus
responsible for AOM has increased and may continue to increase with widespread use of the new 20-valent conjugate pneumococcal vaccine;
therefore, some experts (Ellen Wald) recommend use of amox/clav over amoxicillin as first-line therapy for well-documented AOM.97 The most
current AAP guidelines98 and meta-analyses99,100 suggest that the greatest benefit with therapy occurs in children with bilateral AOM who are
<2 y; for other children, close observation is also an option. AAP guidelines provide an option for non-severe cases, particularly disease in older
children, to provide a prescription to parents but have them fill the prescription only if the child’s condition deteriorates.98 European guidelines
are similar, although somewhat more conservative.101 Although prophylaxis is only rarely indicated, amoxicillin or other antibiotics can be given
at the same milligram per kilogram dose as for treatment but less frequently, either qd or bid, to prevent infections (if the benefits outweigh the
risks of development of resistant organisms for that child).98
– Newborns See Ch 2.
– Infants and children (pneumococcus, Amox/clav (90 mg/kg/day amox component PO div See Ch 18 for dosages. Current data suggest that
H influenzae non–type b, Moraxella bid for unimmunized infants [pneumococcal post-PCV13, H influenzae is now the most

2025 Nelson’s Pediatric Antimicrobial Therapy —

most common)96,97,102 vaccine] but 45 mg/kg/day amox component common pathogen, shifting the recommendation
PO div bid for immunized infants). for empiric therapy from amoxicillin to amox/
Amoxicillin is still a reasonable choice for empiric clav,97,98,102 although retrospective review of out-
therapy, but failures will most likely be caused by comes suggests that amoxicillin is not inferior to
BL-producing Haemophilus (or Moraxella). amox/clav.100 Published data document new but
a. For Haemophilus strains that are BL positive: uncommon emergence of penicillin resistance in
amox/clav, cefdinir, cefpodoxime, cefuroxime, pneumococci isolated in the post-PCV13 era.103,104
ceftriaxone IM, levofloxacin. Return to standard-dosage amoxicillin (45 mg/kg/
day) for AOM.
Tympanocentesis should be performed in children
whose second-line therapy fails.
 Antimicrobial Therapy According to Clinical Syndromes

20 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

D. EAR AND SINUS INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Infants and children (pneumococcus, b. For pen-R pneumococci (much less common in
H influenzae non–type b, Moraxella the PCV13/20 era): high-dosage amoxicillin
most common)96,97,102 (continued) achieves greater middle ear activity than PO
cephalosporins. Options include ceftriaxone
50 mg/kg/day IM q24h for 1–3 doses; OR
levofloxacin 20 mg/kg/day PO div bid for
children ≤5 y and 10 mg/kg PO qd for children
>5 y; OR a macrolide-class antibiotic:
azithromycin PO at 1 of 3 dosages: (1) 10 mg/kg
on day 1, followed by 5 mg/kg qd for days 2–5;
(2) 10 mg/kg qd for 3 days; or (3) 30 mg/kg once.
Caution: Up to 40% of pneumococci are
macrolide resistant.
Sinusitis, acute (H influenzae Same antibiotic therapy as for AOM, as pathogens IDSA sinusitis guidelines recommend amox/clav as
non–type b, pneumococcus, are similar: either amox/clav (90 mg/kg/day first-line therapy108; amoxicillin is still an
group A streptococcus, amox component PO div bid) or amoxicillin option.106 While both represent reasonable and
Moraxella)96,104–107 alone (90 mg/kg/day PO div bid).96 effective therapy, amox/clav provides activity
Therapy of 14 days may be necessary while against BL-positive strains of H influenzae, which
mucosal swelling resolves and ventilation is are more likely to be prevalent in both sinusitis
restored. and otitis in the PCV13/20 era.97 There is no
If high-quality evidence for decreased penicillin controlled evidence to determine whether the
resistance in the PCV13 era becomes available in use of antihistamines, decongestants, or nasal
the future, the dose of amoxicillin required for irrigation is efficacious in children with acute
treatment may decrease.105 sinusitis.107
E. OROPHARYNGEAL INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Dental abscess (mixed aerobic/ Clindamycin 30 mg/kg/day PO, IV, IM div q6–8h OR High-quality prospectively collected data on the value
anaerobic oral flora)109,110 penicillin G 100,000–200,000 U/kg/day IV div of antibiotics have not been published, particularly
q6h and metronidazole 30–40 mg/kg/day IV div regarding the need for antibiotics after dental
q8h (AIII) extraction. Recommendations are based on the
microbiology of dental abscesses.
Amox/clav PO, clindamycin PO are PO options.
Metronidazole has excellent anaerobic activity but
no aerobic activity. Penicillin failures reported.
Other IV options include ceftriaxone and
metronidazole, OR meropenem.
Tooth extraction usually necessary. Erosion of abscess
may occur into facial, sinusitis, deep head, and neck
compartments.
Diphtheria pharyngitis111 Erythromycin 40–50 mg/kg/day PO div qid for DAT, a horse antiserum, is investigational and available

2025 Nelson’s Pediatric Antimicrobial Therapy —

14 days OR penicillin G 150,000 U/kg/day IV div only from the CDC Emergency Operations Center at
q6h; PLUS DAT (AIII) 770-488-7100; www.cdc.gov/diphtheria/hcp/dat/
index.html (accessed September 12, 2024).
Epiglottitis (supraglottitis; Ceftriaxone 50 mg/kg/day IV, IM q24h for Emergency: provide airway.
H influenzae type b in an 7–10 days For suspected S aureus infection (causes only 5% of
unimmunized child; rarely epiglottitis), consider adding clindamycin or
pneumococcus, S aureus)112,113 vancomycin to ceftriaxone or using ceftaroline
single-drug therapy.
 Antimicrobial Therapy According to Clinical Syndromes

22 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

E. OROPHARYNGEAL INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Gingivostomatitis, Acyclovir 80 mg/kg/day PO div qid (max dose Early treatment is likely to be the most effective. Start
herpetic114–116 800 mg) for 7 days (for severe disease, use IV treatment as soon as PO intake is compromised.
therapy at 30 mg/kg/day div q8h) (BIII); OR, for Valacyclovir is the prodrug of acyclovir that provides
infants ≥3 mo, valacyclovir 20 mg/kg/dose PO improved PO bioavailability compared with PO
bid (max dose 1,000 mg; instructions for acyclovir.
preparing liquid formulation with 28-day shelf Extended duration of therapy may be needed for
life included in package insert) (CIII)116 immunocompromised children.
The PO acyclovir dose (80 mg/kg/day div into 4 equal
doses) provided is safe and effective for varicella, but
75 mg/kg/day div into 5 equal doses has been
studied for HSV.115 Max daily acyclovir dose should
not exceed 3,200 mg.
Lemierre syndrome Empiric: meropenem 60 mg/kg/day div q8h (or Anecdotal reports suggest that metronidazole may be
(Fusobacterium necrophorum 120 mg/kg/day div q8h for CNS metastatic foci) effective for apparent failures with other agents.
primarily; also reported with (AIII) OR ceftriaxone 100 mg/kg/day q24h AND Often requires anticoagulation.
MRSA)117–121 metronidazole 40 mg/kg/day div q8h or Metastatic and recurrent abscesses often develop
– Pharyngitis with internal jugular clindamycin 40 mg/kg/day div q6h (BIII). during active, appropriate therapy, requiring multiple
vein septic thrombosis; also ADD empiric vancomycin if MRSA is suspected if debridements and prolonged antibiotic therapy.121
known as postanginal sepsis, clindamycin is not already in the treatment Treatment duration is often ≥4–6 wk.
necrobacillosis regimen or based on local susceptibility data.
Peritonsillar cellulitis or Clindamycin 30 mg/kg/day PO, IV, IM div q8h; for Consider I&D for larger abscess, particularly if no good
abscess (group A streptococcus preschool infants with consideration of enteric initial response to medical therapy.
with mixed oral flora, including bacilli, ADD ceftriaxone 50 mg/kg/day IV q24h Alternatives: meropenem or imipenem or PIP/TAZO.
anaerobes, CA-MRSA)122 (BIII). Amox/clav for convalescent PO therapy (BIII).
See Retropharyngeal; No controlled, prospective data on benefits/risks of
parapharyngeal; lateral steroids.123
pharyngeal cellulitis or abscess
later in this table.
Pharyngitis (group A Amoxicillin 50–75 mg/kg/day PO, qd, bid, or tid for Although penicillin V is the most narrow-spectrum
streptococcus primarily)7,124,125 10 days OR penicillin V 50–75 mg/kg/day PO, qid, treatment, amoxicillin displays better GI absorption
bid, or tid, OR benzathine penicillin 600,000 U IM than PO penicillin V; the suspension is better
for children <27 kg, 1.2 million U IM if >27 kg, as tolerated. These advantages should be balanced by
a single dose (AII) the unnecessary increased spectrum of activity.
For penicillin-allergic children: erythromycin Once-daily amoxicillin dosage: for children 50 mg/kg
(estolate) at 20–40 mg/kg/day PO div bid to qid; (max 1,000–1,200 mg).7
OR 40 mg/kg/day PO div bid to qid for 10 days; A 5-day treatment course is FDA approved for
OR azithromycin 12 mg/kg qd for 5 daysa (AII); azithromycin at 12 mg/kg/day for 5 days, and some
OR clindamycin 30 mg/kg/day PO div tid PO cephalosporins have been approved (cefdinir,
a
Since 1994 this is the dose investigated and FDA cefpodoxime), with rapid clinical response to treat-
approved for children with strep pharyngitis, and ment that can also be seen with other antibiotics; a
it is higher than the standard dose for other RTIs. 10-day course is preferred for prevention of ARF,
particularly in areas where ARF is prevalent, as no
data exist on efficacy of 5 days of therapy for
prevention of ARF, although data support the
treatment of pharyngitis with 5 days of therapy with

2025 Nelson’s Pediatric Antimicrobial Therapy —

cephalosporins and penicillin.7,126,127
Retropharyngeal; Clindamycin 40 mg/kg/day IV div q8h or Consider I&D; possible airway compromise, mediastinitis.
parapharyngeal; lateral vancomycin 40 mg/kg/day IV div q8h AND Alternatives: meropenem or imipenem (BIII); PIP/TAZO.
pharyngeal cellulitis or ceftriaxone 50 mg/kg/day IV q24h Can step down to less broad-spectrum coverage based
abscess (mixed aerobic/ on cultures.
anaerobic flora, now including Amox/clav for convalescent PO therapy (but no activity
CA-MRSA)122,128,129 for MRSA) (BIII).
Tracheitis, bacterial (S aureus, Clindamycin 40 mg/kg/day IV div q8h or For susceptible S aureus, oxacillin/nafcillin or cefazolin
including CA-MRSA; group A vancomycin 40 mg/kg/day IV div q8h AND May represent bacterial superinfection of viral
streptococcus; pneumococcus; ceftriaxone 50 mg/kg/day q24h OR ceftaroline laryngotracheobronchitis, including influenza
H influenzae type b, rarely single-drug therapy: 2 mo–<2 y, 24 mg/kg/day
Pseudomonas)130 IV div q8h; ≥2 y, 36 mg/kg/day IV div q8h (max
single dose 400 mg); >33 kg, either 400 mg/dose
IV q8h or 600 mg/dose IV q12h (BIII)
 Antimicrobial Therapy According to Clinical Syndromes

24 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Abscess, lung
– Primary (a complication of Empiric therapy with ceftriaxone 50–75 mg/ For severe CA-MRSA infections, see Chap 12.
severe, necrotizing CAP caused kg/day q24h AND clindamycin 40 mg/kg/day For presumed Mycoplasma, add FQ (levofloxacin) or
by pneumococcus; S aureus, div q8h or vancomycin 45 mg/kg/day IV div macrolide.
particularly CA-MRSA; group A q8h for ≥14–21 days (AIII) OR (for MRSA) Bronchoscopy may be necessary if abscess fails to drain;
streptococcus, rarely ceftaroline single-drug therapy: 2–<6 mo, surgical excision is rarely necessary for pneumococcus
Mycoplasma pneumoniae)131,132 30 mg/kg/day IV div q8h (each dose given but may be important for CA-MRSA and MSSA.
over 2 h); ≥6 mo, 45 mg/kg/day IV div q8h Focus antibiotic coverage based on culture results.
(each dose given over 2 h) (max single dose For MSSA: oxacillin/nafcillin or cefazolin.
600 mg) (BII)
– Secondary to aspiration (ie, foul Clindamycin 40 mg/kg/day IV div q8h and Alternatives: ceftriaxone AND metronidazole OR amp/sul
smelling; polymicrobial ceftriaxone 50–75 mg/kg/day q24h or OR imipenem IV OR PIP/TAZO IV (BIII)
infection with oral aerobes and meropenem 60 mg/kg/day IV div q8h for PO step-down therapy with clindamycin or amox/clav (BIII)
anaerobes)133 ≥10 days (AIII)
Allergic bronchopulmonary Prednisone 0.5 mg/kg qd for 1–2 wk and then Not all allergic pulmonary disease is associated with true
aspergillosis134 taper (BII) for mild, acute stage illness AND fungal infection. Larger steroid dosages to control
(for more severe disease) voriconazole135 inflammation may lead to tissue invasion by Aspergillus.
18 mg/kg/day PO div q12h load followed Corticosteroids are the cornerstone of therapy for
by 16 mg/kg/day div q12h (AIII) OR exacerbations, and itraconazole and voriconazole have a
itraconazole136 10 mg/kg/day PO div q12h demonstrable corticosteroid-sparing effect.
(BII). Voriconazole and itraconazole require
trough concentration monitoring.
Aspiration pneumonia Clindamycin 40 mg/kg/day IV div q8h; ADD Alternatives: ceftriaxone AND metronidazole OR amp/sul IV
(polymicrobial infection with ceftriaxone 50–75 mg/kg/day q24h for OR imipenem IV OR PIP/TAZO IV (BIII)
oral aerobes and anaerobes)133 additional Haemophilus activity OR, as a PO step-down therapy with clindamycin or amox/clav (BIII)
single agent, meropenem 60 mg/kg/day IV
div q8h; for ≥10 days (BIII).
Atypical pneumonia (See Mycoplasma pneumoniae and Legionnaires disease later in this table under Pneumonias of other established
etiologies.)
Bronchitis (bronchiolitis), For bronchitis/bronchiolitis in children, no With PCR multiplex diagnosis now widely available, a
acute137 antibiotic needed for most cases, as disease nonbacterial diagnosis will allow clinicians to avoid use
is usually viral of antibiotics, but viral/bacterial coinfection can still
occur.
Community-acquired pneumonia (See Pneumonia, community-acquired, later in this table.)
Cystic fibrosis: Seek advice from experts in acute and chronic management. Larger than standard doses of β-lactam antibiotics have been
required in the past to achieve the same blood concentrations as those in children without CF, but in the current era of maximal pulmonary and
nutritional support of CF, most antibiotics eliminated by the kidney can be administered at typical doses to achieve adequate blood concentra-
tions. However, we do not know whether the concentrations of antibiotics achieved at the deep sites of infection in the CF lung are adequate,
particularly with advanced CF disease. The Cystic Fibrosis Foundation posts guidelines for treatment of pulmonary exacerbation (www.cff.org/
medical-professionals/pulmonary-exacerbations-clinical-care-guidelines; reviewed July 2021; accessed September 12, 2024). Dosages of
β-lactams should be designed to achieve their PK/PD goals to increase the chance of response.138,139
– Acute pulmonary exacerbation Cefepime 150–200 mg/kg/day div q8h or Monitor concentrations of aminoglycosides, vancomycin.

2025 Nelson’s Pediatric Antimicrobial Therapy —

(P aeruginosa primarily; also meropenem 120 mg/kg/day div q6h AND Insufficient evidence to recommend routine use of inhaled
Burkholderia cepacia, tobramycin 6–10 mg/kg/day IM, IV div antibiotics for acute exacerbations.146
Stenotrophomonas maltophilia q6–8h for treatment of acute exacerbation Cultures with susceptibility will help select antibiotics, as
[and other non-fermenting (AII); many alternatives: imipenem IV, MDR is common, but synergy testing is not well
GNB]; S aureus [including ceftazidime IV, or ciprofloxacin 30 mg/kg/ standardized.147
CA-MRSA], nontuberculous day PO, IV div tid Combination therapy may provide synergistic killing and
mycobacteria)140–145 For MRSA: ceftaroline 45 mg/kg/day IV div q8h delay the emergence of resistance (BIII). Attempt at early
(each dose given over 2 h) (max single dose eradication of new-onset Pseudomonas may decrease
600 mg) (BIII) OR vancomycin 60–80 mg/kg/ progression of disease.148
day IV div q8h Failure to respond to antibacterials should prompt
Duration of therapy not well-defined: evaluation for appropriate drug doses and for invasive/
10–14 days (BIII)141 allergic fungal disease as well as maximization of
pulmonary hygiene.
 Antimicrobial Therapy According to Clinical Syndromes

26 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Chronic inflammation in CF: Inhaled tobramycin 300 mg bid, cycling Other inhaled antibiotics may also be effective153 (BIII).
impact of inhaled antibiotics 28 days on therapy, 28 days off therapy, is Two newer pwd preparations of inhaled tobramycin are
and azithromycin to minimize effective adjunctive therapy between available.
long-term damage to lung exacerbations, with new data suggesting a Azithromycin does not decrease the benefit of improved
benefit of alternating inhaled tobramycin pulmonary function with inhaled tobramycin in those
with inhaled aztreonam (AI).149,150 with Pseudomonas airway colonization.154
Azithromycin adjunctive chronic therapy,
greatest benefit for those colonized with
Pseudomonas (AII).151,152
Pertussis155,156 Azithromycin: for those ≥6 mo, 10 mg/kg/day Azithromycin and clarithromycin are better tolerated than
on day 1, then 5 mg/kg/day for days 2–5; erythromycin; azithromycin is preferred in young infants
for those <6 mo, 10 mg/kg/day for 5 days to potentially reduce pyloric stenosis risk (see Ch 2).
(recommended dose per CDC); OR Provide prophylaxis to family members.
clarithromycin 15 mg/kg/day div bid for Unfortunately, no adjunctive therapy has been shown to be
7 days; or erythromycin (estolate preferable) beneficial in decreasing the cough.157
40 mg/kg/day PO div qid for 7–10 days (AII)
Alternative: TMP/SMX 8 mg/kg/day of TMP div
bid for 14 days (BIII)
Pneumonia, community-acquired: empiric therapy for bronchopneumonia, lobar consolidation, or complicated pneumonia
with pleural fluid/empyema
– Mild to moderate “chest cold”– No antibiotic therapy unless epidemiologic, Broad-spectrum antibiotics may increase risk of subsequent
like illness (overwhelmingly clinical, or laboratory reasons to suspect infection with antibiotic-resistant pathogens.
viral, especially in preschool bacterial coinfection, or Mycoplasma
children)158
– Moderate to severe illness Empiric therapy Consider next-generation sequencing diagnostic tests,
(pneumococcus; group A For most regions now with high rates of tracheal aspirate, or BAL for Gram stain/culture for severe
streptococcus; S aureus, PCV13/20 vaccine use or low rates of infection in intubated children.
including CA-MRSA; pneumococcal resistance to penicillin (fully For CA-MRSA: if vancomycin is being used rather than
M pneumoniae129,159,160; for those immunized child): ampicillin 150–200 mg/ ceftaroline, check vancomycin serum concentrations and
with aspiration and underlying kg/day div q6h. For milder illness managed renal function, particularly at the higher dosage needed
comorbidities, H influenzae, completely in the outpatient setting, to achieve an AUC:MIC of 400.
non-typeable; and for amoxicillin can be used if S aureus is not a Alternatives to azithromycin for atypical pneumonia
unimmunized children, significant consideration. Standard-dosage include erythromycin IV, PO, or clarithromycin PO, or
H influenzae type b) amoxicillin (for pen-S pneumococci) can doxycycline IV, PO for children >7 y, or levofloxacin IV, PO.
again be used for empiric therapy (45 mg/
kg/day div tid).
For regions with low rates of PCV13/20 vaccine Benefits of combination empiric therapy with a β-lactam
use (or for an unimmunized child), with high and a macrolide are conflicting and may apply only to
rates of pneumococcal resistance to penicil- certain older pediatric populations.161,162
lin: ceftriaxone 50–75 mg/kg/day q24h (AI). Duration of therapy is still not well-defined in
For PO therapy, high-dosage amoxicillin prospective, controlled trials in pediatric community-

2025 Nelson’s Pediatric Antimicrobial Therapy —

80–100 mg/kg/day PO div tid is preferred. acquired bacterial pneumonia. Retrospective data with
For suspected CA-MRSA: ceftaroline: 2–<6 mo, diagnosis based only on clinical examination and
30 mg/kg/day IV div q8h (each dose given radiograph (eg, lots of viral pneumonia included)
over 2 h); ≥6 mo, 45 mg/kg/day IV div q8h suggested that 10 days may be unnecessary for all
(each dose given over 2 h) (max single dose children (5 days or just 3 days may be sufficient, but most
600 mg) (BII),161 OR vancomycin 40–60 mg/ short-course studies do not have a definitive pathogen
kg/day (AIII).3 diagnosis).163,164 Empiric PO outpatient therapy for less
For suspected Mycoplasma/atypical severe illness: standard-dosage amoxicillin may be as
pneumonia agents, particularly in effective as high-dosage amoxicillin 80–100 mg/kg/day
school-aged children, ADD azithromycin PO div tid (NOT bid, which is used for otitis) (BIII).
10 mg/kg IV, PO on day 1, then 5 mg/kg qd
for days 2–5 of treatment (AII).
 Antimicrobial Therapy According to Clinical Syndromes

28 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Pleural fluid/empyema Empiric therapy: ceftaroline single-drug Initial therapy based on Gram stain of empyema fluid;
(same pathogens as for therapy: 2–<6 mo, 30 mg/kg/day IV div q8h; typically, clinical improvement is slow, with persisting but
community-associated ≥6 mo, 45 mg/kg/day IV div q8h (each dose decreasing “spiking” fever for 2–3 wk.
bronchopneumonia) (Based on given over 2 h) (max single dose 600 mg) For antibiotic-pretreated children whose cultures are likely
extent of fluid and symptoms, (BII), OR ceftriaxone 50–75 mg/kg/day q24h to be negative, consider next-generation sequencing
may benefit from chest tube AND vancomycin 40–60 mg/kg/day IV div tests from blood or BAL to allow the spectrum of
drainage with fibrinolysis or q8h (BIII) or clindamycin 40 mg/kg/day IV div antibiotics treatment to be narrowed when test results
­video-assisted thoracoscopic q8h are available.170
surgery.)159,165–169 There are concerns about the effectiveness of vancomycin
monotherapy in influenza-associated MRSA
pneumonia.171
– Interstitial pneumonia If C trachomatis suspected, azithromycin Most often respiratory viral pathogens, CMV, or chlamydial;
syndrome of early infancy 10 mg/kg on day 1, followed by 5 mg/kg/day role of Ureaplasma uncertain
qd for days 2–5 OR erythromycin 40 mg/kg/
day PO div qid for 14 days (BII)
Pneumonia: definitive therapy for pathogens of CAP
– Pneumococcus (may occur No reported failures of ceftriaxone for pen-R
with non-PCV13 pneumococcus; no need to add vancomycin for this
serotypes)131,159–161 reason (CIII).
Levofloxacin is an alternative, particularly for those with
severe allergy to β-lactam antibiotics (BI),172 but due to
theoretical cartilage toxicity concerns for humans, may
not be first-line therapy.
– Pneumococcal, pen-S Penicillin G 250,000–400,000 U/kg/day IV div After improvement (decreased fever, no oxygen needed),
q4–6h for 10 days (BII) OR ampicillin change to amoxicillin 45 mg/kg/day PO div tid OR
150–200 mg/kg/day IV div q6h; for penicillin V 50–75 mg/kg/day div qid. Treat until patient
outpatient management: amoxicillin is clinically asymptomatic and chest radiograph has
45 mg/kg/day PO div tid significantly improved (7–21 days) (BIII).
– Pneumococcal, pen-R Ceftriaxone 100 mg/kg/day q24h or div q12h Addition of vancomycin has not been required for
for 10–14 days (BIII) treatment of pen-R strains.
Ceftaroline is more active against pneumococcus than
ceftriaxone, but with no current ceftriaxone resistance,
ceftaroline is not required.
For PO convalescent therapy, high-dosage amoxicillin
(100–150 mg/kg/day PO div tid), OR clindamycin
(30 mg/kg/day PO div tid), OR linezolid (30 mg/kg/day
PO div tid), OR levofloxacin PO.
– Staphylococcus aureus For MSSA: oxacillin/nafcillin 150 mg/kg/day IV Check vancomycin serum concentrations and renal
(including CA-MRSA) is a rare div q6h or cefazolin 100 mg/kg/day IV div function, particularly at the higher dosage designed to
(1%) cause of pediatric q8h (AII) attain an AUC:MIC of 400 for invasive CA-MRSA disease.
CAP.4,6,131,159,173,174 For suspected CA-MRSA: ceftaroline: 2–<6 mo, For life-threatening disease, optimal therapy for CA-MRSA
30 mg/kg/day IV div q8h (each dose given has not been studied and remains poorly defined:
over 2 h); ≥6 mo, 45 mg/kg/day IV div q8h consider adding gentamicin and/or rifampin for
(each dose given over 2 h) (max single dose combination therapy (CIII).
600 mg) (AII), OR vancomycin 40–60 mg/kg/ Linezolid 30 mg/kg/day IV, PO div q8h is another option,

2025 Nelson’s Pediatric Antimicrobial Therapy —

day (AIII)3; may need addition of rifampin, more effective in adults than vancomycin for MRSA
clindamycin, or gentamicin, but no nosocomial pneumonia175 (follow platelet and WBC
prospective data to validate improved counts weekly).
outcomes (AIII) (See Ch 12.) For influenza-associated MRSA pneumonia, vancomycin
monotherapy was inferior to combination therapies.168
Do NOT use daptomycin for pneumonia (inactivated by
surfactant).
PO convalescent therapy for MSSA: cephalexin PO; for
CA-MRSA: clindamycin or linezolid PO.
Total course for ≥21 days (AIII).
 Antimicrobial Therapy According to Clinical Syndromes

30 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Group A streptococcus Penicillin G 250,000 U/kg/day IV div q4–6h for Change to amoxicillin 75 mg/kg/day PO div tid or
10 days (BII) penicillin V 50–75 mg/kg/day div qid to tid after clinical
improvement (BIII).
Pneumonia: immunosuppressed, neutropenic host
– Immunosuppressed, Antibiotic therapy: cefepime 150 mg/kg/day IV Biopsy/BAL for histology/cultures or serum/BAL for next-
neutropenic host176 div q8h (AII), OR meropenem 60 mg/kg/day generation sequencing testing helps determine need for
(P aeruginosa, other community- div q8h (AII), OR PIP/TAZO 240–300 mg/kg/ antifungal, antiviral, and/or antimycobacterial treatment.
associated or nosocomial GNB, day div q6h; AND if S aureus (including For septic patients, the addition of tobramycin will increase
S aureus, fungi, AFB, MRSA) is suspected clinically, ADD coverage for most gram-negative pathogens.
Pneumocystis, viral [adenovirus, vancomycin 40–60 mg/kg/day IV div q8h For those with mucositis, anaerobic coverage may be need-
CMV, EBV, influenza, RSV, (AIII) OR ceftaroline: 2–<6 mo, 30 mg/kg/day ed, as provided by carbapenems and PIP/TAZO (or with
others]) IV div q8h; ≥6 mo, 45 mg/kg/day IV div q8h the addition of clindamycin or metronidazole to other
For treatment recommendations (max single dose 600 mg) (BIII). agents).
for fungal pathogens, see Ch 5; Antifungal therapy usually started if no Consider use of 2 active agents for definitive therapy for
for viral pathogens, see Ch 7. response to antibiotics within 72–96 h (AmB, Pseudomonas for neutropenic hosts to assist clearing the
In posttransplant patients ≥12 y voriconazole, or caspofungin/micafungin— pathogen and potentially decrease risk of resistance, but
with CMV disease that is see Ch 5). there is no evidence to support better outcomes (BIII).
refractory to treatment with
ganciclovir, valganciclovir, or
foscarnet, maribavir may be
considered.
Pneumonia: nosocomial (health care–associated/ventilator-associated)
– Nosocomial (health Commonly used regimens, but they should be Pathogens that cause nosocomial pneumonia often have
care–associated/ventilator- individualized based on the “flora” of MDR. Cultures are critical. Empiric therapy also based on
associated) (P aeruginosa, the hospital that may colonize (and child’s prior colonization/infection. Do not treat
enteric GNB [Enterobacter, subsequently infect hospitalized children). colonization, though.
Klebsiella, Serratia, Escherichia Meropenem 60 mg/kg/day div q8h, OR PIP/ For MDR GNB, available IV therapy options include CAZ/AVI
coli], Acinetobacter, TAZO 240–300 mg/kg/day div q6–8h, (now FDA approved for children), TOL/TAZ, mero/vabor,
Stenotrophomonas, and OR cefepime 150 mg/kg/day div q8h; cefiderocol, plazomicin, or colistin.
gram-positive organisms ± gentamicin 6.0–7.5 mg/kg/day div q8h Aerosol delivery of antibiotics may be required for MDR
including CA-MRSA and (AIII); ADD vancomycin or ceftaroline for pathogens, but little high-quality controlled data are
Enterococcus)177,178 suspected CA-MRSA (AIII). available for children.179
Pneumonias of other established etiologies (See Ch 3 for treatment by pathogen.)
– Chlamydophila pneumoniae,180 Azithromycin 10 mg/kg on day 1, followed Doxycycline (patients >7 y). Levofloxacin is also effective.
Chlamydophila psittaci, or by 5 mg/kg/day qd for days 2–5 or
Chlamydia trachomatis erythromycin 40 mg/kg/day PO div qid;

2025 Nelson’s Pediatric Antimicrobial Therapy —

for 14 days
– Cytomegalovirus See Ch 7. Bone marrow transplant recipients with CMV pneumonia
(immunocompromised Ganciclovir IV 10 mg/kg/day IV div q12h for whose ganciclovir therapy alone fails may benefit from
host)181,182 (See Chs 2 and 7 for 2 wk (BIII); if needed, continue at 5 mg/kg/ therapy with IV CMV hyperimmune globulin and
CMV infection in newborns and day q24h to complete 4–6 wk total (BIII). ganciclovir given together (BII).183,184
children, respectively.) PO valganciclovir may be used for convalescent therapy
(BIII).
Foscarnet for ganciclovir-resistant isolates. In
posttransplant patients ≥12 y with CMV disease that
is refractory to treatment with ganciclovir, valganciclovir,
or foscarnet, maribavir may be considered.
 Antimicrobial Therapy According to Clinical Syndromes

32 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Enterobacter spp Cefepime 100 mg/kg/day div q12h or Addition of aminoglycoside to 3rd-generation
meropenem 60 mg/kg/day div q8h; OR cephalosporins (ceftriaxone, ceftazidime) may restrict
ceftriaxone 50–75 mg/kg/day q24h AND the emergence of ampC-mediated constitutive high-level
gentamicin 6.0–7.5 mg/kg/day IM, IV div q8h resistance, but concern exists for inadequate
(AIII) aminoglycoside concentration in airways; not an issue
for ampC-stable β-lactams (cefepime, meropenem,
imipenem, or PIP/TAZO).
– Escherichia coli Ceftriaxone 50–75 mg/kg/day q24h (AII) For cephalosporin-R strains (ESBL producers), use
meropenem, imipenem, or ertapenem (AIII). Use
ampicillin if susceptible.
– Francisella tularensis185 Gentamicin 6.0–7.5 mg/kg/day IM, IV div q8h Other alternative for PO therapy for mild disease:
for ≥10 days for more severe disease (AIII); doxycycline PO for 14–21 days (but watch for relapse).
for less severe disease, ciprofloxacin or See www.cdc.gov/tularemia/about/index.html (accessed
levofloxacin (AIII) September 12, 2024).
– Fungi (See Ch 5.) For detailed pathogen-specific For immunocompetent hosts, triazoles (fluconazole,
Community-associated recommendations, see Ch 5. itraconazole, voriconazole, posaconazole, and
pathogens, which vary by For suspected endemic fungi or mucormycosis isavuconazole) are better tolerated than AmB and equally
region (eg, Coccidioides,186,187 in an immunocompromised host,190 treat effective for many community-associated pathogens (see
Histoplasma)188,189 empirically with a lipid AmB and not Ch 6). For dosage, see Ch 5.
Aspergillus; mucormycosis; voriconazole; biopsy needed to guide Check voriconazole trough concentrations; need to be at
other mold infections in therapy. Posaconazole and isavuconazole191 least >2 mcg/mL.
immunocompromised hosts have in vitro activity and clinical efficacy For Coccidioides infection refractory to fluconazole therapy,
(See Ch 5.) data against some Rhizopus spp. consider increasing the dose, switching to other azoles,
For suspected invasive aspergillosis, treat with or switching to AmB.
voriconazole (AI) (load 18 mg/kg/day div
q12h on day 1, then continue 16 mg/kg/day
div q12h).
– Influenza virus.192,193 Empiric therapy, or documented influenza A New published data continue to confirm the effectiveness
– Recent seasonal influenza A and or B of oseltamivir, particularly when started early in the
B strains continue to be resistant Oseltamivir193,194 (AII): clinical course.
to adamantanes. <12 mo: Check for antiviral susceptibility each season at
Full-term infants: www.cdc.gov/flu/hcp/antivirals/index.html (accessed
0–8 mo: 3 mg/kg/dose bid November 6, 2024).
9–11 mo: 3.5 mg/kg/dose bid, although some For children 12–23 mo, the unit dose of oseltamivir of
experts recommend 3 mg/kg/dose bid 30 mg/dose may provide inadequate drug exposure.
≥12 mo: 3.5 mg/kg/dose PO bid has been studied for PK,195 but
≤15 kg: 30 mg PO bid sample sizes were limited.
>15–23 kg: 45 mg PO bid Limited data for oseltamivir in preterm neonates194:
>23–40 kg: 60 mg PO bid <38 wk of PMA (gestational plus chronologic age):
>40 kg: 75 mg PO bid 1.0 mg/kg/dose PO bid
Zanamivir inhaled (AII): for those ≥7 y, 10 mg 38–40 wk of PMA: 1.5 mg/kg/dose PO bid
(two 5-mg inhalations) bid
Peramivir (BII):
6 mo–12 y: single IV dose of 12 mg/kg, up to

2025 Nelson’s Pediatric Antimicrobial Therapy —

600 mg max
>13 y: single IV dose of 600 mg
Baloxavir (BI): The adamantanes (amantadine and rimantadine) had
≥5 y: activity against influenza A before the late 1990s, but all
<20 kg: single dose PO of 2 mg/kg circulating A strains of influenza have been resistant for
20–79 kg: single dose PO of 40 mg many years. Influenza B is intrinsically resistant to
≥80 kg: single dose PO of 80 mg adamantanes.
The CDC does not recommend baloxavir for monotherapy
for severely immunosuppressed people.
– Klebsiella pneumoniae195,196 Ceftriaxone 50–75 mg/kg/day IV, IM q24h For K pneumoniae strains that contain ESBLs or are produc-
(AIII); for ceftriaxone-resistant strains ing ampC BL, other carbapenems, PIP/TAZO, and FQs are
(ESBL and ampC-producing strains), use other options. Data in adults suggest that outcomes with
meropenem 60 mg/kg/day IV div q8h (AIII) PIP/TAZO are inferior to those with carbapenems.195,196
or other carbapenem. For KPC-producing strains that are resistant to meropen-
em, alternatives include CAZ/AVI (FDA approved for
adults and children), FQs, and colistin (BIII). See Ch 12.
 Antimicrobial Therapy According to Clinical Syndromes

34 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Legionnaires disease (Legionella Azithromycin 10 mg/kg PO q24h for 5–10 days Alternatives: clarithromycin, erythromycin, ciprofloxacin,
pneumophila) (AIII) levofloxacin, doxycycline
Longer durations for non-azithromycin regimens and
immunocompromised patients
– Mycobacteria, nontuberculous In a normal host with pneumonia that requires Highly variable susceptibilities of different nontuberculous
(MAC most common)197 therapy, 3 drugs are now recommended: mycobacterial spp. Culture and susceptibility data are
azithromycin PO (or clarithromycin PO) AND important for success.
ethambutol, AND rifampin, given 3×/wk to Check if immunocompromised: HIV or IFN-γ receptor
prevent macrolide/azalide resistance. deficiency.
Duration of treatment is not well-defined; Consider consulting an ID physician.
consider 6–12 wk for susceptible strains but
longer, up to 12 mo, for resistant strains.
For more extensive cavitary or advanced/
severe bronchiectatic disease, ADD amikacin
or streptomycin (AIII).
– Mycobacterium tuberculosis (See Tuberculosis later in this table.)
– Mycoplasma pneumoniae159,198 Azithromycin 10 mg/kg on day 1, followed Mycoplasma often causes self-limited infection and does
by 5 mg/kg/day qd for days 2–5, OR not routinely require treatment (AIII). Little prospective,
clarithromycin 15 mg/kg/day div bid for well-controlled data exist for treatment of documented
7–14 days, OR erythromycin 40 mg/kg/day mycoplasma pneumonia, specifically in children.198
PO div qid for 14 days Doxycycline (patients >7 y) or levofloxacin.
Macrolide-resistant strains have recently developed
worldwide but may respond to doxycycline or
levofloxacin.199
Studies have been difficult without better diagnostic
techniques, but respiratory tract PCR testing is now
available to assist in early identification of possible
infections.
– Paragonimus westermani See Ch 9.
– Pneumocystis jirovecii, formerly Severe disease: preferred regimen is TMP/SMX, Alternatives for TMP/SMX intolerant, or clinical failure:
carinii200; disease in children 15–20 mg/kg/day of TMP IV div q8h for 3 wk pentamidine 3–4 mg IV qd, infused over 60–90 min (AII);
with immunosuppression or HIV (AI). TMP AND dapsone; OR primaquine AND clindamycin; OR
Mild to moderate disease: may start with IV atovaquone.
therapy, then, after acute pneumonitis is Prophylaxis: TMP/SMX 5 mg/kg/day of TMP PO, div in
resolving, TMP/SMX 20 mg/kg/day of TMP 2 doses, q12h, daily or 3×/wk on consecutive days (AI);
PO div qid for 21 days (AII). OR TMP/SMX 5 mg/kg/day of TMP PO as a single dose,
Use steroid adjunctive treatment for more qd, 3×/wk on consecutive days (AI); once-weekly regi-
severe disease (AII). mens have also been successful201; OR dapsone 2 mg/kg
(max 100 mg) PO qd, or 4 mg/kg (max 200 mg) once
weekly; OR atovaquone: 30 mg/kg/day for infants 1–3
mo, 45 mg/kg/day for infants 4–24 mo, and 30 mg/kg/
day for children >24 mo.
– Pseudomonas aeruginosa202,203 Cefepime 150 mg/kg/day IV div q8h ± tobra- Ciprofloxacin IV, or colistin IV for MDR strains of
mycin 6.0–7.5 mg/kg/day IM, IV div q8h (AII). Pseudomonas203 (See Ch 12.)

2025 Nelson’s Pediatric Antimicrobial Therapy —

Alternatives: meropenem 60 mg/kg/day div
q8h, OR PIP/TAZO 240–300 mg/kg/day div
q6–8h (AII) ± tobramycin (BIII).
– Respiratory syncytial virus infec- For immunocompromised hosts, the only FDA- Treat only for severe disease, immunocompromised, severe
tion (bronchiolitis, approved treatment is ribavirin aerosol: underlying cardiopulmonary disease, as aerosol ribavirin
pneumonia)204 6-g vial (20 mg/mL in sterile water), by SPAG- provides only a small benefit. Airway reactivity with inha-
2, over 18–20 h daily for 3–5 days, although lation precludes routine use. We have not personally used
questions remain regarding efficacy. inhaled ribavirin for the past several years.
Palivizumab and nirsevimab (Beyfortus) are not effective
for treatment of an active RSV infection.
RSV antivirals and additional monoclonal antibodies are
currently under investigation.
Monitor for neutropenia and nephrotoxicity.
 Antimicrobial Therapy According to Clinical Syndromes

36 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

F. LOWER RESPIRATORY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Tuberculosis
– Primary pulmonary INH 10–15 mg/kg/day (max 300 mg) PO qd for Obtain baseline LFTs. Consider monthly LFTs for at least
disease15,16,205,206 6 mo AND rifampin 15–20 mg/kg/day (max 3 mo or as needed for symptoms. It is common to have
600 mg) PO qd for 6 mo AND PZA 30–40 mg/ mildly elevated liver transaminase concentrations
kg/day (max 2 g) PO qd for first 2 mo of ther- (2–3 times normal) that do not further increase during
apy only (AII). Twice-weekly treatment, par- the entire treatment interval. Children with obesity may
ticularly with DOT, is acceptable.15 have mild elevation when therapy is started.
If risk factors present for MDR, ADD New recommendations on short-course (4-mo) daily thera-
ethambutol 20 mg/kg/day PO qd OR py for children with non-severe TB come from the WHO
streptomycin 30 mg/kg/day IV, IM div q12h guidelines, March 2022 (www.who.int/publications/i/
initially. item/9789240046764; accessed September 12, 2024).
Contact TB specialist for therapy for drug-resistant TB.205
FQs may play a role in treating MDR strains. Bedaquiline,
in a new drug class for TB therapy, is approved for
adults and children >5 y with MDR TB when used in
combination therapy. Delamanid is not approved by the
FDA as of September 2024 but is approved in the
European Union and many countries in Asia for MDR TB.
DOT preferred; after 2 wk of daily therapy, can change to
twice-weekly dosing double dosage of INH (max
900 mg), PZA (max 2 g), and ethambutol (max 2.5 g);
rifampin remains same dosage (15–20 mg/kg/day, max
600 mg) (AII).
LP ± CT of head for children ≤2 y to rule out occult,
concurrent CNS infection; consider testing for HIV
infection (AIII).
M bovis infection from unpasteurized dairy products is
also called “tuberculosis”; all strains of M bovis are PZA
resistant. Treat 9–12 mo with INH and rifampin.
– Latent TB infection15,16,206,207 (skin Many options now Consider LFTs as needed for symptoms. Stop
test conversion; more recently INH/rifapentine: INH/rifapentine if AST or ALT ≥5 times the ULN
just called “TB infection”15 in Rifampin alone (all ages): 15–20 mg/kg/dose even in the absence of symptoms or ≥3 times the
contrast to “TB disease” for daily (max 600 mg) for 4 mo ULN in the presence of symptoms.
symptomatic TB infection) For children 2–11 y: once-weekly DOT for 12 wk: For children <2 y: INH and rifapentine may be used, but
INH 25 mg/kg/dose (max 900 mg), AND there are less data on safety and efficacy.
rifapentine: For exposure to known INH-resistant but
10.0–14.0 kg: 300 mg rifampin-susceptible strains, use rifampin 6 mo (AIII).
14.1–25.0 kg: 450 mg
25.1–32.0 kg: 600 mg
32.1–49.9 kg: 750 mg
≥50.0 kg: 900 mg (max)
For children 2–11 y: INH 25 mg/kg, rounded up
to nearest 50 or 100 mg (max 900 mg), AND
rifapentine (See above.)
INH/rifampin (all ages): INH 10–15 mg/kg/day
(max 300 mg)/rifampin 15–20 mg/kg/day

2025 Nelson’s Pediatric Antimicrobial Therapy —

(max 600 mg) daily for 3 mo
INH 10–15 mg/kg/day (max 300 mg) PO daily
for 6–9 mo (12 mo for immunocompromised
patients) (AIII); treatment with INH at
20–30 mg/kg twice weekly for 9 mo also
effective (AIII)
– Exposed child <5 y, or Prophylaxis for possible infection for 2–3 mo Alternative regimens:
immunocompromised patient after last exposure, with rifampin 15–20 mg/ INH 10–15 mg/kg PO qd AND rifampin 15–20 mg/kg/dose
(at high risk for dissemination) kg/dose PO qd OR INH 10–15 mg/kg PO qd; qd (max 600 mg) for up to 3 mo.
for at least 2–3 mo (AIII), with repeat skin If PPD or IGRA test remains negative at 8–10 wk and child
test or IGRA test (AIII). Also called “window appears well, consider stopping empiric therapy. PPD
prophylaxis.” may not be reliable in immunocompromised patients.
Not much data to assess reliability of IGRA assays in very
young infants or immunocompromised hosts, but not
likely to be much better or worse than the PPD skin test.
 Antimicrobial Therapy According to Clinical Syndromes

38 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

G. CARDIOVASCULAR INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Bacteremia
– Occult bacteremia/serious In general, hospitalization for late-onset neonatal Current data document the importance of
bacterial infection (late-onset sepsis in the ill-appearing infant, with cultures of ampicillin-resistant E coli in bacteremia and UTI in
neonatal sepsis; fever without blood, urine, and CSF; start ampicillin for GBS infants <90 days.211–213
focus), infants <1–2 mo (GBS, and Listeria at 200 mg/kg/day IV div q6h AND For a nontoxic, febrile infant with good access to
E coli, Listeria, pneumococcus, cefepime or ceftazidime for E coli/enteric bacilli; medical care: blood and urine cultures may be
meningococcus)208–213 use ceftriaxone for those after the first few weeks obtained, and we are getting much closer to
following birth (cefotaxime no longer routinely eliminating LPs in low-risk infants.208 Risk scores
available in the United States); higher dosages if incorporate various combinations of history
meningitis is documented. (previously healthy), no skin or soft tissue infection,
In areas with low (<20%) ampicillin resistance clinical status, and laboratory tests (urinalysis, WBC
in E coli, consider ampicillin and gentamicin count, and, possibly, procalcitonin). Infants may be
(gentamicin will not cover CNS infection follow- discharged home without antibiotics and close
ing bacteremia caused by ampicillin-resistant follow-up if evaluation is negative (Rochester; modi-
E coli when treated with ampicillin and fied Philadelphia criteria)209–213 (BI). Standardizing
gentamicin). evaluation of these infants by collaborating clinicians
can create a local standard of care, as no test or
examination has 100% accuracy for these babies.
– Occult bacteremia/serious Empiric therapy: if unimmunized, febrile, mild to Conjugated vaccines for H influenzae type b and
bacterial infection (fever with- moderate toxic: after blood culture: ceftriaxone pneumococcus have virtually eliminated occult
out focus) in infants from 2–3 to 50 mg/kg IM (BII). bacteremia of infancy by these pathogens.
36 mo of age (H influenzae type b/ For the fully immunized (H influenzae type b and For occult bacteremia, PO convalescent therapy is
pneumococcus in unimmunized pneumococcus) and nontoxic infant, routine selected by susceptibility of blood isolate, following
patients; meningococcus; pneu- empiric outpatient therapy for fever with response to IM/IV treatment, with CNS and other
mococcus [non-vaccine strains]; antibiotics is not recommended, but follow foci ruled out by examination ± laboratory tests
increasingly S aureus)212 closely in case of non-vaccine strain ± imaging. LP is not recommended for routine
pneumococcal infection, vaccine failure, or evaluation of fever but is recommended for
meningococcal bacteremia (BIII).210,212,213 bacteremia in younger infants.208
– Haemophilus influenzae type b, Ceftriaxone IM/IV OR, if BL negative, ampicillin IV, If BL negative: amoxicillin 75–100 mg/kg/day PO div tid
non-CNS infections followed by PO convalescent therapy (AII) (AII).
If positive, consider these options (but there are no
data on treatment of bacteremic infection):
high-dosage cefixime, ceftibuten, cefdinir PO, or
levofloxacin PO (CIII).
– Meningococcus Ceftriaxone IM/IV or penicillin G IV (if susceptible) PO convalescent therapy can be considered for occult
bacteremia or mild infection (AII).
– Pneumococcus, non-CNS Ceftriaxone IM/IV or penicillin G/ampicillin IV (if If pen-S or penicillin-intermediate (MIC is ≤2 or lower):
infections pen-S), followed by PO convalescent therapy (AII) amoxicillin 75–100 mg/kg/day PO div tid (AII).
If pen-R (MIC is ≥4): continue ceftriaxone IM or switch
to clindamycin if susceptible (CIII); linezolid and
levofloxacin may also be options (CIII).
– Staphylococcus aureus4,6,214–217 MSSA: nafcillin or oxacillin/nafcillin IV 150–200 mg/ Usually not necessary to add gentamicin or rifampin,216
usually associated with focal kg/day div q6h ± gentamicin 6 mg/kg/day div although for disseminated MRSA infection,

2025 Nelson’s Pediatric Antimicrobial Therapy —

infection q8h (AII). combination therapy is often used but without
MRSA: ceftaroline: 2 mo–<2 y, 24 mg/kg/day IV div supporting controlled data (AIII).
q8h; ≥2 y, 36 mg/kg/day IV div q8h (max single For persisting bacteremia caused by MRSA, consider
dose 400 mg) (BIII) OR vancomycin215 40–60 mg/ adding gentamicin or rifampin, or changing from
kg/day (CII) IV div q8h OR daptomycin IV218 vancomycin (particularly for MRSA with vancomycin
8–12 mg/kg/day q24h (BII). MIC of >2 mcg/mL) to daptomycin or ceftaroline
Treat for 2 wk (IV + PO) from negative blood cul- (daptomycin will not treat pneumonia).
tures unless endocarditis/endovascular thrombus For toxic shock syndrome, clindamycin should be
is present, which may require up to 6 wk of added for the initial 48–72 h of therapy to decrease
therapy (BIII). toxin production (linezolid may also act this way);
IVIG may be added to bind circulating toxin; no
controlled data exist for these measures.
Watch for the development of metastatic foci of
infection, including endocarditis.
If catheter-related, remove catheter.
 Antimicrobial Therapy According to Clinical Syndromes

40 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

G. CARDIOVASCULAR INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Endocarditis: Prospective, controlled data on therapy for endocarditis in neonates, infants, and children are limited, and many recommendations
are extrapolated from adult studies, in which some level of evidence exists, or from other invasive bacteremia infection studies. Surgical
indications: intractable heart failure; persistent infection; large mobile vegetations; peripheral embolism; and valve dehiscence, perforation,
rupture, or fistula, or a large perivalvular abscess.219–223 Consider community vs nosocomial pathogens based on recent surgeries, prior antibiotic
therapy, and possible entry sites for bacteremia (skin, oropharynx and respiratory tract, GI tract). Children with congenital heart disease and
those with prosthetic valves/materials are more likely to have more turbulent cardiovascular blood flow, which increases risk for endovascular
infection. Catheter-placed bovine jugular valves also seem to increase risk of infection.222,223 Similar guidelines have been published for both the
United States and the European Union.220,221 Immunocompromised hosts may become bacteremic with a wide range of bacteria, fungi, and
mycobacteria.
– Native valve219–221
– Empiric therapy for presumed Ceftriaxone IV 100 mg/kg q24h OR amp/sul Combination (β-lactam + gentamicin) provides
endocarditis (viridans 300 mg/kg/day div q4–6h AND gentamicin IV, bactericidal activity against most strains of viridans
streptococci, S aureus, HACEK IM 6 mg/kg/day div q8h (AII). streptococci, the most common pathogens in
group) For more acute, severe infection, ADD vancomycin infective endocarditis. Cefepime is recommended for
40–60 mg/kg/day IV div q8h to cover S aureus adults,219 but resistance data in enteric bacilli in
(AIII) (insufficient data to recommend ceftaroline children suggest that ceftriaxone remains a
for endocarditis). reasonable choice. Amp/sul adds extended anaerobic
activity and BL stability that is not likely to be
needed.
May administer gentamicin with a qd regimen (CIII).
For β-lactam allergy, use vancomycin 45 mg/kg/day IV
div q8h AND gentamicin 6 mg/kg/day IV div q8h.
– Culture-negative native valve endocarditis: treat 4–6 wk (obtain advice from an ID specialist for an appropriate regimen that is based on likely
pathogens).219,220
– Viridans streptococci: follow echocardiogram for evidence of worsening vegetation; β-lactam allergy: vancomycin.
 Copyright © 2025. American Academy of Pediatrics. All rights reserved.
Created from aut on 2025-05-21 21:08:49.

2025ch01-Nelson-2025_001-074.indd
Pediatrics, 2025. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/aut/detail.action?docID=3208859
Nelson's Pediatric Antimicrobial Therapy,

Fully susceptible to penicillin Ceftriaxone 50 mg/kg IV, IM q24h for 4 wk OR The AHA recommends higher dosage of ceftriaxone
penicillin G 200,000 U/kg/day IV div q4–6h for similar to that of penicillin non-susceptible strains,
4 wk (BII); OR penicillin G or ceftriaxone but for fully susceptible strains, standard-dose
ceftriaxone provides the necessary PD exposure.
Relatively resistant to penicillin Penicillin G 300,000 U/kg/day IV div q4–6h for Gentamicin is used for the first 2 wk for a total of 4 wk
4 wk, or ceftriaxone 100 mg/kg IV q24h for 4 wk; of therapy for relatively resistant strains.
AND gentamicin 6 mg/kg/day IM, IV div q8h for Vancomycin-containing regimens should use at least a
the first 2 wk (AIII) 4-wk treatment course, with gentamicin used for the
entire course.
41

– Enterococcus (dosages for native or prosthetic valve infections)

edited by Debra L. Palazzi, et al., American Academy of

Ampicillin-susceptible Ampicillin 300 mg/kg/day IV, IM div q6h or Combined treatment with cell wall active antibiotic
(gentamicin-S) penicillin G 300,000 U/kg/day IV div q4–6h; AND plus aminoglycoside used to achieve bactericidal
gentamicin 6 mg/kg/day IV div q8h; for 4–6 wk activity. Children are not as likely to develop renal
(AII) toxicity from gentamicin as adults.
For β-lactam allergy: vancomycin.
Ampicillin-resistant (gentamicin-S) Vancomycin 40 mg/kg/day IV div q8h AND Little data exist in children for daptomycin, ceftaroline,
gentamicin 6 mg/kg/day IV div q8h; for 6 wk or linezolid.
(AIII) For gentamicin-resistant strains, use streptomycin or
Vancomycin-resistant Daptomycin IV if also ampicillin resistant (dose other aminoglycoside if susceptible. If ampicillin-
(gentamicin-S) is age dependent; see Ch 18 for doses) susceptible gentamicin-resistant, can combine
± gentamicin 6 mg/kg/day IV div q8h; for ampicillin and ceftriaxone.
4–6 wk (AIII)
2/18/25
 Antimicrobial Therapy According to Clinical Syndromes

42 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

G. CARDIOVASCULAR INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Staphylococci: S aureus, MSSA or MSSE: nafcillin or oxacillin/nafcillin Surgery may be necessary in acute phase; conflicting
including CA-MRSA; 150–200 mg/kg/day IV div q6h for 4–6 wk AND data on efficacy of 1st-generation cephalosporins,
Staphylococcus epidermidis6,215 gentamicin 6 mg/kg/day div q8h for first 14 days. although more recent data suggest equivalence to
Consider continuing therapy at CA-MRSA or MRSE: daptomycin IV218 8–12 mg/kg/ penicillins.
end of 6 wk if vegetations day q24h (BII), OR vancomycin 40–60 mg/kg/day The AHA suggests gentamicin for only the first
increase on echocardiogram or IV div q8h AND gentamicin for 6 wk; consider for 3–5 days for MSSA or MSSE and optional gentamicin
there is a concern for abscess. slow response, ADD rifampin 20 mg/kg/day IV for MRSA.
Consider septic thrombophlebitis: div q8–12h. Daptomycin dose is age dependent (see Ch 18 for
the risk of persisting organisms Insufficient data to recommend ceftaroline for doses).
is not defined in deep venous MRSA endocarditis.
thromboses that may be “seed-
ed” as a result of bacteremia.
– Pneumococcus, gonococcus, Penicillin G 200,000 U/kg/day IV div q4–6h for 4 wk For gonococcal endocarditis: ceftriaxone alone,
group A streptococcus (BII); alternatives: ceftriaxone or vancomycin 1–2 g IV q24h for >4 wk.59
For penicillin non-susceptible strains of pneumococcus,
consult with ID specialist but should be able to use
high-dosage penicillin G 300,000 U/kg/day IV div
q4–6h or high-dosage ceftriaxone 100 mg/kg IV
q12h or q24h for 4 wk, if supported by PD (eg, the
time that penicillin or ceftriaxone is above the MIC of
the organism, during the dosing interval).
– HACEK (Haemophilus, Usually susceptible to ceftriaxone 100 mg/kg IV Some organisms will be ampicillin susceptible. Usually
Aggregatibacter [formerly q24h for 4 wk (BIII) do not require the addition of gentamicin.
Actinobacillus], Cardiobacterium,
Eikenella, Kingella spp)
– Enteric GNB Antibiotics specific to pathogen (usually For ESBL organisms, carbapenems or β-lactam/BLI
ceftriaxone plus initial treatment with combinations, PLUS gentamicin initially, should be
gentamicin until clinical/microbiologic effective. See Ch 12.
improvement); duration at least 6 wk (AIII) No controlled data on the benefit of gentamicin in
combination.
– Pseudomonas aeruginosa Antibiotic specific to susceptibility: cefepime or Both cefepime and meropenem are more active
meropenem PLUS tobramycin against Pseudomonas and less likely to allow
BL-resistant pathogens to emerge than ceftazidime.
– Prosthetic valve/ Follow echocardiogram for resolution of
material219,222,223 vegetation.
For β-lactam allergy: vancomycin.
– Viridans streptococci
Fully susceptible to penicillin Ceftriaxone 100 mg/kg IV, IM q24h for 6 wk OR
penicillin G 300,000 U/kg/day IV div q4–6h for
6 wk (AII); OR penicillin G or ceftriaxone AND

2025 Nelson’s Pediatric Antimicrobial Therapy —

gentamicin 6 mg/kg/day IM, IV div q8h for first
2 wk of 6-wk course (AII)
Relatively resistant to penicillin Penicillin G 300,000 U/kg/day IV div q4–6h for Obtain the MIC of the strep spp to the antibiotic used
6 wk, or ceftriaxone 100 mg/kg IV q24h for 6 wk; for treatment; based on expected or measured serum
AND gentamicin 6 mg/kg/day IM, IV div q8h for antibiotic concentrations, assess PD (ability to
6 wk (AIII) achieve the desired time that penicillin [or
ceftriaxone] is above the MIC of the organism, during
the dosing supported by the interval). See Ch 11.
Gentamicin is used for all 6 wk of therapy for prosthetic
valve/material endocarditis caused by relatively
resistant strains.
– Enterococcus (See dosages earlier in this table under Native Valve.) Treatment course is at least 6 wk, particularly if vancomycin is used.215,219
 Antimicrobial Therapy According to Clinical Syndromes

44 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

G. CARDIOVASCULAR INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Staphylococci: S aureus, MSSA or MSSE: nafcillin or oxacillin/nafcillin Daptomycin dose is age and weight dependent (see
including CA-MRSA; 150–200 mg/kg/day IV div q6h for ≥6 wk AND Ch 18 for doses).
S epidermidis6,219 gentamicin 6 mg/kg/day div q8h for first 14 days. Valve replacement for prosthetic valve endocarditis
Consider continuing therapy at CA-MRSA or MRSE: daptomycin IV218 8–12 mg/kg/ caused by S aureus is preferable in most patients, if
end of 6 wk if vegetations day q24h (BII), OR vancomycin 40–60 mg/kg/day not all.
persist or increase on IV div q8h AND gentamicin for ≥6 wk; ADD
echocardiogram. rifampin 20 mg/kg/day IV div q8–12h.
– Candida85,219,220 AmB lipid formulation, 3–5 mg/kg q24h with/ Poor prognosis; obtain advice from an ID specialist.
without flucytosine 100 mg/kg/day div q6h Surgery may be required to resect infected valve.
(there is more experience with AmB preparations Long-term suppressive therapy with fluconazole.
[no comparative trials against echinocandins]),
OR micafungin 2–4 mg/kg/day (BIII). Do not use
fluconazole as initial therapy because of inferior
fungistatic effect.
– Culture-negative prosthetic valve endocarditis: treat at least 6 wk.
Endocarditis antibiotic prophylaxis220,221,224: Endocarditis is rarely caused by dental/GI procedures, and antibiotic prophylaxis for procedures
prevents an exceedingly small proportion of endocarditis cases; therefore, the risks of antibiotic prophylaxis outweigh the benefits. Highest-risk
conditions currently recommended for prophylaxis for children undergoing procedures: (1) prosthetic heart valve (or prosthetic material used to
repair a valve); (2) previous endocarditis; (3) cyanotic congenital heart disease that is unrepaired (or palliatively repaired with shunts and
conduits); (4) congenital heart disease that is repaired but with defects at the site of repair adjacent to prosthetic material; (5) completely
repaired congenital heart disease by using prosthetic material, for the first 6 mo after repair; or (6) cardiac transplant patients with valvulopathy.
Routine prophylaxis is no longer required for children with native valve abnormalities. Assessment of recent prophylaxis guidelines does not
document an increase in endocarditis.225
– In highest-risk patients: dental Amoxicillin 50 mg/kg PO 60 min before procedure If penicillin allergy: clindamycin 20 mg/kg PO (60 min
procedures that involve OR ampicillin or ceftriaxone or cefazolin, all at before) or IV (30 min before); OR azithromycin
manipulation of the gingival or 50 mg/kg IM/IV 30–60 min before procedure 15 mg/kg or clarithromycin 15 mg/kg, 60 min before
periodontal region of teeth (little data to support alternative regimens)
– Genitourinary and GI procedures None No longer recommended
Lemierre syndrome Empiric: meropenem 60 mg/kg/day div q8h (or Anecdotal reports suggest that metronidazole may be
(F necrophorum primarily; also 120 mg/kg/day div q8h for CNS metastatic foci) effective for apparent failures with other agents.
reported with MRSA)119–121 (AIII) OR ceftriaxone 100 mg/kg/day q24h AND Often requires anticoagulation.
– Pharyngitis with internal jugular metronidazole 40 mg/kg/day div q8h or Metastatic and recurrent abscesses often develop
vein septic thrombosis; also clindamycin 40 mg/kg/day div q6h (BIII). during active, appropriate therapy, requiring multiple
known as postanginal sepsis, ADD empiric vancomycin if MRSA is suspected if debridements and prolonged antibiotic therapy.122
necrobacillosis clindamycin is not already in the treatment Treat until CRP is close to normal (AIII).
regimen or local susceptibility data indicate that
vancomycin use is preferred.
Purulent pericarditis
– Empiric (acute, bacterial: Ceftaroline: 2–<6 mo, 30 mg/kg/day IV div q8h; For presumed staph infection, consider adding
S aureus [including MRSA], ≥6 mo, 45 mg/kg/day IV div q8h (max single gentamicin pending cultures (AIII).
group A streptococcus, dose 600 mg) (BIII), OR vancomycin 40 mg/kg/ Increasingly uncommon with immunization against
pneumococcus, meningococcus; day IV div q8h and ceftriaxone 50–75 mg/kg/day pneumococcus and H influenzae type b.227
in unimmunized children, q24h (AIII) Pericardiocentesis is essential to establish diagnosis.
H influenzae type b)226,227 Surgical drainage of pus with pericardial window or

2025 Nelson’s Pediatric Antimicrobial Therapy —

pericardiectomy is important to prevent tamponade.
– Staphylococcus aureus For MSSA: oxacillin/nafcillin 150–200 mg/kg/day IV Continue therapy with gentamicin until clinically
div q6h OR cefazolin 100 mg/kg/day IV div q8h. improved; consider use of rifampin in severe cases
Treat for 2–3 wk after drainage (BIII). due to tissue penetration characteristics.
For CA-MRSA: continue ceftaroline or vancomycin.
Treat for 3–4 wk after drainage (BIII).
– Haemophilus influenzae type b in Ceftriaxone 50 mg/kg/day q24h for 10–14 days Ampicillin for BL-negative strains
unimmunized children (AIII)
– Pneumococcus, meningococcus, Penicillin G 200,000 U/kg/day IV, IM div q6h for Ceftriaxone for penicillin non-susceptible pneumococci
group A streptococcus 10–14 days OR ceftriaxone 50 mg/kg qd for
10–14 days (AIII)
 Antimicrobial Therapy According to Clinical Syndromes

46 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

G. CARDIOVASCULAR INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Coliform bacilli Ceftriaxone 50–75 mg/kg/day q24h for ≥3 wk (AIII) Alternative drugs depending on susceptibilities; for
Enterobacter, Serratia, or Citrobacter, use cefepime or
meropenem. For ESBL E coli or Klebsiella, use a
carbapenem.
– Tuberculous15,16 INH 10–15 mg/kg/day (max 300 mg) PO, IV qd for For those at highest risk for restrictive pericarditis,
6 mo AND rifampin 10–20 mg/kg/day (max steroids may provide benefit. For children:
600 mg) PO, IV qd for 6 mo. ADD PZA 20–40 mg/ prednisone 2 mg/kg/day for 4 wk, then 0.5 mg/kg/
kg/day PO qd for first 2 mo of therapy; if day for 4 wk, then 0.25 mg/kg/day for 2 wk, then
suspected MDR, also add ethambutol 20 mg/kg/ 0.1 mg/kg/day for 1 wk.
day PO qd (AIII).

H. GASTROINTESTINAL INFECTIONS (See Ch 9 for parasitic infections.)

Clinical Diagnosis Therapy (evidence grade) Comments
Diarrhea/Gastroenteritis
Note on E coli and diarrheal disease: Antibiotic susceptibility of E coli varies considerably from region to region. For mild to moderate disease,
TMP/SMX may be started as initial therapy, but for more severe disease and for locations with rates of TMP/SMX resistance >10%–20%,
azithromycin, a PO 3rd-generation cephalosporin (eg, cefixime, cefdinir, ceftibuten), or ciprofloxacin should be used (AIII). Diagnostic testing
by traditional cultures with antibiotic susceptibility testing is recommended for significant disease (AIII). New molecular tests (particularly
multiplex PCR tests) are commercially available and quite helpful to diagnose specific pathogens or presence of enterotoxins, but they do not
provide susceptibility information or distinguish between viable and nonviable organisms.
– Empiric therapy for community- Azithromycin 10 mg/kg qd for 3 days (BII); OR Alternatives: 3rd-generation cephalosporins (eg,
associated diarrhea in the ciprofloxacin 30 mg/kg/day PO div bid for 3 days; ceftriaxone); have been shown effective in
United States (E coli [STEC, OR cefixime 8 mg/kg/day PO qd (BII). uncomplicated Salmonella typhi infections.
including O157:H7 strains; ETEC; Current recommendation is to avoid treatment of Rifaximin is a nonabsorbable rifamycin in tab form not
and EPEC], Salmonella, Shiga toxin–containing (STEC O157:H7) strains.228 to be used for invasive bacterial enteritis: 600 mg/
Campylobacter, and Shigella day div tid for 3 days (for nonfebrile, non-bloody
predominate; Yersinia and diarrhea in children ≥12 y).
parasites cause <5%; viral Most retrospective data support withholding treatment
pathogens are far more of O157:H7 strains to avoid HUS.230–232 Antitoxins and
common, especially for children immune globulins are under investigation.233
<3 y.)228,229
– Travelers diarrhea: empiric For mild diarrhea, treatment is not Susceptibility patterns of E coli, Campylobacter,
therapy (E coli, Campylobacter, recommended.237 Salmonella, and Shigella vary widely by country, with
Salmonella, and Shigella, plus Azithromycin 10 mg/kg qd for 1–3 days (AII); OR increasing resistance to commonly used antibiotics;
many other pathogens, rifaximin 200 mg PO tid for 3 days (age ≥12 y) check the CDC and country-specific data for
including protozoa)234–240 (BIII); OR ciprofloxacin 30 mg/kg/day PO div bid departing or returning travelers. Azithromycin
The CDC provides updated advice for 3 days (BII). preferable to ciprofloxacin for travelers to Southeast

2025 Nelson’s Pediatric Antimicrobial Therapy —

both pretravel and post-travel at Asia given high prevalence of quinolone-resistant
wwwnc.cdc.gov/travel/page/ Campylobacter.
clinician-information-center Rifaximin, not to be used for invasive bacterial enteritis.
(reviewed November 3, 2022; For adults who travel and take antibiotics (mostly FQs),
accessed September 12, 2024). colonization with ESBL-positive E coli is more
See 2017 guidelines from frequent on return home.241
International Society of Travel Adjunctive therapy with loperamide (antimotility) is
Medicine.237 not recommended for children <2 y and should be
used only in cases of nonfebrile, non-bloody
diarrhea.235,239,242 May shorten symptomatic illness
by about 24 h.
 Antimicrobial Therapy According to Clinical Syndromes

48 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

H. GASTROINTESTINAL INFECTIONS (See Ch 9 for parasitic infections.)
Clinical Diagnosis Therapy (evidence grade) Comments
– Travelers diarrhea: Prophylaxis: early self-treatment with agents listed previously is preferred over long-term prophylaxis, but
prophylaxis234,235,237 may use prophylaxis for a short-term (<14 days) visit to very high-risk region: rifaximin (for children ≥12 y),
azithromycin (BIII). FQs should not be used for prevention, due to potential cartilage toxicity.
– Aeromonas hydrophila243 Ciprofloxacin 30 mg/kg/day PO div bid for 5 days Not all strains produce enterotoxins and diarrhea; role
OR cefixime 8 mg/kg/day PO qd (BIII) in diarrhea questioned.243 Resistance to TMP/SMX
about 10%–15%. Choose narrowest-spectrum agent
based on in vitro susceptibilities.
– Campylobacter jejuni244,245 Azithromycin 10 mg/kg/day for 3 days (BII) or Alternatives: doxycycline or ciprofloxacin (high rate of
erythromycin 40 mg/kg/day PO div qid for 5 days FQ resistance in Thailand, India, and now the United
(BII) States).
Single-dose azithromycin (1 g, once) is effective in adults.
– Cholera246,247 Azithromycin 20 mg/kg once; OR erythromycin Ciprofloxacin or TMP/SMX (if susceptible)
50 mg/kg/day PO div qid for 3 days; OR doxycy-
cline 4.4 mg/kg/day (max 200 mg/day) PO div
bid, for all ages
– Clostridioides (formerly Treatment stratified by severity and recurrence Adult guidelines recommend fidaxomicin as first-line
Clostridium) difficile First episode: therapy, where available; is approved for children
(antibiotic-associated Mild to moderate illness: metronidazole 30 mg/kg/ down to age 6 mo.251
colitis)248–252 day PO div qid; OR vancomycin 40 mg/kg/day PO Attempt to stop antibiotics that may have caused
div qid. C difficile infection.
Severe illness: vancomycin 40 mg/kg/day PO div Vancomycin is more effective for severe infection.248,249
qid for 7 days. Many infants and children aged <2 y may have
Severe and complicated/systemic: vancomycin PO asymptomatic colonization with C difficile.249
AND metronidazole IV; consider vancomycin Higher risk for relapse in children with multiple
enema (500 mg/100 mL physiologic [normal] comorbidities.
saline) soln q8h until improvement).248,249 Fecal microbiota transplant for failure of medical
For relapsing C difficile enteritis, consider pulse therapy in recurrent enteritis.
therapy (1 wk on/1 wk off for 3–4 cycles) or Bezlotoxumab (IV infusion) is approved for age ≥12 mo to
prolonged tapering therap red ce the chance of rec rrence in high risk patients
– Escherichia coli
Enterotoxigenic (etiology of most Azithromycin 10 mg/kg qd for 3 days (AII); OR Most illnesses are brief and self-limited and may not
TD)235,236 ciprofloxacin 30 mg/kg/day PO div bid for 3 days require treatment.
(BII); OR cefixime 8 mg/kg/day PO qd for 3 days Alternatives: rifaximin 600 mg/day div tid for 3 days
(CIII) (for nonfebrile, non-bloody diarrhea in children
≥12 y, as rifaximin is not absorbed systemically); OR
TMP/SMX.
Resistance increasing worldwide; check country-
specific rates at the CDC traveler website: wwwnc.
cdc.gov/travel/page/clinician-information-center.
Enterohemorrhagic (O157:H7; Recommendation to avoid treatment of STEC Animal model data suggest that some antibiotics
STEC, etiology of HUS)228,230–233 O157:H7 strains.228 (rifamycins) are less likely to increase toxin
Most retrospective data support withholding production than FQs.253
treatment of O157:H7 strains to avoid HUS.230–232 Injury to colonic mucosa may lead to invasive bacterial
colitis that does require antimicrobial therapy.

2025 Nelson’s Pediatric Antimicrobial Therapy —

– Gastritis, peptic ulcer disease Triple-agent therapy in areas of low clarithromycin Resistance to clarithromycin is as high as 20% in some
(Helicobacter pylori)254–256 resistance (or known clarithromycin regions.254,257
susceptibility): clarithromycin 7.5 mg/kg/dose Current use of bismuth in regimens for known or
2–3 times each day, AND amoxicillin 40 mg/kg/ suspected clarithromycin resistance, with bismuth
dose (max 1 g) PO bid AND omeprazole 0.5 mg/ (262 mg qid for those aged <10 y; 524 mg qid
kg/dose PO bid for 14 days (BII), OR if suscep­ ≥10 y), amoxicillin, metronidazole, and
tibilities unknown or clarithromycin resistant: omeprazole.254
quadruple-agent therapy clarithromycin, amoxi- Metronidazole resistance reported.254
cillin, omeprazole, AND metronidazole Newer, FQ-based treatment combinations used in
(15 mg/kg/day div bid)254–257 adults with clarithromycin resistance.255
 Antimicrobial Therapy According to Clinical Syndromes

50 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

H. GASTROINTESTINAL INFECTIONS (See Ch 9 for parasitic infections.)
Clinical Diagnosis Therapy (evidence grade) Comments
– Giardiasis (see Ch 9) (Giardia Tinidazole (for age ≥3 y) 50 mg/kg/day (max 2 g)
259
If therapy is unsuccessful, another course of the same
intestinalis, formerly lamblia)258 for 1 day (BII); OR nitazoxanide PO (take with agent is usually curative.
food), age 12–47 mo, 100 mg/dose bid for Alternatives: metronidazole 20–30 mg/kg/day PO div
3 days; age 4–11 y, 200 mg/dose bid for 3 days; tid for 7–10 days (BII); OR paromomycin OR
age ≥12 y, 1 tab (500 mg) bid for 3 days (BII) albendazole (CII), OR mebendazole OR furazolidone.
Prolonged or combination drug courses may be need-
ed for immunocompromised conditions.
Treatment of asymptomatic carriers is controversial but
recommended in the United States (per AAP Red
Book).
– Salmonellosis260,261 (See Travelers diarrhea: prophylaxis earlier in this section of the table, and Ch 9.)
Non-typhoid strains260,261 Usually none for self-limited diarrhea in Alternatives: ciprofloxacin 30 mg/kg/day PO div bid for
immunocompetent child (diarrhea is often much 5 days (AI).
improved by the time culture results are Carriage of strains may be prolonged in treated
available). children, but a current systematic review did not
Treat children with persisting symptomatic support this earlier observation.260
infection and all infants <3 mo (greater risk for For bacteremic infection, ceftriaxone IM/IV may be
bacteremia): azithromycin 10 mg/kg PO qd for initially used until secondary sites of infection (bone/
3 days (AII); OR ceftriaxone 75 mg/kg/day IV, IM joint, liver/spleen, CNS) are ruled out, for a total of
q24h for 5 days (AII); OR cefixime 20–30 mg/kg/ 7–10 days.261
day PO for 5–7 days (BII); OR for susceptible
strains: TMP/SMX 8 mg/kg/day of TMP PO div bid
for 14 days (AI).
Typhoid fever261–265 Azithromycin 20 mg/kg qd for 5 days (AII); OR Most strains are FQ resistant.
ceftriaxone 75 mg/kg/day IV, IM q24h for 5 days Increasing cephalosporin resistance.261,266 For newly
(AII); OR cefixime 20–30 mg/kg/day PO div q12h emergent MDR strains, may require a carbapenem
for 14 days (BII); OR for susceptible strains: (especially if recent travel to Pakistan).
ampicillin OR TMP/SMX 8 mg/kg/day of TMP Amoxicillin does not achieve high colonic intraluminal
PO div bid for 14 days (AI) or ciprofloxacin concentrations or high intracellular concentrations.
30 mg/kg/day div bid Longer treatment courses for focal invasive disease
(eg, osteomyelitis).
Corticosteroids may be indicated for severe,
life-threatening disease.
– Shigellosis238,267–269 Mild episodes do not require treatment. Alternatives for susceptible strains: TMP/SMX 8 mg/kg/
Azithromycin 10 mg/kg/day PO for 3 days (AII); OR day of TMP PO div bid for 5 days; OR ampicillin (not
ciprofloxacin 30 mg/kg/day PO div bid for amoxicillin).
3–5 days (BII); OR cefixime238 8 mg/kg/day PO qd Ceftriaxone 50 mg/kg/day IM, IV if parenteral therapy
for 5 days (AII). necessary, for 2–5 days.
Avoid antiperistaltic drugs.
Treatment for the improving child is not usually

2025 Nelson’s Pediatric Antimicrobial Therapy —

necessary to hasten recovery, but some experts
would treat to decrease communicability.
– Yersinia enterocolitica270–272 Antimicrobial therapy probably not of value for High rates of resistance to ampicillin.
mild disease in normal hosts. May mimic appendicitis in older children.
TMP/SMX PO, IV; OR ciprofloxacin PO, IV (BIII). Limited clinical data exist on PO therapy.
Parenteral therapy for more severe infection:
ceftriaxone plus gentamicin.
 Antimicrobial Therapy According to Clinical Syndromes

52 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

H. GASTROINTESTINAL INFECTIONS (See Ch 9 for parasitic infections.)
Clinical Diagnosis Therapy (evidence grade) Comments
Intra-abdominal infection (abscess, peritonitis secondary to bowel/appendix contents)
– Appendicitis, bowel-associated Source control is critical to curing this infection. Many other regimens may be effective. Because report-
(enteric GNB, Bacteroides spp, Newer data suggest that stratification of cases is ed retrospective data are published from
Enterococcus spp, Pseudomonas important to assess the effect of surgical and different centers, be aware that the patient
spp)273–278 medical therapy on outcomes, and using just a populations, extent of disease, and surgical approach
one-size-fits-all antibiotic recommendation may to treatment are not standardized across hospitals, so
not be the best approach.273–275,278,279 antibiotic(s) that work in institution A may not be as
Meropenem 60 mg/kg/day IV div q8h or imipenem effective in institution B.274,275
60 mg/kg/day IV div q6h; OR PIP/TAZO 240 mg/ Options include ampicillin 150 mg/kg/day div q8h AND
kg/day PIP component div q6h; for 4–5 days for gentamicin 6.0–7.5 mg/kg/day IV, IM div q8h AND
patients with adequate source control,277 metronidazole 40 mg/kg/day IV div q8h; OR
≥7–10 days if suspicion of persisting ceftriaxone 50 mg/kg q24h AND metronidazole
intra-abdominal abscess (AII). 40 mg/kg/day IV div q8h.
Pseudomonas is found consistently in up to Narrow the spectrum of antibiotics as soon as
20%–30% of children,274,277,280 providing susceptibility data are available; susceptibility data
evidence to document the need for empiric use of are particularly useful for PO step-down therapy if
an antipseudomonal drug (preferably one with appropriate for the child.
anaerobic activity), such as a carbapenem or PIP/ Data support IV outpatient therapy or PO step-down
TAZO, unless the surgery was highly effective at therapy278,280,284 when clinically improved, particularly
drainage/source control (gentamicin is not active in when PO therapy can be focused on the most
an abscess), which may explain successful out- prominent, invasive cultured pathogens.
comes in retrospective studies that did not include Publications on outcomes of antibiotic therapy
antipseudomonal coverage.278,279,281–283 regimens (IV or PO) without culture data cannot be
accurately interpreted.
– Tuberculosis, abdominal INH 10–15 mg/kg/day (max 300 mg) PO qd for Corticosteroids have been routinely used as
(M bovis, from unpasteurized 6–9 mo AND rifampin 10–20 mg/kg/day (max adjunctive therapy to decrease morbidity from
dairy products in the United 600 mg) PO qd for 6–9 mo (AII) AND, for inflammation.286,287
States,15,16,285 and in parts of the abdominal infection caused by M tuberculosis, DOT preferred; after 2+ wk of daily therapy, can change
world as a complication of ADD PZA 30–40 mg/kg/day (max 2 g) PO qd for to twice-weekly dosing double dosage of INH (max
systemic TB caused by first 2 mo of therapy only 900 mg); rifampin remains same dosage (10–20 mg/
 Some experts recommend routine empiric use of LP ± CT of head for children ≤2 y with active disease
ethambutol, based on local resistance data. to rule out occult, concurrent CNS infection (AIII).
If risk factors are present for MDR, ADD ethambutol No published prospective comparative data on a 6-mo
20 mg/kg/day PO qd OR an FQ (moxifloxacin or vs 9-mo treatment course in children.
levofloxacin).
Perirectal abscess (Bacteroides Ceftriaxone or ciprofloxacin AND metronidazole Surgical drainage alone may be curative. Obtaining
spp, other anaerobes, enteric (BIII). In high-risk or health care–associated infec- cultures and susceptibilities is increasingly important
bacilli)288 tion, PIP/TAZO OR cefepime AND metronidazole. with rising resistance to cephalosporins in
community E coli isolates.
May represent inflammatory bowel disease.
Peritonitis
– Peritoneal dialysis indwelling Antibiotic added to dialysate in concentrations Selection of antibiotic based on organism isolated from
catheter infection approximating those attained in serum for peritoneal fluid; systemic antibiotics if there is
(staphylococci; enteric GNB; systemic disease (eg, 4 mcg/mL for gentamicin, accompanying systemic signs of infection, including
yeast)289,290 25 mcg/mL for vancomycin, 125 mcg/mL for bacteremia/fungemia

2025 Nelson’s Pediatric Antimicrobial Therapy —

cefazolin, 25 mcg/mL for ciprofloxacin) after a
larger LD (AII)290
– Primary spontaneous bacterial Ceftriaxone 50 mg/kg/day q24h; if pen-S, then Other antibiotics according to culture and susceptibility
peritonitis (pneumococcus or penicillin G 150,000 U/kg/day IV div q6h; for tests. Spontaneous pneumococcal peritonitis now
group A streptococcus)291 7–10 days (AII) infrequent in PCV13/20-immunized children.
– Also a complication in children
with cirrhosis, with a wide range
of pathogens, many of which
can be MDR
 Antimicrobial Therapy According to Clinical Syndromes

54 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

I. GENITAL AND SEXUALLY TRANSMITTED INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Consider testing for HIV and other STIs in a child with one documented STI; consider sexual abuse in prepubertal children. The recommendations
below focus on adult and adolescent infections as per the CDC STI treatment guidelines (2021),59 which are posted online at www.cdc.gov/std/
treatment-guidelines/STI-Guidelines-2021.pdf (accessed September 12, 2024), with supplemental data published in 2022.56 Neonatal and child
recommendations can be found on the same web page.
Chancroid (Haemophilus Azithromycin 1 g PO as single dose OR ceftriaxone Alternative: erythromycin 1.5 g/day PO div tid for
ducreyi)59 250 mg IM as single dose 7 days; OR ciprofloxacin 1,000 mg PO qd, div bid for
3 days
Chlamydia trachomatis Doxycycline (patients >7 y) 4.4 mg/kg/day (max Alternatives: levofloxacin 500 mg PO q24h for 7 days
(cervicitis, urethritis)59 200 mg/day) PO div bid for 7 days; OR
azithromycin 20 mg/kg (max 1 g) PO for 1 dose
Epididymitis (associated with Ceftriaxone 50 mg/kg/day q24h for 7–10 days AND Microbiology not well studied in children; in infants,
positive urine cultures and (for older children) doxycycline 200 mg/day div also associated with urogenital tract anomalies.
STIs)59,292 bid for 10 days Postviral inflammation may be one etiology of
epididymitis in boys.292
Treat infants for S aureus and E coli; may resolve
spontaneously; in STI, treat for Chlamydia and
gonococcus.
Gonorrhea59,293,294 Antibiotic resistance is an ongoing problem, with new data suggesting the emergence of global azithromycin
resistance.56,293,294
– Newborns See Ch 2.
– Genital infections 2021 CDC guidelines for uncomplicated GC59: Increased dose of ceftriaxone to reflect small decreases
(uncomplicated vulvovaginitis, ceftriaxone 25–50 mg/kg IV/IM in a single dose, in documented in vitro susceptibility for GC;
cervicitis, urethritis, or proctitis) not to exceed 250 mg in children ≤45 kg or azithromycin no longer recommended, with 4% of
and pharyngitis56,59,293,294 500 mg in those >45 kg. For adults, the CDC no strains overall with resistance, but highest resistance
longer recommends azithromycin (1 g PO for rates found in isolates from MSM.
1 dose). Doxycycline 200 mg/day div q12h for If ceftriaxone is unavailable, give gentamicin 240 mg
7 days if chlamydia has not been excluded. IM as a single dose plus azithromycin 2 g PO as a
single dose OR cefixime 800 mg PO as a single
dose.59
FQs are not recommended due to resistance.
– Conjunctivitis59 Ceftriaxone 1g IM for 1 dose Lavage the eye with saline.
– Disseminated gonococcal Ceftriaxone 50 mg/kg/day IM, IV q24h (max 1 g) No studies in children: increase dosage for meningitis.
infection59 AND azithromycin 1 g PO for 1 dose; total course
for 7 days
Granuloma inguinale Azithromycin 1 g PO once weekly or 500 mg qd Primarily in tropical regions of India, Pacific, and Africa.

2025 Nelson’s Pediatric Antimicrobial Therapy —

(donovanosis; Klebsiella for at least 3 wk and until all lesions have Options: doxycycline 4.4 mg/kg/day div bid (max
[formerly Calymmatobacterium] completely healed 200 mg/day) PO for at least 3 wk OR erythromycin
granulomatis)59 base 500 mg PO qid for at least 3 wk OR TMP/SMX
1 DS (160-mg/800-mg) tab PO bid for at least
3 wk; all regimens continue until all lesions have
completely healed.
Herpes simplex virus, genital Acyclovir 20 mg/kg/dose (max 400 mg) PO tid for For recurrent episodes: treat with acyclovir PO,
infection (first 7–10 days (first episode) (AI); OR valacyclovir valacyclovir PO, or famciclovir PO, immediately when
episode)59,295,296 20 mg/kg/dose (directions for extemporaneous symptoms begin, for 5 days.
suspension on package label), max 1 g PO bid for For suppression: acyclovir 20 mg/kg/dose (max
7–10 days (first episode) (AI); OR famciclovir 400 mg) PO bid; OR valacyclovir 20 mg/kg/dose PO
250 mg PO tid for 7–10 days (AI); for more severe qd (max 500 mg to start, or 1 g for difficult to
infection: acyclovir 15 mg/kg/day IV div q8h as suppress).
1-h infusion for 7–10 days (AII) Important issues for HSV in pregnancy for the fetus/
newborn.295 Prophylaxis is recommended by ACOG in
pregnant women.296
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56 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

I. GENITAL AND SEXUALLY TRANSMITTED INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Lymphogranuloma venereum Doxycycline 4.4 mg/kg/day (max 200 mg/day) PO Alternatives: erythromycin 2 g/day PO div qid for
(C trachomatis)59 (patients >7 y) div bid for 21 days 21 days; OR azithromycin 1 g PO once weekly for 3 wk
Pelvic inflammatory disease Ceftriaxone 250 mg IM for 1 dose AND both Optional regimen: cefoxitin 2 g IV q6h; AND
(Chlamydia or gonococcus, plus doxycycline 200 mg/day PO div bid and doxycycline 200 mg/day PO or IV div bid; OR
anaerobes)59,297 metronidazole 1 g/day PO div bid for 14 days clindamycin 900 mg IV q8h AND gentamicin 1.5 mg/
OR cefotetan 2 g IV q12h AND doxycycline 100 mg kg IV, IM q8h, OR amp/sul (3 g IV q6h) AND
PO or IV q12h doxycycline (100 mg bid).
After clinical improvement with parenteral therapy,
transition to PO therapy with doxycycline 100 mg
2 times/day and metronidazole 500 mg 2 times/day
is recommended to complete 14 days of therapy.
Initial IM + PO therapy (similar to above) can be
considered for mild to moderate disease.
Syphilis59,298 (Test for HIV.) Penicillin G regimens provided below are
preferred.59
– Congenital See Ch 2.
– Neurosyphilis (positive CSF VDRL Penicillin G crystalline 200,000–300,000 U/kg/day For adults: penicillin G procaine 2.4 million U IM daily
or CSF pleocytosis with (max 24 million U/day) div q6h for 10–14 days PLUS probenecid 500 mg PO qid, for 10 to 14 days
serologic diagnosis of syphilis) (AIII) OR ceftriaxone 2 g IV daily for 10 to 14 days
– Primary, secondary Penicillin G benzathine 50,000 U/kg (max Follow-up serologic tests at 6, 12, and 24 mo; 15% may
2.4 million U) IM as a single dose (AIII); do not remain seropositive despite adequate treatment.
use benzathine-procaine penicillin mixtures. Alternatives if penicillin-allergic: doxycycline (patients
>7 y) 4.4 mg/kg/day (max 200 mg) PO div bid for
14 days, OR ceftriaxone 1 g daily for 10 days.
CSF examination should be performed for children
being treated for primary or secondary syphilis to
rule out asymptomatic neurosyphilis.
Test for HIV.
– Syphilis lasting for ≤1 y, Penicillin G benzathine 50,000 U/kg Alternative if allergy (nonpregnant) to penicillin:
without clinical symptoms (early (max 2.4 million U) IM ×1 (AIII) doxycycline (patients >7 y) 4.4 mg/kg/day
latent syphilis) (max 200 mg/day) PO div bid for 14 days
– Syphilis lasting for >1 y, without Penicillin G benzathine 50,000 U/kg Alternative if allergy (nonpregnant) to penicillin:
clinical symptoms (late latent (max 2.4 million U) IM weekly for 3 doses (AIII) doxycycline (patients >7 y) 4.4 mg/kg/day
syphilis) or syphilis lasting for (max 200 mg/day) PO div bid for 28 days.
unknown duration Look for neurologic, eye, and aortic complications of
tertiary syphilis.
Trichomoniasis59 Tinidazole 50 mg/kg (max 2 g) PO for 1 dose (BII)
OR metronidazole 500 mg PO bid for 7 days
(preferred for women) OR metronidazole 2 g PO
for 1 dose (BII)
Urethritis, nongonococcal Azithromycin 20 mg/kg (max 1 g) PO for 1 dose, OR Erythromycin, levofloxacin, or ofloxacin
(See Gonorrhea earlier in this doxycycline (patients >7 y) 4.4 mg/kg/day (max Increasing resistance noted in Mycoplasma
table for gonorrhea 200 mg/day) PO div bid for 7 days (AII) genitalium299

2025 Nelson’s Pediatric Antimicrobial Therapy —

therapy.)59,299
Vaginitis60
– Bacterial vaginosis59,300 Metronidazole 500 mg PO bid for 7 days OR Alternative: tinidazole 1 g PO qd for 5 days, OR
metronidazole vaginal gel (0.75%) qd for 5 days, clindamycin 300 mg PO bid for 7 days
OR clindamycin vaginal cream for 7 days Recurrence common; new approaches to prevention of
new infections under study300
Caused by synergy of Gardnerella with anaerobes
– Candidiasis, vulvovaginal59,301 Topical vaginal cream/tabs/suppositories For uncomplicated vulvovaginal candidiasis, no topical
(alphabetic order): butoconazole, clotrimazole, agent is clearly superior.
econazole, fenticonazole, miconazole, For severe acute Candida vulvovaginitis, fluconazole
sertaconazole, terconazole, or tioconazole for (max 150 mg) given q72h for a total of 2 or 3 doses.
3–7 days (AI); OR fluconazole 10 mg/kg (max Avoid azoles during pregnancy.
150 mg) as a single dose (AII) For recurring disease,301 consider 10–14 days of
induction with topical agent or fluconazole, followed
by fluconazole once weekly for 6 mo (AI).
 Antimicrobial Therapy According to Clinical Syndromes

58 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

I. GENITAL AND SEXUALLY TRANSMITTED INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Prepubertal vaginitis302,303
No prospective studies Cultures from symptomatic prepubertal girls are
statistically more likely to yield E coli, enterococcus,
coagulase-negative staphylococci, and streptococci
(viridans streptococcus and group A streptococcus),
but these organisms may also be present in
asymptomatic girls.
Consider the presence of a foreign body.
– Streptococcus, group A304 Penicillin V 50–75 mg/kg/day PO div tid for 10 days Amoxicillin 50–75 mg/kg/day PO div tid

J. CENTRAL NERVOUS SYSTEM INFECTIONS

Clinical Diagnosis Therapy (evidence grade) Comments
Abscess, brain (respiratory tract Until etiology is established, use empiric therapy Surgery for abscesses ≥2 cm in diameter.
flora, skin flora, or bowel flora, for presumed mixed-flora infection with origins For single pathogen abscess, use a single agent in
depending on the pathogenesis from the respiratory tract, skin, and/or bowel, doses that will achieve effective CNS exposure. The
of infection [direct extension or based on individual patient evaluation and risk blood-brain barrier is not intact in brain abscesses.
bacteremia]; rarely for brain abscess. Initial coverage should include If CA-MRSA suspected, ADD vancomycin 60 mg/kg/day
parasitic)305,306 respiratory tract flora (including anaerobes), skin IV div q6–8h ± rifampin 20 mg/kg/day IV div q12h,
flora (including MSSA/MRSA), and bowel flora pending culture results. We have successfully treated
(gram-positive, gram-negative, anaerobes), MRSA intracranial infections with ceftaroline, but no
particularly for children with structural heart prospective data exist.
disease with right-to-left intracardiac shunting. If secondary to chronic otitis, include meropenem or
Many antibiotic combinations will be effective, cefepime in regimen for anti-Pseudomonas activity.
particularly for antibiotics used to treat For enteric GNB, consider ESBL-producing E coli and
meningitis. Klebsiella that are resistant to ceftriaxone and require
meropenem.
 Meropenem 120 mg/kg/day div q8h (AIII); OR Seizure potential is less for meropenem than
nafcillin 150–200 mg/kg/day IV div q6h AND imipenem.
ceftriaxone 100 mg/kg/day IV q24h AND
metronidazole 30 mg/kg/day IV div q8h (BIII); for
2–3 wk after successful drainage (depending on
pathogen, size of abscess, and response to
therapy); longer course if no surgery (3–6 wk)
(BIII). Follow resolution by imaging.
Encephalitis307 (may be infectious or immune-complex mediated, not distinguishable clinically308)
– Amebic (Naegleria fowleri, See Amebiasis in Table 9B.
Balamuthia mandrillaris, and
Acanthamoeba)
– Cytomegalovirus See Cytomegalovirus in Ch 7. Not well studied in Follow quantitative PCR in CSF for CMV DNA.
children. Consider ganciclovir 10 mg/kg/day IV Reduce dose for renal insufficiency. Monitor for
div q12h; for severe immunocompromised, ADD neutropenia.

2025 Nelson’s Pediatric Antimicrobial Therapy —

foscarnet 180 mg/kg/day IV div q8h for 3 wk.
– Enterovirus Supportive therapy; no antivirals currently FDA Pocapavir and pleconaril309 have not been approved by
approved the FDA as of August 2024. Pocapavir can be used
under an expanded access IND, but pleconaril is not
available for compassionate use.

– Epstein-Barr virus310 Not studied in a controlled comparative trial. Follow quantitative PCR in CSF for EBV DNA. Efficacy of
Consider ganciclovir 10 mg/kg/day IV div q12h antiviral therapy not well-defined.
or acyclovir 60 mg/kg/day IV div q8h for 3 wk.
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60 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

J. CENTRAL NERVOUS SYSTEM INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Herpes simplex virus (See
311
Acyclovir 60 mg/kg/day IV as 1- to 2-h infusion div Ongoing study (NCT03084783) to assess the risks/
Ch 2 for neonatal infection.) q8h for 21 days for ≤4 mo; for those >4 mo, benefits of dexamethasone.
45 mg/kg/day IV for 21 days (AIII) Perform CSF HSV PCR near end of 21 days of therapy,
and continue acyclovir until PCR negative.
Safety of high-dosage acyclovir (60 mg/kg/day) not
well-defined beyond the neonatal period; can be
used, but monitor for neurotoxicity and
nephrotoxicity; the FDA has approved acyclovir at
this dosage for encephalitis for children up to 12 y.
Monitor for neutropenia and nephrotoxicity.
– Toxoplasma (See Ch 2 for See Ch 9.
neonatal congenital infection.)
– Arbovirus (flavivirus—Japanese Supportive therapy Investigational only (antiviral, interferon, immune
encephalitis, Zika, West Nile, St globulins).
Louis encephalitis, tick-borne No specific antiviral agents are yet commercially
encephalitis; togavirus—west- available for any of the arboviruses, including Zika or
ern equine encephalitis, eastern West Nile.
equine encephalitis; bunyavirus—
La Crosse encephalitis, California
encephalitis)307,312,313
Meningitis, bacterial, community-associated
NOTES
– Pediatric community-associated bacterial meningitis is quite uncommon in the era of conjugate vaccines. Rare cases caused by non-vaccine
strains of pneumococcus, or occurring in immunocompromised children, may still occur. The incidence of highly resistant pneumococci in
invasive pediatric infections is so low that vancomycin is no longer needed for empiric therapy (toxicity of exposure is no longer justified).
Ceftriaxone resistance is not a public health issue at this time.
– Dexamethasone 0.6 mg/kg/day IV div q6h for 2 days as an adjunct to antibiotic therapy decreases hearing deficits and other neurologic sequelae in
adults and children (for Haemophilus; unproven benefit for pneumococcus; not prospectively studied in children for meningococcus or E coli). The
first dose of de amethasone is gi en before or conc rrent ith the first dose of antibiotic probabl little benefit if gi en ≥1 h after the antibiotic 314
– Empiric therapy315 Ceftriaxone 100 mg/kg/day IV q24h (AII) Vancomycin may not be needed for empiric treatment
of possible pen-R pneumococcus given current,
exceedingly high ceftriaxone susceptibility in North
America.316 The blood barrier is not competent early
in the antibiotic treatment course, allowing increased
penetration as culture/susceptibility results are
pending. The first case of ceftriaxone treatment
failure 30 y ago initially responded to our treatment
with ceftriaxone.317
– Haemophilus influenzae type b315 Ceftriaxone 100 mg/kg/day IV q24h; for 10 days Alternative: ampicillin 200–400 mg/kg/day IV div q6h
in unimmunized children (AI) (for BL-negative strains).
Add dexamethasone (0.6 mg/kg/day IV div q6h) before
or with first dose of antibiotics.
– Meningococcus (Neisseria Penicillin G 250,000 U/kg/day IV div q4h; or Meningococcal prophylaxis: rifampin 10 mg/kg PO
meningitidis)315 ceftriaxone 100 mg/kg/day IV q24h, or q12h for 4 doses OR ceftriaxone 125–250 mg IM once
cefotaxime 200 mg/kg/day IV div q6h; treatment OR ciprofloxacin 500 mg PO once (adolescents and

2025 Nelson’s Pediatric Antimicrobial Therapy —

course for 7 days (AI) adults)
– Neonatal See Ch 2.
– Pneumococcus For pen-S and cephalosporin-susceptible strains: Some pneumococci may be resistant to penicillin but
(S pneumoniae)315,316 penicillin G 250,000 U/kg/day IV div q4–6h, OR still be susceptible to ceftriaxone and may be treated
ceftriaxone 100 mg/kg/day IV q24h; for 10 days with the cephalosporin alone. In parts of the world
(AI). without widespread use of conjugate pneumococcal
For pen-R pneumococci (assuming ceftriaxone vaccines, with widespread penicillin- and
susceptibility): continue ceftriaxone IV for total ceftriaxone-resistant strains, add vancomycin to
course (AIII). ceftriaxone pending cultures and susceptibilities.
With the efficacy of current pneumococcal conjugate
vaccines, primary bacterial meningitis is uncommon,
and penicillin resistance for all invasive
pneumococcal infections has decreased substantially.
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62 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

J. CENTRAL NERVOUS SYSTEM INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Meningitis, TB (M tuberculosis; For non-immunocompromised children: INH M bovis strains are intrinsically resistant to PZA.
M bovis)16 15 mg/kg/day PO, IV div q12–24h AND rifampin Instead of streptomycin, amikacin or kanamycin can be
20–30 mg/kg/day PO, IV div q12–24h for 12 mo used. Aminoglycosides are rapidly bactericidal for
AND PZA 30 mg/kg/day PO div q12–24h for first mycobacteria.
2 mo of therapy, AND streptomycin 30 mg/kg/ Ethionamide is used to ensure multidrug coverage and
day IV, IM div q12h or ethionamide or can be stopped if strain is fully susceptible to usual
moxifloxacin/levofloxacin for first 4–8 wk of therapy.
therapy; followed by INH and rifampin Hyponatremia from inappropriate ADH secretion is
combination therapy to complete at least common; ventricular drainage may be necessary for
12 mo for the total course. Streptomycin or obstructive hydrocephalus.
ethionamide is used instead of ethambutol in Administer corticosteroids (can use same
children, primarily infants, who have this dexamethasone dose as for bacterial meningitis,
infection. 0.6 mg/kg/day IV div q6h) for 4 wk until
neurologically stable, then taper dose for 1–3 mo to
decrease neurologic complications and improve
prognosis by decreasing incidence of infarction.318
Watch for rebound CNS inflammation during taper; if
present, then increase dose to previously effective
level, then taper more slowly.
For recommendations for drug-resistant strains and
treatment of TB in HIV-infected patients, visit the CDC
website for TB: www.cdc.gov/tb (accessed September
12, 2024).
Shunt infections: The use of antibiotic-impregnated shunts has decreased the frequency of this infection.319 Shunt removal is usually necessary
for cure, with placement of a new external ventricular drain; intraventricular injection of antibiotics should be considered in children responding
poorly to systemic antibiotic therapy. Duration of therapy varies by pathogen and response to treatment.315
– Empiric therapy pending Gram Vancomycin 60 mg/kg/day IV div q8h, AND If Gram stain shows only gram-positive cocci, can start
stain and culture315,320 cefepime 50 mg/kg IV q8h (AII) with vancomycin alone.
For ESBL-containing GNB, meropenem should be used
as the preferred carbapenem for CNS infection.
– Staphylococcus epidermidis or Vancomycin (for S epidermidis and CA-MRSA) For children who cannot tolerate vancomycin,
Staphylococcus aureus315,320 60 mg/kg/day IV div q8h; OR nafcillin (if ceftaroline has anecdotally been successful:
organisms susceptible) 150–200 mg/kg/day ceftaroline320: 2–<6 mo, 30 mg/kg/day IV div q8h
AND rifampin; for 10–14 days (AIII) (each dose given over 2 h); ≥6 mo, 45 mg/kg/day IV
div q8h (each dose given over 2 h) (max single dose
600 mg) (BIII). Linezolid, daptomycin, and TMP/SMX
are other untested options.
– Gram-negative bacilli315 Empiric therapy with meropenem 120 mg/kg/day Remove shunt. Select appropriate therapy based on in
IV div q8h OR cefepime 150 mg/kg/day IV div vitro susceptibilities.
q8h (AIII) Meropenem, ceftriaxone, and cefepime have all been
For E coli (without ESBLs): ceftriaxone 100 mg/kg/ studied in pediatric meningitis.
day IV q12h for at least 14 days but preferably Systemic gentamicin as combination therapy is not

2025 Nelson’s Pediatric Antimicrobial Therapy —

21 days routinely recommended with carbapenems and
cefepime.
Intrathecal therapy with aminoglycosides not routinely
necessary with highly active β-lactam therapy and
shunt removal.
See Ch 12.
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64 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

K. URINARY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
NOTE: Antibiotic susceptibility profiles of E coli, the most common cause of UTI, vary considerably. Check your local microbiology laboratory for
susceptibilities from urinary tract isolates in your clinic (community-acquired) and your hospital (nosocomially acquired). For mild disease, TMP/
SMX may be initial empiric therapy if local susceptibility is ≥80%, and up to a 20% failure rate is acceptable. Amoxicillin resistance in most
communities is >50%. For moderate to severe disease (possible pyelonephritis), obtain cultures and begin a PO 2nd- or 3rd-generation
cephalosporin (cefuroxime, cefaclor, cefprozil, cefixime, ceftibuten, cefdinir, cefpodoxime), ciprofloxacin PO, or ceftriaxone IM. Given the high
urine concentrations demonstrated by β-lactam antibiotics (penicillins, cephalosporins, carbapenems), and the fact that susceptibility reporting
from the microbiology laboratory may be based on achievable serum concentrations, not urine concentrations, situations may exist for which an
antibiotic that is reported as R (resistant) will actually be effective therapy and easily achieve concentrations in urine (100-fold higher than
serum) that can inhibit pathogens to cure an infection.321 Although we are reluctant to recommend an antibiotic that the laboratory reports as R,
if your patient is improving on your empiric treatment, it is reasonable to continue that treatment and follow the progress closely. In that context,
cephalexin may be more effective against E coli for UTI than one might expect from the hospital antibiogram report based on serum
concentrations. Antibiotic susceptibility testing will help direct you to the most narrow-spectrum agent.
Cystitis, acute (E coli)322,323 For mild to moderate disease: TMP/SMX 8 mg/kg/ Alternative: amoxicillin 30–45 mg/kg/day PO div tid OR
day of TMP PO div bid for 3 days (see NOTE amox/clav PO if susceptible (BII); ciprofloxacin
above about resistance rates to TMP/SMX), OR 20–30 mg/kg/day PO div bid for suspected or
cephalexin 50–75 mg/kg/day div q8–12h. documented resistant (including ESBL-producing)
In children with moderate to severe disease, it is organisms for both cystitis and complicated UTI.324
often difficult to distinguish between upper tract Ciprofloxacin is approved for complicated UTIs for
and lower tract infections: cefixime 8 mg/kg/day children ≥12 mo.
PO qd; OR ceftriaxone 50 mg/kg IM q24h for Gentamicin is another option with excellent activity
3–5 days (with normal anatomy) (BII); but narrow against community strains of E coli, but it is only IM
the spectrum of antibiotic, if possible, based on or IV and is nephrotoxic.
urine culture data. For children who do not
respond to treatment, obtain follow-up culture
after 36–48 h. Routine follow-up cultures of urine
are not needed for the child who responds to
treatment.
Nephronia, lobar Ceftriaxone 50 mg/kg/day IV, IM q24h. Nephronia, a complication of pyelonephritis, is an
Escherichia coli and other enteric Duration depends on resolution of renal cellulitis invasive, consolidative parenchymal infection; it can
rods (also called “focal bacterial vs development of abscess (10–21 days) (AIII). evolve into renal abscess. Step-down therapy with
nephritis”)325,326 For ESBL-positive E coli, carbapenems and FQs PO cephalosporins once cellulitis/abscess has initially
are often active agents. responded to therapy.
Pyelonephritis, acute Ceftriaxone 50 mg/kg/day IV, IM q24h OR For mild to moderate infection, shorter courses and PO
(E coli)196,322–324,327–331 gentamicin 5–6 mg/kg/day IV, IM q24h (yes, qd). therapy are likely to be as effective as IV/IM therapy
For documented or suspected ceftriaxone-resistant for a standard duration of 7–14 days, for susceptible
ESBL-positive strains, use meropenem IV, strains, down to 3 mo of age.327,328,330
imipenem IV, or ertapenem IV196,328,329; OR In children, it is often difficult to distinguish between
gentamicin IV/IM OR TOL/TAZ. upper tract and lower tract infections.
Switch to PO therapy following clinical response If bacteremia documented and infant <2–3 mo, rule
(BII). If organism resistant to amoxicillin and out meningitis and treat 10–14 days IV + PO (AIII).
TMP/SMX, use a PO 1st-, 2nd-, or 3rd-generation Aminoglycosides at any dose are more nephrotoxic
cephalosporin (BII); if cephalosporin-R or for than β-lactams but represent effective therapy (AI).
Pseudomonas, can use ciprofloxacin PO 30 mg/ For dosing of gentamicin, qd is preferred to tid.327
kg/day div q12h (up to 40 mg/kg/day)324 (BIII); The duration of treatment is a function of the extent of

2025 Nelson’s Pediatric Antimicrobial Therapy —

for 7–14 days total (depending on response to infection (with potential renal abscess formation in
therapy). severe pyelonephritis); no prospective data collection
See Ch 12. has addressed the extent of infection at the time of
diagnosis. Early renal cellulitis should respond to
5–7 days of therapy; renal abscesses may take
≥14 days to resolve.328
 Antimicrobial Therapy According to Clinical Syndromes

66 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

K. URINARY TRACT INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Recurrent UTI, Only for those with grade III–V reflux or with Prophylaxis is not recommended for patients with
prophylaxis322,330,332–335 recurrent febrile UTI: TMP/SMX 2 mg/kg/dose of grade I–II reflux and no evidence of renal damage
TMP PO qd OR nitrofurantoin 1–2 mg/kg PO qhs; (although the RIVUR study334 included these children,
more rapid resistance may develop by using and they may also benefit), but early treatment of
β-lactams (BII). new infection is recommended for these children.
Cranberries can prevent UTI.333
Resistance eventually develops to every antibiotic; follow
resistance patterns for each patient. The use of
periodic urine cultures is controversial, as there are
no comparative data to guide management of
asymptomatic bacteriuria in a child at high risk for
recurrent UTI.
Although one can prevent febrile UTIs, it is not clear
that one can prevent renal scar formation.336

L. MISCELLANEOUS SYSTEMIC INFECTIONS

Clinical Diagnosis Therapy (evidence grade) Comments
Actinomycosis337–339 Penicillin G 250,000 U/kg/day IV div q6h, OR ampicillin Surgery with debridement as indicated.
150 mg/kg/day IV div q8h until improved (often up Alternatives: amoxicillin, doxycycline (for children
to 6 wk for extensive infection); then long-term >7 y), clarithromycin, erythromycin, ceftriaxone
convalescent therapy with penicillin V 100 mg/kg/ IM/IV, or meropenem IV.
day (up to 4 g/day) PO for 6–12 mo (AII) Long-term therapy is needed to prevent relapse.
Anaplasmosis340,341 (human Doxycycline 4.4 mg/kg/day IV, PO (max 200 mg/day) No contraindication for doxycycline treatment in
granulocytotropic anaplasmosis, div bid for 7–10 days (regardless of age) (AIII) ANY age-group. For mild disease, consider
Anaplasma phagocytophilum) rifampin 20 mg/kg/day PO div bid for 7–10 days
(BIII)
Anthrax, sepsis/pneumonia, For community-associated anthrax infection, For invasive infection after bioterror exposure,
community vs bioterror amoxicillin 75 mg/kg/day div q8h OR doxycycline for 2 or 3 antibiotics may be required.17
exposure (inhalation, children >7 y For PO step-down therapy, can use PO
cutaneous, GI, For bioterror-associated exposure (regardless of age): ciprofloxacin or doxycycline; if susceptible, can
meningoencephalitis)17 ciprofloxacin 20–30 mg/kg/day IV div q12h, OR use penicillin, amoxicillin, or clindamycin.
levofloxacin 16 mg/kg/day IV div q12h not to exceed May require long-term PEP after bioterror event
250 mg/dose (AIII); OR doxycycline 4.4 mg/kg/day PO due to inhalation of spores that have not yet
(max 200 mg/day) div bid germinated and to ongoing exposure to spores
in the environment that was exposed.
Appendicitis (See Appendicitis, bowel-associated, in Table 1H under Intra-abdominal infection.)
Brucellosis342,343 Doxycycline 4.4 mg/kg/day PO (max 200 mg/day) div Combination therapy with rifampin will decrease
bid (for children >7 y) AND rifampin (15–20 mg/kg/ the risk of relapse. For more serious infections,
day div q12h) (BIII); OR for children <8 y: TMP/SMX ADD gentamicin 6.0–7.5 mg/kg/day IV, IM div
10 mg/kg/day of TMP IV, PO div q12h AND rifampin q8h for the first 1–2 wk of therapy to further
15–20 mg/kg/day div q12h (BIII); for at least 6 wk decrease risk of relapse (BIII), particularly for
endocarditis, osteomyelitis, or meningitis.

2025 Nelson’s Pediatric Antimicrobial Therapy —

Prolonged treatment for 4–6 mo and surgical
debridement may be necessary for deep
infections (AIII).
Cat-scratch disease (Bartonella Supportive care for adenopathy (I&D of infected lymph This dosage of azithromycin has been documented
henselae)344–346 node); azithromycin 12 mg/kg/day PO qd for 5 days to be safe and effective for strep pharyngitis and
shortens the duration of adenopathy (AIII). may offer greater deep tissue exposure than the
No prospective data exist for invasive CSD: gentamicin dosage used in early studies8 and used for otitis
(for 14 days) AND TMP/SMX AND rifampin for media.
hepatosplenic disease and osteomyelitis (AIII). For Alternatives: ciprofloxacin, doxycycline.
CNS infection, use ceftriaxone AND gentamicin
± TMP/SMX (AIII).
Chickenpox/shingles (VZV) See Varicella-zoster virus in Ch 7.
COVID-19 (acute SARS-CoV-2 See Coronavirus (SARS-CoV-2) in Table 7C.
infection)
 Antimicrobial Therapy According to Clinical Syndromes

68 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

L. MISCELLANEOUS SYSTEMIC INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Ehrlichiosis (human monocytic Doxycycline 4.4 mg/kg/day IV, PO div bid (max 100 mg/ For mild disease, consider rifampin 20 mg/kg/day
ehrlichiosis, caused by Ehrlichia dose) for 7–10 days (regardless of age) (AIII) PO div bid (max 300 mg/dose) for 7–10 days
chaffeensis, and Ehrlichia (BIII).
ewingii)340,341,347,348
Febrile, neutropenic patient Cefepime 150 mg/kg/day div q8h (AI); OR meropenem Alternatives: other anti-Pseudomonas β-lactams
(empiric therapy for invasive 60 mg/kg/day div q8h (AII); OR PIP/TAZO (300 mg/ (imipenem) AND antistaphylococcal antibiotics,
infection: Pseudomonas, enteric kg/day PIP component div q8h for infants/children including ceftaroline for MRSA.
GNB, staphylococci, >9 mo; 240 mg/kg/day div q8h for infants 2–9 mo), If no response within 72–96 h and no alternative
streptococci, yeast, OR ceftazidime 150 mg/kg/day IV div q8h AND etiology demonstrated, begin additional empiric
fungi)176,349–352 tobramycin 6 mg/kg/day IV q8h (AII). therapy with antifungals (BII)176; dosages and for-
ADD vancomycin 40 mg/kg/day IV div q8h if clinically mulations outlined in Ch 5.
unstable, or MRSA or coagulation-negative staph Increasingly resistant pathogens (ESBL E coli and
infection suspected (eg, central catheter infection) KPC Klebsiella) will require alternative empiric
(AIII). therapy if MDR organisms are colonizing the
ADD metronidazole to ceftazidime or cefepime if patient, caused a previous infection in the child,
colitis, head/neck space infection, or other deep or present on the child’s hospital unit.
anaerobic infection suspected (AIII). For low-risk patients with negative cultures and
close follow-up, alternative management
strategies have been explored: PO therapy with
amox/clav and ciprofloxacin may be used, with
cautious discontinuation of antibiotics (even in
those without marrow recovery).176,353
HIV infection See Ch 7.
Infant botulism354 Botulism immune globulin for infants (BabyBIG) See www.infantbotulism.org for information for
50 mg/kg IV for 1 dose (AI); BabyBIG can be obtained physicians and parents. Website organized by the
from the California Department of Public Health at California Department of Public Health (accessed
www.infantbotulism.org, through your state health September 12, 2024).
department. Aminoglycosides should be avoided because they
potentiate the neuromuscular effect of botulinum
Kawasaki syndrome355–358 No antibiotics; IVIG 2 g/kg as a single dose (AI)359; may Aspirin 80–100 mg/kg/day div qid in acute febrile
need to repeat dose in up to 15% of children for phase; once afebrile for 24–48 h, high-dose
persisting fever that lasts 24 h after completion of aspirin may no longer add benefit, but dose is
the IVIG infusion (AII). Corticosteroids as primary changed to low-dose antiplatelet therapy.
adjunctive therapy in the acute phase of Kawasaki Role of corticosteroids, anakinra, infliximab, etaner-
syndrome can be associated with reduced coronary cept, calcineurin inhibitors, and antithrombotic
artery abnormalities, reduced inflammatory markers, therapy, as well as methotrexate, for IVIG-resistant
and shorter duration of hospital stay when compared Kawasaki syndrome is under investigation, and
to no corticosteroids.356,357 Consult an ID physician, a some interventions are likely to improve outcome
rheumatologist, or a pediatric cardiologist. in severe cases.357–360 Infliximab may decrease
Adjunctive therapy with corticosteroids for those at acute symptoms in patients whose IVIG fails but
high risk for the development of aneurysms.356,357 may not decrease the risk for coronary artery
abnormalities. Similar findings were noted with
another tumor necrosis factor inhibitor, etaner-
cept, in the overall population, although subsets
of children within the study may have benefited.
Leprosy (Hansen disease)361 Dapsone 1 mg/kg/day PO qd AND rifampin Consult the HRSA National Hansen’s Disease

2025 Nelson’s Pediatric Antimicrobial Therapy —

10 mg/kg/day PO qd; ADD (for multibacillary disease) (Leprosy) Program at www.hrsa.gov/
clofazimine 1 mg/kg/day PO qd; for 12 mo for hansens-disease (reviewed August 2024;
paucibacillary disease; for 24 mo for multibacillary accessed September 12, 2024) for advice about
disease (AII). treatment and free antibiotics: 800-642-2477.
Leptospirosis362,363 Penicillin G 250,000 U/kg/day IV div q6h, OR ceftriax- Alternative: for those with mild disease, intolerant
one 50 mg/kg/day IV, IM q24h; for 7 days (BII) of doxycycline, azithromycin 20 mg/kg on day 1,
For mild disease in all age-groups, doxycycline 10 mg/kg for days 2 and 3, or amoxicillin
(>7 y) 4.4 mg/kg/day (max 200 mg/day) PO div bid
for 7–10 days (BII)
Lyme disease (Borrelia Neurologic evaluation, including LP, if there is clinical
burgdorferi)364,365 suspicion of CNS involvement
– Early localized disease Doxycycline 4.4 mg/kg/day (max 200 mg/day) PO div Alternative: cefuroxime, 30 mg/kg/day (max
(erythema migrans, single or bid for 10 days for all ages (AII) OR amoxicillin 50 mg/ 1,000 mg/day) PO, in 2 div doses for 14 days OR
multiple) (any age) kg/day (max 1.5 g/day) PO div tid for 14 days (AII) azithromycin 10 mg/kg/day PO qd for 7 days
 Antimicrobial Therapy According to Clinical Syndromes

70 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

L. MISCELLANEOUS SYSTEMIC INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
– Arthritis (no CNS disease) PO therapy as outlined in early localized disease but for Persistent or recurrent joint swelling after
28 days (AIII) treatment: repeat a 4-wk course of PO antibiotics
or give ceftriaxone 50–75 mg/kg IV q24h for
14–28 days.
For persisting arthritis after 2 defined antibiotic
treatment courses, use symptomatic therapy.
– Isolated facial (Bell) palsy Doxycycline as outlined in early localized disease, for LP is not routinely required unless CNS symptoms
14 days (AIII); efficacy of amoxicillin unknown develop. Treatment to prevent late sequelae; will
not provide a quick response for palsy.
– Carditis PO therapy as outlined in early localized disease,
for 14 days (range 14–21 days) OR ceftriaxone
50–75 mg/kg IV q24h for 14 days (range 14–21 days)
(AIII)
– Neuroborreliosis Doxycycline 4.4 mg/kg/day (max 200 mg/day) PO div
bid for 14–21 days (AII) OR ceftriaxone 50–75 mg/kg
IV q24h OR penicillin G 300,000 U/kg/day IV div q4h;
for 14–21 days (AIII)
Melioidosis (Burkholderia Acute sepsis: meropenem 75 mg/kg/day div q8h; OR Alternative convalescent therapy: amox/clav
pseudomallei)366,367 ceftazidime 150 mg/kg/day IV div q8h; followed by (90 mg/kg/day of amox div tid, not bid) for
TMP/SMX (10 mg/kg/day of TMP) PO div bid for children ≤7 y, or doxycycline for children >7 y;
3–6 mo for 20 wk (AII).
MDR strains may be susceptible to cefiderocol IV.
Mycobacteria, nontuberculous9,11,12,197
– Adenitis in normal host (See Excision usually curative (BII); azithromycin PO OR Antibiotic susceptibility patterns are quite variable;
Adenitis entries in Table 1A.) clarithromycin PO for 6–12 wk (with or without cultures should guide therapy; medical therapy
rifampin or ethambutol) if susceptible (BII) is 60%–70% effective. Data suggest that toxicity
of antimicrobials may not be worth the small
clinical benefit.
For more resistant organisms, other antibiotics may
be active, including TMP/SMX, FQs, doxycycline,
or, for parenteral therapy, amikacin, meropenem,
or cefoxitin. See Ch 3 for specific mycobacterial
pathogens.
– Pneumonia or disseminated The more severe the infection, the more aggressive the Outcomes particularly poor for Mycobacterium
infection in normal or treatment: usually treated with 3 or 4 active drugs abscessus.369,370
compromised hosts (HIV, (eg, clarithromycin OR azithromycin, AND See Ch 18 for dosages; cultures are essential, as the
IFN-γ receptor deficiency, ethambutol, AND amikacin, cefoxitin, or susceptibility patterns of nontuberculous
CF)11,197,368,369 meropenem). Also test for ciprofloxacin, TMP/SMX, mycobacteria are varied.

2025 Nelson’s Pediatric Antimicrobial Therapy —

rifampin, linezolid, clofazimine, and doxycycline (BII).
Nocardiosis (Nocardia asteroides TMP/SMX 8 mg/kg/day of TMP div bid or sulfisoxazole Wide spectrum of disease, from skin lesions to
and Nocardia brasiliensis)371,372 120–150 mg/kg/day PO div qid for ≥6–12 wk. For brain abscess.
severe infection, particularly in immunocompromised Surgery when indicated.
hosts, IN ADDITION to TMP/SMX, use amikacin 15– Alternatives: doxycycline (for children >7 y), amox/
20 mg/kg/day IM, IV div q8h OR imipenem or clav, or linezolid.
meropenem (not ertapenem) (AIII). For susceptible Immunocompromised children may require
strains, ceftriaxone. months of therapy.
 Antimicrobial Therapy According to Clinical Syndromes

72 — Chapter 1. Antimicrobial Therapy According to Clinical Syndromes

L. MISCELLANEOUS SYSTEMIC INFECTIONS
Clinical Diagnosis Therapy (evidence grade) Comments
Plague (Yersinia pestis) 373–375
Gentamicin 7.5 mg/kg/day IV div q8h (AII) OR A complete listing of treatment options and doses
doxycycline 4.4 mg/kg/day (max 200 mg/day) PO div for children is provided on the CDC website
bid OR ciprofloxacin 30 mg/kg/day PO div bid. (www.cdc.gov/plague/about/index.html;
Gentamicin is poorly active in abscesses; consider accessed September 12, 2024).
alternatives for bubonic plague.
Q fever (Coxiella burnetii)376,377 Acute stage: doxycycline 4.4 mg/kg/day (max 200 mg/ Follow doxycycline and hydroxychloroquine serum
day) PO div bid for 14 days (AII) for children of any age. concentrations during endocarditis/chronic
Endocarditis and chronic disease (ongoing symptoms disease therapy.
for 6–12 mo): doxycycline for children >7 y AND CNS: use FQ (no prospective data) (BIII).
hydroxychloroquine for 18–36 mo (AIII). Clarithromycin may be an alternative based on
Seek advice from pediatric ID specialist for children limited data (CIII).
≤7 y: may require TMP/SMX 8–10 mg/kg/day of TMP
div q12h with doxycycline; OR levofloxacin with
rifampin for 18 mo.
Rocky Mountain spotted Doxycycline 4.4 mg/kg/day (max 200 mg/day) PO div Start empiric therapy early.
fever (fever, petechial rash with bid for 7–10 days (AI) for children of any age
centripetal spread; Rickettsia
rickettsii)378,379
Tetanus (Clostridium tetani)380,381 Metronidazole 30 mg/kg/day IV, PO div q8h OR Wound debridement essential; may infiltrate
penicillin G 100,000 U/kg/day IV div q6h for wound with a portion of TIG dose, but not well
10–14 days; AND TIG 500 U IM (AII) studied; IVIG may provide antibody to toxin if TIG
not available.
Immunize with Td or Tdap.
See Ch 15 for prophylaxis recommendations.
Toxic shock syndrome Empiric: oxacillin/nafcillin 150 mg/kg/day IV div q6h Clindamycin added for the initial 48–72 h of
(toxin-producing strains of AND vancomycin 45 mg/kg/day IV div q8h (for therapy to decrease toxin production.
S aureus, including MRSA, or MRSA); OR ceftaroline single-drug therapy (MSSA/ Ceftaroline is an option for MRSA treatment,
group A streptococcus)3,6,7,382,383 MRSA): 2 mo–<2 y, 24 mg/kg/day IV div q8h; ≥2 y, particularly with renal injury from shock and
36 mg/kg/day IV div q8h (max single dose 400 mg); vancomycin (BIII).
>33 kg, either 400 mg/dose IV q8h or 600 mg/dose IVIG may provide additional benefit by binding
IV q12h (BI) AND clindamycin 30–40 mg/kg/day div circulating toxin (CIII).
q8h (to decrease toxin production) for 7–10 days For MSSA: oxacillin/nafcillin AND clindamycin
(AIII) ± gentamicin.
For CA-MRSA: ceftaroline (or vancomycin) AND
clindamycin ± gentamicin.
For group A streptococcus: penicillin G AND
clindamycin.
Tularemia (F tularensis)185,384 Gentamicin 6.0–7.5 mg/kg/day IM, IV div q8h; for Doxycycline as an alternative, although relapse
10–14 days (AII) rates may be higher than with other antibiotics.
Alternative for mild disease: ciprofloxacin (for 10 days) See www.cdc.gov/tularemia/hcp/clinical-care/
index.html (accessed October 14, 2024).

2025 Nelson’s Pediatric Antimicrobial Therapy —

 2025 Nelson’s Pediatric Antimicrobial Therapy — 75

Antimicrobial Therapy for Neonates

OTES
2
A list of table abbreviations and acronyms can be found at the start of this publication.

Antimicrobial Therapy for Neonates

Prospectively collected neonatal antimicrobial pharmacokinetic (PK), safety, and
efficacy data continue to become available, thanks in large part to federal legislation
(especially the US Food and Drug Administration [FDA] Safety and Innovation Act of
2012 that mandates neonatal studies). In situations of inadequate data, suggested doses
in this chapter are based on efficacy, safety, and pharmacologic data from older chil-
dren or adults. These may not account for the effect of developmental changes (effect
of ontogeny) on drug metabolism and, hence, are not optimal, particularly for the
unstable preterm neonate.1
For those drugs with an intramuscular (IM) route, an assumption is being made that
the IM absorption in neonates is similar to that in older children or adults in whom
that route has been better studied. The IM and intravenous (IV) routes are not equiva-
lent. The IM route is reasonable as post-initial IV therapy in hemodynamically stable
neonates with difficult-to-maintain IV access whose infection has been microbiologi-
cally controlled and who are clinically recovering.
Oral (PO) convalescent therapy for neonatal infections has not been well studied but
may be used cautiously in non–life-threatening infections in adherent families with
ready access to medical care.2,3
Substitution for cefotaxime in neonates and very young infants: Since 2018, US
pharmaceutical companies have discontinued manufacturing and marketing cefo-
taxime. The FDA is allowing importation of cefotaxime from a Canadian distributor
(877-404-3338). For centers without cefotaxime readily available, we are recommend-
ing the following 3 agents as substitutes:
eftazidime has evidence supporting use and is FDA approved for neonates. The FDA-
pproved dosage differs from what we are recommending in Table 2B.
efepime has been FDA approved for infants 2 months and older and for children
nce 1999. Although neonatal PK and safety studies have been published, the original
anufacturer did not seek approval from the FDA for neonates and infants younger than
months, so the FDA has not evaluated data or approved cefepime for neonates. Both
fepime and ceftazidime have activity against gram-negative bacilli, including Pseudo-
onas aeruginosa, and against Neisseria meningitidis, and both would be expected to
enetrate neonatal cerebrospinal fluid to treat neonatal meningitis. Cefepime is more
tive in vitro against enteric bacilli (Escherichia coli) and Pseudomonas than ceftazidime
nd is stable against ampC β-lactamase often expressed by enteric bacilli, most often
nterobacter cloacae, Klebsiella aerogenes, and Citrobacter freundii. Cefepime is stable
many, but not all, extended-spectrum β-lactamases (ESBLs), although it is routinely
ported as resistant to ESBL-containing gram-negative bacteria. Cefepime also has more
 — Chapter 2. Antimicrobial Therapy for Neonates

vitro activity than ceftazidime against some gram-positive bacteria such as group B
reptococci and methicillin-susceptible Staphylococcus aureus. There are no meaningful
fferences in the safety profiles or therapeutic monitoring of cefepime and ceftazidime.4
eftriaxone is FDA approved for neonates with the following 2 caveats:
1. N
 eonates with hyperbilirubinemia should not be treated with ceftriaxone due to the
potential for ceftriaxone to displace albumin-bound bilirubin, creating more free
bilirubin that can diffuse into the brain and increase the risk for kernicterus. Our
recommendation is to avoid ceftriaxone in any at-risk neonates with hyperbilirubi-
nemia, particularly those who are unstable or acidotic and particularly preterm neo-
nates and infants up to a postmenstrual age of 41 weeks (gestational + chronologic
age).5 Full-term neonates and infants with total bilirubin concentrations less than
10 mg/dL and falling (usually older than 1 week) may be considered for treatment,
but no prospective data exist to support this bilirubin cutoff.6
 eftriaxone is contraindicated in neonates younger than 28 days if they require
2. C
concomitant treatment with calcium-containing IV solutions. Neonates should not
receive IV ceftriaxone while receiving IV calcium-containing products, including
parenteral nutrition, by the same or different infusion catheters. Fatal reactions with
ceftriaxone-calcium precipitates in lungs and kidneys in neonates have occurred.
There are no data on interactions between IV ceftriaxone and PO calcium-
containing products or between IM ceftriaxone and IV or PO calcium-containing
products.7
A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
Conjunctivitis
– Chlamydial8–11 Azithromycin 10 mg/kg/day PO for 1 day, Macrolides PO preferred to topical eye drops to prevent development
then 5 mg/kg/day PO for 4 days (AII), or of pneumonia; association of macrolides and pyloric stenosis in
erythromycin ethylsuccinate PO for young neonates.12
10–14 days (AII) Alternative: 3-day course of higher-dose azithromycin at 10 mg/kg/
dose qd, although safety not well-defined in neonates (CIII).
PO sulfonamides may be used after the immediate neonatal period for
infants who do not tolerate erythromycin.
– Gonococcal13–17 Ceftriaxone 25–50 mg/kg (max 250 mg) IV, For adults, ceftriaxone in higher doses is recommended as
IM once (AIII) single-agent therapy.
Ceftriaxone should be used for neonates with no risk for
hyperbilirubinemia5 or IV calcium-drug interactions.7 Cefotaxime or

2025 Nelson’s Pediatric Antimicrobial Therapy —

cefepime is preferred for neonates with hyperbilirubinemia5 and
those with risk for calcium-drug interactions (see Notes).
Saline irrigation of eyes.
Evaluate for chlamydial infection if maternal chlamydial infection not
excluded.
All neonates born to mothers with untreated gonococcal infection
(regardless of symptoms) require therapy. Cefixime and
ciprofloxacin not recommended for maternal empiric therapy.
– Staphylococcus Topical therapy is sufficient for mild S aureus Aminoglycoside ophth drops or oint, polymyxin/TMP drops
aureus18–20 cases (AII), but PO or IV therapy may be No prospective data for MRSA conjunctivitis (BIII)
considered for moderate to severe Cephalexin PO for mild to moderate disease caused by MSSA
conjunctivitis. Increased S aureus resistance with ciprofloxacin/levofloxacin ophth
MSSA: oxacillin/nafcillin IV or cefazolin (for formulations (AII)
non-CNS infections) IM, IV for 7 days.
MRSA: vancomycin IV or ceftaroline IV.
 Antimicrobial Therapy for Neonates

78 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Pseudomonas Cefepime/ceftazidime IV or tobramycin/ Aminoglycoside or polymyxin B–containing ophth drops or oint as
aeruginosa21–23 gentamicin IV, IM for 7–10 days adjunctive therapy
(alternatives: meropenem, PIP/TAZO,
amikacin) (BIII)
– Other gram-negative Aminoglycoside or polymyxin B–containing Duration of therapy dependent on clinical course and may be as short
ophth drops or oint if mild (AII) as 5 days if clinically resolved
Systemic therapy if moderate to severe or
unresponsive to topical therapy (AIII)
Cytomegalovirus
– Congenital24–28 For moderately to severely symptomatic Benefit for hearing loss and neurodevelopmental outcomes (AI).
neonates with congenital CMV disease: PO Treatment recommended for neonates with either moderate to severe
valganciclovir at 16 mg/kg/dose bid for symptomatic congenital CMV disease (with or without CNS
6 mo27 (AI); IV ganciclovir at 6 mg/kg/dose involvement) or isolated sensorineural hearing loss. Note that the
q12h can be used for some or all of the durations of therapy differ for these, with 6 mo recommended for the
first 6 wk of therapy if PO therapy not former and 6 wk recommended for the latter. Ideally, treatment
advised but provides no added benefit should start within 1 mo; treatment after age 1 mo did not improve
over PO valganciclovir (AII).29 An “induction hearing outcomes in clinical trials (AIII).28
period” starting with IV ganciclovir is not Treatment is not routinely recommended for “mildly symptomatic”
recommended if PO valganciclovir can be neonates congenitally infected with CMV (eg, only 1 or perhaps
tolerated. 2 manifestations of congenital CMV infection, which are mild in scope
For isolated sensorineural hearing loss [eg, isolated IUGR, mild hepatomegaly] or transient and mild in
secondary to congenital CMV infection: PO nature [eg, a single platelet count of 80,000 μL or an ALT of 130 U/L,
valganciclovir at 16 mg/kg/dose bid for with these numbers serving only as examples]), as the risks of
6 wk (AI).30 treatment may not be balanced by benefits in mild disease.28
 Treatment for asymptomatic neonates congenitally infected with CMV
should not be given.
Neutropenia develops in 20% (PO valganciclovir) to 68% (IV ganciclovir)
of neonates receiving long-term therapy (responds to G-CSF or
temporary discontinuation of therapy).
CMV-IVIG not recommended for infants.
– Perinatally or Ganciclovir 12 mg/kg/day IV div q12h for Antiviral treatment has not been studied in this population but can be
postnatally acquired26 14–21 days (AIII) considered in patients with acute, severe visceral (end-organ)
disease, such as pneumonitis, hepatitis, encephalitis, NEC, or
persistent thrombocytopenia. If such patients are treated with
parenteral ganciclovir, a reasonable approach is to treat for 2 wk and
then reassess responsiveness to therapy. If clinical and laboratory
data suggest benefit of treatment, an additional 1 wk of parenteral
ganciclovir can be considered if symptoms and signs have not fully
resolved. PO valganciclovir is not recommended in these more
severe disease manifestations. Observe for possible relapse after
completion of therapy (AIII).

2025 Nelson’s Pediatric Antimicrobial Therapy —

 Antimicrobial Therapy for Neonates

80 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
Fungal infections (See also Ch 5.)
– Candidiasis31–40 Treatment Neonates have high risk for urinary tract and CNS infections,
AmB-D (1 mg/kg/day) is recommended problematic for echinocandins with poor penetration at those sites;
therapy (AII). therefore, AmB-D is preferred, followed by fluconazole.
Fluconazole (25 mg/kg on day 1, then Echinocandins are discouraged, despite their fungicidal activity.
12 mg/kg q24h) is an alternative if the Infants with invasive candidiasis should be evaluated for other sites of
patient has not been receiving fluconazole infection: CSF analysis, echocardiogram, abdominal ultrasound to
prophylaxis (AII).41 include bladder, retinal eye examination (AIII).
For treatment of neonates and young infants CT or ultrasound imaging of genitourinary tract, liver, and spleen
(<120 days) receiving ECMO, fluconazole should be performed if blood culture results are persistently positive
LD is 35 mg/kg on day 1, then 12 mg/kg (AIII).
q24h (BII).42 Meningoencephalitis in the neonate occurs at a higher rate than in
AmB lipid formulation is an alternative but older children/adults.
carries a theoretical risk of decreasing Central venous catheter removal strongly recommended.
urinary tract penetration compared with Infected CNS devices, including ventriculostomy drains and shunts,
AmB-D (CIII).43 should be removed, if possible.
Duration of therapy for candidemia without Length of therapy dependent on disease (BIII), usually 2 wk after all
obvious metastatic complications is 2 wk clearance.
after documented clearance and Antifungal susceptibility testing is suggested with persistent disease.
resolution of symptoms (therefore, Candida krusei is inherently resistant to fluconazole; Candida
generally 3 wk total). parapsilosis may be less susceptible to echinocandins; there is
increasing resistance of Candida glabrata to fluconazole and
echinocandins.
Prophylaxis No proven benefit for combination antifungal therapy in candidiasis.
In nurseries with high rates of candidiasis Change from AmB or fluconazole to echinocandin if cultures
(>10%),44 IV or PO fluconazole prophylaxis persistently positive (BIII) despite source control.
(AI) (3–6 mg/kg twice weekly for 6 wk) in Although fluconazole prophylaxis has been shown to reduce
high-risk neonates (birth weight <1,000 g) colonization, it has not reduced mortality.34
is recommended. PO nystatin, Echinocandins should be used with caution and generally limited to
100,000 U tid for 6 wk, is an alternative to salvage therapy or situations in which resistance or toxicity
fluconazole in neonates with birth weights precludes use of AmB-D or fluconazole (CIII).
<1,500 g if availability or resistance Role of flucytosine in neonates with meningitis is questionable and
precludes fluconazole use (CII). not routinely recommended due to toxicity concerns. The addition
Prophylaxis of neonates and children of flucytosine (100 mg/kg/day div q6h) may be considered as
receiving ECMO: fluconazole 12 mg/kg on salvage therapy in patients who have not had a clinical response to
day 1, then 6 mg/kg/day (BII). initial AmB therapy, but adverse effects are frequent (CIII).
Serum flucytosine concentrations should be obtained after 3–5 days
to achieve a 2-h post-dose peak <100 mcg/mL (ideally 30–80 mcg/
mL) to prevent neutropenia.
See Skin and soft tissues later in this table for management of

2025 Nelson’s Pediatric Antimicrobial Therapy —

congenital cutaneous candidiasis.
 Antimicrobial Therapy for Neonates

82 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Aspergillosis (usually Voriconazole dosing never studied in Aggressive antifungal therapy and early debridement of skin lesions,
cutaneous infection neonates but likely initial dosing same or which are a common manifestation in neonatal aspergillosis (AIII).
with systemic higher as pediatric ≥2 y: 18 mg/kg/day IV Voriconazole is preferred primary antifungal therapy for all clinical
dissemination)27,45–47 div q12h for an LD on the first day, then forms of aspergillosis (AI). Early initiation of therapy in patients with
16 mg/kg/day IV div q12h as a strong suspicion of disease is important while a diagnostic
maintenance dose. Continued dosing is evaluation is conducted.
guided by monitoring of trough serum Therapeutic voriconazole trough serum concentrations of 2–5 mg/L
concentrations (AII). are important for success. It is critical to monitor trough
When patient’s condition is stable, may concentrations to guide therapy due to high inter-patient
switch from voriconazole IV to variability.28 Low voriconazole concentrations are a leading cause of
voriconazole PO 18 mg/kg/day div bid clinical failure. A second agent (eg, AmB) may be added until
(AII). Unlike in adults, PO bioavailability in voriconazole levels are therapeutic.
children is about only 60%. PO Neonatal and infant voriconazole dosing is not well-defined, but
bioavailability in neonates has never been doses required to achieve therapeutic troughs are generally higher
studied. Trough monitoring is crucial after than in children >2 y (AIII).48
switch.26 Limited experience with posaconazole and no experience with
Alternatives for primary therapy when isavuconazole in neonates.49
voriconazole cannot be administered: Total treatment course is a minimum of 6–12 wk, largely dependent
L-AmB 5 mg/kg/day (AII). ABLC is another on the degree and duration of immunosuppression and evidence of
alternative. Echinocandin primary disease improvement.
monotherapy should not be used for Salvage antifungal therapy options after failed primary therapy
treating invasive aspergillosis (CII). AmB-D include a change of antifungal class (using L-AmB or an
should be used only in resource-limited echinocandin), a switch to posaconazole (trough concentrations
settings in which no alternative agent is >1 mcg/mL [see Ch 18 for pediatric dosing]), or use of combination
available (AII). antifungal therapy.
Combination therapy with voriconazole + an echinocandin may be
considered in select patients.
In vitro data suggest some synergy with 2 (but not 3) drug
combinations: an azole + an echinocandin is the most well studied.
If combination therapy is used, this is likely best done initially when
 Routine susceptibility testing is not recommended but is suggested
for patients who are suspected of having an azole-resistant isolate
or who are unresponsive to therapy.
Azole-resistant Aspergillus fumigatus is increasing. If local
epidemiology suggests >10% azole resistance, initial empiric
therapy should be voriconazole + echinocandin OR + L-AmB, and
subsequent therapy guided based on antifungal susceptibilities.50
Micafungin likely has equal efficacy to caspofungin against
aspergillosis.32
Gastrointestinal infections
– Necrotizing Ampicillin IV AND gentamicin AND Surgical drainage (AII). Possible benefit of laparotomy over peritoneal
enterocolitis or metronidazole IV for ≥10 days (All). drain in one randomized controlled trial.56
peritonitis secondary to Clindamycin may be used in place of Definitive antibiotic therapy based on blood culture results (aerobic,
bowel rupture51–55 metronidazole (AII). anaerobic, and fungal); meropenem for ESBL-positive GNRs or
Alternatives: meropenem (AI); PIP/TAZO ± cefepime for inducible ampC cephalosporinase–producing GNRs;
gentamicin (All). vancomycin rather than ampicillin if MRSA prevalent. Bacteroides

2025 Nelson’s Pediatric Antimicrobial Therapy —

ADD fluconazole if known to have GI colonization may occur as early as the first week after birth (AIII).
colonization with susceptible Candida spp Duration of therapy dependent on clinical response and risk for
(BIII). persisting IAI abscess (AIII).
Probiotics may prevent NEC in preterm neonates, but the optimal
strain(s), dose, duration, safety, and target subgroups are not fully
known.57,58 Until a product is FDA approved, administration of
probiotics to prevent NEC should be limited to participation in a
clinical trial.
– Salmonella (non- Ampicillin IM, IV (if susceptible) OR Observe for focal complications (eg, meningitis, arthritis) (AIII). TMP/
typhoid and typhi)59 ceftriaxone or cefepime IM, IV for SMX for focal GI infection and low risk for unconjugated
7–10 days (AII) hyperbilirubinemia due to interaction between sulfa and
bilirubin-albumin binding.
 Antimicrobial Therapy for Neonates

84 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
Herpes simplex infection
– Central nervous system Acyclovir 60 mg/kg/day div q8h IV for If CNS involvement, perform CSF HSV PCR near end of 21 days of
and disseminated 21 days (AII). therapy and continue IV acyclovir until PCR negative.
disease60–62 ALT may help identify early disseminated Monitor early in treatment of acute kidney injury, particularly in sicker
infection. infants and those receiving additional nephrotoxins.63
Infuse over 1 h and maintain adequate infant hydration to decrease
– Skin, eye, or mouth Acyclovir 60 mg/kg/day div q8h IV for risk for crystal nephropathy.
disease60–62 14 days (AII). Involve ophthalmologist when acute ocular HSV disease suspected. If
Obtain CSF PCR for HSV to assess for CNS present, ADD topical 1% trifluridine or 0.15% ganciclovir ophth gel
infection. (AII) (see Ch 18 for pediatric dosing).
Acyclovir PO (300 mg/m2/dose tid) suppression for 6 mo
recommended following parenteral therapy (AI).64 Observe for
possible cutaneous or CNS relapse after completion of therapy (or,
more rarely, during suppression therapy) (BII).65 Monitor for
neutropenia.
Different IV acyclovir dosages have been modeled,66 but no clinical
data are available in humans to support their use.
Use foscarnet for acyclovir-resistant disease (see Ch 18 for pediatric
dosing).
HIV prophylaxis following perinatal exposure67,68
– Prophylaxis following ZDV for the first 4 wk of age (AI). May reduce For detailed information: https://clinicalinfo.hiv.gov/en/guidelines/
low-risk exposure to 2 wk for some low-risk situations (BII). perinatal/whats-new (updated January 31, 2024; accessed August 7,
(mother who had HIV GA ≥35 wk: ZDV 8 mg/kg/day PO div q12h 2024).
infection before OR 6 mg/kg/day IV div q8h. UCSF Clinician Consultation Center (888-448-8765) provides free
pregnancy, received GA 30–34 wk: ZDV 4 mg/kg/day PO (OR clinical consultation.
ART during pregnancy, 3 mg/kg/day IV) div q12h. Increase at 2 wk Start prevention therapy as soon after delivery as possible but by
and sustained viral of age to 6 mg/kg/day PO (OR 4.5 mg/kg/ 6–8 h of age for best effectiveness (AII).
suppression within day IV) div q12h. Monitor CBC at birth and 4 wk (AII).
4 wk of delivery) GA ≤29 wk: ZDV 4 mg/kg/day PO (OR 3 mg/ Perform HIV-1 DNA PCR or RNA assays at 14–21 days, 1–2 mo, and
kg/day IV) div q12h. Increase at 4 wk of 4–6 mo (AI).
age to 6 mg/kg/day PO (OR 4.5 mg/kg/day Initiate TMP/SMX prophylaxis for PCP at 6 wk of age if HIV infection
IV) div q12h. not yet excluded (AII). TMP/SMX dosing is 2.5–5 mg/kg/dose of TMP
The preventive ZDV doses listed for neonates component PO q12h.
are also treatment doses for infants with
diagnosed HIV infection.
Treatment of HIV-infected neonates should

2025 Nelson’s Pediatric Antimicrobial Therapy —

be considered only with expert
consultation.
 Antimicrobial Therapy for Neonates

86 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Prophylaxis following Presumptive HIV treatment (BII): Delivery management varies for women with HIV who are receiving
higher-risk perinatal ZDV and 3TC for 6 wk ART and have viral loads between 20 and 999 copies/mL. Data do
exposure (mother who AND EITHER not show a clear benefit to IV ZDV and cesarean delivery for these
had primary HIV NVP or RAL women. Decisions about the addition of NVP, 3TC, or RAL for infants
infection during ZDV dosing as above; in infants ≥35 wk of born to these mothers should be made in consultation with a
pregnancy OR who was gestation, the dosage should be increased pediatric ID specialist.
not treated before to 12 mg/kg/day PO div q12h once the NVP dosing and safety not established for infants with birth weight
delivery OR who was infant is >4 wk of age. <1,500 g.
treated but did not 3TC dosing (≥32 wk of gestation at The HIV Guidelines Committee recommends using “treatment” ARV
achieve viral birth): regimens for high-risk, exposed neonates in an attempt to preclude
suppression within Birth–4 wk: 4 mg/kg/day PO div q12h infection or to increase the chance of HIV remission or cure. This was
4 wk of delivery, >4 wk: 8 mg/kg/day PO div q12h initially stimulated by the experience of a baby from Mississippi:
especially if delivery NVP dosing: high-risk neonate treated within first 2 days after birth with
was vaginal) ≥37 wk of gestation at birth: subsequent infection documentation; off therapy at 18 mo of age
Birth–4 wk: NVP 12 mg/kg/day PO div q12h. without evidence of circulating virus until 4 y of age, at which point
>4 wk: NVP 400 mg/m2/day of BSA PO div HIV became detectable.69 Clinical trials are ongoing to study these
q12h; make this dose increase only for issues further.
infants with confirmed HIV infection. When empiric treatment is used for high-risk infants and HIV infection
≥34–<37 wk of gestation at birth: is subsequently excluded, NVP, 3TC, and/or RAL can be discontinued
Birth–1 wk: NVP 8 mg/kg/day PO div q12h. and ZDV can be continued for 6 wk total.
1–4 wk: NVP 12 mg/kg/day PO div q12h. If HIV infection is confirmed, see Ch 7 for treatment recommendations.
>4 wk: NVP 400 mg/m2/day of BSA PO div Consider consultation with a pediatric ID specialist, especially when
q12h; make this dose increase only for considering use of RAL (CIII).
infants with confirmed HIV infection. If the mother has taken RAL within 2–24 h before delivery, the
RAL dosing: neonate’s first dose of RAL should be delayed until 24–48 h after
≥37 wk of gestation at birth and birth; other ARV drugs should be started as soon as possible.
≥2,000 g in weight:
 Birth–1 wk: qd dosing at about 1.5 mg/kg/
dose: 2–<3 kg: 0.4 mL (4 mg) qd; 3–<4 kg:
0.5 mL (5 mg) qd; 4–<5 kg: 0.7 mL (7 mg)
qd
1–4 wk: bid dosing at about 3 mg/kg/dose:
2–<3 kg: 0.8 mL (8 mg) bid; 3–<4 kg: 1 mL
(10 mg) bid; 4–<5 kg: 1.5 mL (15 mg) bid
4–6 wk: bid dosing at about 6 mg/kg/dose:
3–<4 kg: 2.5 mL (25 mg) bid; 4–<6 kg:
3 mL (30 mg) bid; 6–<8 kg: 4 mL (40 mg)
bid
Influenza A and B viruses70–73
Treatment Oseltamivir: Oseltamivir chemoprophylaxis is not recommended for infants <3 mo
Preterm, <38 wk of PMA: 1 mg/kg/dose PO unless the situation is judged critical because of limited safety and
bid efficacy data in this age-group.
Preterm, 38–40 wk of PMA: 1.5 mg/kg/dose Parenteral peramivir is approved in the United States for use in

2025 Nelson’s Pediatric Antimicrobial Therapy —

PO bid children ≥6 mo; no PK or safety data exist in neonates.75
Preterm, >40 wk of PMA: 3 mg/kg/dose PO PO baloxavir is approved in the United States for use in people ≥5 y;
bid71 no PK or safety data exist in neonates.76
Full-term, birth–8 mo: 3 mg/kg/dose PO
bid71,74
9–11 mo: 3.5 mg/kg/dose PO bid72
Omphalitis and funisitis
– Empiric therapy for Cefepime OR gentamicin, AND clindamycin Appropriate wound management for infected cord and necrotic tissue
omphalitis and OR metronidazole for ≥10 days (AII) (AIII).
necrotizing funisitis; Need to culture to direct therapy.
direct therapy against Alternatives for coliform coverage if resistance likely: cefepime,
coliform bacilli, S aureus meropenem.
(consider MRSA), and For suspect MRSA: ADD ceftaroline or vancomycin.
anaerobes77–79 Alternative for combined MSSA and anaerobic coverage: PIP/TAZO.
 Antimicrobial Therapy for Neonates

88 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Group A or B Penicillin G IV for ≥7–14 days (shorter course Group A streptococcus usually causes “wet cord” without pus and with
streptococcus80 for superficial funisitis without invasive minimal erythema; single dose of penicillin benzathine IM
infection) (AII) adequate.
Consultation with pediatric ID specialist recommended for necrotizing
fasciitis (AII).
– Staphylococcus aureus79 MSSA: oxacillin/nafcillin IV, IM for ≥5–7 days Assess for bacteremia and other focus of infection.
(shorter course for superficial funisitis Alternatives for MRSA: clindamycin (if susceptible) (BIII) or linezolid
without invasive infection) (AIII) (CIII).
MRSA: vancomycin (AIII) or ceftaroline (BII)
– Clostridium or Metronidazole OR clindamycin OR Crepitation and rapidly spreading cellulitis around umbilicus
Bacteroides spp81 penicillin G IV for ≥10 days, with additional Foul-smelling umbilical drainage
agents based on culture results (AII) Mixed infection with other gram-positive and gram-negative bacteria
common
Osteomyelitis, suppurative arthritis81–84
Obtain cultures (aerobic; fungal if NICU) of bone or joint fluid before antibiotic therapy.
Duration of therapy dependent on causative organism and normalization of ESR and CRP levels; minimum for osteomyelitis 3 wk and arthritis
therapy 2–3 wk if no organism identified (AIII).
Surgical drainage of pus (AIII); physical therapy may be needed (BIII).
– Empiric therapy Nafcillin/oxacillin IV (or vancomycin or Alternatives for MRSA: clindamycin (if susceptible) or linezolid
ceftaroline if MRSA is a concern) AND
cefepime OR gentamicin IV, IM (AIII)
– Coliform bacteria (eg, For E coli and Klebsiella: cefepime OR Meropenem for ESBL-producing coliforms (AIII)
E coli, Klebsiella spp, ceftazidime OR ampicillin (if susceptible)
Enterobacter spp) (AIII)
For Enterobacter, Serratia, or Citrobacter:
cefepime OR ceftazidime IV (AIII)
– Gonococcal arthritis Ceftriaxone IV, IM ± azithromycin 10 mg/kg Ceftriaxone no longer recommended as empiric single-agent therapy
and tenosynovitis14–17 PO q24h for 5 days (AIII; see Comments). due to increasing cephalosporin resistance; therefore, addition of
azithromycin recommended until susceptibilities are known (no
data in neonates; azithromycin dose is that recommended for
pertussis). Cefotaxime or cefepime is preferred for neonates with
hyperbilirubinemia and those with risk for calcium-drug interactions
(see Notes).
– Staphylococcus aureus MSSA: oxacillin/nafcillin IV (AII) Alternative for MSSA: cefazolin (AIII).
MRSA: vancomycin IV (AIII) OR ceftaroline IV Alternatives for MRSA: clindamycin (if susceptible) (BIII) or linezolid
(BII) (CIII). Addition of rifampin if persistently positive cultures.
– Group B streptococcus Ampicillin or penicillin G IV (AII)
– Haemophilus influenzae Ampicillin IV OR cefepime/ceftazidime IV, IM Start with IV therapy and switch to PO therapy when clinically stable.
if ampicillin resistant Amox/clav PO OR amoxicillin PO if susceptible (AIII).
Otitis media85
No controlled treatment trials in neonates; if no response, obtain middle ear fluid for culture.

2025 Nelson’s Pediatric Antimicrobial Therapy —

– Empiric therapy86 Cefepime/ceftazidime OR oxacillin/nafcillin Start with IV therapy and switch to amox/clav PO when clinically
AND gentamicin stable (AIII).
– Escherichia coli (therapy Cefepime/ceftazidime Start with IV therapy and switch to PO therapy when clinically stable.
for other coliforms In addition to pneumococcus and Haemophilus, coliforms and S aureus
based on susceptibility may also cause AOM in neonates (AIII).
testing) For ESBL-producing strains, use meropenem (AII).
Amox/clav if susceptible (AIII).
– Staphylococcus aureus MSSA: oxacillin/nafcillin IV (AII) Start with IV therapy and switch to PO therapy when clinically stable.
MRSA: vancomycin IV (AIII) OR ceftaroline IV MSSA: cephalexin PO for 10 days or cloxacillin PO (AIII).
(BII) Alternatives for MRSA: clindamycin (if susceptible) (BIII) or linezolid
(CIII).
– Group A or B Penicillin G or ampicillin IV, IM Start with IV therapy and switch to PO therapy when clinically stable.
streptococcus Amoxicillin 30–40 mg/kg/day PO div q8h for 10 days.
 Antimicrobial Therapy for Neonates

90 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
Parotitis, Oxacillin/nafcillin IV AND gentamicin IV, IM Usually staph but occasionally coliform.
suppurative87 for 10 days; consider vancomycin if MRSA Antimicrobial regimen without I&D is adequate in >75% of cases.88
suspected (AIII).
Pulmonary infections
– Empiric therapy for the Ampicillin IV, IM AND gentamicin or For neonates with no additional risk factors for bacterial infection (eg,
neonate with early ceftazidime/cefepime for 7–10 days; maternal chorioamnionitis) who (1) have negative blood cultures,
onset of pulmonary consider treating low-risk neonates for (2) have no need for >8 h of oxygen, and (3) are asymptomatic at
infiltrates (within the <7 days (see Comments). 48 h into therapy, 4 days may be sufficient therapy, based on babies
first 48–72 h after birth) with clinical pneumonia, none of whom had positive cultures.89
– Aspiration pneumonia90 Ampicillin IV, IM AND gentamicin IV, IM for Early-onset neonatal pneumonia may represent aspiration of amniotic
7–10 days (AIII) fluid, particularly if fluid is not sterile.
Mild aspiration episodes may not require antibiotic therapy.
– Chlamydia trachomatis91 Azithromycin PO, IV q24h for 5 days OR Association of erythromycin and azithromycin with pyloric stenosis in
erythromycin ethylsuccinate PO for infants treated <6 wk of age92
14 days (AII)
– Mycoplasma hominis93,94 Clindamycin PO, IV for 7–10 days (resistant Pathogenic role in pneumonia not well-defined and clinical efficacy
to macrolides) unknown; no association with BPD (BIII)
– Pertussis95 Azithromycin 10 mg/kg PO, IV q24h for Association of erythromycin and azithromycin with pyloric stenosis in
5 days OR erythromycin ethylsuccinate PO infants treated <6 wk of age92
for 14 days (AII) Alternatives: for >1 mo of age, clarithromycin for 7 days; for >2 mo of
age, TMP/SMX for 14 days
– Pseudomonas Cefepime IV, IM for 7–10 days (AIII) Alternatives: ceftazidime AND tobramycin, meropenem, OR PIP/TAZO
aeruginosa96 AND tobramycin
– Respiratory syncytial Treatment (see Comments). Aerosol ribavirin (6-g vial to make 20-mg/mL soln in sterile water),
virus97 Prophylaxis: nirsevimab is approved and aerosolized over 18–20 h daily for 3–5 days (BII), provides little
recommended over palivizumab. benefit and should be considered for use only in life-threatening RSV
Shortages of nirsevimab during the infection. Difficulties in administration, complications with airway
2023–2024 RSV season have led the reactivity, concern for potential toxicities to health care professionals,
manufacturer to use a reservation program and lack of definitive evidence of benefit preclude routine use.
for the 2024–2025 season, but we are still Neither palivizumab nor nirsevimab provides benefit in the treatment
giving palivizumab recommendations in of an active RSV infection.
this edition. Nirsevimab is recommended for all infants during their first RSV season,
Nirsevimab, 50 mg/dose (<5 kg at dose) or including well infants. Only those at high risk should receive a second
100 mg/dose (≥5 kg at dose) IM once per dose before their second RSV season.
season (a) within the first week after birth For situations where nirsevimab is not available, palivizumab should
for all infants born during October–March continue to be used as follows:
and (b) when entering first RSV season and • Palivizumab prophylaxis may be considered for children <24 mo who
<8 mo of age for all infants born during will be profoundly immunocompromised during the RSV season.
April–September. • Palivizumab prophylaxis is not recommended in the second year after
Alternative: palivizumab (a monoclonal birth except for children who required at least 28 days of
antibody) 15 mg/kg IM monthly (max supplemental oxygen after birth and who continue to require

2025 Nelson’s Pediatric Antimicrobial Therapy —

5 doses). medical support (supplemental oxygen, chronic corticosteroid
For high-risk infants: therapy, or diuretic therapy) during the 6-mo period before the start
In first year after birth, recommended for of the second RSV season.
infants born before 29 wk 0 days’ • Monthly prophylaxis should be discontinued in any child who
gestation. experiences a breakthrough RSV hospitalization.
Not recommended for otherwise healthy • Children with pulmonary abnormality or neuromuscular disease that
infants born at ≥29 wk 0 days’ gestation. impairs the ability to clear secretions from the upper airways may be
In first year after birth, recommended for considered for prophylaxis in the first year after birth.
preterm infants with CLD of prematurity, Insufficient data are available to recommend palivizumab or nirsevimab
defined as birth at <32 wk 0 days’ prophylaxis for children with CF or Down syndrome.
gestation and a requirement for >21% The burden of RSV disease and costs associated with transport from
oxygen for at least 28 days after birth or at remote locations may result in a broader use of palivizumab or
36 wk of PMA. nirsevimab for RSV prevention in Alaska Native populations and
Clinicians may administer in the first year possibly in select other American Indian populations.98,99
after birth to certain infants with Palivizumab or nirsevimab prophylaxis is not recommended for
hemodynamically significant heart disease. prevention of health care–associated RSV disease.
RSV antivirals are currently investigational for neonates and young infants
 Antimicrobial Therapy for Neonates

92 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– SARS-CoV-2 (COVID-19) Remdesivir (AII) Must be ≥28 days of age and ≥3 kg in weight, with a positive result on
5 mg/kg on day 1, then 2.5 mg/kg/day for up SARS-CoV-2 viral testing.
to 10 days Consider corticosteroids.
– Staphylococcus MSSA: oxacillin/nafcillin IV (AIII). Alternative for MSSA: cefazolin IV
aureus20,100–102 MRSA: ceftaroline IV (BIII) OR vancomycin IV Alternatives for MRSA: clindamycin (if susceptible) (BIII) or linezolid
(BII). (CIII)
Duration of therapy depends on extent of Addition of rifampin or linezolid if persistently positive cultures (AIII)
disease (pneumonia vs pulmonary Thoracostomy drainage of empyema
abscesses vs empyema) and should be
individualized with therapy up to
≥21 days.
– Group B Penicillin G IV OR ampicillin IV, IM for 10 days For serious infections, ADD gentamicin for synergy until clinically
streptococcus103,104 (AIII) improved.
No prospective, randomized data on the efficacy of a 7-day treatment
course.
– Ureaplasma spp Azithromycin106 IV 20 mg/kg qd for 3 days Pathogenic role of Ureaplasma not well-defined and BPD prophylaxis
(urealyticum or (BII)107 not currently recommended. Clinical trials have not shown benefit
parvum)105 to azithromycin treatment of Ureaplasma-colonized preterm
infants.108
If only the nasogastric route is available, 10 mg/kg PO q12h × 6 can be
trialed instead of 20 mg/kg to improve GI tolerability, but the
absorption has not been evaluated and this approach may not
achieve the same concentrations as IV.
Many Ureaplasma spp resistant to erythromycin.
Association of erythromycin and pyloric stenosis in young infants.
Sepsis and meningitis102,109,110
Duration of therapy: 10 days for sepsis without a focus (AIII); minimum of 21 days for gram-negative meningitis (or at least 14 days after CSF is
sterile) and 14–21 days for GBS meningitis and other gram-positive bacteria (AIII).
There are no prospective, controlled studies on 5- or 7-day courses for mild or presumed sepsis.
– Initial therapy, Ampicillin IV AND a second agent, either Gentamicin preferred over cephalosporins for empiric therapy for
organism unknown cefepime/ceftazidime IV or gentamicin IV, sepsis when meningitis has been ruled out.
IM (AII) Cephalosporin preferred if meningitis suspected or cannot be
excluded clinically or by LP (AIII). For locations with a high rate
(≥10%) of ESBL-producing E coli, and in which meningitis is
suspected, empiric therapy with meropenem is preferred over
cephalosporins.
Initial empiric therapy for nosocomial infection should be based on
each hospital’s pathogens and susceptibilities.
Essential: Always narrow antibiotic coverage once susceptibility data
are available.
– Bacteroides fragilis Metronidazole or meropenem IV, IM (AIII) Alternative: clindamycin, but increasing resistance reported

2025 Nelson’s Pediatric Antimicrobial Therapy —

– Carbapenem-resistant CAZ/AVI IV 40 mg/kg q8h (see Ch 18) (BIII) Combination options: amikacin, colistin IV 2.5 mg/kg q12h.112
GNR111 ADD aztreonam if MBL producing (such as NDM or VIM, not currently
prevalent in NICUs in the United States).
Alternative: high-dose meropenem if CRO with MIC 4–8 mg/L.
Consultation with ID specialist strongly recommended to assist with
drug selection, monitoring, and acquisition of investigational agents
if needed for emergency use (eg, mero/vabor, IMI/REL, fosfomycin,
plazomicin).
– Enterococcus spp Ampicillin IV, IM AND gentamicin IV, IM (AIII); Gentamicin needed with ampicillin or vancomycin for bactericidal
for ampicillin-resistant organisms: activity; continue until clinical and microbiologic response
vancomycin AND gentamicin IV (AIII) documented (AIII).
For vancomycin-resistant enterococci that are also ampicillin resistant:
linezolid (AIII).
 Antimicrobial Therapy for Neonates

94 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Enterovirus Supportive therapy; no antivirals currently Pocapavir PO is currently under investigation for enterovirus (poliovirus)
FDA approved (see Ch 7) and can be used under an expanded access IND.
Pleconaril PO is currently under consideration for submission to the
FDA for approval to treat neonatal enteroviral sepsis syndrome.113 As
of June 2024, it is not available for compassionate use.
– Escherichia coli109,110 Cefepime/ceftazidime IV or gentamicin IV, IM Cephalosporin preferred if meningitis suspected or cannot be
(AII) excluded by LP (AIII)
For locations with a high rate (≥10%) of ESBL-producing E coli, and in
which meningitis is suspected, empiric therapy with meropenem
preferred over cephalosporins
– Group A streptococcus Penicillin G or ampicillin IV (AII) Penicillin resistance increasingly reported for Streptococcus mitis
or viridans streptococci isolates; alternatives: vancomycin or linezolid if not cephalosporin
susceptible
– Group B Penicillin G or ampicillin IV AND gentamicin Continue gentamicin until clinical and microbiologic response
streptococcus103 IV, IM (AI) documented (AIII).
Duration of therapy: 10 days for bacteremia/sepsis (AII); minimum of
14 days for meningitis (AII).
– Listeria Ampicillin IV, IM AND gentamicin IV, IM (AIII) Gentamicin is synergistic in vitro with ampicillin. Continue until
monocytogenes114 clinical and microbiologic response documented (AIII).
– Neisseria gonorrhoeae115 Ceftriaxone OR cefepime OR ceftazidime IV Duration of therapy: 7 days for bacteremia/sepsis (AII), 10–14 days if
(AI) meningitis is suspected or confirmed (BII).
See Gonococcal earlier in this table for recommendations.
– Neisseria meningitidis Ceftriaxone OR cefepime OR ceftazidime IV Duration of therapy: 7 days for bacteremia/sepsis (AII), 10–14 days if
(AI) meningitis is suspected or confirmed (BII)
– Pseudomonas Cefepime IV, IM OR ceftazidime IV, IM AND Meropenem is a suitable alternative (AIII). PIP/TAZO should not be
aeruginosa tobramycin IV IM (AIII) used for CNS infection
– Staphylococcus Vancomycin IV (AIII) Add rifampin if cultures persistently positive.116
epidermidis (or any Alternatives: linezolid, ceftaroline.
coagulase-negative
staphylococci)
– Staphylococcus MSSA: oxacillin/nafcillin IV, IM or cefazolin IV, Alternatives for MRSA: clindamycin (if susceptible), linezolid
aureus20,100–102,117–119 IM (AII)
MRSA: vancomycin IV or ceftaroline IV (AIII)
Skin and soft tissues
– Breast abscess120 Oxacillin/nafcillin IV, IM (for MSSA) OR Gram stain of expressed pus guides empiric therapy; vancomycin or
vancomycin IV or ceftaroline IV (for MRSA). ceftaroline if MRSA prevalent in community; other alternatives:
ADD cefepime/ceftazidime OR gentamicin if clindamycin, linezolid; may need surgical drainage to minimize
GNRs seen on Gram stain (AIII). damage to breast tissue.
Treatment duration individualized until clinical findings have
completely resolved (AIII).
– Congenital cutaneous AmB for 14 days, or 10 days if CSF culture Treat promptly with full IV treatment dose, not prophylactic dosing or

2025 Nelson’s Pediatric Antimicrobial Therapy —

candidiasis121 negative (AII) topical therapy.
Alternative: fluconazole if Candida albicans Diagnostic workup includes aerobic cultures of skin lesions, blood,
or other Candida spp with known and CSF. Pathology examination of placenta and umbilical cord if
fluconazole susceptibility possible.
– Erysipelas (and other Penicillin G IV for 5–7 days, followed by PO Alternative: ampicillin.
group A strep therapy (if bacteremia not present) to GBS may produce similar cellulitis or nodular lesions.
infections) complete a 10-day course (AIII)
– Impetigo neonatorum MSSA: oxacillin/nafcillin IV, IM OR cephalexin Systemic antibiotic therapy not usually required for superficial
(AIII) impetigo; local chlorhexidine cleansing may help with or without
MRSA: vancomycin IV or ceftaroline IV for topical mupirocin (MRSA) or bacitracin (MSSA).
5 days (AIII) Alternatives for MRSA: clindamycin IV, PO or linezolid IV, PO.
 Antimicrobial Therapy for Neonates

96 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Staphylococcus MSSA: oxacillin/nafcillin IV, IM (AII) Surgical drainage may be required.
aureus20,100,102,122 MRSA: ceftaroline IV (AIII) or vancomycin IV Alternatives for MRSA: clindamycin (if susceptible) IV, linezolid IV.
Convalescent PO therapy if infection responds quickly to IV therapy.
– Group B Penicillin G IV OR ampicillin IV, IM Usually no pus formed
streptococcus103 Treatment duration dependent on extent of infection, 7–14 days
Syphilis, congenital (≤1 mo of age)123
When availability of penicillin is compromised, contact the CDC.
Evaluation and treatment do not depend on mother’s HIV status.
Obtain follow-up serology q2–3mo until nontreponemal test nonreactive or decreased 4-fold.
– Proven or highly Aqueous penicillin G 50,000 U/kg/dose q12h Evaluation to determine type and duration of therapy: CSF analysis
probable disease: (day after birth 1–7), q8h (>7 days) IV OR (VDRL, cell count, protein), CBC, and platelet count. Other tests, as
(1) abnormal physical procaine penicillin G 50,000 U/kg IM q24h clinically indicated, including long-bone radiography, chest
examination; (2) serum for 10 days (AII) radiography, LFTs, cranial ultrasonography, ophthalmologic
quantitative examination, and hearing test (ABR).
nontreponemal Infants with positive CSF VDRL test(s) do not routinely need repeat LP
serologic titer 4-fold unless their serum nontreponemal test(s) remain elevated at age
higher than mother’s 6–12 mo. If CSF parameters remain abnormal without an alternative
titer; or (3) positive dark explanation, re-treat.
field or fluorescent If >1 day of therapy is missed, entire course is restarted.
antibody test of body
fluid(s)
– Normal physical Evaluation abnormal or not done Evaluation: CSF analysis, CBC with platelet count, long-bone
examination, serum completely: aqueous penicillin G 50,000 U/ radiographs.
quantitative kg/dose q12h (day after birth 1–7), q8h If >1 day of therapy is missed, entire course is restarted.
nontreponemal (>7 days) IV OR procaine penicillin G Reliable follow-up important if only a single dose of penicillin
serologic titer ≤ 50,000 U/kg IM q24h for 10 days (AII) benzathine given.
maternal titer, and Evaluation normal: aqueous penicillin G
maternal treatment 50,000 U/kg/dose q12h (day after birth
was (1) none, 1–7), q8h (>7 days) IV OR procaine
inadequate, or penicillin G 50,000 U/kg IM q24h for
undocumented; (2) 10 days; OR penicillin G benzathine
erythromycin, 50,000 U/kg/dose IM in a single dose (AIII)
azithromycin, or other
non-penicillin regimen;
or (3) <4 wk before
delivery.
– Normal physical Penicillin G benzathine 50,000 U/kg/dose IM No evaluation required.
examination, serum in a single dose (AIII) Some experts would not treat but provide close serologic follow-up.

2025 Nelson’s Pediatric Antimicrobial Therapy —

quantitative
nontreponemal
serologic titer ≤
maternal titer, mother
treated adequately
during pregnancy and
>4 wk before delivery;
no evidence of
reinfection or relapse in
mother
 Antimicrobial Therapy for Neonates

98 — Chapter 2. Antimicrobial Therapy for Neonates

A. RECOMMENDED THERAPY FOR SELECT NEONATAL CONDITIONS
Therapy (evidence grade) See Tables
Condition 2B–2D for neonatal dosages. Comments
– Normal physical No treatment No evaluation required.
examination, serum Some experts would treat with penicillin G benzathine 50,000 U/kg as
quantitative a single IM injection, particularly if follow-up is uncertain.
nontreponemal
serologic titer ≤
maternal titer, mother
treated adequately
before pregnancy
Syphilis, congenital Aqueous penicillin G crystalline 200,000– Evaluation to determine type and duration of therapy: CSF analysis
(>1 mo of age)123 300,000 U/kg/day IV div q4–6h for 10 days (VDRL, cell count, protein), CBC, and platelet count. Other tests as
(AII) clinically indicated, including long-bone radiography, chest
radiography, LFTs, neuroimaging, ophthalmologic examination, and
hearing evaluation. If there are no clinical manifestations of disease,
CSF examination is normal, and CSF VDRL test result is nonreactive,
some specialists will treat with up to 3 weekly doses of penicillin G
benzathine 50,000 U/kg IM.
Some experts will provide a single dose of penicillin G benzathine
50,000 U/kg IM after 10 days of parenteral treatment, but value of
this additional therapy is not well-documented.
Tetanus Metronidazole IV, PO (alternative: penicillin G Wound cleaning and debridement vital; IVIG (200–400 mg/kg) is an
neonatorum124 IV) for 10–14 days (AIII) alternative if TIG not available; equine tetanus antitoxin not
Human TIG 500 U IM for 1 dose (AIII) available in the United States but is alternative to TIG.
Toxoplasmosis, Sulfadiazine 100 mg/kg/day PO div q12h Corticosteroids (1 mg/kg/day div q12h) if active chorioretinitis or CSF
congenital125,126 AND pyrimethamine 2 mg/kg PO daily for protein >1 g/dL (AIII).
2 days (LD), then 1 mg/kg PO q24h for Round sulfadiazine dose to 125 or 250 mg (¼ or ½ of 500-mg tab);
2–6 mo, then 3×/wk (M-W-F) up to 1 y (AII) round pyrimethamine dose to 6.25 or 12.5 mg (¼ or ½ of 25-mg
tab). OK to crush tabs to give with feeding.
 Folinic acid (leucovorin) 10 mg 3×/wk Start sulfadiazine after neonatal jaundice has resolved.
continuing for 1 wk after pyrimethamine Clindamycin is an alternative to sulfadiazine in patients with G6PD
(AII) deficiency or intolerance.
Therapy is effective against only active trophozoites, not cysts.
Urinary tract infection127
No prophylaxis for grades 1–3 reflux.128,129
In neonates with reflux, prophylaxis reduces recurrences but increases likelihood of recurrences being due to resistant organisms. Prophylaxis does
not affect renal scarring.128
– Initial therapy, Ampicillin AND gentamicin; OR ampicillin Renal ultrasound and VCUG indicated after first UTI to identify
organism unknown AND cefepime/ceftazidime, pending abnormalities of urinary tract
culture and susceptibility test results, for PO therapy acceptable once neonate asymptomatic and culture sterile
7–10 days
– Coliform bacteria (eg, Cefepime/ceftazidime IV, IM OR, in absence Ampicillin or cefazolin used for susceptible organisms
E coli, Klebsiella, of renal or perinephric abscess, gentamicin
Enterobacter, Serratia) IV, IM for 7–10 days (AII)

2025 Nelson’s Pediatric Antimicrobial Therapy —

– Enterococcus Ampicillin IV, IM for 7 days for cystitis (may Aminoglycoside needed with ampicillin or vancomycin for synergistic
need 10–14 days for pyelonephritis), add bactericidal activity (assuming organisms are susceptible to an
gentamicin until cultures are sterile (AIII); aminoglycoside)
for ampicillin resistance, use vancomycin,
add gentamicin until cultures are sterile.
– Pseudomonas Cefepime IV, IM, OR ceftazidime IV, IM OR, in Meropenem is an alternative.
aeruginosa absence of renal or perinephric abscess,
tobramycin IV, IM for 7–10 days (AIII)
– Candida spp36–38 See Candidiasis earlier in this table under
Fungal infections.
 Antimicrobial Therapy for Neonates

100 — Chapter 2. Antimicrobial Therapy for Neonates

B. ANTIMICROBIAL DOSAGES FOR NEONATES—Lead author Jason Sauberan, assisted by the editors and John Van Den Anker
Dosages (mg/kg/day) and Intervals of Administration
Chronologic Age ≤28 days
Body Weight ≤2,000 g Body Weight >2,000 g Chronologic Age
Antimicrobial Route 0–7 days old 8–28 days old 0–7 days old 8–28 days old 29–60 days
NOTE: This table contains empiric dosage recommendations for each agent listed. See Table 2A for more details of dosages for specific pathogens
in specific tissue sites and for information on anti-influenza and ARV drug dosages.
Acyclovir (treatment of acute IV 60 div q8h 60 div q8h 60 div q8h 60 div q8h 60 div q8h
disease)
Acyclovir (suppression following PO — 900/m2/day div — 900/m2/day div 900/m2/day div
treatment of acute disease) q8h q8h q8h
Only IV acyclovir should be used for the treatment of acute neonatal HSV disease. PO suppression therapy for a duration of 6 mo after completion
of initial IV treatment.
Amoxicillina PO — 75 div q12h 100 div q12h 100 div q12h 100 div q12h
Amoxicillin/clavulanateb PO — — 30 div q12h 30 div q12h 30 div q12h
Amphotericin B
– Deoxycholate IV 1 q24h 1 q24h 1 q24h 1 q24h 1 q24h
– Lipid complex IV 5 q24h 5 q24h 5 q24h 5 q24h 5 q24h
– Liposomal IV 5 q24h 5 q24h 5 q24h 5 q24h 5 q24h
Ampicillin IV, IM 100 div q12h 150 div q12h 150 div q8h 150 div q8h 200 div q6h
Ampicillin (GBS meningitis) IV 300 div q8h 300 div q6h 300 div q8h 300 div q6h 300 div q6h
Azithromycinc IV, PO 10 q24h 10 q24h 10 q24h 10 q24h 10 q24h
Aztreonam IV, IM 60 div q12h 90 div q8h d
90 div q8h 120 div q6h 120 div q6h
Cefazolin (Enterobacterales)e IV, IM 50 div q12h 75 div q8h 100 div q12h 150 div q8h 100–150 div q6–8h
Cefazolin (MSSA) IV, IM 50 div q12h 50 div q12h 75 div q8h 75 div q8h 75 div q8h
Cefepime IV, IM 60 div q12h 60 div q12h 100 div q12h 100 div q12h 150 div q8hf
Cefotaxime IV, IM 100 div q12h 150 div q8h 100 div q12h 150 div q6h 200 div q6h
Ceftaroline IV, IM 12 div q12h g
18 div q8h g
18 div q8h 18 div q8h 18 div q8h
Ceftazidimeh IV, IM 100 div q12h 150 div q8hd 100 div q12h 150 div q8h 150 div q8h
Ceftazidime/avibactami IV 60 div q8hi 60 div q8hi 60 div q8h 60 div q8h 90 div q8h
Ceftolozane/tazobactam IV — — 60 div q8h 60 div q8h 60 div q8h
Ceftriaxonej IV, IM — — 50 q24h 50 q24h 50 q24h
Ciprofloxacin IV 15 div q12h 15 div q12h 25 div q12h 25 div q12h 25 div q12h
Clindamycin IV, IM, 15 div q8h 15 div q8h 21 div q8h 27 div q8h 30 div q8h

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

PO
Dalbavancin IV 22.5 once 22.5 once 22.5 once 22.5 once 22.5 once
Daptomycin (Potential neurotoxicity; IV 12 div q12h 12 div q12h 12 div q12h 12 div q12h 12 div q12h
use cautiously if no other options.)
Erythromycin IV, PO 40 div q6h 40 div q6h 40 div q6h 40 div q6h 40 div q6h
Fluconazole
– Treatmentk IV, PO 12 q24h 12 q24h 12 q24h 12 q24h 12 q24h
– Prophylaxis IV, PO 6 mg/kg/dose 6 mg/kg/dose 6 mg/kg/dose 6 mg/kg/dose 6 mg/kg/dose
twice weekly twice weekly twice weekly twice weekly twice weekly
Flucytosinel PO 75 div q8h 100 div q6hd 100 div q6h 100 div q6h 100 div q6h
Ganciclovir IV 12 div q12h 12 div q12h 12 div q12h 12 div q12h 12 div q12h
Linezolid IV PO 20 div q12h 30 div q8h 30 div q8h 30 div q8h 30 div q8h
 Antimicrobial Therapy for Neonates

102 — Chapter 2. Antimicrobial Therapy for Neonates

B. ANTIMICROBIAL DOSAGES FOR NEONATES—Lead author Jason Sauberan, assisted by the editors and John Van Den Anker
Dosages (mg/kg/day) and Intervals of Administration
Chronologic Age ≤28 days
Body Weight ≤2,000 g Body Weight >2,000 g Chronologic Age
Antimicrobial Route 0–7 days old 8–28 days old 0–7 days old 8–28 days old 29–60 days
Meropenem
– Sepsis, IAIm IV 40 div q12h 60 div q8hm 60 div q8h 90 div q8hm 90 div q8h
– Meningitis IV 80 div q12h 120 div q8h m
120 div q8h 120 div q8h 120 div q8h
– Carbapenem-resistant organism
with MIC 4–8 mg/L
Metronidazolen IV, PO 15 div q12h 15 div q12h 22.5 div q8h 30 div q8h 30 div q8h
Micafungin IV 10 q24h 10 q24h 10 q24h 10 q24h 10 q24h
Nafcillin,o oxacillino IV, IM 50 div q12h 75 div q8hd 75 div q8h 100 div q6h 150 div q6h
Penicillin G benzathine IM 50,000 U 50,000 U 50,000 U 50,000 U 50,000 U
Penicillin G crystalline (GBS sepsis, IV 100,000 U div 150,000 U div 100,000 U div 150,000 U div 200,000 U div
congenital syphilis) q12h q8h q12h q8h q6h
Penicillin G crystalline (GBS IV 450,000 U div 500,000 U div 450,000 U div 500,000 U div 500,000 U div
meningitis) q8h q6h q8h q6h q6h
Penicillin G procaine IM 50,000 U q24h 50,000 U q24h 50,000 U q24h 50,000 U q24h 50,000 U q24h
Piperacillin/tazobactam IV 300 div q8h 320 div q6hp 320 div q6h 320 div q6h 320 div q6h
Rifampin q
IV, PO 10 q24h 15 q24h 10 q24h 15 q24h 15 q24h
Valganciclovir PO Insufficient Insufficient 32 div q12h 32 div q12h 32 div q12h
data data
Voriconazoler IV 12 div q12h 12 div q12h 12 div q12h 12 div q12h 16 div q12h
 Zidovudine IV 3 div q12hs 3 div q12hs 6 div q12h 6 div q12h See HIV prophylaxis in
Table 2A.
PO 4 div q12hs 4 div q12hs 8 div q12h 8 div q12h See HIV prophylaxis in
Table 2A.
a
For streptococcal and enterococcal infections.
b
FDA approved doses for susceptible H influenzae non-CNS infections are shown in the table. Higher dosing 75 mg/kg/day div q8h recommended for IV to PO step-down
treatment of susceptible E coli (MIC ≤8 mg/L). May use 25- or 50-mg/mL formulation.
c
See Table 2A for pathogen-specific dosing.
d
Use 0–7 days old dosing until 14 days old if birth weight <1,000 g.
e
If isolate MIC 4 mg/L and no CNS focus. If MIC ≤2 mg/L, can use MSSA dosing.
f
Infusion over 3 h, or 200 mg/kg/day div q6h, to treat organisms with MIC 8 mg/L.
g
Serum concentration (is available commercially). Goal exposure is a concentration > MIC (usually 0.5 or 1 mg/L) at 60% of the dosing interval.
h
For treating susceptible Pseudomonas infection. If treating non–AmpC-producing Enterobacterales with MIC ≤4 mg/L (eg, susceptible E coli or Klebsiella), can use one-half
the dose given in the table.
i
FDA approved for GA ≥31 wk. Case reports suggest safety of the 60 mg/kg div q8h dosage for <31 wk. Considering the safety record of ceftazidime alone in very preterm
neonates, and the high stakes of a CAZ/AVI-worthy infection, it is reasonable to use this dosage in all neonates up to 28 days postnatally.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

j
Usually avoided in neonates. Can be considered for transitioning to outpatient treatment of GBS bacteremia in well-appearing neonates with low risk for
hyperbilirubinemia. Contraindicated if concomitant IV calcium (see Notes at beginning of chapter).
k
LD 25 mg/kg followed 24 h later by maintenance dose listed if GA ≥30 wk or LD 9 mg/kg if <30 wk.
l
Desired serum concentrations peak 60–80 mg/L, trough 5–10 mg/L to achieve time-above-MIC of >40% for invasive candidiasis, and trough 10–20 mg/L for Cryptococcus.
Dose range 50–100 mg/kg/day. Always use in combination with other agents; be alert to development of resistance.
m
Adjust dosage after 14 days of age rather than after 7 days of age.
n
LD 15 mg/kg.
o
Double the dose for meningitis.
p
When PMA reaches >30 wk.
q
For either Staphylococcus bacteremia or primary TB.
r
Adjust dose to target trough 2–5 mg/L (see Aspergillosis in Table 2A under Fungal infections).
s
Starting dose if GA <35 wk 0 days and PNA ≤14 days. See HIV prophylaxis in Table 2A for ZDV dosage after 2 wk of age and for NVP and 3TC recommendations.
 Antimicrobial Therapy for Neonates

104 — Chapter 2. Antimicrobial Therapy for Neonates

C. AMINOGLYCOSIDES
Empiric Dosage (mg/kg/dose) by Gestational and Postnatal Ages
<30 wk 30–34 wka ≥35 wka
Medication Route 0–14 days >14 days 0–10 days >10 days 0–7 days >7 days
Amikacinb IV, IM 15 q48h 15 q36h 15 q36h 15 q24h 15 q24h 17.5 q24h
Gentamicinc IV, IM 5 q48h 5 q36h 5 q36h 5 q24h 4 q24h 5 q24h
Tobramycin c
IV, IM 5 q48h 5 q36h 5 q36h 5 q24h 4 q24h 5 q24h
a
If >60 days of age, see Ch 18.
b
Desired serum or plasma concentrations: 20–35 mg/L or 10 × MIC (peak), <7 mg/L (trough).
c
Desired serum or plasma concentrations: 6–12 mg/L or 10 × MIC (peak), <2 mg/L (trough). A 7.5 mg/kg dose q48h, or q36h if ≥30 wk of GA and >7 days of PNA, more likely
to achieve desired concentrations if pathogen MIC = 1 mg/L.130
 2025 Nelson’s Pediatric Antimicrobial Therapy — 105

D. VANCOMYCINa
Empiric Dosage by Gestational Age and SCr
Begin with a 20 mg/kg LD. 2
≤28 wk of GA >28 wk of GA

Antimicrobial Therapy for Neonates

SCr (mg/dL) Dose (mg/kg) Frequency SCr (mg/dL) Dose (mg/kg) Frequency
<0.5 15 q12h <0.7 15 q12h
0.5–0.7 20 q24h 0.7–0.9 20 q24h
0.8–1.0 15 q24h 1.0–1.2 15 q24h
1.1–1.4 10 q24h 1.3–1.6 10 q24h
>1.4 15 q48h >1.6 15 q48h
a
SCr concentrations normally fluctuate and are partly influenced by transplacental maternal creatinine in the first
week after birth. Cautious use of creatinine-based dosing strategy with frequent reassessment of renal function and
vancomycin serum concentrations is recommended in neonates ≤7 days old. Desired serum concentrations: a
24-h AUC:MIC of at least 400 mg·h/L can be considered based on adult studies of invasive MRSA infections. The AUC
is best calculated from 2 concentrations (ie, peak and trough) rather than 1 trough serum concentration. When AUC
calculation is not feasible, a trough concentration ≥10 mg/L is very highly likely (>90%) to achieve the goal AUC
target in neonates when the MIC is 1 mg/L. However, troughs as low as 7 mg/L can still achieve an AUC ≥400 in some
preterm neonates due to their slower clearance. Thus, AUC is preferred over trough monitoring to prevent unnecessary
overexposure. For centers where invasive MRSA infection is relatively common or where MRSA with MIC of 1 mg/L is
common, an online dosing tool is available that may improve the likelihood of empirically achieving AUC ≥400,
compared with Table 2D (https://neovanco.insight-rx.com); accessed October 18, 2024). If >60 days of age,
see Ch 18.

E. Use of Antimicrobials During Pregnancy or Breastfeeding

The use of antimicrobials during pregnancy and lactation should balance benefit to the
mother with the risk for fetal and neonatal toxicity (including anatomic anomalies with
fetal exposure). A number of factors determine the degree of transfer of antibiotics across
the placenta: lipid solubility, degree of ionization, molecular weight, protein binding,
placental maturation, and placental and fetal blood flow. The Pregnancy and Lactation
Labeling Rule of 2014 began replacing the traditional A to X risk categories with narrative
summaries of risks associated with the use of a drug during pregnancy and lactation for
the mother, the fetus, and the breastfeeding newborn/infant/child. The risk categories
from A to X were felt to be too simplistic. This transition was completed in 2020. Risks are
now all clearly noted, and for drugs with high fetal risk, black box warnings are included
(eg, ribavirin).131 Fetal serum antibiotic concentrations (or cord blood concentrations)
following maternal administration have not been systematically studied, but new PK
models of transplacental drug transfer and fetal metabolism have recently been developed
to provide some insight into fetal drug exposure.132–134 The following commonly used
drugs appear to achieve fetal concentrations that are equal to or only slightly less than
those in the mother: penicillin G, amoxicillin, ampicillin, sulfonamides, trimethoprim,
 106 — Chapter 2. Antimicrobial Therapy for Neonates

tetracyclines, and oseltamivir. The aminoglycoside concentrations in fetal serum are 20%
to 50% of those in maternal serum. Cephalosporins, carbapenems, nafcillin, oxacillin,
2
clindamycin, and vancomycin penetrate poorly (10%–30%), and fetal concentrations of
erythromycin and azithromycin are less than 10% of those in the mother.
Antimicrobial Therapy for Neonates

The most current updated information on the PK and safety of antimicrobials and other
agents in human milk can be found at the National Library of Medicine LactMed website
(www.ncbi.nlm.nih.gov/books/NBK501922; accessed August 7, 2024).135
In general, neonatal exposure to antimicrobials in human milk is minimal or insignifi-
cant. Aminoglycosides, β-lactams, ciprofloxacin, clindamycin, macrolides, fluconazole,
and agents for tuberculosis are considered safe for the mother to take during breastfeed-
ing.136,137 The most commonly reported neonatal side effect of maternal antimicrobial
use during breastfeeding is increased stool output.138 Clinicians should recommend that
mothers alert their pediatric health care professional if stool output changes occur. Mater-
nal treatment with sulfa-containing antibiotics should be approached with caution in the
breastfed infant who is jaundiced or ill.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 107

3. Preferred Therapy for Specific Bacterial and Mycobacterial Pathogens

NOTES
• A list of table abbreviations and acronyms can be found at the start of this publication
• For fungal, viral, and parasitic infections, see Chapters 5, 7, and 9, respectively. 3
• Limitations of space do not permit listing of all possible alternative antimicrobials.

Preferred Therapy for Bacterial & Mycobacterial Pathogens

• Again this year, cefotaxime, a third-generation cephalosporin approved by the US
Food and Drug Administration for children more than 3 decades ago, is not given as
an option for therapy for pathogens, as it is not routinely available in the United States
and we believe that it may not return. Ceftriaxone has a virtually identical antibacterial
spectrum of activity to cefotaxime; cefepime is very similar in gram-positive activ-
ity but adds Pseudomonas aeruginosa (and some enhanced activity for Enterobacter,
Serratia, and Citrobacter) to the gram-negative activity of cefotaxime; ceftazidime
adds Pseudomonas activity but loses gram-positive activity, compared with cefotaxime.
Cefepime, ceftazidime, and, of course, ceftriaxone have been documented to be effec-
tive in pediatric meningitis clinical trials. We are not aware if these alternative antibiot-
ics, compared with cefotaxime, have resulted in an increased failure rate in treating
children, although problems with ceftriaxone and the biliary tract with prolonged
therapy, known since the original approval of ceftriaxone, continue to be reported.
 108 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

A. COMMON BACTERIAL PATHOGENS AND USUAL PATTERN OF

SUSCEPTIBILITY TO ANTIBIOTICS (GRAM POSITIVE)
Commonly Used Antibiotics (One Agent per Class Listed)
(scale — to ++ defined in footnote)
3 Ampicillin/ Amoxicillin/ Methicillin/
Penicillin Amoxicillin Clavulanate Oxacillin
Preferred Therapy for Bacterial & Mycobacterial Pathogens

Enterococcus faecalisa ++ ++ + —
Enterococcus faeciuma ++ ++ + —
Nocardia spp b
— — ± —
Staphylococcus, coagulase- — — — ±
negative
Staphylococcus aureus, — — — —
methicillin-resistant
Staphylococcus aureus, — — — ++
methicillin-susceptible
Streptococcus pneumoniae ++ ++ ++ +
Streptococcus pyogenes ++ ++ ++ ++
NOTE: ++ = preferred; + = acceptable; ± = possibly effective (see text for further discussion); — = unlikely to be
effective.
a
Need to add gentamicin or other aminoglycoside to ampicillin/penicillin or vancomycin for in vitro bactericidal
activity.
b
Nocardia is usually susceptible to TMP/SMX, carbapenems (meropenem), and amikacin.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 109

Commonly Used Antibiotics (One Agent per Class Listed)

(scale — to ++ defined in footnote)
Cefazolin/ 3
Cephalexin Vancomycin Clindamycin Linezolid Daptomycin Ceftaroline

Preferred Therapy for Bacterial & Mycobacterial Pathogens

— + — + + —
— + — + + —
— — — + — —
± ++ + ++ ++ ++

— ++ ++ ++ ++ ++

++ ++ + ++ ++ ++

++ + + ++ + ++
++ + ++ + ++ ++
 110 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

B. COMMON BACTERIAL PATHOGENS AND USUAL PATTERN OF

SUSCEPTIBILITY TO ANTIBIOTICS (GRAM NEGATIVE)a
Antibiotics (One Agent per Class Listed)
(scale — to ++ defined in footnote)
3 Ampicillin/ Amoxicillin/ Cefazolin/
Amoxicillin Clavulanate Cephalexin Cefuroxime Ceftriaxone CAZ/AVI Cefiderocol
Preferred Therapy for Bacterial & Mycobacterial Pathogens

Acinetobacter spp — — — — + + ++
Burkholderia — — — — — ++ ++
cepacia
Citrobacter spp — — — + + ++ ++
Enterobacter sppb — — — ± + ++ ++
Escherichia coli c
+ + + ++ d
++ d
++ ++
Haemophilus + ++ + ++ ++ ++ ++
influenzaef
Klebsiella sppc — — + ++ ++ ++ ++
Neisseria ++ ++ + ++ +
meningitidis
Pseudomonas — — — — — ++ ++
aeruginosab
Salmonella, non- + ++ ++ ++ ++
typhoid spp
Serratia sppb — — — ± + ++ ++
Shigella spp + ++ + + ++ ++ ++
Stenotrophomonas — — — — — + ++
maltophilia
NOTE: ++ = preferred; + = acceptable; ± = possibly effective (see text for further discussion); — = unlikely to be
effective; [blank cell] = untested.
a
CDC (NARMS) statistics for each state, by year, are found for many enteric pathogens on the CDC website at https://
wwwn.cdc.gov/narmsnow and are also provided by the SENTRY surveillance system (JMI Laboratories); we also use
current pediatric hospital antibiograms from the editors’ hospitals to assess pediatric trends. When sufficient data are
available, pediatric community isolate susceptibility data are used. Nosocomial resistance patterns may be quite
different, usually with increased resistance, particularly in adults; please check your local/regional hospital
antibiogram for your local susceptibility patterns.
b
AmpC will be constitutively produced in low frequency in every population of organisms and will be selected out
during therapy with 3rd-generation cephalosporins if used as single-agent therapy.
c
Rare carbapenem-resistant isolates in pediatrics (KPC, NDM strains).
d
Will be resistant to virtually all current cephalosporins if ESBL producing.
e
Follow the MIC, not the report for susceptible (S), intermediate (I), or resistant (R), as some ESBL producers will have
low MICs and can be effectively treated with higher dosages.
f
Will be resistant to ampicillin/amoxicillin if BL producing.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 111

Antibiotics (One Agent per Class Listed)

(scale — to ++ defined in footnote)
Meropenem/ Piperacillin/ TMP/ 3
Ceftazidime Cefepime Imipenem Tazobactam SMX Ciprofloxacin Gentamicin

Preferred Therapy for Bacterial & Mycobacterial Pathogens

+ + + + + + —
+ + + — +d — —

+ ++ ++ + ++ ++ +
+ ++ ++ + ++ ++ +
++ d
++ e
++ ++ + ++ +
++ ++ ++ ++ ++ ++ ±

++ ++e ++ ++ ++ ++ ++
+ ++ ++ ++ +

+ ++ ++ ++ — ++ +

++ ++ ++ ++ ++ ++ +

+ ++ ++ + ++ ++ ++
++ ++ ++ ++ ± ++
+ ± — ± ++ + —
 112 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

C. COMMON BACTERIAL PATHOGENS AND USUAL PATTERN OF

SUSCEPTIBILITY TO ANTIBIOTICS (ANAEROBES)
Commonly Used Antibiotics (One Agent per Class Listed)
(scale — to ++ defined in footnote)
3 Ampicillin/ Amoxicillin/
Penicillin Amoxicillin Clavulanate Cefazolin Cefoxitin
Preferred Therapy for Bacterial & Mycobacterial Pathogens

Anaerobic streptococci ++ ++ ++ ++ ++
Bacteroides fragilis ± ± ++ — +
Clostridia (eg, tetani, ++ ++ ++ +
perfringens)
Clostridioides (formerly — — — —
Clostridium) difficile
NOTE: ++ = preferred; + = acceptable; ± = possibly effective (see text for further discussion); — = unlikely to be
effective; [blank cell] = untested.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 113

Commonly Used Antibiotics (One Agent per Class Listed)

(scale — to ++ defined in footnote)
Ceftriaxone/ Meropenem/ Piperacillin/ 3
Cefepime Imipenem Tazobactam Metronidazole Clindamycin Vancomycin

Preferred Therapy for Bacterial & Mycobacterial Pathogens

++ ++ ++ ++ ++ ++
— ++ ++ ++ +

± ++ ++ ++ + ++

— ++ ++ — ++
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

114 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Acinetobacter baumannii1–7 Sepsis, meningitis, nosocomial Cefepime; meropenem (BIII) or Multiple mechanisms of resistance
pneumonia, wound infection other carbapenem. exist, with no single antibiotic
Use culture results to guide that will be routinely effective
therapy. Consult an ID specialist against all strains. Possible
for highly MDR strains. options: ceftazidime ± avibactam,
amp/sul, PIP/TAZO, TMP/SMX,
ciprofloxacin, tigecycline/
eravacycline, colistin/polymyxin B.
Cefiderocol3 and durlobactam/
sulbactam,1,2 approved for adults,
are currently under active
pediatric investigation.
Watch for emergence of resistance
during therapy, including to
colistin.
Consider combination therapy for
life-threatening infection.7
Inhaled colistin for pneumonia
caused by MDR strains (BIII).
Actinomyces israelii8,9 Actinomycosis (cervicofacial, Penicillin G; ampicillin (CIII) Amoxicillin, doxycycline,
thoracic, abdominal) clindamycin, ceftriaxone,
meropenem, PIP/TAZO, linezolid
Aeromonas hydrophila10 Diarrhea Ciprofloxacin (CIII) TMP/SMX, ceftriaxone, cefepime
Sepsis, cellulitis, necrotizing fasciitis Cefepime (BIII); ciprofloxacin (BIII) Meropenem, TMP/SMX
Aggregatibacter (formerly Periodontitis, abscesses (including Ceftriaxone (CIII) Ampicillin/amoxicillin for BL-negative
Actinobacillus) brain), endocarditis strains, or amox/clav, doxycycline,
actinomycetemcomitans11 TMP/SMX, ciprofloxacin
One of the HACEK organisms that
cause endocarditis
Aggregatibacter (formerly Sepsis, endocarditis, abscesses Ceftriaxone (AII); OR ampicillin (if BL Ciprofloxacin, amox/clav (for strains
Haemophilus) aphrophilus12 (including brain) negative) AND gentamicin (BII) resistant to ampicillin)
One of the HACEK organisms that
cause endocarditis
Anaplasma (formerly Ehrlichia) Human granulocytic anaplasmosis Doxycycline (all ages) (AII) Rifampin, levofloxacin
phagocytophilum13,14
Arcanobacterium haemolyticum15 Pharyngitis, cellulitis, Lemierre Azithromycin (BIII) Erythromycin, ceftriaxone,
syndrome clindamycin, vancomycin
Cephalosporin with or without
gentamicin or macrolide for
invasive disease

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Bacillus anthracis16 Anthrax (cutaneous, GI, Ciprofloxacin (regardless of age) Doxycycline, amoxicillin, levofloxacin,
inhalational, (AIII). clindamycin, penicillin G,
meningoencephalitis) For invasive systemic infection, use vancomycin, meropenem.
combination therapy. Wild-type Bioterror strains may be antibiotic
strains are likely to be susceptible resistant.
to penicillin.
Bacillus cereus or subtilis17,18 Sepsis; toxin-mediated Vancomycin (BIII) Clindamycin, meropenem,
gastroenteritis ciprofloxacin, linezolid, daptomycin
Bacteroides fragilis19,20 Peritonitis, sepsis, abscesses Metronidazole (AI) Meropenem or imipenem (AI); PIP/
TAZO (AI); amox/clav (BII).
Recent surveillance suggests
resistance of up to 25%–50%
globally for clindamycin.
Rarely reported carbapenem
resistance.
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

116 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Bacteroides, other spp19,20 Pneumonia, sepsis, abscesses Metronidazole (BII) Meropenem or imipenem; penicillin G
or ampicillin if BL negative
Bartonella henselae21,22 CSD Azithromycin for lymph node Ciprofloxacin, doxycycline
disease (BII); gentamicin AND
TMP/SMX AND rifampin for
hepatosplenic disease and
osteomyelitis (BIII). For CNS
infection, use ceftriaxone AND
gentamicin ± TMP/SMX (BIII).
Bartonella quintana22,23 Bacillary angiomatosis, peliosis Gentamicin plus rifampin, OR Azithromycin, doxycycline
hepatis, endocarditis doxycycline plus rifampin (BIII);
erythromycin; ciprofloxacin (BIII)
Bordetella pertussis, Pertussis Azithromycin (AIII); erythromycin Clarithromycin, TMP/SMX,
parapertussis24,25 (BII) ciprofloxacin (in vitro data)
Borrelia burgdorferi, Lyme Treatment based on stage of Doxycycline for all ages (AII); Azithromycin.
disease26,27 infection (see Lyme disease in amoxicillin or cefuroxime can be A single course of doxycycline is
Table 1L), and prophylaxis after used in children ≤7 y (AIII); not associated with detectable
high-risk exposure ceftriaxone IV for CNS/meningitis tooth staining in children.
(AII).
Borrelia hermsii, turicatae, parkeri; Relapsing fever Doxycycline for all ages (AIII) Penicillin or erythromycin in children
tick-borne relapsing fever28,29 intolerant of doxycycline (BIII).
A single course of doxycycline is not
associated with detectable tooth
staining in children.
Borrelia recurrentis, louse-borne Relapsing fever Single-dose doxycycline for all ages Penicillin or erythromycin in
relapsing fever28 (AIII) children intolerant of doxycycline
(BIII). Amoxicillin; ceftriaxone.
A single course of doxycycline is
not associated with detectable
tooth staining in children.
Brucella spp30–32 Brucellosis Doxycycline AND rifampin (BIII); OR, For serious infection: doxycycline
See Ch 1. for children ≤7 y: TMP/SMX AND AND gentamicin AND rifampin; or
rifampin (BIII) TMP/SMX AND gentamicin AND
rifampin (AIII). May require
extended therapy (months).
Burkholderia cepacia complex33–36 Pneumonia, sepsis in children with Meropenem (BIII) for severe Cefiderocol, CAZ/AVI, TOL/TAZ,
immunocompromise; pneumonia disease, if susceptible. Consider doxycycline, minocycline,
in children with CF36 CAZ/AVI or cefiderocol for severe ceftazidime, TMP/SMX.
disease if carbapenem resistant Aerosolized antibiotics may provide
(AIII). higher concentrations in lung.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Burkholderia pseudomallei37–39 Melioidosis Meropenem (AIII) or ceftazidime TMP/SMX, doxycycline, or amox/
(BIII), followed by prolonged clav for chronic disease
TMP/SMX for 12 wk (AII)
Campylobacter fetus40–42 Sepsis, meningitis in the neonate, Meropenem (BIII) Ampicillin, gentamicin,
endovascular infection erythromycin, ciprofloxacin
Campylobacter jejuni42,43 Diarrhea Azithromycin (BII); erythromycin Amox/clav, doxycycline,
(BII) ciprofloxacin (very high rates of
ciprofloxacin-resistant strains in
Thailand, Hong Kong, and Spain)
Capnocytophaga canimorsus44,45 Sepsis after dog bite (increased risk Meropenem OR PIP/TAZO; amox/ Clindamycin, penicillin G,
with asplenia) clav (BIII) imipenem, linezolid, ceftriaxone,
amp/sul
Capnocytophaga ochracea46,47 Neonatal sepsis, abscesses Ampicillin, ceftriaxone (BIII); amox/ Meropenem, PIP/TAZO
clav (BIII)
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

118 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Cellulosimicrobium (formerly Wound infection; catheter infection Vancomycin ± rifampin (AIII) Linezolid; resistant to β-lactams,
Oerskovia) cellulans48 macrolides, clindamycin,
aminoglycosides
Chlamydia trachomatis49–51 Lymphogranuloma venereum Doxycycline (AII) Azithromycin, erythromycin
Urethritis, cervicitis Doxycycline (AII) Azithromycin, erythromycin, ofloxacin
Inclusion conjunctivitis of newborn Azithromycin (AIII) Erythromycin
Pneumonia of infancy Azithromycin (AIII) Erythromycin, ampicillin
Trachoma Azithromycin (AI) Doxycycline, erythromycin
Chlamydophila (formerly Pneumonia Azithromycin (AII); erythromycin Doxycycline, levofloxacin
Chlamydia) pneumoniae49,50,52 (AII)
Chlamydophila (formerly Psittacosis, pneumonia Doxycycline (AII) for >7 y; Levofloxacin
Chlamydia) psittaci53 azithromycin (AIII) OR
erythromycin (AIII) for ≤7 y
Chromobacterium violaceum54–56 Sepsis, pneumonia, abscesses Meropenem ± ciprofloxacin Susceptibility is variable. Other options
depending on severity of the may include TMP/SMX, cefepime,
disease (AIII) amikacin, imipenem, ceftriaxone,
ceftazidime, and PIP/TAZO.
Citrobacter koseri (formerly Meningitis, sepsis C freundii may develop ampC- Ciprofloxacin, PIP/TAZO, ceftriaxone
diversus), freundii57,58 mediated resistance to AND gentamicin, TMP/SMX,
3rd-generation cephalosporins colistin
after exposure to these antibiotics; Carbapenem-resistant strains now
cefepime should be active against reported; may be susceptible to
most ampC BL-expressing strains; CAZ/AVI, mero/vabor, IMI/REL, or
meropenem will be active against cefiderocol5,57
both ampC and ESBL-expressing
strains.
Clostridioides (formerly Clostridium) Antibiotic-associated colitis Treatment stratified by severity and Stop the predisposing antimicrobial
difficile59–61 See Clostridioides difficile in Table recurrence therapy, if possible.
1H under Diarrhea/ For the initial episode For relapsing C difficile enteritis,
Gastroenteritis. Mild to moderate illness: consider pulse therapy with
metronidazole PO or vancomycin vancomycin (1 wk on/1 wk off for
PO 3–4 cycles) or prolonged tapering
Severe illness: vancomycin PO or therapy.
fidaxomicin PO62 No pediatric data on fecal
Severe and complicated/systemic transplant for recurrent disease.
illness: vancomycin PO or Bezlotoxumab can be considered to
fidaxomicin PO AND reduce the chance of recurrence
metronidazole IV ± vancomycin in high-risk patients.
per rectum
Clostridium botulinum63–65 Botulism: foodborne; wound; Botulism antitoxin heptavalent For more information, call your
potentially bioterror related (equine) types A–G FDA state health department or the
approved in 2013 CDC clinical emergency botulism
No antibiotic treatment except for service, 770-488-7100 (www.cdc.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

wound botulism when gov/botulism/treatment/index.
debridement and treatment for html; accessed October 21, 2024).
vegetative organisms should be For bioterror public exposure,
provided after antitoxin is treatment recommendations will
administered (penicillin G or be emergently posted on the
metronidazole) (no controlled CDC website.
data)
Infant botulism Human botulism immune globulin BabyBIG available nationally from
for infants (BabyBIG) (AII) the California Department of
No antibiotic treatment Public Health at 510-231-7600
(https://infantbotulism.org;
accessed November 11, 2024).
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

120 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Clostridium perfringens66,67 Gas gangrene/necrotizing fasciitis/ Penicillin G AND clindamycin for Meropenem, metronidazole,
sepsis (also caused by Clostridium invasive infection (BII); no clindamycin monotherapy
sordellii, septicum, novyi) antimicrobials indicated for No defined benefit of hyperbaric
Food poisoning foodborne illness. The oxygen over aggressive surgery/
clindamycin is recommended by antibiotic therapy
some experts to inhibit toxin
production.
Clostridium tetani68–70 Tetanus TIG 500 U (previously 3,000– Prophylaxis for contaminated
6,000 U) IM, with part injected wounds: 250 U IM for those with
directly into the wound (IVIG at <3 tetanus immunizations.
200–400 mg/kg if TIG not Start/continue immunization for
available) tetanus.
Metronidazole (AIII) OR penicillin G Alternative antibiotics: meropenem;
(BIII) doxycycline, clindamycin.
Corynebacterium diphtheriae71 Diphtheria Diphtheria equine antitoxin Antitoxin protocol: www.cdc.gov/
(available through the CDC diphtheria/downloads/protocol.
Emergency Operations Center, pdf (version 12.0; February 9,
770-488-7100, under an 2023; accessed October 21, 2024)
investigational protocol [www.
cdc.gov/diphtheria/hcp/dat/
index.html; accessed October 21,
2024) AND erythromycin or
penicillin G (AIII)
Corynebacterium jeikeium72,73 Sepsis, endocarditis, nosocomial Vancomycin (AIII) Daptomycin (emerging resistance
infections reported), tigecycline, linezolid
Corynebacterium minutissimum74,75 Erythrasma; bacteremia in Erythromycin or clindamycin PO for Topical 1% clindamycin for
compromised hosts erythrasma (BIII); OR, for cutaneous infection; meropenem,
bacteremia,75 vancomycin OR penicillin/ampicillin, ciprofloxacin
Coxiella burnetii76,77 Q fever Acute infection: doxycycline (all Alternative for acute infection:
See Q fever in Table 1L. ages) (AII) TMP/SMX
Chronic infection or endocarditis Alternative for chronic infection:
(course not well-defined): TMP/SMX AND doxycycline (BII);
doxycycline for children >7 y OR levofloxacin AND rifampin
AND hydroxychloroquine for
18–36 mo
Cutibacterium (formerly In addition to acne, invasive Penicillin G (AIII); vancomycin (AIII) Ceftriaxone, doxycycline,
Propionibacterium) acnes78,79 infection: sepsis, postoperative clindamycin, linezolid,
wound/shunt infection daptomycin
Resistant to metronidazole
Ehrlichia chaffeensis,14,80 muris80,81 Human monocytic ehrlichiosis Doxycycline (all ages) (AII) Rifampin
Ehrlichia ewingii14,80 E ewingii ehrlichiosis Doxycycline (all ages) (AII) Rifampin
Eikenella corrodens82,83 Human bite wounds; respiratory Amox/clav PO; ceftriaxone; PIP/TAZO, amp/sul, ciprofloxacin
tract and GI tract abscesses, meropenem/imipenem Resistant to clindamycin,

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

meningitis, endocarditis For BL-negative strains: ampicillin; cephalexin, erythromycin
penicillin G (BIII)
Elizabethkingia (formerly Sepsis, meningitis (particularly in Levofloxacin; TMP/SMX (BIII) PIP/TAZO, minocycline, vancomycin.
Chryseobacterium) neonates) Rifampin may be added to another
meningoseptica84,85 active drug.
Enterobacter spp5,57,58,86–89 Sepsis, pneumonia, wound Cefepime; meropenem; PIP/TAZO CAZ/AVI, ertapenem, imipenem,
infection, UTI (BII) ceftriaxone AND gentamicin,
TMP/SMX, ciprofloxacin
Emerging carbapenem-resistant
strains worldwide89
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

122 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Enterococcus spp90–92 Endocarditis, UTI, intra-abdominal Ampicillin AND gentamicin (AI), OR For strains resistant to gentamicin
abscess vancomycin AND gentamicin (for on synergy testing, use
ampicillin-resistant strains); streptomycin or other active
bactericidal activity present only aminoglycoside for invasive
with combination infections. For vancomycin-
Ampicillin AND ceftriaxone in resistant strains that are also
combination also effective92,93 ampicillin resistant: daptomycin
OR linezolid.91,92
Erysipelothrix rhusiopathiae94 Cellulitis (erysipeloid), sepsis, Invasive infection: ampicillin (BIII); Resistance to penicillin reported.
abscesses, endocarditis penicillin G; ceftriaxone, Ciprofloxacin, erythromycin.
meropenem (BIII) Resistant to vancomycin,
Cutaneous infection: penicillin V; daptomycin, TMP/SMX.
amoxicillin; cephalexin;
clindamycin
Escherichia coli (See Ch 1 for specific UTI, community acquired, not A 1st-, 2nd-, or 3rd-generation Amoxicillin; TMP/SMX if susceptible.
infection entities and references.) hospital acquired cephalosporin PO, IM as empiric Ciprofloxacin if resistant to other
Increasing resistance to therapy (BI) options.
3rd-generation cephalosporins due For hospital-acquired UTI, review
to ESBLs and to carbapenems due hospital antibiogram for best
to carbapenemases (KPC)4,5,88,89 empiric choices.
See Ch 12. TD Azithromycin (AII) Rifaximin (for nonfebrile, non-
bloody diarrhea for children
>11 y); cefixime, ciprofloxacin
 Sepsis, pneumonia, hospital- A 2nd-, 3rd-, or 4th-generation For AmpC-producing strains
acquired UTI cephalosporin IV (BI) (ceftriaxone-resistant): cefepime;
for ESBL-producing strains:
meropenem (AIII) or other
carbapenem; PIP/TAZO and
ciprofloxacin if resistant to other
antibiotics
For KPC-producing strains
(meropenem-resistant): CAZ/AVI
Meningitis Ceftriaxone or cefepime (AIII) For ESBL-producing strains:
meropenem (AIII)
Francisella tularensis95,96 Tularemia Gentamicin (AII) for invasive disease Convalescent PO therapy, or
treatment of mild disease with
doxycycline, ciprofloxacin.
Resistant to β-lactam antibiotics.
Watch for relapse.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Fusobacterium spp97–99 Sepsis, soft tissue infection, Metronidazole (AIII) or clindamycin Penicillin G, PIP/TAZO.
Lemierre syndrome (See Ch 1.) AND ceftriaxone; meropenem Combinations often used for
monotherapy is a reasonable Lemierre syndrome.
option (BIII). Anticoagulation for ongoing
thromboembolic complications.
Gardnerella vaginalis51,100 Bacterial vaginosis Metronidazole (BII) Tinidazole, clindamycin,
metronidazole gel, clindamycin
cream/gel
Haemophilus ducreyi51 Chancroid Azithromycin (AIII); ceftriaxone (BIII) Erythromycin, ciprofloxacin
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

124 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Haemophilus influenzae101 Nonencapsulated strains: URTIs BL negative: ampicillin IV (AI); Levofloxacin, azithromycin, TMP/
(otitis media, sinusitis) amoxicillin PO (AI) SMX
BL positive: ceftriaxone IV, IM (AI);
amox/clav (AI) OR 2nd- or
3rd-generation cephalosporins
PO (AI)
Type b strains in unimmunized BL negative: ampicillin IV (AI); Other regimens: meropenem IV,
children: meningitis, arthritis, amoxicillin PO (AI) levofloxacin IV
cellulitis, epiglottitis, pneumonia BL positive: ceftriaxone IV, IM (AI) or Full IV course (10 days) for
cefepime IV; amox/clav (AI) OR meningitis, but PO step-down
2nd- or 3rd-generation therapy well-documented after
cephalosporins PO (AI) response to treatment of non-
CNS infections
Levofloxacin PO as step-down
therapy for BL-positive strains
Helicobacter pylori102–104 Gastritis, peptic ulcer Triple-agent therapy: clarithromycin For clarithromycin/metronidazole
See Gastritis in Table 1H under (susceptible strains) AND resistance, tetracycline for
Diarrhea/Gastroenteritis. amoxicillin AND omeprazole (AII); children >7 y. Other regimens
ADD metronidazole for suspected include bismuth in addition to
resistance to clarithromycin. other proton pump inhibitors.
Kingella kingae105,106 Osteomyelitis, arthritis Ampicillin; penicillin G (AII) Cefazolin, ceftriaxone, TMP/SMX,
cefuroxime, ceftaroline,
ciprofloxacin. Resistant to
clindamycin, vancomycin,
linezolid.
Klebsiella spp (Klebsiella UTI A 2nd- or 3rd-generation Use most narrow-spectrum agent
pneumoniae, oxytoca)88,89,107–110 cephalosporin (AII) active against pathogen: TMP/
Increasing resistance to SMX, ciprofloxacin, gentamicin.
3rd-generation cephalosporins ESBL producers should be treated
(ESBLs) and carbapenems (KPC), as with a carbapenem (meropenem,
well as to colistin ertapenem, imipenem), but KPC
See Ch 12. (carbapenemase)-containing
bacteria may require
ciprofloxacin, CAZ/AVI,
colistin.108,109
Sepsis, pneumonia, meningitis, Ceftriaxone; cefepime (AIII) Carbapenem or ciprofloxacin if
hospital-acquired infection For carbapenem-resistant KPC resistant to other routine
strains: CAZ/AVI, mero/vabor, or antibiotics.
IMI/REL. Meningitis caused by ESBL
For carbapenem-resistant NDM producer: meropenem if
strains, use aztreonam AND CAZ/ susceptible.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

AVI. KPC (carbapenemase) producers:
ciprofloxacin, colistin, cefiderocol,
OR CAZ/AVI (approved by the
FDA for children in 2019 and
active against current strains of
KPC108–110).
NDMs, VIMs, and IMPs are MBLs
resistant to CAZ/AVI, requiring
both aztreonam (stable to MBL)
AND CAZ/AVI (stable to AmpC
and ESBL).
Klebsiella granulomatis51 Granuloma inguinale Azithromycin (AII) Doxycycline, TMP/SMX, ciprofloxacin
Legionella spp111 Legionnaires disease Azithromycin (AI) OR levofloxacin Erythromycin, clarithromycin, TMP/
(AII) SMX, doxycycline
Leptospira spp112 Leptospirosis Penicillin G IV (AII); ceftriaxone IV PO therapy: amoxicillin,
(AII) doxycycline, azithromycin
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

126 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Leuconostoc113 Bacteremia Penicillin G (AIII); ampicillin (BIII) Clindamycin, erythromycin,
doxycycline (uniformly resistant
to vancomycin)
Listeria monocytogenes114 Sepsis, meningitis in compromised Ampicillin (ADD gentamicin for Ampicillin AND TMP/SMX;
host; neonatal sepsis severe infection, compromised ampicillin AND linezolid;
hosts including neonates [new levofloxacin
retrospective data in hospitalized Resistant to cephalosporins
adults suggest no benefit from including ceftriaxone
added gentamicin].)115 (AII)
Moraxella catarrhalis116 Otitis, sinusitis, bronchitis Amox/clav (AI), as most are BL TMP/SMX; a 2nd- or 3rd-generation
positive cephalosporin
Morganella morganii57,58,87,117,118 UTI, neonatal sepsis, wound Cefepime (AIII); meropenem (AIII); Intrinsically resistant to penicillin/
infection levofloxacin (BIII) ampicillin and colistin.
PIP/TAZO, ceftriaxone AND
gentamicin, ciprofloxacin, TMP/
SMX.
Has intrinsic inducible ampC BL;
3rd-generation cephalosporins
may be selected for resistance.
MBLs resistant to CAZ/AVI,
requiring both aztreonam (stable
to MBL) AND CAZ/AVI (stable to
AmpC and ESBL), are now
emerging.
Mycobacterium abscessus119–125 Skin and soft tissue infections; All clinical illness presentations: For patients with pulmonary
3 subspecies now identified pneumonia initial treatment depends on disease, the decision to treat is
(abscessus, bolletii, massiliense) whether there is marcrolide (eg, based on clinical symptoms,
clarithromycin or azithromycin) comorbidities, and radiographic
resistance. For susceptible and microbiologic findings. All
isolates, initial therapy should patients with non-pulmonary
include azithromycin OR disease should be treated.
clarithromycin plus amikacin OR Consider consulting an ID
imipenem OR cefoxitin plus 2 of physician. Should test for
the following: omadacycline OR susceptibility to all possible
tigecycline, tedizolid OR linezolid, antibiotic options listed as well as
clofazimine. cefoxitin. May need pulmonary
For macrolide-resistant isolates, resection. Initial intensive phase
initial therapy should include of therapy followed by months of
amikacin plus imipenem OR “maintenance” therapy.
cefoxitin plus 2 of the following:
omadacycline OR tigecycline,

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

tedizolid OR linezolid,
clofazimine.
For pneumonia: same as above for
initial treatment.
Continuation phase: may consider
nebulized amikacin AND 2–3 of
the following antibiotics guided
by drug susceptibility results and
patient tolerance: clofazimine,
linezolid PO OR tedizolid PO,
omadacycline OR, possibly,
bedaquiline.120,123,125
Treatment is for at least 12 mo after
sputum cultures become
negative. All other forms of
disease are treated for at least
6–12 mo.
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

128 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Mycobacterium avium Cervical adenitis Clarithromycin (AII); azithromycin Surgical excision is more likely than
complex119,124,126 (AII) sole medical therapy to lead to
cure.
May increase cure rate with addition
of rifampin or ethambutol.
Pneumonia For pneumonia, ADD rifampin AND Depending on susceptibilities and
ethambutol AND, for severe severity of the illness, ADD
disease, amikacin (AIII).123 amikacin ± ciprofloxacin.
Disseminated disease in competent Clarithromycin or azithromycin Depending on susceptibilities and
host, or disease in AND ethambutol AND rifampin severity of the illness, ADD
immunocompromised host (AIII), AND, for severe disease, additional agents.
amikacin
Mycobacterium bovis127–129 TB (historically not INH AND rifampin (AII); ADD M bovis is always resistant to PZA.
microbiologically or clinically ethambutol for suspected Consider ADDING streptomycin for
differentiated from resistance (AIII). severe infection.
Mycobacterium tuberculosis
infection; causes adenitis,
abdominal TB, meningitis)
Mycobacterium chelonae119,130 Abscesses; catheter infection Clarithromycin or azithromycin Also test for susceptibility to
(AIII); ADD amikacin for invasive tigecycline, TMP/SMX, doxycycline,
disease, ± imipenem if tobramycin, imipenem (more
susceptible (AIII). active than meropenem),130
moxifloxacin, linezolid.
Mycobacterium fortuitum Skin and soft tissue infections; Amikacin AND cefoxitin ± Also test for susceptibility to
complex118,119,124,126,130 catheter infection levofloxacin (AIII) clarithromycin, imipenem,
tigecycline, minocycline,
sulfonamides, doxycycline,
linezolid
Mycobacterium leprae131 Leprosy Dapsone AND rifampin for Consult HRSA (National Hansen’s
paucibacillary (1–5 patches) (AII). Disease [Leprosy] Program) at
ADD clofazimine for lepromatous, www.hrsa.gov/hansens-disease
multibacillary (>5 patches) for advice about treatment and
disease (AII). free antibiotics: 800-642-2477
(reviewed August 2024; accessed
October 21, 2024).
Mycobacterium marinum, Papules, pustules, abscesses Clarithromycin ± ethambutol (AIII) TMP/SMX AND rifampin;
balnei119,132 (swimming pool granuloma) ethambutol AND rifampin,
doxycycline ± 1 or 2 additional
antibiotics
Surgical debridement
Mycobacterium tuberculosis127,133 TB (pneumonia; meningitis; cervical For active infection in children Add streptomycin for severe
See Tuberculosis in Ch 1 for detailed adenitis; mesenteric adenitis; without risk factors for resistance: infection.
recommendations for active osteomyelitis) INH AND rifampin AND PZA (AI); For MDR TB, bedaquiline is FDA
infection, latent infection, and ADD ethambutol for suspected approved for adults and for

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

exposures in high-risk children. resistance. children ≥5 y. The 3-drug PO
For latent infection: INH AND combination of pretomanid,
rifapentine once weekly for 12 wk bedaquiline, and linezolid has
(AII) OR rifampin daily for 4 mo, orphan drug approval for MDR TB
OR INH/rifampin combination in adults, to be taken together for
daily (all ages) for 3 mo OR INH 26 wk.
daily or biweekly for 9 mo (AII). Corticosteroids should be added to
regimens for meningitis,
mesenteric adenitis, and
endobronchial infection (AIII).
Mycoplasma hominis51,134,135 Neonatal infection including Neonates: doxycycline; Usually erythromycin resistant
meningitis/ventriculitis; moxifloxacin
nongonococcal urethritis Urethritis: clindamycin (AIII)
Mycoplasma pneumoniae136,137 Pneumonia Azithromycin (AI); erythromycin Doxycycline and FQs are usually
(BI); macrolide resistance active against macrolide-
emerging worldwide138 susceptible and macrolide-
it t t i
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

130 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Neisseria gonorrhoeae51,139 Gonorrhea; arthritis Formerly, ceftriaxone AND PO cefixime as single-drug therapy
See Gonorrhea in Table 1I. azithromycin or doxycycline (AIII), is no longer routinely
but in 2020, due to increasing recommended due to increasing
resistance to azithromycin (4% in resistance but can be used when
adults), only ceftriaxone is now ceftriaxone cannot.139
routinely recommended. Gentamycin IM + azithromycin for
type I allergy to cephalosporins.
Neisseria meningitidis140,141 Sepsis, meningitis Ceftriaxone (AI) Penicillin G or ampicillin if
susceptible with amoxicillin step-
down therapy for non-CNS
infection
For prophylaxis following exposure:
rifampin or ciprofloxacin
(ciprofloxacin-resistant strains are
now reported). Azithromycin may
be less effective.
Nocardia asteroides, brasiliensis142,143 Pneumonia with abscess, TMP/SMX (AII); sulfisoxazole (BII); Linezolid, ceftriaxone,
cutaneous cellulitis/abscess, brain for severe infection, ADD clarithromycin, minocycline,
abscess imipenem or meropenem AND levofloxacin, tigecycline, amox/
amikacin (AII). clav
Pasteurella multocida144,145 Sepsis, abscesses, animal bite Penicillin G (AIII); ampicillin (AIII); Amox/clav, PIP/TAZO, doxycycline,
wound amoxicillin (AIII) ceftriaxone, cefpodoxime,
cefuroxime, TMP/SMX,
levofloxacin.
Cephalexin may not demonstrate
adequate activity.
Not usually susceptible to
clindamycin or erythromycin.
Peptostreptococcus146 Sepsis, deep head/neck space and Penicillin G (AII); ampicillin (AII) Clindamycin, vancomycin,
IAI meropenem, imipenem,
metronidazole
Plesiomonas shigelloides147,148 Diarrhea, neonatal sepsis, Antibiotics may not be necessary to Meropenem
meningitis treat diarrhea: amox/clav PO or Increasing resistance to TMP/SMX
ciprofloxacin PO (BIII); 2nd- and
3rd-generation cephalosporins
(AIII); azithromycin (BIII). For
meningitis/sepsis: ceftriaxone.
Prevotella (formerly Bacteroides) Deep head/neck space abscess; Metronidazole or clindamycin (AII) PIP/TAZO, cefoxitin, meropenem or
spp,149 melaninogenica dental abscess imipenem (AII)
Propionibacterium (now In addition to acne, invasive Penicillin G (AIII); vancomycin (AIII) Ceftriaxone, doxycycline,
Cutibacterium) acnes78,79 infection: sepsis, postoperative clindamycin, linezolid,
wound/shunt infection daptomycin
Resistant to metronidazole

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Proteus mirabilis150 UTI, sepsis, meningitis Ceftriaxone (AII) for AmpC- PIP/TAZO; cefiderocol; increasing
negative, ESBL-negative strains; resistance to TMP/SMX and FQs,
cefepime for AmpC-positive, particularly in nosocomial isolates
ESBL-negative strains; Rarely contain plasmid-mediated
carbapenem for ESBL-positive ampC BL
strains Colistin resistant
PO therapy: amox/clav; TMP/SMX,
ciprofloxacin
Proteus vulgaris, other spp (indole- UTI, sepsis, meningitis Cefepime for AmpC-positive, ESBL- Imipenem, ertapenem, TMP/SMX,
positive strains)4–6,57,58,88 negative strains; meropenem for cefiderocol, CAZ/AVI for
ESBL producers. Ciprofloxacin; carbapenem resistance
gentamicin if susceptible (BIII). Colistin resistant
Potential ampC hyperproducer (and
some strains with ESBLs), so at
risk for resistance to
3rd-generation cephalosporins.
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

132 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Providencia spp57,58,151 Sepsis Cefepime; ciprofloxacin, PIP/TAZO, Meropenem or other carbapenem
gentamicin (BIII) for ESBL producer; TMP/SMX;
CAZ/AVI for carbapenem
resistance
Colistin and tigecycline resistant
Pseudomonas aeruginosa152–154 UTI Ceftazidime or cefepime (AII); other Amikacin, ciprofloxacin
antipseudomonal β-lactams;
tobramycin
Nosocomial sepsis, pneumonia Cefepime (AI), OR meropenem (AI), Ciprofloxacin AND tobramycin;
OR PIP/TAZO AND tobramycin cefiderocol; colistin.57
(BI), OR ceftazidime AND There is controversy regarding
tobramycin (BII) additional clinical benefit in
outcomes with combination
therapy (including β-lactam/
aminoglycoside combinations or
double β-lactam combinations),
but combinations may increase
the likelihood of empiric active
coverage and decrease the
emergence of resistance.155–157
Prolonged infusion of β-lactam
antibiotics will allow greater
therapeutic exposure to high-MIC
pathogens.
 Pneumonia in CF158–161 Cefepime (AII) or meropenem (AI); Inhalational antibiotics for
See Cystic Fibrosis in Table 1F. OR ceftazidime AND tobramycin prevention of acute
(BII) (AI). exacerbations (but insufficient
Azithromycin provides benefit in evidence to recommend for
prolonging interval between treatment of exacerbation):
exacerbations. tobramycin; aztreonam; colistin.
Many organisms are MDR.
Pseudomonas cepacia, mallei, pseudomallei (See Burkholderia entries earlier in this table.)
Ralstonia162 Bacteremia, pneumonia, Ciprofloxacin, meropenem, Often resistant to β-lactams,
meningitis, osteomyelitis ceftazidime, TMP/SMX aminoglycosides. Data lacking on
preferred therapeutic regimen.
Rhodococcus (formerly equi) Necrotizing pneumonia Vancomycin AND imipenem for Ciprofloxacin or levofloxacin AND
hoagii163 immunocompromised hosts, azithromycin or rifampin;
single-drug therapy for normal doxycycline; linezolid
hosts (AIII)

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Rickettsia164,165 Rocky Mountain spotted fever, Doxycycline (all ages) (AII) Chloramphenicol is less effective
Q fever, typhus, rickettsialpox, than doxycycline.
Ehrlichia infection, Anaplasma A single course of doxycycline is
infection not associated with detectable
dental staining.
Salmonella, non-typhoid spp166–168 Gastroenteritis (may not require Azithromycin (AII) OR ciprofloxacin For susceptible strains when culture
See Salmonellosis in Table 1H under therapy if clinically improving OR ceftriaxone (AII) results are available: cefixime
Diarrhea/Gastroenteritis. and not immunocompromised). (AII), TMP/SMX; ampicillin
Consider treatment for those with
higher risk for invasion (<1 y [or,
with highest risk, those <3 mo],
immunocompromised, and with
focal infections or bacteremia).
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

134 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Salmonella typhi167,169,170 Typhoid fever Azithromycin (AII); ceftriaxone (AII); Obtain blood and stool cultures
See Salmonellosis in Table 1H under cefixime (AII); TMP/SMX (AII); before treatment to allow for
Diarrhea/Gastroenteritis. ciprofloxacin (AII) selection of most narrow-
spectrum antibiotic. Prefer
antibiotics with high intracellular
concentrations (eg, TMP/SMX,
FQs). Amoxicillin acceptable for
susceptible strains.
Serratia marcescens57,58,87–89 Nosocomial sepsis, pneumonia Cefepime; meropenem; PIP/TAZO One of the enteric bacilli that have
(BII) inducible chromosomal AmpC
Potential AmpC constitutive BLs (active against 1st-, 2nd-, and
producer (and some strains with 3rd-generation cephalosporins)
ESBLs) that may be constitutively
produced by organisms within a
population; ertapenem,
imipenem, TMP/SMX,
ciprofloxacin, ceftriaxone AND
gentamicin
Resistant to colistin
Shewanella spp171,172 Wound infection, nosocomial Ceftazidime (AIII) Cefepime, meropenem, PIP/TAZO,
pneumonia, peritoneal-dialysis amp/sul, ciprofloxacin,
peritonitis, ventricular shunt gentamicin
infection, neonatal sepsis Resistant to TMP/SMX and colistin
Shigella spp173–176 Enteritis, UTI, prepubertal vaginitis Mild episodes of enteritis do not Substantial (>30%) resistance to
require treatment. azithromycin now reported in the
Azithromycin (unless local United States, with ciprofloxacin
resistance is high) OR resistance up to 15% but
ciprofloxacin OR cefixime OR ceftriaxone resistance low at
ceftriaxone.176 5%.176 Use most narrow-spectrum
agent active against pathogen:
PO ampicillin (not amoxicillin for
enteritis); TMP/SMX.
Sphingomonas paucimobilis177,178 Bacteremia, wound infection, Antipseudomonal penicillins, Aminoglycosides, TMP/SMX
ocular infection, osteomyelitis carbapenems (BIII)
Spirillum minus179 Rat-bite fever (sodoku) Penicillin G IV (AII); for endocarditis, Ampicillin, doxycycline, ceftriaxone,
ADD gentamicin or streptomycin vancomycin, streptomycin
(AIII).
Staphylococcus aureus (See Ch 1 for specific infections.)180,181

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

– Mild to moderate infections Skin infections, mild to moderate MSSA: a 1st-generation For MSSA: amox/clav.
cephalosporin (cefazolin IV, For CA-MRSA: linezolid IV, PO;
cephalexin PO) (AI); oxacillin/ daptomycin IV has been studied
nafcillin IV (AI), dicloxacillin and FDA approved for use in
PO (AI) children >1 y.183
MRSA: clindamycin (if susceptible)
IV or PO, ceftaroline IV,182
vancomycin IV, or TMP/SMX
PO (AII)
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

136 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
– Moderate to severe infections, Pneumonia, sepsis, myositis, MSSA: oxacillin/nafcillin IV (AI); a For CA-MRSA: linezolid (AII); OR
empiric treatment of CA-MRSA osteomyelitis, etc 1st-generation cephalosporin daptomycin185 for non-pulmonary
(cefazolin IV) (AI) ± gentamicin infection (AII) (studies published
(AIII) on use in children); ceftaroline IV
MRSA: clindamycin (if susceptible) (FDA approved for children)
(AII) OR ceftaroline (AII) OR Approved for adults (primarily for
vancomycin if MIC is ≤2 (AII)184 treatment of MRSA): dalbavancin
Combination therapy with (once-weekly dosing), oritavancin
gentamicin and/or rifampin not (once-weekly dosing), tedizolid
prospectively studied (See Ch 12.)
Staphylococcus, coagulase- Nosocomial bacteremia (neonatal Empiric: vancomycin (AII) OR If susceptible: linezolid; ceftaroline
negative186,187 bacteremia), infected ceftaroline (AII) IV; daptomycin for age >1 y (but
intravascular catheters, CNS not for pneumonia)
shunts, UTI
Stenotrophomonas maltophilia188–190 Sepsis TMP/SMX (AII) Levofloxacin, doxycycline,
minocycline, tigecycline, colistin,
and cefiderocol.190
Consider CAZ/AVI plus aztreonam
for severe infection.88
Streptobacillus moniliformis179,191 Rat-bite fever (Haverhill fever) Penicillin G (AIII); ampicillin (AIII); Doxycycline, ceftriaxone,
for endocarditis, ADD gentamicin carbapenems, clindamycin,
or streptomycin (AIII). vancomycin
Streptococcus, group A192 Pharyngitis, impetigo, adenitis, Penicillin (AI); amoxicillin (AI) A 1st-generation cephalosporin
cellulitis, necrotizing fasciitis (cefazolin or cephalexin) (AI),
clindamycin (AI), a macrolide (AI),
vancomycin (AIII).
For recurrent strep pharyngitis,
clindamycin or amox/clav, or the
addition of rifampin to the last 4
days of penicillin therapy (AIII).
The addition of clindamycin or
linezolid may decrease toxin
production in overwhelming
infection.
Streptococcus, group B193 Neonatal sepsis, pneumonia, Penicillin (AII) or ampicillin (AII) Gentamicin can be used until a
meningitis clinical/microbiologic response
has been documented (AIII).
Streptococcus milleri/anginosus Pneumonia, sepsis, skin and soft Penicillin G (AIII); ampicillin (AIII); Clindamycin, vancomycin

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

group (intermedius, anginosus, tissue infection,194,195 sinusitis,197 ADD gentamicin for serious
and constellatus; includes some arthritis, brain abscess, epidural infection (AIII); ceftriaxone.
ß-hemolytic group C and group G abscess, subdural empyema, Many strains show decreased
streptococci)194–196 meningitis susceptibility to penicillin,
requiring higher dosages to
achieve adequate antibiotic
exposure, particularly in the CNS.
Streptococcus, viridans group Endocarditis198; oropharyngeal, Penicillin G ± gentamicin (AII) OR Vancomycin
(α-hemolytic streptococci, most deep head/neck space infections ceftriaxone ± gentamicin (AII)
commonly Streptococcus
sanguinis, oralis [mitis], salivarius,
mutans, morbillorum)
 Preferred Therapy for Bacterial & Mycobacterial Pathogens

138 — Chapter 3. Preferred Therapy for Bacterial & Mycobacterial Pathogens

D. PREFERRED THERAPY FOR SPECIFIC BACTERIAL AND MYCOBACTERIAL PATHOGENS; PLEASE CHECK CULTURE
SUSCEPTIBILITY PANEL RESULTS FOR INDIVIDUAL CHILDREN
Organism Clinical Illness Drug of Choice (evidence grade) Alternatives
Streptococcus pneumoniae199–201 Sinusitis, otitis (outpatient)202 Amoxicillin, with or without Consider initial use of amoxicillin at
With widespread use of conjugate clavulanate, for first-line therapy. high dosage (90 mg/kg/day div
pneumococcal vaccines, (Adult guidelines recommend bid), especially for children at risk
antibiotic resistance in amox/clav as first-line therapy.) for pen-R strains or more than
pneumococci has decreased.201 “mild” infection. Other options
include cefdinir, with or without
clindamycin; doxycycline
(age >8 y); or levofloxacin.
Meningitis Ceftriaxone (AI): consider addition Penicillin G alone for pen-S strains;
of vancomycin (ie, ceftriaxone- ceftriaxone alone for ceftriaxone-
resistant strains are not common susceptible strains, but can be
in the post-PCV13 era [AIII]). given qd for outpatient
Vancomycin may not be required. management for pen-S strains.
If started, discontinue as soon as Corticosteroids may be considered
susceptibilities are available. if given concurrently with the first
dose of antimicrobial agents,
although data are lacking to
support this approach.
Pneumonia, osteomyelitis/ Ampicillin (AII); ceftriaxone (AI) Penicillin G alone for pen-S strains;
arthritis,199,201 sepsis ceftriaxone alone for ceftriaxone-
susceptible strains and for
outpatient management
Treponema pallidum51,202 Syphilis Penicillin G (AII) Desensitize to penicillin preferred
See Chs 1 and 2. to alternative therapies.
Doxycycline, ceftriaxone.
Ureaplasma urealyticum51,203 Genitourinary infections Azithromycin (AII) Erythromycin; doxycycline, a
quinolone (for adolescent genital
infections)
Neonatal pneumonia Azithromycin (AIII) (effective
clearing of U urealyticum cultures
in preterm neonates
demonstrated, but randomized
trial to treat pneumonia not yet
performed203)
Vibrio cholerae204,205 Cholera Doxycycline (AI), single-dose A single treatment course of
doxycycline is not associated
with tooth staining.
If susceptible, azithromycin (AII):
ciprofloxacin (AII).
Vibrio vulnificus206–208 Sepsis, necrotizing fasciitis Doxycycline AND ceftriaxone (AII) Doxycycline or ciprofloxacin for
or ciprofloxacin AND ceftriaxone. severe diarrhea.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

TMP/SMX AND aminoglycoside as
an alternative.
Ceftazidime may be used in place
of ceftriaxone.
Yersinia enterocolitica209,210 Diarrhea, mesenteric enteritis, TMP/SMX for enteritis (AIII); Gentamicin, doxycycline
reactive arthritis, sepsis ceftriaxone or ciprofloxacin for
invasive infection (AIII)
Yersinia pestis211–213 Plague Gentamicin (AII) OR ciprofloxacin Levofloxacin, streptomycin
See Plague in Table 1L. (AII) for septicemic plague; OR Dual therapy for more severe
doxycycline for bubonic plague disease or for bioterrorism-
related infection
Yersinia pseudotuberculosis209 Mesenteric adenitis; Far East Ceftriaxone, TMP/SMX, or Gentamicin
scarlet-like fever214; reactive ciprofloxacin (AIII)
arthritis
 2025 Nelson’s Pediatric Antimicrobial Therapy — 141

4. Choosing Among Antibiotics Within a Class: β-Lactams and β-Lactamase

Inhibitors, Macrolides, Aminoglycosides, and Fluoroquinolones
Antibiotics should be compared with others regarding (1) antimicrobial spectrum;
(2) degree of antibiotic exposure (a function of the pharmacokinetics [PK] of the
nonprotein-bound drug at the site of infection and the pharmacodynamic impact of
the drug); (3) demonstrated efficacy in adequate and well-controlled clinical trials;
(4) tolerance, toxicity, and side effects; and (5) cost. When a new antibiotic is first 4
approved by regulatory agencies, it is helpful to compare the new agent with other

Choosing Among Antibiotics Within a Class

agents based on publicly available data from controlled clinical trials, particularly
relevant to antibiotics in the same class if already approved for children. If there is
no substantial benefit for efficacy or safety for one antimicrobial over another for the
isolated or presumed bacterial pathogen(s), one should opt for using an older, more
extensively used agent (with presumably better-defined efficacy and safety) that is usu-
ally less expensive and is preferably narrower in its spectrum of activity. If, however,
newer agents provide an enhanced spectrum of activity against antibiotic-resistant
isolates, they may be necessary for empiric or definitive therapy.
β-Lactams and β-Lactamase Inhibitors
β-Lactam/β-Lactamase Inhibitor (BLI) Combinations. Increasingly studied and
approved by the US Food and Drug Administration (FDA) are β-lactam/BLI combina-
tions that target antibiotic resistance for pathogens with resistance to current β-lactams
based on the presence of many newly emerging β-lactamases (BLs). The β-lactam
antibiotic may have initially demonstrated activity against a pathogen, but if a new BL
is present in that pathogen, it will hydrolyze the β-lactam ring structure and inactivate
the antibiotic. The BLI is usually a β-lactam structure, which explains why it binds
readily to certain BLs and can inhibit their activity; however, the BLI does not usually
demonstrate direct antibiotic activity itself (although some BLIs, like sulbactam, which
demonstrates antibacterial activity against Acinetobacter, have recently been approved
in adults and are being studied in children). Just as different β-lactam antibiotics bind
bacterial target sites with varying affinity (creating a range of susceptibilities based on
their ability to bind and inhibit function), different BLIs will bind the different bacterial
BLs with varying affinity. A BLI that binds well to the Haemophilus influenzae BL may
not bind to and inhibit a Staphylococcus aureus BL or may not bind well to one of the
many Pseudomonas BLs. As amoxicillin and ampicillin were used extensively against
H influenzae following their approval, resistance increased based on the presence of
a BL that hydrolyzes the β-lactam ring of amoxicillin/ampicillin (with up to 40% of
isolates currently demonstrating resistance in some regions). Clavulanate, a BLI that
binds to and inactivates the H influenzae BL, allows amoxicillin/ampicillin to “survive”
and inhibit cell wall formation, leading to the death of the organism. The first oral (PO)
β-lactam/BLI combination of amoxicillin/clavulanate, originally known as Augmentin,
has been very effective. Similar combinations, primarily intravenous (IV), have now
 142 — Chapter 4. Choosing Among Antibiotics Within a Class

been studied, pairing penicillins, cephalosporins, and carbapenems with BLIs such as
tazobactam, sulbactam, avibactam, and relebactam as well as with new increasingly
broad-spectrum BLIs including vaborbactam, durlobactam, taniborbactam, and many
others in development.
β-Lactam Antibiotics
Oral Cephalosporins (cephalexin, cefadroxil, cefaclor, cefprozil, cefuroxime, cefix-
4 ime, cefdinir, cefpodoxime, cefditoren [tablet only], and ceftibuten). As a class, the
PO cephalosporins have the advantage over PO penicillins of somewhat greater
Choosing Among Antibiotics Within a Class

spectrum of activity. The serum half-lives of cefpodoxime, ceftibuten, and cefixime are
greater than 2 hours. The spectrum of activity for gram-negative organisms increases
as one goes from the first-generation cephalosporins (cephalexin and cefadroxil), to
the second-generation (cefaclor, cefprozil, and cefuroxime) that demonstrate activ-
ity against H influenzae (including BL-producing strains), to the third-generation
(cefixime, cefdinir, cefpodoxime, cefditoren, and ceftibuten) that have enhanced
coverage of many enteric gram-negative bacilli (GNB; eg, Escherichia coli, Klebsiella
species). However, ceftibuten and cefixime, in particular, have a disadvantage of less
activity against Streptococcus pneumoniae than the others, particularly against penicillin
non-susceptible strains. Currently, no PO cephalosporins exist with activity against
the extended-­spectrum β-lactamases (ESBLs) of E coli/Klebsiella, Pseudomonas, or
methicillin-resistant Staphylococcus aureus (MRSA).
Parenteral Cephalosporins. First-generation cephalosporins, such as cefazolin, are
used mainly for treatment of gram-positive infections caused by S aureus (excluding
MRSA) and group A streptococcus and for surgical prophylaxis; the gram-negative
spectrum is limited but more extensive than for ampicillin. Cefazolin is well tolerated
by intramuscular or IV injection.
A second-generation cephalosporin (cefuroxime) and the cephamycins (cefoxitin and
cefotetan) provide increased activity against many gram-negative organisms, particu-
larly H influenzae and E coli. Cefoxitin has additional activity against up to 80% of
strains of Bacteroides fragilis. In empiric therapy for mild to moderate infections at low
risk of being caused by B fragilis, cefoxitin can be considered for use in place of the
more active agents such as metronidazole or carbapenems.
Third-generation cephalosporins (ceftriaxone and ceftazidime) have enhanced
potency against many enteric GNB. As with all cephalosporins, though, they are
less active against enterococci and Listeria at readily achievable serum concentra-
tions. Only ceftazidime has significant activity against Pseudomonas. Ceftriaxone
has been used very successfully to treat meningitis caused by pneumococcus (mostly
penicillin-susceptible strains), H influenzae type b, meningococcus, and susceptible
strains of E coli. Because ceftriaxone is excreted to a large extent by the liver, it
can be used with little dosage adjustment in patients with renal failure. With a
serum half-life of 4 to 7 hours, it can be given once a day for infections caused by
susceptible organisms. Of great importance, ceftazidime has been paired with the
 2025 Nelson’s Pediatric Antimicrobial Therapy — 143

broad-spectrum BLI avibactam, which allows activity against both cephalosporin-

resistant (ESBL-producing) and carbapenem-resistant (Klebsiella pneumoniae car-
bapenemase [KPC]–producing) gram-negative pathogens.
Cefepime, a fourth-generation cephalosporin approved for use in children in 1999,
exhibits (1) enhanced antipseudomonal activity over ceftazidime; (2) the gram-positive
activity of second-generation cephalosporins; (3) better activity than earlier generations
against enteric GNB; and (4) stability against the inducible ampC BLs of Enterobacter 4
(and some strains of Citrobacter, Proteus, and Serratia) that can hydrolyze third-

Choosing Among Antibiotics Within a Class

generation cephalosporins. It can be used as single-drug antibiotic therapy against
these pathogens. However, cefepime is hydrolyzed by many of the most widely circulat-
ing ESBL enzymes (and carbapenemases) and should not be used if an ESBL E coli or
Klebsiella is suspected.
Ceftaroline and ceftobiprole are fifth-generation cephalosporins, with activity against
MRSA. Ceftaroline was approved by the FDA for adults in 2010, approved for chil-
dren in 2016 for treatment of complicated skin infections (including MRSA) and
community-­acquired pneumonia (CAP), and approved for neonates in 2019. Cefto-
biprole was approved on April 3, 2024, for CAP in children down to 3 months of age,
but it is also approved for S aureus bacteremia, endocarditis, and skin infections in
adults.1 The PK of ceftaroline have been evaluated in all pediatric age-groups, including
neonates, and in children with cystic fibrosis (CF); clinical studies for pediatric CAP
and complicated skin infection are published.2,3 Based on these published data and
postmarketing experience for infants and children, we believe that ceftaroline should
be as effective as and perhaps safer than vancomycin for treatment of MRSA infec-
tions. Just as β-lactams such as cefazolin are preferred treatment over vancomycin for
methicillin-susceptible S aureus infections, ceftaroline may be preferred over vanco-
mycin for MRSA infection. Neither renal function nor drug levels need to be followed
with ceftaroline therapy. Limited PK and clinical data also support the use of ceftaroline
in neonates in which coagulase-negative staphylococci are the most common patho-
gens causing catheter-related bloodstream infections. Experience with ceftobiprole in
children is currently limited. Although ceftobiprole is likely to be comparable in efficacy
to ceftaroline, it does not provide significant benefits over ceftaroline, so for now, we
continue to recommend ceftaroline as the preferred fifth-generation drug.
Cefiderocol4,5 is an advanced-spectrum cephalosporin, approved for adults with
complicated urinary tract infections (cUTIs) and nosocomial pneumonia (including
ventilator-associated pneumonia), with a unique mechanism of entry into bacterial
cells. It covers some difficult-to-treat multidrug-resistant gram-negative pathogens,
including Acinetobacter, Pseudomonas, and Stenotrophomonas, so we are looking for-
ward to approval for children, hopefully by next year. Neonatal studies have started.
Penicillinase-Resistant Penicillins (dicloxacillin [capsules only]; nafcillin and oxacillin
[parenteral only]). “Penicillinase” refers specifically to the BL produced by S aureus
in this case and not those produced by gram-negative bacteria. These antibiotics are
 144 — Chapter 4. Choosing Among Antibiotics Within a Class

active against penicillin-resistant (pen-R) S aureus but not against MRSA. Nafcillin
differs pharmacologically from the others because it is excreted primarily by the liver
rather than by the kidneys, which may explain the relative lack of nephrotoxicity when
this penicillin is compared with methicillin, which is no longer available in the United
States. Nafcillin PK are erratic in people with liver disease, and the drug often causes
painful phlebitis with IV infusion.
4 Antipseudomonal and Anti-Enteric Gram-Negative β-Lactams (ceftazidime,
cefepime, meropenem, imipenem, ertapenem, aztreonam, piperacillin/tazobactam
Choosing Among Antibiotics Within a Class

[PIP/TAZO], ceftazidime/avibactam [CAZ/AVI], and ceftolozane/tazobactam [TOL/

TAZ]). Still under investigation in children, but approved for adults, are cefiderocol,
imipenem/relebactam (IMI/REL), meropenem/vaborbactam, sulbactam/durlobac-
tam, and cefepime/enmetazobactam. The BLI (tazobactam, avibactam, vaborbactam,
durlobactam, or enmetazobactam in these combinations) binds irreversibly to and
neutralizes specific BL enzymes produced by the organism. The combination adds to
the spectrum of the original antibiotic only when the mechanism of resistance is a BL
enzyme and only when the BLI is capable of binding to and inhibiting that particular
organism’s BL enzyme(s). The combinations extend the spectrum of activity of the pri-
mary antibiotic to include many BL-positive bacteria, including some strains of enteric
GNB (E coli, Klebsiella, Enterobacter, and Serratia), S aureus, and B fragilis. Strains of
Pseudomonas may still be resistant to PIP/TAZO, TOL/TAZ, CAZ/AVI, and IMI/REL
and other β-lactam/BLI combinations because of many other non-BL mechanisms of
resistance.
In general, use ceftazidime and cefepime over meropenem and imipenem, given the
narrower spectrum of activity. However, Pseudomonas has an intrinsic capacity to
develop resistance following exposure to any antibiotic, including β-lactam antibiotics,
based on multiple mechanisms of resistance: inducible chromosomal BLs, upregulated
efflux pumps, changes in the permeability of the cell wall, and mutational changes in the
antibacterial target sites. Because development of resistance during therapy can occur
(particularly BL-mediated resistance against ceftazidime), close monitoring is recom-
mended. Cefepime, meropenem, and imipenem are relatively more stable to the BLs, but
resistance can still develop to these agents based on other mechanisms. For carbapenem
resistance, speak with an infectious diseases specialist, but CAZ/AVI is stable to the more
common serine carbapenemases and cefiderocol to the increasingly common metallo-
carbapenemases (see Carbapenems later in this section of the chapter).
Aminopenicillins (amoxicillin and amoxicillin/clavulanate [PO formulations only, in
the United States], ampicillin [PO and parenteral], and ampicillin/sulbactam [paren-
teral only]). Amoxicillin is very well absorbed, good tasting, and associated with very
few side effects. Augmentin is a combination of amoxicillin and clavulanate (as noted
previously) that is available in several fixed proportions that permit amoxicillin to
remain active against many BL-producing bacteria, including H influenzae and S aureus
(but not MRSA). Amoxicillin/clavulanate has undergone many changes in formulation
since its introduction in 1985. The ratio of amoxicillin to clavulanate was originally 4:1,
 2025 Nelson’s Pediatric Antimicrobial Therapy — 145

based on susceptibility data of pneumococcus and Haemophilus during the 1970s. With
the emergence of pen-R pneumococcus, recommendations for increasing the dosage of
amoxicillin were made, particularly for upper respiratory tract infections. If, however,
one increases the dosage of clavulanate, the incidence of diarrhea increases. By keeping
the dosage of clavulanate constant while increasing the dosage of amoxicillin, one can
treat the relatively resistant pneumococci while not increasing gastrointestinal side
effects of the combination. The original 4:1 ratio is present in suspensions containing
4
125 and 250 mg of amoxicillin per 5 mL and the 125- and 250-mg chewable tablets. A
higher 7:1 ratio is present in the suspensions containing 200 and 400 mg of amoxicil-

Choosing Among Antibiotics Within a Class

lin per 5 mL and in the 200- and 400-mg chewable tablets. A still higher ratio of 14:1
is present in the suspension formulation Augmentin ES-600 that contains 600 mg of
amoxicillin per 5 mL; this preparation is designed to deliver
90 mg/kg/day of amoxicillin, divided twice daily, for the treatment of ear (and sinus)
infections. The high serum and middle ear fluid concentrations achieved with
45 mg/kg/dose, combined with the long middle ear fluid half-life (4–6 hours) of amoxi-
cillin, allow for a therapeutic antibiotic exposure to pathogens in the middle ear with
a twice-daily regimen. However, the prolonged half-life in the middle ear fluid is not
necessarily found in other infection sites (eg, skin, lung tissue, joint tissue), for which
dosing of amoxicillin and Augmentin should continue to be 3 times daily for most
susceptible pathogens.
For older children who can swallow tablets, the amoxicillin to clavulanate ratios are as
follows: 500-mg tablet (4:1); 875-mg tablet (7:1); 1,000-mg tablet (16:1).
Sulbactam, another BLI similar to clavulanate, is combined with ampicillin in a
parenteral formulation. The relatively narrow spectrum of activity of ampicillin
against enteric bacilli limits the activity of this combination, compared with the more
broad spectrum of activity of agents such as piperacillin, ceftazidime, ceftolozane, or
carbapenems when used in β-lactam/BLI combinations. Sulbactam, as a BLI, does not
increase the spectrum of activity beyond what ampicillin can potentially achieve in
organisms without BLs.
Carbapenems. Meropenem, imipenem, and ertapenem are currently available
carbapenems with a broader spectrum of activity than of any other class of β-lactam
currently available. Meropenem, imipenem, and ertapenem are approved by the
FDA for use in children. At present, we recommend them for treatment of infections
caused by bacteria resistant to standard therapy or for mixed infections involving
aerobes and anaerobes. Imipenem has greater central nervous system (CNS) irritabil-
ity than other carbapenems, leading to an increased risk for seizures in children with
meningitis, but this is not clinically significant in children without underlying CNS
inflammation or other predisposing factors. Meropenem was not associated with an
increased rate of seizures, compared with cefotaxime in children with meningitis.
Imipenem and meropenem are active against virtually all coliform bacilli, includ-
ing ceftriaxone-­resistant (ESBL- or ampC-producing) strains; against Pseudomonas
aeruginosa (including most ceftazidime-resistant strains); and against anaerobes,
 146 — Chapter 4. Choosing Among Antibiotics Within a Class

including B fragilis. While ertapenem lacks the excellent activity against P aeruginosa
of the other carbapenems, it has the advantage of a prolonged serum half-life, which
allows for once-daily dosing in adults and children 13 years and older and twice-daily
dosing in younger children. Increasingly emerging strains of K pneumoniae (and E coli)
may contain KPCs that degrade and inactivate all the carbapenems. Less common in
North America are the New Delhi metallo–β-lactamase (NDM)–carrying enteric bacilli
(E coli and Klebsiella) that are also resistant to carbapenems. Multidrug-resistant strains
4
have spread to many parts of the world, reinforcing the need to keep track of your
local antibiotic susceptibility patterns. Carbapenems have been paired with BLIs (eg,
Choosing Among Antibiotics Within a Class

vaborbactam, relebactam) that inhibit serine carbapenemases like KPC but that do not
inhibit the metallo-BL enzymes like NDM. New BLIs that can inhibit NDM are under
investigation, but cefiderocol, currently approved for adults and under investigation in
children, is stable to most metallo-BL like NDM.
Macrolides
Erythromycin is the prototype of macrolide antibiotics. Almost 30 macrolides have
been produced, but only 3 are FDA approved for children in the United States: eryth-
romycin, azithromycin (also called an “azalide”), and clarithromycin, while a fourth,
telithromycin (also called a “ketolide”), is approved for adults and available only in
tablet form. As a class, these drugs achieve greater concentrations intracellularly than
in serum, particularly with azithromycin and clarithromycin. As a result, measuring
serum concentrations is usually not clinically useful. Gastrointestinal intolerance to
erythromycin is caused by the breakdown products of the macrolide. This is much less
of a problem with azithromycin and clarithromycin. Azithromycin, clarithromycin,
and telithromycin extend the clinically relevant activity of erythromycin to include
Haemophilus; azithromycin and clarithromycin also have substantial activity against
certain mycobacteria. Azithromycin is also active in vitro and effective against many
enteric gram-negative pathogens, including Salmonella and Shigella, when given PO.
For many infections, the ability of azithromycin to concentrate intracellularly with drug
accumulation over multiple doses allows dosing just once daily for 3 to 5 days to create
site-of-infection concentrations that are equivalent to 7 to 10 days for more traditional
antibiotics.
Aminoglycosides
Although 5 aminoglycoside antibiotics are available in the United States, only 3 are
widely used for systemic therapy for aerobic gram-negative infections and for synergy
in the treatment of certain infections: gentamicin, tobramycin, and amikacin. Strepto-
mycin and kanamycin have more limited utility than the other agents due to increased
toxicity. Resistance in GNB to aminoglycosides is caused by bacterial enzymes that
adenylate, acetylate, or phosphorylate the aminoglycoside, resulting in inactivity. The
specific activities of each enzyme against each aminoglycoside in each pathogen are
highly variable. As a result, antibiotic susceptibility tests must be done for each ami-
noglycoside drug separately. There are small differences between aminoglycosides in
toxicity to the kidneys and eighth cranial nerve hearing/vestibular function, although
 2025 Nelson’s Pediatric Antimicrobial Therapy — 147

it is uncertain whether these small differences are clinically significant. For all children
receiving a full treatment course of a week or more, it is advisable to monitor peak
and trough serum concentrations early in the course of therapy, as the degree of drug
exposure correlates with toxicity and the elevated trough concentrations may predict
impending drug accumulation. With amikacin, desired peak concentrations are 20 to
35 mcg/mL and trough drug concentrations are less than 10 mcg/mL; for gentamicin
and tobramycin, depending on the frequency of dosing (every 8, 12, or 24 hours), peak
4
concentrations should be 5 to 10 mcg/mL and trough concentrations less than 2 mcg/mL.
Decades ago, children with CF required much greater dosages to achieve equivalent

Choosing Among Antibiotics Within a Class

therapeutic serum concentrations due to enhanced renal clearance, although with
improvements in nutrition and pulmonary function, the differences are far less promi-
nent. Inhaled tobramycin has been very successful in children with CF as prophylaxis
for GNB infections. The role of inhaled aminoglycosides in treatment or prevention
of other gram-negative pneumonias (eg, ventilator-associated pneumonia) has not yet
been defined.
Once-Daily Dosing of Aminoglycosides. Once-daily dosing of 5 to 7.5 mg/kg of gen-
tamicin or tobramycin has been studied in adults and in some neonates and children;
peak serum concentrations are greater than those achieved with dosing 3 times daily.
Aminoglycosides demonstrate concentration-dependent killing of pathogens, suggest-
ing a potential benefit to higher serum concentrations achieved with once-daily dosing.
Regimens giving the daily dosage as a single infusion (rather than as traditionally split
doses every 8 hours) are effective and safe for normal adults and immunocompro-
mised hosts with fever and neutropenia and may be less toxic than 8-hourly dosing.
Experience with once-daily dosing in children is increasing, with similar encouraging
results as noted for adults. A recent Cochrane review for children (and adults) with CF
comparing once-daily with 3-times-daily administration showed equal efficacy with
decreased toxicity in children.3 Once-daily dosing should be considered as effective as
multiple, smaller doses per day and is likely to be safer for children; therefore, it should
be the preferred regimen for treatment.
Fluoroquinolones
Fluoroquinolone (FQ) toxicity to cartilage in weight-bearing joints of experimental
juvenile animals was first documented to be dose and duration-of-therapy dependent
more than 40 years ago. Pediatric studies were therefore not initially undertaken with
ciprofloxacin or other FQs. However, with increasing antibiotic resistance in pediatric
pathogens and an accumulating database in pediatrics suggesting that joint toxicity
may be uncommon, the FDA allowed prospective studies to proceed in 1998. As of
July 2024, no cases of FQ-attributable joint toxicity have been documented to occur
in children with FQs that are approved for use in the United States. Limited published
data are available from prospective, blinded studies to accurately assess this risk. Retro-
spective published data are always difficult to interpret but continue to suggest caution.6
A prospective, randomized, double-blind study of moxifloxacin for intra-abdominal
infection, with 1-year follow-up specifically designed to assess tendon/joint toxicity,
 148 — Chapter 4. Choosing Among Antibiotics Within a Class

demonstrated no concern for toxicity.7 Unblinded studies with levofloxacin for respira-
tory tract infections (RTIs) and unpublished randomized studies comparing cipro-
floxacin with other agents for cUTI suggest the possibility of an uncommon, reversible
FQ-attributable arthralgia, but these data should be interpreted with caution. The use of
FQs for antibiotic-resistant infections where no other active agent is available is reason-
able, while weighing the benefits of treatment against the low risk for toxicity from this
class of antibiotics. The use of a PO FQ when the only alternative is parenteral therapy
4
is also justified.8 For clinicians reading this book, a well-documented case of FQ joint
toxicity in a child is publishable (and reportable to the FDA), and the editors would be
Choosing Among Antibiotics Within a Class

very happy to support such a report. Feel free to contact us if you have a case.
Ciprofloxacin usually has very good gram-negative activity (with great regional varia-
tion in susceptibility) against enteric bacilli (E coli, Klebsiella, Enterobacter, Salmonella,
and Shigella) and against P aeruginosa. However, it lacks substantial gram-positive
coverage and should not be used to treat streptococcal, staphylococcal, or pneumococ-
cal infections. Levofloxacin and moxifloxacin are more active against these pathogens;
levofloxacin has documented efficacy and safety in pediatric clinical trials for RTIs,
acute otitis media, and CAP. Children with any question of joint/tendon/bone toxicity
in the levofloxacin studies were followed up to 5 years after treatment, with no differ-
ence in joint/tendon outcomes compared to the outcomes of standard FDA-approved
antibiotics used in these studies.9 None of the newer-generation FQs are significantly
more active against gram-negative pathogens than ciprofloxacin. Quinolone antibiotics
are bitter tasting. Ciprofloxacin and levofloxacin are currently available in a suspension
form; ciprofloxacin is FDA approved in pediatrics for cUTIs and inhalation anthrax,
while levofloxacin is approved for plague and inhalation anthrax. Regarding levofloxa-
cin, Johnson & Johnson chose not to apply to the FDA for approval for pediatric RTI
indications, despite successful clinical trials in children. For reasons of safety and to
prevent the emergence of widespread resistance, FQs should not be used for primary
therapy for pediatric infections and should be limited to situations in which safe and
effective alternative PO therapy does not exist.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 149

5. Preferred Therapy for Specific Fungal Pathogens

NOTES
• A list of table abbreviations and acronyms can be found at the start of this publication.
• See Chapter 6 for discussion of the differences between polyenes, azoles, and
echinocandins.

Preferred Therapy for Fungal Pathogens

 Preferred Therapy for Fungal Pathogens

150 — Chapter 5. Preferred Therapy for Fungal Pathogens

A. OVERVIEW OF MORE COMMON FUNGAL PATHOGENS AND THEIR USUAL PATTERN OF ANTIFUNGAL
SUSCEPTIBILITIES
Caspofungin,
Micafungin,
Amphotericin B Anidulafungin,
Fungal Species Formulations Fluconazole Itraconazole Voriconazole Posaconazole Isavuconazole Flucytosine and Rezafungin
Aspergillus ++ — — — — — — ++
calidoustus
Aspergillus + — ± ++ + ++ — +
fumigatus
Aspergillus terreus — — + ++ + ++ — +
Blastomyces ++ + ++ + + + — —
dermatitidis
Candida albicans + ++ + + + + + ++
Candida auris ± — ± ± + + ± ++
Candida ++ ++ + + + + + +
parapsilosis
Candida tropicalis + + + + + + + ++
Clavispora — ++ + + + + + +
(Candida)
lusitaniae
Coccidioides ++ ++ + + ++ + — —
immitis
Cryptococcus spp ++ + + + + + ++ —
Fusarium spp ± — — ++ + + — —
Histoplasma ++ + ++ + + + — —
capsulatum
Lomentospora — — ± ± ± ± — ±
(formerly
Scedosporium)
prolificans
Meyerozyma + ± + + + + + ±
(Candida)
guilliermondii
Mucor spp ++ — ± — + ++ — —
Nakaseomyces + — ± ± ± ± + ±
(Candida)
glabrata
Paracoccidioides + + ++ + + + — —
spp
Penicillium spp ± — ++ + + + — —

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Pichia kudriavzevii + — — + + + + ++
(Candida krusei)
Rhizopus spp ++ — — — + + — —
Scedosporium — — ± + + + — ±
apiospermum
Sporothrix spp + + ++ + + + — —
Trichosporon spp — + + ++ + + — —
NOTE: ++ = preferred; + = acceptable; ± = possibly effective (see text for further discussion); — = unlikely to be effective.
 Preferred Therapy for Fungal Pathogens

152 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Infection
When treating invasive fungal disease with azoles, it is important to document therapeutic serum concentrations, particularly when using PO
therapy. The editors use laboratories that provide high-performance liquid chromatography/mass spectrometry techniques with more rapid
results than from the older microbiologic techniques. One laboratory that provides this service is the University of Texas Health Science Center at
the San Antonio Fungus Testing Laboratory (https://lsom.uthscsa.edu/pathology/reference-labs/fungus-testing-laboratory/antifungal-drug-levels
[accessed September 9, 2024]; 210-567-4029).
Therapy (evidence grade) Comments
Prophylaxis
Prophylaxis of invasive Caspofungin was superior to fluconazole in a Fluconazole is not effective against molds and some strains of
fungal infection in randomized controlled trial of neutropenic children Candida. Posaconazole PO, voriconazole PO, and
patients with with acute myeloid leukemia (AI),12 yet compared to micafungin IV are effective in adults in preventing yeast
hematologic triazoles, caspofungin did not significantly reduce and mold infections but are not all well studied in children
malignancies1–11 incidence of invasive fungal disease in pediatric for this indication.15
recipients of allogeneic hematopoietic cell
transplants.13 Micafungin is safe and effective as
prophylaxis in pediatric autologous hematopoietic
stem cell transplant (AII).14 Fluconazole 6 mg/kg/day
for prevention of infection (AII). Posaconazole for
prevention of infection has been well studied in
adults (AI) and offers anti-mold coverage.4
Prophylaxis of invasive Fluconazole 6 mg/kg/day for prevention of infection AmB, caspofungin, micafungin, voriconazole, or posaconazole
fungal infection in (AII) may be effective in preventing infection.
patients with solid-
organ transplants16–20
Treatment
Aspergillosis1,21–32 Voriconazole (AI) 18 mg/kg/day IV div q12h as LD on Voriconazole is the current guideline-recommended primary
first day, then 16 mg/kg/day IV div q12h as antifungal therapy for all clinical forms of aspergillosis. A
maintenance dose for children aged 2–12 y or 12– recent randomized controlled trial showed that
14 y and weighing <50 kg. In children aged ≥15 y or posaconazole is non-inferior to voriconazole for invasive
12–14 y and weighing >50 kg, use adult dosing (load aspergillosis (AI).35 An earlier randomized controlled trial
12 mg/kg/day IV div q12h on first day, then 8 mg/kg/ showed that isavuconazole was non-inferior to voriconazole
day div q12h as maintenance dose) (AII). When for invasive aspergillosis (AI).30
patient’s condition is stable, may switch from Early initiation of therapy in patients with strongly suspected
voriconazole IV to voriconazole PO at a dose of disease is important while a diagnostic evaluation is
18 mg/kg/day div bid for children 2–12 y and at least conducted.
400 mg/day div bid for children >12 y (AII). Dosing in Optimal voriconazole trough serum concentrations (generally
children <2 y is less clear, but doses are generally thought to be 2–5 mcg/mL) are essential. Check trough
higher due to more rapid clearance (AIII). These are level 2–5 days after initiation of therapy, and repeat the
only initial dosing recommendations; it is critical to following week to verify and 4 days after a change of
understand that continued dosing in all ages is dose.32 It is critical to monitor trough concentrations to

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

guided by close monitoring of trough serum guide therapy due to high inter-patient variability.36 Low
voriconazole concentrations in individual patients voriconazole concentrations are a consistent leading cause
(AII). Unlike in adults, voriconazole PO bioavailability of clinical failure. Younger children (especially <3 y) often
in children is about only 50%–60%, so trough levels have lower trough voriconazole levels and need much
are crucial when using PO.33 higher dosing. Dosing for younger children should begin as
Alternatives for primary therapy when voriconazole listed but will invariably need to be increased.
cannot be administered: isavuconazole (AI), Total treatment course is a minimum of 6 wk, largely
posaconazole (AI), or L-AmB 5 mg/kg/day (AII). dependent on the degree and duration of
Dosing of isavuconazole in children <13 y is 10 mg/ immunosuppression and evidence of disease improvement.
kg (q8h on days 1 and 2 and qd thereafter).34 ABLC is A recent expert panel agreed that primary therapy, with
another alternative. Echinocandin primary confirmed appropriate therapeutic drug levels, should be
monotherapy should not be used for treating given for at least 8 days to show an effect.37
invasive aspergillosis (CII). AmB-D should be used
only in resource-limited settings in which no
alternative agent is available (AII).
(Continued on next page)
 Preferred Therapy for Fungal Pathogens

154 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
Aspergillosis1,21–32 Current guidelines recommend that salvage antifungal
(continued) therapy options after failed primary therapy include a
change of antifungal class (by using L-AmB or an
echinocandin), a switch to isavuconazole, a switch to
posaconazole (serum trough concentrations ≥1 mcg/mL),
or use of combination antifungal therapy. Most experts
would recommend a switch to L-AmB.
Azole monotherapy is not usually recommended after azole
prophylaxis has failed.
Combination antifungal therapy with voriconazole plus an
echinocandin may be considered in select patients. The
addition of anidulafungin to voriconazole as combination
therapy showed some statistical benefit to the combination
over voriconazole monotherapy in only certain patients.38
In vitro data suggest some synergy with 2 (but not 3) drug
combinations: an azole plus an echinocandin is the most
well studied. If combination therapy is used, this is likely
best done initially, when voriconazole trough
concentrations may not yet be appropriate.
Routine antifungal susceptibility testing is not recommended
but is suggested for patients who are suspected of having
an azole-resistant isolate or who are unresponsive to
therapy.
Azole-resistant A fumigatus is increasing. If local
epidemiology suggests >10% azole resistance, initial
empiric therapy should be voriconazole + echinocandin OR
+ L-AmB, and subsequent therapy should be guided by
antifungal susceptibilities.39
Micafungin likely has equal efficacy to caspofungin against
aspergillosis.40
 Return of immune function is paramount to treatment
success; for children receiving corticosteroids, decreasing
the corticosteroid dosage or changing to steroid-sparing
protocols is important.
Bipolaris, Voriconazole (AI) 18 mg/kg/day IV div q12h as LD on Aggressive surgical debulking/excision is essential for CNS
Cladophialophora, first day, then 16 mg/kg/day IV div q12h as lesions.
Curvularia, Exophiala, maintenance dose for children aged 2–12 y or 12– These can be highly resistant infections, so strongly
Alternaria, and other 14 y and weighing <50 kg. In children aged ≥15 y or recommend antifungal susceptibility testing to guide
agents of 12–14 y and weighing >50 kg, use adult dosing (load therapy and consultation with a pediatric ID expert.
phaeohyphomycosis 12 mg/kg/day IV div q12h on first day, then 8 mg/kg/ Antifungal susceptibilities are often variable, but empiric
(dematiaceous, day div q12h as maintenance dose) (AII). When therapy with voriconazole is the best start.
pigmented molds)41–48 patient’s condition is stable, may switch from Optimal voriconazole trough serum concentrations (generally
voriconazole IV to voriconazole PO at a dose of thought to be 2–5 mcg/mL) are important for success.
18 mg/kg/day div bid for children 2–12 y and at least Check trough level 2–5 days after initiation of therapy and
400 mg/day div bid for children >12 y (AII). Dosing in repeat the following week to verify and 4 days after a
children <2 y is less clear, but doses are generally change of dose. It is critical to monitor trough

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

higher due to more rapid clearance (AIII). These are concentrations to guide therapy due to high inter-patient
only initial dosing recommendations; continued variability.36 Low voriconazole concentrations are a leading
dosing in all ages is guided by close monitoring of cause of clinical failure. Younger children (especially <3 y)
trough serum voriconazole concentrations in often have lower voriconazole levels and need much higher
individual patients (AII). Unlike in adults, dosing. Some experts will recommend higher trough levels
voriconazole PO bioavailability in children is about for difficult CNS lesions.
only 50%–60%, so trough levels are crucial. 33

Alternatives could include posaconazole (trough

concentrations >1 mcg/mL) or combination therapy
with an echinocandin + azole or an echinocandin +
L-AmB (BIII).
 Preferred Therapy for Fungal Pathogens

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B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
Blastomycosis (North For moderate to severe pulmonary disease: L-AmB New international guidelines exist.56 All forms of
American)49–55 5 mg/kg IV daily for 1–2 wk or until improvement blastomycosis should be treated. Itraconazole PO soln
noted, then step-down therapy with itraconazole PO provides greater and more reliable absorption than caps,
soln 10 mg/kg/day div bid (max 400 mg/day) for a and only the PO soln should be used (on an empty
total of 6–12 mo (AIII). ABLC is an alternative stomach); serum concentrations of itraconazole should be
formulation if L-AmB is not available. Itraconazole LD determined 5 days after start of therapy to ensure adequate
(double dose for first 2 days) is recommended in drug exposure. For blastomycosis, maintain trough
adults but has not been studied in children (but is itraconazole concentrations 1–2 mcg/mL (values for both
likely helpful). itraconazole and hydroxyl-itraconazole are added together).
For mild to moderate pulmonary disease: itraconazole If only itraconazole caps are available, use 20 mg/kg/day
PO soln 10 mg/kg/day div bid (max 400 mg/day) for div q12h taken with cola drink to increase gastric acidity
a total of 6–12 mo (AIII). Itraconazole LD (double and bioavailability.
dose for first 2 days) is recommended in adults but Alternative to itraconazole: 12 mg/kg/day fluconazole (BIII)
has not been studied in children (but is likely after an LD of 25 mg/kg/day. A case series has shown that
helpful). outcomes of voriconazole are similar to those of
For CNS blastomycosis: L-AmB or ABLC (preferred over itraconazole, and there is little experience with
AmB-D) for 4–6 wk, followed by an azole posaconazole or isavuconazole.
(fluconazole is preferred, at 12 mg/kg/day after an Patients with extrapulmonary blastomycosis should receive at
LD of 25 mg/kg; alternatives for CNS disease are least 12 mo of total therapy; long courses are
voriconazole or itraconazole), for a total of at least recommended for CNS or bone involvement.
12 mo and until resolution of CSF abnormalities (AII). If induction with L-AmB alone is failing, add itraconazole or
Some experts suggest combination therapy with high-dose fluconazole until clinical improvement. Lifelong
L-AmB/ABLC plus high-dose fluconazole as induction itraconazole if immunosuppression cannot be reversed.
therapy in CNS blastomycosis until clinical
improvement (BIII).
Candidiasis57–61
(See Ch 6.)
– Cutaneous Topical therapy (alphabetic order): ciclopirox, Fluconazole 6 mg/kg/day PO qd for 5–7 days
clotrimazole, econazole, haloprogin, ketoconazole, Relapse common with chronic mucocutaneous disease, and
miconazole, oxiconazole, sertaconazole, sulconazole antifungal susceptibilities critical to drive appropriate
– Disseminated infection, An echinocandin is recommended as initial therapy. Prompt removal of an infected IV catheter or any infected
acute (including catheter Caspofungin 70 mg/m2 IV LD on day 1 (max dose devices is absolutely critical to success (AII). Biofilms form
fungemia) 70 mg), followed by 50 mg/m2 IV (max dose 70 mg) early, so prompt removal is preferred.
on subsequent days (AII); OR micafungin 2 mg/kg/ For infections with C krusei or C glabrata, an echinocandin is
day q24h (children weighing <40 kg), with max dose preferred; however, there are increasing reports of some
100 mg/day (AII).62 ABLC or L-AmB 5 mg/kg/day IV C glabrata resistance to echinocandins (treatment would,
q24h (BII) is an effective but less attractive therefore, be L-AmB or ABLC) (BIII). There are increasing
alternative due to potential toxicity (AII). reports of some C tropicalis resistance to fluconazole.
Fluconazole (12 mg/kg/day q24h, after an LD of 25 mg/ L-AmB (5 mg/kg daily) is a reasonable alternative if there is
kg/day) is an alternative for patients who are not intolerance, limited availability, or resistance to other
critically ill and have had no prior azole exposure antifungal agents (AI). Transition from a lipid AmB to
(CIII). A fluconazole LD is standard of care in adult fluconazole is recommended after 5–7 days among patients
patients but has been studied only in infants (not yet who have isolates that are susceptible to fluconazole, who
in children)63; however, it is very likely that the are clinically stable, and in whom repeat cultures during
beneficial effect of an LD extends to children. antifungal therapy are negative (AI).
Fluconazole can be used as step-down therapy in Voriconazole (18 mg/kg/day div q12h LD, followed by 16 mg/
stable neutropenic patients with susceptible isolates kg/day div q12h) is effective for candidemia but offers little

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

and documented bloodstream clearance (CIII). For advantage over fluconazole as initial therapy. Voriconazole
children of all ages receiving ECMO, fluconazole is is recommended as PO step-down therapy for select cases
dosed as a 35 mg/kg LD on day 1, followed by of candidemia due to C krusei or if mold coverage is
12 mg/kg/day (BII).64 needed.
Transition from an echinocandin to fluconazole (usually Follow-up blood cultures should be performed qd or qod to
within 5–7 days) is recommended for non- establish the time point at which candidemia has been
neutropenic patients who are clinically stable, have cleared (AIII).
isolates that are susceptible to fluconazole (eg, Duration of therapy is for 2 wk AFTER negative cultures in
C albicans), and have negative repeat blood cultures pediatric patients without obvious metastatic
following initiation of antifungal therapy (AII). complications and after symptom resolution (AII).
In neutropenic patients, ophthalmologic findings of choroidal
and vitreous infection are minimal until recovery from
neutropenia; therefore, dilated funduscopic examinations
should be performed within the first week after recovery
from neutropenia (AIII).
(Continued on next page)
 Preferred Therapy for Fungal Pathogens

158 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
– Disseminated infection, For CNS infections: L-AmB/ABLC (5 mg/kg/day), and All non-neutropenic patients with candidemia should ideally
acute (including catheter AmB-D (1 mg/kg/day) as an alternative, combined have a dilated ophthalmologic examination, preferably
fungemia) (continued) with or without flucytosine 100 mg/kg/day PO div performed by an ophthalmologist, within the first week
q6h (AII) until initial clinical response, then step- after diagnosis (AIII).
down therapy with fluconazole (12 mg/kg/day q24h,
after an LD of 25 mg/kg/day); echinocandins do not
achieve therapeutic concentrations in CSF.
– Disseminated infection, Initial therapy with lipid formulation AmB (L-AmB or If chemotherapy or hematopoietic cell transplant is required,
chronic (hepatosplenic) ABLC, 5 mg/kg daily) OR an echinocandin it should not be delayed because of the presence of chronic
(caspofungin 70 mg/m2 IV LD on day 1 [max dose disseminated candidiasis, and antifungal therapy should be
70 mg], followed by 50 mg/m2 IV [max dose 70 mg] continued throughout the period of high risk to prevent
on subsequent days OR micafungin 2 mg/kg/day relapse (AIII).
q24h in children weighing <40 kg [max dose
100 mg]) for several weeks, followed by PO
fluconazole in patients unlikely to have a
fluconazole-resistant isolate (12 mg/kg/day q24h,
after an LD of 25 mg/kg/day) (AIII).
Therapy should continue until lesions resolve on repeat
imaging; they usually resolve after several months.
Premature discontinuation of antifungal therapy can
lead to relapse (AIII).
– Neonatal60 AmB-D (1 mg/kg/day) is recommended therapy (AII).65 In nurseries with high rates of candidiasis (>10%), IV or PO
See Ch 2. Fluconazole (12 mg/kg/day q24h, after an LD of 25 mg/ fluconazole prophylaxis (AI) (3–6 mg/kg twice weekly for
kg/day) is an alternative if patient has not been 6 wk) in high-risk neonates (birth weight <1,000 g) is
receiving fluconazole prophylaxis (AII).66 For recommended. PO nystatin, 100,000 U tid for 6 wk, is an
treatment of neonates and young infants alternative to fluconazole in neonates with birth weights
(<120 days) receiving ECMO, fluconazole is loaded <1,500 g when availability or resistance precludes the use
with 35 mg/kg on day 1, followed by 12 mg/kg/day of fluconazole (CII).
q24h (BII).
 L-AmB is an alternative but carries a theoretical risk of LP and dilated retinal examination recommended for
penetrating the urinary tract less than AmB-D (CIII) neonates with cultures positive for Candida spp from blood
would. and/or urine (AIII). Same recommended for all neonates
Duration of therapy for candidemia without obvious with birth weight <1,500 g with candiduria with or without
metastatic complications is for 2 wk AFTER candidemia (AIII).
documented clearance and resolution of symptoms CT or ultrasound imaging of genitourinary tract, liver, and
(therefore, generally 3 wk total). spleen should be performed if blood cultures are
Echinocandins should be used with caution and persistently positive (AIII).
generally limited to salvage therapy or to situations Meningoencephalitis in the neonate occurs at a higher rate
in which resistance or toxicity precludes the use of than in older children/adults.
AmB-D or fluconazole (CIII). A recent randomized Central venous catheter removal is strongly recommended.
trial of caspofungin vs AmB-D showed similar fungal- Infected CNS devices, including ventriculostomy drains and
free survival.67 shunts, should be removed if possible.
Role of flucytosine in neonates with meningitis is
questionable and not routinely recommended due
to toxicity concerns. The addition of flucytosine
(100 mg/kg/day div q6h) may be considered as

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

salvage therapy in patients who have not had a
clinical response to initial AmB therapy, but adverse
effects are frequent (CIII).
– Oropharyngeal, Mild oropharyngeal disease: clotrimazole 10-mg A meta-analysis showed that clotrimazole is less effective
esophageal57 troches PO 5 times daily OR nystatin 100,000 U/mL, than fluconazole but as effective as other topical
4–6 mL qid for 7–14 days. therapies.68
Alternatives also include miconazole mucoadhesive For fluconazole-refractory oropharyngeal or esophageal
buccal 50-mg tab to the mucosal surface over the disease: itraconazole PO soln OR posaconazole OR AmB IV
canine fossa qd for 7–14 days OR 1–2 nystatin OR an echinocandin for up to 28 days (AII).
pastilles (200,000 U each) qid for 7–14 days (AII). Esophageal disease always requires systemic antifungal
Moderate to severe oropharyngeal disease: fluconazole therapy. A diagnostic trial of antifungal therapy for
6 mg/kg PO qd for 7–14 days (AII). esophageal candidiasis is appropriate before performing an
Esophageal candidiasis: PO fluconazole (6–12 mg/kg/ endoscopic examination (AI).
day, after an LD of 25 mg/kg/day) for 14–21 days (AI). Chronic suppressive therapy (3×/wk) with fluconazole is
If cannot tolerate PO therapy, use fluconazole IV OR recommended for recurrent infections (AI).
ABLC/L-AmB/AmB-D OR an echinocandin (AI).
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160 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
– Urinary tract infection Cystitis: fluconazole 6 mg/kg qd IV or PO for 2 wk (AII). Treatment is NOT recommended in asymptomatic candiduria
For fluconazole-resistant C glabrata or C krusei, unless high risk for dissemination; neutropenic low birth
AmB-D for 1–7 days (AIII). weight neonate (<1,500 g); or patient to undergo urologic
Pyelonephritis: fluconazole 12 mg/kg qd IV or PO for manipulation (AIII).
2 wk (AIII) after an LD of 25 mg/kg/day. For Neutropenic patients and low birth weight neonates should
fluconazole-resistant C glabrata or C krusei, AmB-D be treated as recommended for candidemia (AIII).
with or without flucytosine for 1–7 days (AIII). Removing Foley catheter, if present, may lead to a
spontaneous cure in the normal host; check for additional
upper urinary tract disease.
AmB-D bladder irrigation is not generally recommended due
to high relapse rate (an exception may be in fluconazole-
resistant Candida) (CIII). For renal collecting-system fungus
balls, surgical debridement may be required in non-
neonates (BIII).
Echinocandins have poor urinary concentrations. AmB-D has
greater urinary penetration than L-AmB/ABLC.
– Vulvovaginal66 Topical vaginal cream/tabs/suppositories (alphabetic For uncomplicated vulvovaginal candidiasis, no topical agent
order): butoconazole, clotrimazole, econazole, is clearly superior.
fenticonazole, miconazole, sertaconazole, Avoid azoles during pregnancy.
terconazole, or tioconazole for 3–7 days (AI) OR For severe disease, fluconazole 150 mg given q72h for
fluconazole 10 mg/kg (max 150 mg) as a single dose 2–3 doses (AI).
(AII) For recurring disease, consider 10–14 days of induction with
topical agent or fluconazole, followed by fluconazole once
weekly for 6 mo (AI).
In a phase 2 study, ibrexafungerp was effective and well
tolerated (AII).69
Chromoblastomycosis Itraconazole PO soln 10 mg/kg/day div bid for 12– Alternative: terbinafine plus surgery; heat and potassium
(SUBQ infection by 18 mo, in combination with surgical excision or iodide; posaconazole.
dematiaceous fungi)70–74 repeat cryotherapy (AII). Lesions are recalcitrant and difficult to treat.
Itraconazole PO soln provides greater and more
reliable absorption than caps, and only the PO soln
should be used (on an empty stomach); serum
concentrations of itraconazole should be determined
5 days after start of therapy to ensure adequate drug
exposure. Maintain trough itraconazole
concentrations 1–2 mcg/mL (values for both
itraconazole and hydroxyl-itraconazole are added
together).

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

 Preferred Therapy for Fungal Pathogens

162 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
Coccidioidomycosis75–83 For moderate infections: fluconazole 12 mg/kg IV/PO New international guidelines exist.56 Mild pulmonary disease
q24h (AII) after an LD of 25 mg/kg/day. does not require routine therapy in the normal host and
For severe pulmonary disease: AmB-D 1 mg/kg/day IV only requires periodic reassessment. Treatment with
q24h OR ABLC/L-AmB 5 mg/kg/day IV q24h (AIII) as fluconazole or itraconazole should be given to all patients
initial therapy for several weeks until clear with underlying immunosuppression, prolonged infection,
improvement, followed by a PO azole for total underlying cardiopulmonary comorbidities, or complement
therapy of at least 12 mo, depending on genetic or fixation titers of ≥1:32.
immunocompromised risk factors. There is experience with posaconazole for disease in adults
For meningitis: fluconazole 12 mg/kg/day IV q24h (AII) but little experience in children. Isavuconazole experience
after an LD of 25 mg/kg/day (AII). Itraconazole has in adults is increasing.
also been effective (BIII). If no response to azole, use Treat until titers of serum cocci complement fixation drop to
intrathecal AmB-D (0.1–1.5 mg/dose) with or 1:8 or 1:4, at about 3–6 mo.
without fluconazole (AIII). Lifelong azole suppressive Disease in immunocompromised hosts may need to be
therapy required due to high relapse rate. Adjunctive treated longer, including potentially lifelong azole
corticosteroids in meningitis have resulted in less secondary prophylaxis. Watch for relapse up to 1–2 y after
secondary cerebrovascular events.84 therapy.
For extrapulmonary (non-meningeal), particularly for
osteomyelitis, a PO azole such as fluconazole or
itraconazole soln 10 mg/kg/day div bid for at least
12 mo (AIII), and L-AmB/ABLC as an alternative (less
toxic than AmB-D) for severe disease or if worsening.
Itraconazole PO soln provides greater and more
reliable absorption than caps, and only the PO soln
should be used (on an empty stomach); serum
concentrations of itraconazole should be determined
5 days after start of therapy to ensure adequate drug
exposure. Maintain trough itraconazole
concentrations 1–2 mcg/mL (values for both
itraconazole and hydroxyl-itraconazole are added
together).
Cryptococcosis85–89 For mild to moderate pulmonary disease: fluconazole New international guidelines exist.90
12 mg/kg/day (max 400 mg) IV/PO q24h after an LD Serum flucytosine concentrations should be obtained after
of 25 mg/kg/day for 6–12 mo (AII). Itraconazole is an 3–5 days to achieve a 2-h post-dose peak <100 mcg/mL
alternative if cannot tolerate fluconazole. (ideally 30–80 mcg/mL) to prevent neutropenia.
For meningitis or severe pulmonary disease: induction For HIV-positive patients, continue maintenance therapy with
therapy with L-AmB 3–4 mg/kg/day q24h; AND fluconazole (6 mg/kg/day) indefinitely. Initiate HAART 2–
flucytosine 100 mg/kg/day PO div q6h for a 10 wk after commencement of antifungal therapy to avoid
minimum of 2 wk and a repeat CSF culture is immune reconstitution inflammatory syndrome.
negative. In low-resource settings, use L-AmB 10 mg/ In organ transplant recipients, continue maintenance
kg as a single dose and flucytosine. This is followed fluconazole (6 mg/kg/day) for 6–12 mo after consolidation
by consolidation therapy with fluconazole (12 mg/ therapy with higher-dose fluconazole.
kg/day with max dose 400–800 mg after an LD of For cryptococcal relapse, restart induction therapy (this time
25 mg/kg/day) for a minimum of 8 more wk (AI). for 4–10 wk), repeat CSF analysis q2wk until sterile, and
Then use maintenance therapy with fluconazole determine antifungal susceptibility of relapse isolate.
(6 mg/kg/day) or 200 mg daily for 12 mo (AI). Successful use of voriconazole, posaconazole, and
Alternative induction therapies for meningitis or severe isavuconazole for cryptococcosis has been reported in adult
pulmonary disease (order of preference): AmB patients.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

product for 4–6 wk (AII); AmB product plus In resource-limited settings, a recent clinical trial of a single
fluconazole for 2 wk, followed by fluconazole for 10 mg/kg dose of L-AmB plus 14 days of flucytosine +
8 wk (BII); fluconazole plus flucytosine for 6 wk (BII). fluconazole was non-inferior to standard therapy.91
Cryptococcosis85–89 For mild to moderate pulmonary disease: fluconazole New international guidelines exist.90
12 mg/kg/day (max 400 mg) IV/PO q24h after an LD Serum flucytosine concentrations should be obtained after
of 25 mg/kg/day for 6–12 mo (AII). Itraconazole is an 3–5 days to achieve a 2-h post-dose peak <100 mcg/mL
alternative if cannot tolerate fluconazole. (ideally 30–80 mcg/mL) to prevent neutropenia.
For meningitis or severe pulmonary disease: induction For HIV-positive patients, continue maintenance therapy with
therapy with L-AmB 3–4 mg/kg/day q24h; AND fluconazole (6 mg/kg/day) indefinitely. Initiate HAART 2–
flucytosine 100 mg/kg/day PO div q6h for a 10 wk after commencement of antifungal therapy to avoid
minimum of 2 wk and a repeat CSF culture is immune reconstitution inflammatory syndrome.
negative. In low-resource settings, use L-AmB 10 mg/ In organ transplant recipients, continue maintenance
kg as a single dose and flucytosine. This is followed fluconazole (6 mg/kg/day) for 6–12 mo after consolidation
by consolidation therapy with fluconazole (12 mg/ therapy with higher-dose fluconazole.
kg/day with max dose 400–800 mg after an LD of For cryptococcal relapse, restart induction therapy (this time
25 mg/kg/day) for a minimum of 8 more wk (AI). for 4–10 wk), repeat CSF analysis q2wk until sterile, and
Then use maintenance therapy with fluconazole determine antifungal susceptibility of relapse isolate.
(6 mg/kg/day) or 200 mg daily for 12 mo (AI). Successful use of voriconazole, posaconazole, and
Alternative induction therapies for meningitis or severe isavuconazole for cryptococcosis has been reported in adult
pulmonary disease (order of preference): AmB patients.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

product for 4–6 wk (AII); AmB product plus In resource-limited settings, a recent clinical trial of a single
fluconazole for 2 wk, followed by fluconazole for 10 mg/kg dose of L-AmB plus 14 days of flucytosine +
8 wk (BII); fluconazole plus flucytosine for 6 wk (BII). fluconazole was non-inferior to standard therapy.91
 Preferred Therapy for Fungal Pathogens

164 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
Fusarium, Lomentospora Voriconazole (AII) 18 mg/kg/day IV div q12h as LD on These can be highly resistant infections, so strongly
(formerly Scedosporium) first day, then 16 mg/kg/day IV div q12h as recommend antifungal susceptibility testing against a wide
prolificans, maintenance dose for children aged 2–12 y or 12– range of agents to guide specific therapy and consultation
Pseudallescheria boydii 14 y and weighing <50 kg. In children aged ≥15 y or with a pediatric ID expert.
(and its asexual form, 12–14 y and weighing >50 kg, use adult dosing (load Optimal voriconazole trough serum concentrations (generally
Scedosporium 12 mg/kg/day IV div q12h on first day, then 8 mg/kg/ thought to be 2–5 mcg/mL) are important for success.
apiospermum),41,92–96 day div q12h as maintenance dose) (AII). Check trough level 2–5 days after initiation of therapy and
and other agents of When patient’s condition is stable, may switch from repeat the following week to verify and 4 days after a
hyalohyphomycosis voriconazole IV to voriconazole PO at a dose of change of dose. It is critical to monitor trough
18 mg/kg/day div bid for children 2–12 y and at least concentrations to guide therapy due to high inter-patient
400 mg/day div bid for children >12 y (AII). Dosing in variability.36 Low voriconazole concentrations are a leading
children <2 y is less clear, but doses are generally cause of clinical failure. Younger children (especially <3 y)
higher due to more rapid clearance (AIII). These are often have lower voriconazole levels and need much higher
only initial dosing recommendations; continued dosing.
dosing in all ages is guided by close monitoring of Often resistant to AmB in vitro.
trough serum voriconazole concentrations in Alternatives: posaconazole (trough concentrations >1 mcg/
individual patients (AII). Unlike in adults, mL) can be active; echinocandins have been reportedly
voriconazole PO bioavailability in children is about successful as salvage therapy in combination with azoles;
only 50%–60%, so trough levels are crucial at this while there are reports of promising in vitro combinations
stage.33 with terbinafine, terbinafine does not obtain therapeutic
tissue concentrations required for these disseminated
infections; miltefosine (for leishmaniasis) use has been
reported. Olorofim is an investigational agent with
excellent activity against these recalcitrant pathogens.
Histoplasmosis97–99 For severe acute pulmonary disease: ABLC/L-AmB New international guidelines exist.56 Mild pulmonary disease
5 mg/kg/day q24h for 1–2 wk, followed by may not require therapy and, in most cases, resolves in
itraconazole 10 mg/kg/day div bid (max 400 mg 1 mo.
daily) to complete a total of 12 wk (AIII). Add CNS histoplasmosis requires initial L-AmB/ABLC (less toxic
methylprednisolone (0.5–1.0 mg/kg/day) for first 1– than AmB-D) therapy for 4–6 wk, followed by itraconazole
2 wk in patients with hypoxia or significant for at least 12 mo and until CSF antigen resolution.
respiratory distress. Itraconazole PO soln provides greater and more reliable
For mild to moderate acute pulmonary disease: if absorption than caps, and only the PO soln should be used
symptoms persist for >1 mo, itraconazole PO soln (on an empty stomach); serum concentrations of
10 mg/kg/day div bid for 6–12 wk (AIII). itraconazole should be determined 5 days after start of
For progressive disseminated histoplasmosis: therapy to ensure adequate drug exposure. Maintain
ABLC/L-AmB 5 mg/kg/day q24h for 4–6 wk; trough itraconazole concentrations at >1–2 mcg/mL
alternative treatment is L-AmB for 1–2 wk followed (values for both itraconazole and hydroxyl-itraconazole are
by itraconazole 10 mg/kg/day div bid (max 400 mg added together). If only itraconazole caps are available, use
daily) to complete a total of at least 12 mo (AIII). 20 mg/kg/day div q12h taken with cola drink to increase
gastric acidity and bioavailability.
Potential lifelong suppressive itraconazole if cannot reverse

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

immunosuppression.
Corticosteroids recommended for 2 wk for pericarditis with
hemodynamic compromise.
Voriconazole and posaconazole use has been reported.
Fluconazole is inferior to itraconazole.
 Preferred Therapy for Fungal Pathogens

166 — Chapter 5. Preferred Therapy for Fungal Pathogens

B. SYSTEMIC INFECTIONS
Therapy (evidence grade) Comments
Mucormycosis (previously Aggressive surgical debridement combined with Latest international mucormycosis guidelines recommend
known as induction antifungal therapy: L-AmB at 5–10 mg/kg/ L-AmB as primary therapy.110
zygomycosis)31,100–106 day q24h (AII) for 3 wk. Lipid formulations of AmB Following clinical response with AmB, long-term PO step-
are preferred to AmB-D due to increased penetration down therapy with posaconazole (trough concentrations
and decreased toxicity. ideally for mucormycosis at >2 mcg/mL) can be attempted
Some experts advocate induction or salvage for 2–6 mo.
combination therapy with combination of L-AmB Dosing of isavuconazole in children <13 y is 10 mg/kg (q8h
plus posaconazole107 or L-AmB plus an echinocandin on days 1 and 2 and qd thereafter).34
(although data are largely in diabetic patients with Voriconazole has NO activity against mucormycosis or other
rhinocerebral disease) (CIII).108 zygomycetes.
For salvage therapy, isavuconazole (AII)109 or Return of immune function is paramount to treatment
posaconazole (AIII). success; for children receiving corticosteroids, decreasing
Following successful induction antifungal therapy (for the corticosteroid dosage or changing to steroid-sparing
at least 3 wk), can continue consolidation therapy protocols is also important.
with posaconazole (or use intermittent L-AmB) (BII). Antifungal susceptibility is key if it can be obtained.
CNS disease likely benefits from higher doses such as L-AmB
at 10 mg/kg/day q24h. Likely no benefit at >10 mg/kg/day
and only increased toxicity.
Paracoccidioido- Itraconazole PO soln 10 mg/kg/day (max 400 mg daily) New international guidelines exist.56 Alternatives: fluconazole;
mycosis111–114 div bid for 6 mo (AIII) OR voriconazole (for dosing, isavuconazole; sulfadiazine or TMP/SMX for 3–5 y.
see Aspergillosis earlier in this table under Voriconazole is similarly efficacious and useful in cases with
Treatment) (BI). Itraconazole is superior to TMP/SMX. CNS involvement.
AmB is recommended for immunocompromised patients.
Pneumocystis jirovecii Severe disease: preferred regimen is TMP/SMX Alternatives: TMP AND dapsone; OR primaquine AND
(formerly carinii) 15–20 mg TMP component/kg/day IV div q8h (AI) clindamycin; OR atovaquone.
pneumonia115–117 OR, for TMP/SMX intolerance or TMP/SMX treatment Prophylaxis: preferred regimen is TMP/SMX (5 mg TMP
failure, pentamidine isethionate 4-mg base/kg/day IV component/kg/day) PO div bid 3×/wk on consecutive days;
qd (BII), for 3 wk. OR same dose, given qd; OR atovaquone: 30 mg/kg/day for
Mild to moderate disease: start with IV therapy, then, infants 1–3 mo; 45 mg/kg/day for infants/children 4–
after acute pneumonitis is resolved, TMP/SMX 20 mg 24 mo; and 30 mg/kg/day for children >24 mo; OR dapsone
TMP component/kg/day PO div qid for 3-wk total 2 mg/kg (max 100 mg) PO qd, OR dapsone 4 mg/kg (max
treatment course (AII). 200 mg) PO once weekly.
Use steroid therapy for more severe disease.
Sporotrichosis118,119 For cutaneous/lymphocutaneous: itraconazole PO soln New international guidelines exist.56 If no response for
10 mg/kg/day div bid for 2–4 wk after all lesions cutaneous disease, treat with higher itraconazole dose,
gone (generally total of 3–6 mo) (AII) terbinafine, or saturated soln of potassium iodide.
For serious pulmonary or disseminated infection or Fluconazole is less effective.
disseminated sporotrichosis: ABLC/L-AmB at 5 mg/ Obtain serum concentrations of itraconazole after 2 wk of
kg/day q24h until favorable response, then step- therapy; want serum trough concentration >1 mcg/mL.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

down therapy with itraconazole PO for at least a total For meningeal disease, initial L-AmB/ABLC (less toxic than
of 12 mo (AIII) AmB-D) should be 4–6 wk before change to itraconazole for
For less severe disease, itraconazole for 12 mo at least 12 mo of therapy.
Surgery may be necessary in osteoarticular or pulmonary
disease.
 Preferred Therapy for Fungal Pathogens

168 — Chapter 5. Preferred Therapy for Fungal Pathogens

C. LOCALIZED MUCOCUTANEOUS INFECTIONS
Infection Therapy (evidence grade) Comments
Dermatophytoses
– Scalp (tinea capitis, Griseofulvin ultramicrosize 10–15 mg/kg/day or Griseofulvin is superior for Microsporum infections, but
including kerion)120–125 microsize 20–25 mg/kg/day PO qd for 6–12 wk terbinafine is superior for Trichophyton infections.126
(AII) (taken with milk or fatty foods to augment Trichophyton tonsurans predominates in the United States.
absorption) generally for 8 wk. No need to routinely follow LFTs in healthy children taking
For kerion, treat concurrently with prednisone (1– griseofulvin.
2 mg/kg/day for 1–2 wk) (AIII). Alternatives: itraconazole PO soln 5 mg/kg qd or fluconazole.
Terbinafine can be used for only 2–4 wk. 2.5% selenium sulfide shampoo, or 2% ketoconazole shampoo,
Terbinafine dosing is 62.5 mg/day (<20 kg), 2–3×/wk should be used concurrently to prevent recurrences.
125 mg/day (20–40 kg), or 250 mg/day (>40 kg)
(AII).
– Tinea corporis (infection Topical agents (alphabetic order): butenafine, For unresponsive tinea lesions, use griseofulvin PO in dosages
of the trunk/limbs/face) ciclopirox, clotrimazole, econazole, haloprogin, provided for scalp (tinea capitis, including kerion); fluconazole
– Tinea cruris (infection of ketoconazole, miconazole, naftifine, oxiconazole, PO; itraconazole PO; OR terbinafine PO.
the groin) sertaconazole, sulconazole, terbinafine, and For tinea pedis: terbinafine PO or itraconazole PO is preferred
– Tinea pedis (infection of tolnaftate (AII); apply daily for 4 wk. over other PO agents.
the toes/feet) Keep skin as clean and dry as possible, particularly for tinea cruris
and tinea pedis.
– Tinea unguium Terbinafine 62.5 mg/day (<20 kg), 125 mg/day Recurrence or partial response common.
(onychomycosis)122,127,128 (20–40 kg), or 250 mg/day (>40 kg). Use for at Pulse terbinafine (1 wk per mo or 1 wk q3mo) or itraconazole has
least 6 wk (fingernails) or 12–16 wk (toenails) similar efficacy to that of continuous treatment.129,130
(AII). Alternative: itraconazole pulse therapy with 10 mg/kg/day div
q12h for 1 wk per mo. Two pulses for fingernails and 3 pulses
for toenails.
Alternatives: fluconazole, griseofulvin.
– Tinea versicolor (also Apply topically: selenium sulfide 2.5% lotion or 1% For lesions that fail to clear with topical therapy or for extensive
called “pityriasis shampoo daily, leave on 30 min, then rinse; for lesions: fluconazole PO or itraconazole PO is equally effective.
versicolor”)122,131,132 7 days, then monthly for 6 mo (AIII); OR ciclopirox Recurrence common.
1% cream for 4 wk (BII); OR terbinafine 1% soln
(BII); OR ketoconazole 2% shampoo daily for 5
days (BII).
For small lesions, topical clotrimazole, econazole,
haloprogin, ketoconazole, miconazole, or
naftifine.

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

 2025 Nelson’s Pediatric Antimicrobial Therapy — 171

6. Choosing Among Antifungal Agents: Polyenes, Azoles, and

Echinocandins
Separating antifungal agents by class, much like navigating the myriad of antibacterial
agents, allows one to best understand the underlying mechanisms of action and then
appropriately choose which agent is optimal for empiric therapy or a targeted approach.
There are certain helpful generalizations that should be considered; for example, echino-
candins are fungicidal against yeasts and fungistatic against molds, while azoles are the
opposite. Coupled with these concepts is the need for continued surveillance for fungal
epidemiology and resistance patterns. While some fungal species are inherently or very
often resistant to specific agents or even classes, there are an increasing number of fungal
isolates that are developing resistance due to environmental pressure or chronic use in 6
individual patients. Additionally, new (often resistant) fungal species emerge that deserve

Choosing Among Antifungal Agents

special attention, such as Candida auris, which can be multidrug resistant. In 2024, there
are now 17 individual antifungal agents approved by the US Food and Drug Administra-
tion (FDA) for systemic use, including entirely new classes. That includes several recently
approved agents, such as rezafungin and oteseconazole. In addition, many new antifun-
gals are currently in development, likely to be approved and available soon (fosmano-
gepix, olorofim, encochleated amphotericin B [AmB], opelconazole, and others). This
chapter focuses on only the most commonly used systemic agents and will not highlight
the many anticipated new agents until they are approved for use in patients. For each
agent, there are sometimes several formulations, each with unique pharmacokinetics (PK)
that one must understand to optimize the agent, particularly in patients who are critically
ill. Therefore, it is more important than ever to establish a firm conceptual foundation in
understanding both how these antifungal agents work to optimize PK and pharmacody-
namics (PD) and where they work best to target fungal pathogens most appropriately.
Polyenes
Amphotericin B is a polyene antifungal antibiotic that has been available since 1958. A
Streptomyces species, isolated from the soil in Venezuela, produced 2 antifungals whose
names originated from the drug’s amphoteric property of reacting as an acid as well as a
base. Amphotericin A was not as active as AmB, so only AmB is used clinically. Nystatin
is another polyene antifungal, but, due to systemic toxicity, it is used only in topical
preparations. Nystatin was named after the New York State Department of Health, where
the discoverers were working at the time. AmB remains the most broad-spectrum
antifungal available for clinical use. This lipophilic drug binds to ergosterol, the major
sterol in the fungal cell membrane, and for years it was thought to create transmembrane
pores that compromise the integrity of the cell membrane and create a rapid fungicidal
effect through osmotic lysis. However, new biochemical studies suggest a mechanism
of action more related to inhibiting ergosterol synthesis. Toxicity is likely due to
cross-reactivity with the human cholesterol bi-lipid membrane, which resembles fungal
ergosterol. The toxicity of the conventional formulation, amphotericin B deoxycholate
(AmB-D)—the parent molecule coupled with an ionic detergent for clinical use—can be
substantial from the standpoints of systemic reactions (eg, fever, rigors) and acute and
 172 — Chapter 6. Choosing Among Antifungal Agents

chronic renal toxicity. Premedication with acetaminophen, diphenhydramine, and

meperidine has historically been used to prevent systemic reactions during infusion.
Renal dysfunction develops primarily as decreased glomerular filtration with a rising
serum creatinine concentration, but substantial tubular nephropathy is associated with
potassium and magnesium wasting, requiring supplemental potassium for many neonates
and children, regardless of clinical symptoms associated with infusion. Fluid loading with
saline pre– and post–AmB-D infusion seems to somewhat mitigate renal toxicity. A
recent age analysis suggests that there is a greater chance of adverse events in patients
older than 13 months, suggesting that this potentially toxic agent is somewhat compara-
tively less toxic in the smallest children.1
6 Three lipid preparations approved in the mid-1990s decrease toxicity with no apparent
decrease in clinical efficacy. Decisions on which lipid AmB preparation to use should,
Choosing Among Antifungal Agents

therefore, largely focus on side effects and costs. Two clinically useful lipid formulations
exist: one in which ribbonlike lipid complexes of AmB are created (amphotericin B lipid
complex [ABLC]), Abelcet, and one in which AmB is incorporated into true liposomes
(liposomal amphotericin B [L-AmB], AmBisome). The classic clinical dosage used of
these preparations is 5 mg/kg/day, in contrast to the 1 mg/kg/day of AmB-D. In most
studies, the side effects of L-AmB were somewhat less than for ABLC, but both have
significantly fewer side effects than AmB-D. The advantage of the lipid preparations is the
ability to safely deliver a greater overall dose of the parent AmB drug. The cost of
conventional AmB-D is substantially less than for either lipid formulation. A colloidal
dispersion of AmB in cholesteryl sulfate, Amphotec, which is no longer available in the
United States, with decreased nephrotoxicity but infusion-related side effects, is closer to
AmB-D than to the lipid formulations and precludes recommendation for its use. The
decreased nephrotoxicity of the 3 lipid preparations is thought to be due to the preferen-
tial binding of its AmB to high-density lipoproteins, compared to AmB-D binding to
low-density lipoproteins. Despite in vitro concentration-dependent killing, a clinical trial
comparing L-AmB at doses of 3 mg/kg/day with 10 mg/kg/day showed no efficacy benefit
for the higher dose and only greater toxicity.2 Recent PK analyses of L-AmB showed that
while children receiving L-AmB at lower doses exhibit linear PK, a significant proportion
of children receiving L-AmB at daily doses greater than 5 mg/kg/day exhibit nonlinear PK
with significantly higher peak concentrations and some toxicity.3,4 Therefore, it is
generally not recommended to use any lipid AmB preparations at very high dosages
(>5 mg/kg/day), as it will likely incur only greater toxicity with no real therapeutic
advantage. There are reports of using higher dosing in very difficult infections where a
lipid AmB formulation is the first-line therapy (eg, mucormycosis), and while experts
remain divided on this practice, it is clear that at least 5 mg/kg/day of a lipid AmB
formulation should be used in such a setting. AmB has a long terminal half-life, and,
coupled with the concentration-dependent killing, the agent is best used as single daily
doses. These PK/PD explain the use in some studies of once-weekly, or even once-
every-2-weeks,5 AmB for antifungal prophylaxis or preemptive therapy, albeit with mixed
clinical results. If the overall AmB exposure needs to be decreased due to toxicity, it is best
 2025 Nelson’s Pediatric Antimicrobial Therapy — 173

to increase the dosing interval (eg, move from daily to only 3 times weekly) but retain the
full milligram per kilogram dose for optimal PK for concentration-dependent killing.
There are ongoing efforts to develop novel delivery mechanisms for AmB, such as
nanoparticles with encochleated AmB as an oral (PO) formulation, which are not ready
for clinical use yet.
AmB-D has been used for nonsystemic purposes, such as bladder washes, intraventricu-
lar instillation, intrapleural instillation, and other modalities, but there are no firm data
supporting those clinical indications, and it is likely that the local toxicities outweigh
the theoretic benefits. One exception is aerosolized AmB for antifungal prophylaxis (not
treatment) in lung transplant recipients due to the different pathophysiology of invasive
aspergillosis (often originating at the bronchial anastomotic site, more so than parenchy- 6
mal disease) in that specific patient population. This aerosolized prophylaxis approach,

Choosing Among Antifungal Agents

while indicated for lung transplant recipients, has not been shown to be effective in
other patient populations. Due to the lipid chemistry, the L-AmB does not interact well
with renal tubules and L-AmB is recovered from the urine at lower levels than AmB-D,
so there is a theoretic concern for decreased microbiologic efficacy when using a lipid
formulation, as opposed to AmB-D, in the treatment of isolated urinary fungal disease.
This theoretic concern is likely outweighed by the real concern of toxicity with AmB-D.
Most experts believe AmB-D should be reserved for use in resource-limited settings
in which no alternative agents (eg, lipid formulations) are available. An exception is in
neonates, for whom limited retrospective data suggest that the AmB-D formulation has
better efficacy for invasive candidiasis.6 Importantly, there are several pathogens that are
inherently or functionally resistant to AmB, including Candida lusitaniae, Trichosporon
species, Aspergillus terreus, Fusarium species, and Pseudallescheria boydii (Scedosporium
apiospermum) or Lomentospora prolificans.
Azoles
This class of systemic agents was first approved in 1981 and is divided into imidazoles
(ketoconazole), triazoles (fluconazole and itraconazole), and second-generation triazoles
(voriconazole, posaconazole, and isavuconazole) based on the number of nitrogen atoms
in the azole ring. All the azoles work by inhibition of ergosterol synthesis (fungal cyto-
chrome P450 [CYP] sterol 14-demethylation) that is required for fungal cell membrane
integrity. While the polyenes are rapidly fungicidal, the azoles are fungistatic against
yeasts and fungicidal against molds. However, it is important to note that ketoconazole
and fluconazole have no mold activity. The only systemic imidazole is ketoconazole,
which is primarily active against Candida species and is available in a PO formulation.
Three azoles (itraconazole, voriconazole, and posaconazole) need therapeutic drug moni-
toring (TDM) with trough levels within the first 4 to 7 days (when the patient is at a PK
steady state); at present, it is unclear if isavuconazole will require drug-level monitoring,
but an increasing number of reports suggest it might be needed. It is less clear if TDM is
required during primary azole prophylaxis, although low levels have been associated with
a higher probability of breakthrough infection.
 174 — Chapter 6. Choosing Among Antifungal Agents

Fluconazole is active against a broader range of fungi than ketoconazole and includes
clinically relevant activity against Cryptococcus, Coccidioides, and Histoplasma. The
pediatric treatment dose is 12 mg/kg/day, which targets exposures that are observed in
critically ill adults who receive 800 mg of fluconazole per day. Like most other azoles, flu-
conazole requires a loading dose (LD) on the first day, and this approach is routinely used
in adult patients. An LD of 25 mg/kg on the first day has been nicely studied in infants7,8
but has not been definitively studied in all children; yet it is likely also beneficial and the
patient will reach steady-state concentrations more quickly based on adult and neonatal
studies. The exception where it has been formally studied is children of all ages receiv-
ing extracorporeal membrane oxygenation, for whom, because of the higher volume
of distribution, a higher LD (35 mg/kg) is required to achieve comparable exposure.9,10
6
Compared with AmB, fluconazole achieves relatively high concentrations in urine and
cerebrospinal fluid (CSF) due to its low lipophilicity, with urinary concentrations often so
Choosing Among Antifungal Agents

high that treatment against even “resistant” pathogens that are isolated only in the urine is
possible. Fluconazole remains one of the most active and, so far, one of the safest systemic
antifungal agents for the treatment of most Candida infections. Candida albicans remains
generally susceptible to fluconazole, although resistance is increasingly present in many
non-albicans Candida species as well as in C albicans in children repeatedly exposed to
fluconazole. Candida krusei is considered inherently resistant to fluconazole, Candida
glabrata demonstrates dose-dependent resistance to fluconazole (and, usually, voricon-
azole), Candida tropicalis is developing more resistant strains, and the newly identified
C auris is generally fluconazole resistant. Fluconazole is available in parenteral and PO
(with >90% bioavailability) formulations, and toxicity is unusual and primarily hepatic.
Itraconazole is active against an even broader range of fungi and, unlike fluconazole,
includes molds such as Aspergillus. It is currently available as a capsule or a PO solu-
tion (the intravenous [IV] form was discontinued); the PO solution provides about 30%
higher and more consistent serum concentrations than capsules and should be used
preferentially. Absorption using itraconazole PO solution is improved on an empty
stomach and not influenced by gastric pH (unlike with the capsule form, which is best
administered under fed conditions or with a more acidic cola beverage to increase
absorption). Monitoring itraconazole serum concentrations, as with most azole antifun-
gals, is a key principle in management. Generally, itraconazole serum trough levels should
be 1 to 2 mcg/mL, greater than 1 mcg/mL for treatment, and greater than 0.5 mcg/mL
for prophylaxis; trough levels greater than 5 mcg/mL may be associated with increased
toxicity. Concentrations should be checked after 5 days of therapy to ensure adequate
drug exposure. When measured by high-pressure liquid chromatography, itraconazole
and its bioactive hydroxy-itraconazole metabolite are reported, the sum of which should
be considered in assessing drug levels. In adult patients, itraconazole is loaded at 200 mg
twice daily for 2 days, followed by 200 mg daily starting on the third day. Loading dose
studies have not been performed in children. Itraconazole in children requires twice-daily
dosing throughout treatment, compared with once-daily maintenance dosing in adults,
and the key to treatment success is following drug levels. Limited PK data are available
 2025 Nelson’s Pediatric Antimicrobial Therapy — 175

in children; itraconazole has not been approved by the FDA for pediatric indications.
Itraconazole is indicated in adults for therapy for mild to moderate disease with blasto-
mycosis, histoplasmosis, and others. Although it possesses some mold antifungal activity,
itraconazole is not indicated as primary therapy against invasive aspergillosis, as voricon-
azole is a far superior option. Itraconazole is not active against mucormycosis. A recent
guideline on allergic bronchopulmonary aspergillosis (ABPA) in children and adolescents
with asthma suggests that itraconazole is preferred over voriconazole due to the increased
toxicity seen with voriconazole.11 Revised worldwide clinical practice guidelines for ABPA
reaffirm itraconazole preference. Toxicity in adults is primarily hepatic.12
Voriconazole was approved in 2002 and is FDA approved for children 2 years and older.13
Voriconazole is a fluconazole derivative, so think of it as having the greater tissue and CSF 6
penetration of fluconazole but the added antifungal spectrum of itraconazole to include

Choosing Among Antifungal Agents

molds. While the bioavailability of voriconazole in adults is about 96%, multiple studies
have shown that it is about only 50% to 60% in children, requiring clinicians to carefully
monitor voriconazole trough concentrations in patients taking the PO formulation,
further complicated by great inter-patient variability in clearance. Voriconazole serum
concentrations are tricky to interpret, but monitoring these concentrations is essential to
using this drug, as with all azole antifungals, and is especially important in circumstances
of suspected treatment failure or possible toxicity. Most experts suggest voriconazole
trough concentrations of 2 mcg/mL (at a minimum, 1 mcg/mL) or greater, which would
generally exceed the pathogen’s minimum inhibitory concentration. Generally, toxicity
will not be seen until concentrations of about 6 mcg/mL or greater. Trough levels should
be monitored 2 to 5 days after initiation of therapy and monitored again the following
week to confirm that the patient remains in the therapeutic range or again 4 days after a
change of dose. One important point is the acquisition of an accurate trough concentra-
tion, one obtained just before the next dose is due (not hours before solely for phlebotomy
convenience) and not obtained through a catheter infusing the drug. These simple trough
parameters will make interpretation possible. The fundamental voriconazole PK are
different in adults versus children; in adults, voriconazole is metabolized in a nonlinear
fashion, whereas in children, the drug is metabolized in a linear fashion. This explains the
increased pediatric loading dosing for voriconazole at 9 mg/kg/dose versus loading with
6 mg/kg/dose in adult patients. Younger children, especially those younger than 2 years,
require even higher dosages of voriconazole and have a larger therapeutic window for
dosing. The youngest patients (aged <2 years) likely also require higher initial starting
doses.14 However, many studies have shown an inconsistent relationship, on a population
level, between dosing and levels, highlighting the need for close monitoring after the
initial dosing scheme and then dose adjustment as needed in the individual patient. A
recent study highlighted the need for not only larger doses but often multiple dose
adjustments in children to obtain therapeutic trough concentrations.15 For children
younger than 2 years, some studies have even proposed 3-times-daily dosing to achieve
sufficient serum levels.16 Given the poor clinical and microbiologic response of
Aspergillus infections to AmB, voriconazole is clearly the treatment of choice for invasive
 176 — Chapter 6. Choosing Among Antifungal Agents

aspergillosis and many other invasive mold infections (eg, pseudallescheriasis, fusariosis).
Importantly, infections with mucormycosis are resistant to voriconazole. Voriconazole
retains activity against most Candida species, including some that are fluconazole
resistant, but it is unlikely to replace fluconazole for treatment of fluconazole-susceptible
Candida infections. Importantly, there are increasing reports of C glabrata resistance to
voriconazole. Voriconazole produces some unique transient visual field abnormalities in
about 10% of adults and children. There are an increasing number of reports, seen in as
high as 20% of patients, of a photosensitive sunburn-like erythema that is not prevented
by sunscreen (only sun avoidance). In some rare long-term use (mean of 3 years of
therapy) cases, voriconazole phototoxicity has developed into cutaneous squamous cell
carcinoma. Discontinuing voriconazole is recommended in patients experiencing chronic
6
phototoxicity. Rash is the most common indication for switching from voriconazole to
posaconazole/isavuconazole if a triazole antifungal is required. Other voriconazole
Choosing Among Antifungal Agents

chronic toxicities reported include fluorosis and periostitis. Hepatotoxicity is uncommon,

occurring in only 2% to 5% of patients. Voriconazole is CYP metabolized (CYP2C19),
and allelic polymorphisms in the population could lead to personalized dosing.17 Results
have shown that some patients of certain ethnicities will face higher toxic serum
concentrations than other patients, again reiterating the need for close trough level
monitoring. Voriconazole also interacts with many similarly P450-metabolized drugs to
produce some profound changes in serum concentrations of many concurrently
administered drugs.
Posaconazole, an itraconazole derivative, was FDA approved in 2006 as a PO suspen-
sion for adolescents 13 years and older. A delayed-release (DR) tablet formulation was
approved in November 2013, also for adolescents 13 years and older, and an IV formula-
tion was approved in March 2014 for patients 18 years and older. Effective absorption of
the PO suspension strongly requires taking the medication with food, ideally a high-fat
meal; taking posaconazole on an empty stomach will result in about one-fourth of the
absorption as in the fed state. In one study, the PO suspension had only 16% bioavailabil-
ity.18 The tablet formulation has significantly better absorption (66% in one study)19 due
to its delayed release in the small intestine, but absorption will still be slightly increased
with food. If the patient can take the (relatively large) tablets, the DR tablet is the much-
preferred form due to the ability to easily obtain higher and more consistent drug levels.
Due to the low pH (<5) of IV posaconazole, a central venous catheter is required for
administration. The IV formulation contains only slightly lower amounts of the cyclo-
dextrin vehicle than voriconazole, so similar theoretic renal accumulation concerns exist.
The pediatric PO suspension dose recommended by some experts for treating invasive
disease is estimated to be at least 18 mg/kg/day divided 3 times daily, but even that dose
has not achieved target levels.20 A study with a new pediatric formulation for suspension,
essentially the tablet form that is able to be suspended, has recently been completed and
showed good tolerability. In that study, a dose of 6 mg/kg (given twice daily as an LD on
the first day and then once daily) as an IV or formulation for PO suspension achieved tar-
get exposures that were necessary for antifungal prophylaxis, with a safety profile similar
 2025 Nelson’s Pediatric Antimicrobial Therapy — 177

to that for adult patients.21 In that study, the IV formulation led to greater levels than the
formulation for suspension, but both achieved target levels. Pharmacokinetic modeling
also revealed that 6-mg/kg dosing was appropriate, and for those patients weighing more
than 40 kg, the 300-mg/day tablet was predicted to be effective.22 A subsequent study
suggests that posaconazole dosing for the DR tablets and IV formulation requires likely
greater daily doses for children younger than 13 years.23 However, the exact pediatric
dosing for posaconazole requires consultation with a pediatric infectious disease expert.
Importantly, the DR tablet cannot be broken for use due to its chemical coating. Pediatric
dosing with the current IV or extended-release (ER) tablet dosing is not yet fully defined,
but adolescents can likely follow the adult dosing schemes. In adult patients, IV posacon-
azole is loaded at 300 mg twice daily on the first day and then 300 mg once daily starting
6
on the second day. Similarly, in adult patients, the ER tablet is dosed as 300 mg twice
daily on the first day and then 300 mg once daily starting on the second day. In adult

Choosing Among Antifungal Agents

patients, the maximum amount of posaconazole PO suspension given is 800 mg/day due
to its excretion, and that has been given as 400 mg twice daily or 200 mg 4 times daily
in severely ill patients due to saturable absorption and findings of a marginal increase in
exposure with more frequent dosing. Greater than 800 mg/day is not indicated in any
patient. As with voriconazole and itraconazole, trough levels should be monitored, and
most experts feel that posaconazole levels for treatment should be greater than or equal
to 1 mcg/mL (and >0.7 mcg/mL for prophylaxis). Monitor posaconazole trough levels on
day 5 of therapy or soon after. For in vitro activity against Candida species, posaconazole
is better than fluconazole and equivalent to voriconazole. For overall in vitro antifungal
activity against Aspergillus, posaconazole is also equivalent to voriconazole, but, notably,
it is the first triazole with substantial activity against some mucormycosis pathogens,
including Rhizopus species and Mucor species, as well as activity against Coccidioides,
Histoplasma, and Blastomyces and the pathogens of phaeohyphomycosis. Posaconazole
treatment of invasive aspergillosis in patients with chronic granulomatous disease appears
to be superior to voriconazole in this specific patient population for an unknown reason.
Posaconazole is eliminated by hepatic glucuronidation but does demonstrate inhibition
of the CYP3A4 enzyme system, leading to many drug interactions with other P450-
metabolized drugs. It is currently approved for prophylaxis of Candida and Aspergillus
infections in high-risk adults and for treatment of Candida oropharyngeal disease or
esophagitis in adults. Posaconazole, like itraconazole, has generally poor CSF penetration.
Isavuconazole is a new triazole that was FDA approved in March 2015 for treatment
of invasive aspergillosis and invasive mucormycosis with PO (capsules only) and IV
formulations. Isavuconazole has not only a similar antifungal spectrum as voriconazole
but also, very importantly, activity against mucormycosis. A phase 3 clinical trial in adult
patients demonstrated non-inferiority versus voriconazole against invasive aspergillosis
and other mold infections,24 and an open-label study showed activity against mucor-
mycosis.25 New international mucormycosis guidelines recommend isavuconazole in
the setting of preexisting renal compromise (when L-AmB, the recommended primary
therapy, is, therefore, not recommended).26 Isavuconazole is actually dispensed as the
 178 — Chapter 6. Choosing Among Antifungal Agents

prodrug isavuconazonium sulfate. Dosing in adult patients is loading with isavuconazole

at 200 mg (equivalent to 372-mg isavuconazonium sulfate) every 8 hours for 2 days
(6 doses), followed by 200 mg once daily for maintenance dosing. A recently completed
pediatric PK study reports that a dose of 10 mg/kg (every 8 hours on days 1 and 2 and
once daily thereafter) resulted in similar exposures and safety as seen in adults.27 The
half-life is long (>5 days), there is 98% bioavailability in adults, and there is no reported
food effect with PO isavuconazole. The manufacturer suggests no need for TDM, but
some experts suggest trough levels may be needed in difficult-to-treat infections, and,
absent well-defined therapeutic targets, the mean concentrations from phase II/III studies
suggest that a range of 2 to 3 mcg/mL after day 5 is adequate exposure. Another study
suggests a range of 2 to 5 mcg/mL.28 To date, it seems that isavuconazole requires less
6
dose modifications than voriconazole. Unlike voriconazole, the IV formulation does
not contain the vehicle cyclodextrin, a difference that could make it more attractive in
Choosing Among Antifungal Agents

patients with renal failure. Early experience suggests a much lower rate of photosensitivity
and skin disorders as well as visual disturbances, compared with voriconazole. Pediatric
studies for treatment of invasive aspergillosis and mucormycosis are currently ongoing.
Oteseconazole is a PO azole approved in 2022 to reduce the incidence of recurrent vul-
vovaginal candidiasis. However, this agent is contraindicated in females of reproductive
potential based on animal studies in that it may cause fetal harm when administered to a
pregnant woman or potential harm to the breastfed infant.
Echinocandins
This class of systemic antifungal agents was first approved in 2001. The echinocandins
inhibit cell wall formation (in contrast to acting on the cell membrane by the polyenes
and azoles) by noncompetitively inhibiting beta-1,3-glucan synthase, an enzyme present
in fungi but absent in mammalian cells. These agents are generally very safe, as there is
no beta-1,3-glucan in humans. The echinocandins are not metabolized through the CYP
system, so fewer drug interactions occur, compared with the azoles. There is no need to
adjust dose in renal failure, but one needs a lower dosage in the setting of very severe
hepatic dysfunction. As a class, these antifungals generally have poor CSF penetration,
although animal studies have shown adequate brain parenchyma levels, and do not con-
centrate well in the urine. While the 3 clinically available echinocandins each individu-
ally have some unique and important dosing and PK parameters, especially in children,
efficacy is generally equivalent. Opposite the azole class, the echinocandins are fungicidal
against yeasts but fungistatic against molds. The fungicidal activity against yeasts has
elevated the echinocandins to the preferred therapy against invasive candidiasis. Echi-
nocandins are best used against invasive aspergillosis only as salvage therapy if a triazole
fails or in a patient with suspected triazole resistance, never as primary monotherapy
against invasive aspergillosis or any other invasive mold infection. Improved efficacy with
combination therapy with the echinocandins and triazoles against Aspergillus infections
is unclear, with disparate results in multiple smaller studies and a definitive clinical trial
 2025 Nelson’s Pediatric Antimicrobial Therapy — 179

demonstrating minimal benefit over voriconazole monotherapy in only certain patient

populations. Some experts have used combination therapy in invasive aspergillosis with a
triazole plus echinocandin only during the initial phase of waiting for triazole drug levels
to be appropriately high. There are reports of echinocandin resistance in Candida species,
as high as 12% in C glabrata in some studies, and the echinocandins as a class have previ-
ously been shown to be somewhat less active against Candida parapsilosis isolates (about
10%–15% respond poorly, but most are still susceptible, and guidelines still recommend
echinocandin empiric therapy for invasive candidiasis). There is no TDM required for the
echinocandins.
Caspofungin received FDA approval for children and teens aged 3 months to 17 years in
2008 for empiric therapy for presumed fungal infections in febrile, neutropenic patients; 6
treatment of candidemia as well as Candida esophagitis, peritonitis, and empyema;

Choosing Among Antifungal Agents

and salvage therapy for invasive aspergillosis. A study in children with acute myeloid
leukemia demonstrated that caspofungin prophylaxis resulted in significantly lower
incidence of invasive fungal disease, compared with fluconazole prophylaxis.29 A study
comparing caspofungin with triazole prophylaxis in pediatric allogeneic hematopoietic
cell transplant recipients showed no difference in the agents.30 Due to its earlier approval,
there are generally more reports with caspofungin than with the other echinocandins.
Caspofungin dosing in children is calculated according to body surface area (BSA), with
an LD on the first day of 70 mg/m2, followed by daily maintenance dosing of 50 mg/m2,
and not to exceed 70 mg regardless of the calculated dose. Dose adjustment is unneces-
sary in children with mild liver dysfunction.31 Significantly higher doses of caspofungin
have been studied in adult patients without any clear added benefit in efficacy, but if the
50 mg/m2 dose is tolerated and does not provide adequate clinical response, the daily dose
can be increased to 70 mg/m2. One study suggested a cutoff of a BSA of 1.3 m2, whereby
below that size, a BSA-based LD is indicated, and above that size, a fixed LD is indicated.32
Dosing for caspofungin in neonates is 25 mg/m2/day.
Micafungin was approved in 2005 for adults for treatment of candidemia, Candida
esophagitis and peritonitis, and prophylaxis of Candida infections in stem cell transplant
recipients and in 2013 for pediatric patients 4 months and older. Micafungin has the most
pediatric and neonatal data available of all 3 echinocandins, including more extensive
PK studies surrounding dosing and several efficacy studies.33–35 Micafungin dosing in
children is age dependent, as clearance increases dramatically in the younger age-groups
(especially neonates), necessitating higher doses for younger children. Dosages for
children are generally thought to be 2 mg/kg/day, with higher dosages likely needed for
neonates, infants,36 and younger patients and 10 mg/kg/day given to preterm neonates.
Adult micafungin dosing (100 or 150 mg once daily) is used in patients who weigh more
than 40 kg. Unlike with the other echinocandins, an LD is not required for micafungin.
Micafungin twice-weekly dosing for prophylaxis has been initially shown to be effective
in children,37 and a prospective pediatric study showed that micafungin prophylaxis was
safe and effective in children with autologous hematopoietic stem cell transplant.38
 180 — Chapter 6. Choosing Among Antifungal Agents

Anidulafungin was approved for adults for candidemia and Candida esophagitis in 2006
and is not officially approved for pediatric patients. Like the other echinocandins, anidu-
lafungin is not P450 metabolized and has not demonstrated significant drug interactions.
Limited pediatric PK data suggest weight-based dosing (3 mg/kg/day LD, followed by
1.5 mg/kg/day maintenance dosing).39 This dosing achieves similar exposure levels in
neonates and infants.39 The adult dose for invasive candidiasis is an LD of 200 mg on the
first day, followed by 100 mg daily. An open-label study of pediatric invasive candidiasis
in children showed similar efficacy and minimal toxicity, comparable to those of the other
echinocandins.40 An additional study showed similar and acceptable PK in patients
1 month to 2 years of age.41
6 Rezafungin was approved in 2023 for adults with limited or no alternative options for
treatment of candidemia or candidiasis. Administration is unique in that it consists of
Choosing Among Antifungal Agents

an LD of 400 mg followed by a once-weekly 200-mg dose. The ReSTORE randomized,

double-blind clinical trial investigators studied a total of 199 patients and compared
rezafungin administered once weekly to caspofungin administered daily in the treatment
of candidemia and candidiasis and found rezafungin to be non-inferior, with rezafungin
(59%) and caspofungin (61%) showing similar global cure rates at 14 days.42 There are no
completed trials in pediatrics, but a phase 1 pediatric PK study is in development.
Triterpenoid
Ibrexafungerp was approved in June 2021 for adults with vulvovaginal candidiasis fol-
lowing 2 phase III studies (VANISH 203 and VANISH 306). This is the first new class
of antifungals (also called “fungerps”) approved since 2001. Enfumafungin, structurally
distinct from the echinocandins, was discovered through screening of natural products
and modified to develop this semisynthetic derivative for clinical use. Like the echino-
candins, ibrexafungerp not only noncompetitively inhibits beta-1,3-glucan synthase but
also destroys the fungi Candida and inhibits the fungi Aspergillus. The binding site on the
glucan-synthase enzyme is not the same as on the echinocandins. Resistance or reduced
susceptibility to the echinocandins is largely through 2 hot spot alterations in the FKS1
gene, while many resistance alterations to ibrexafungerp are due to the FKS2 gene, and
ibrexafungerp has activity against some echinocandin-resistant isolates. Ibrexafungerp
is the first PO available glucan-synthase inhibitor and has a long half-life, suggesting
once-daily dosing for clinical use. A liposomal IV formulation is in clinical development.
As with the echinocandins, initial studies show limited to no distribution to the central
nervous system and variable distribution to the eye. In a phase II study, ibrexafungerp as
step-down therapy following initial echinocandin therapy for invasive candidiasis was
well tolerated and achieved a favorable global response, like the standard of care.43 There
is an ongoing coadministration study with voriconazole in pulmonary invasive asper-
gillosis (SCYNERGIA), as well as an ongoing recurrent vulvovaginal candidiasis study
(CANDLE), yet no completed or ongoing pediatric studies.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 181

7. Preferred Therapy for Specific Viral Pathogens

NOTE
• A list of table abbreviations and acronyms can be found at the start of this publication.

Preferred Therapy for Viral Pathogens

 Preferred Therapy for Viral Pathogens

182 — Chapter 7. Preferred Therapy for Viral Pathogens

A. OVERVIEW OF NON-HIV, NON–HEPATITIS B OR C VIRAL PATHOGENS AND USUAL PATTERN OF SUSCEPTIBILITY
TO ANTIVIRALS

Virus Acyclovir Baloxavir Cidofovir Famciclovir Foscarnet Ganciclovir

Cytomegalovirus + + +
Herpes simplex virus ++ + + +
Influenza A and B viruses +
SARS-CoV-2
Varicella-zoster virus ++ + + +

Nirmatrelvir
Virus Letermovir Maribavir Plus Ritonavir Oseltamivir Peramivir Remdesivir Valacyclovir Valganciclovir Zanamivir
Cytomegalovirus + + ++
Herpes simplex ++ +
virus
Influenza A and ++ + +
B viruses
SARS-CoV-2 ++ ++
Varicella-zoster ++
virus
NOTE: ++ = preferred; + = acceptable; [blank cell] = untested.
 B. OVERVIEW OF HEPATITIS B OR C VIRAL PATHOGENS AND USUAL PATTERN OF SUSCEPTIBILITY TO ANTIVIRALS
Virus Elbasvir/Grazoprevir (Zepatier) Entecavir Glecaprevir/Pibrentasvir (Mavyret) Interferon Alfa-2b
Hepatitis B virus ++ +
Hepatitis C virusa +b,c ++d,e

Pegylated Interferon Sofosbuvir/Ledipasvir Sofosbuvir (Sovaldi) Plus

Virus Lamivudine Alfa-2a (Harvoni) Ribavirin
Hepatitis B virus + +
Hepatitis C virusa ++d,f ++d,g

Virus Sofosbuvir/Velpatasvir (Epclusa) Sofosbuvir/Velpatasvir/Voxilaprevir (Vosevi) Tenofovir

Hepatitis B virus ++

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

Hepatitis C virusa ++d,e +e,h
NOTE: ++ = preferred; + = acceptable; [blank cell] = untested.
a
HCV treatment guidelines from the IDSA and the AASLD available at www.hcvguidelines.org (accessed August 15, 2024).
b
Approved ≥12 y of age.
c
Treats genotypes 1 and 4.
d
Approved ≥3 y of age.
e
Treats genotypes 1 through 6.
f
Treats genotypes 1, 4, 5, and 6.
g
In children, treats genotypes 2 and 3; in adults, 1 through 4.
h
Not approved for children.
 Preferred Therapy for Viral Pathogens

184 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
Adenovirus (pneumonia or Cidofovir and ribavirin are active in vitro, but no Brincidofovir, the PO bioavailable lipophilic derivative of
disseminated infection in prospective clinical data exist and both have cidofovir, has been evaluated for the treatment of
immunocompromised hosts)1 significant toxicity. adenovirus in immunocompromised hosts. It has been
Two cidofovir dosing schedules have been used approved for use in smallpox and is available only in the
in clinical settings: (1) 5 mg/kg/dose IV once US stockpile for use in the event of a bioterrorism attack.
weekly or (2) 1–1.5 mg/kg/dose IV 3×/wk. If
parenteral cidofovir is used, IV hydration and
PO probenecid should be used to reduce renal
toxicity.
Coronavirus (SARS-CoV-2) Remdesivir is approved for use in patients aged Treatment duration for remdesivir is 10 days for hospitalized
≥28 days and weighing at least 3 kg with patients requiring invasive mechanical ventilation and/or
positive results of direct SARS-CoV-2 viral ECMO.
testing, who are hospitalized or who are not Treatment duration for remdesivir is 5 days for hospitalized
hospitalized and have mild to moderate patients not requiring invasive mechanical ventilation
COVID-19 and risk factors for progression to and/or ECMO (can be extended for up to 5 additional days
severe COVID-19: based on initial clinical response).
Adults and pediatric patients weighing ≥40 kg: Treatment duration for remdesivir is 3 days for nonhospitalized
single IV LD of 200 mg on day 1, followed by patients diagnosed with mild to moderate COVID-19 and
maintenance IV doses of 100 mg qd on and having risk factors for progression to severe COVID-19.
after day 2 Nirmatrelvir/ritonavir (Paxlovid) has numerous drug-drug
Pediatric patients aged ≥28 days and weighing interactions. Consult the listing on the FDA or Pfizer
3–<40 kg: single IV LD of 5.0 mg/kg on day 1, website before prescribing.
followed by maintenance IV doses of 2.5 mg/
kg qd on and after day 2
Nirmatrelvir/ritonavir (Paxlovid) is approved for
use in adults to treat mild to moderate COVID-
19; in people aged 12–17 y weighing ≥40 kg,
it is available by EUA from the FDA: 300 mg
nirmatrelvir with 100 mg ritonavir PO bid for
5 days
Cytomegalovirus
– Congenital and postnatal2 See Ch 2.
– Immunocompromised (HIV, For induction: ganciclovir 10 mg/kg/day IV div Use foscarnet or cidofovir for ganciclovir-resistant strains; for
chemotherapy, transplant- q12h for 14–21 days (AII) (may be increased HIV-positive children undergoing HAART, CMV may resolve
related)3–15 to 15 mg/kg/day IV div q12h). without anti-CMV therapy.
For maintenance: 5 mg/kg IV q24h for 5–7 days Also used for prevention of CMV disease posttransplant for
per week. Duration dependent on degree of 100–120 days.
immunosuppression (AII). Data on valganciclovir dosing in young children for
CMV hyperimmune globulin may decrease treatment of retinitis are unavailable, but consideration
morbidity in bone marrow transplant patients can be given to transitioning from IV ganciclovir to PO
with CMV pneumonia (AII). valganciclovir after improvement of retinitis is noted.
Limited data on PO valganciclovir in infants16,17 (32 mg/kg/
day PO div bid) and children (dosing by BSA [dose
(milligrams) = 7 × BSA × CrCl]).5
Maribavir (400 mg PO bid) is approved for the treatment of
adult and pediatric patients (aged ≥12 y and weighing at

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

least 35 kg) with posttransplant CMV infection/disease
that is refractory to treatment (with or without genotypic
resistance) with ganciclovir, valganciclovir, cidofovir, or
foscarnet.
 Preferred Therapy for Viral Pathogens

186 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
– Prophylaxis of infection in Ganciclovir 5 mg/kg IV daily (or 3×/wk) (started Neutropenia is a complication with ganciclovir and
immunocompromised hosts4,18 at engraftment for stem cell transplant valganciclovir prophylaxis and may be addressed with
patients) (BII) G-CSF.
Valganciclovir at total dose in milligrams = 7 × Prophylaxis and preemptive treatment strategies are
BSA × CrCl (use max CrCl 150 mL/min/ effective, but preemptive treatment in high-risk adult liver
1.73 m2) PO qd with food for children and transplant recipients is superior to prophylaxis.9
teens 4 mo–16 y (max dose 900 mg/day) for Letermovir being studied in children, but no dosing
primary prophylaxis in HIV patients19 who are information available at this time.
CMV antibody positive and have severe
immunosuppression (CD4 count <50/mm3 in
children ≥6 y; CD4 percentage <5% in
children <6 y) (CIII)
Letermovir (adults ≥18 y, CMV-seropositive
recipients [R+] of an allogeneic hematopoietic
stem cell transplant) 480 mg administered PO
qd or as IV infusion over 1 h through 100 days
posttransplant (BI)20
Ebola Atoltivimab/maftivimab/odesivimab-ebgn For treatment of Zaire ebolavirus infections
(brand name: Inmazeb)
Ansuvimab-zykl (brand name: Ebanga)
Enterovirus Supportive therapy; no antivirals currently FDA Pocapavir PO is currently under investigation for enterovirus
approved (poliovirus) and can be used under an expanded access
IND.
Pleconaril PO is currently under consideration for submission
to the FDA for approval to treat neonatal enteroviral sepsis
syndrome.21 As of August 2024, it is not available for
compassionate use.
Epstein-Barr virus
– Mononucleosis, encephalitis22–24 Limited data suggest small clinical benefit of No prospective data on benefits of acyclovir IV or ganciclovir
valacyclovir in adolescents for mononucleosis IV in EBV clinical infections of normal hosts.
(3 g/day div tid for 14 days) (CIII). Patients suspected to have infectious mononucleosis should
For EBV encephalitis: ganciclovir IV OR acyclovir not be given ampicillin or amoxicillin, which causes
IV (AIII). nonallergic morbilliform rashes in a high proportion of
patients with active EBV infection (AII).
Therapy with short-course corticosteroids (prednisone 1 mg/
kg/day PO [max 20 mg/day] for 7 days with subsequent
tapering) may have a beneficial effect on acute symptoms
in patients with marked tonsillar inflammation with
impending airway obstruction, massive splenomegaly,
myocarditis, hemolytic anemia, or hemophagocytic
lymphohistiocytosis (BIII).
– Posttransplant Ganciclovir (AIII) Decrease immunosuppression if possible, as this approach
lymphoproliferative disorder25,26 has the most effect on control of EBV; rituximab,

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

methotrexate have been used but without controlled data.
Preemptive treatment with ganciclovir may decrease PTLD in
solid-organ transplants.
 Preferred Therapy for Viral Pathogens

7
C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS

188 — Chapter 7. Preferred Therapy for Viral Pathogens

Infection Therapy (evidence grade) Comments
Hepatitis B virus (chronic)27–45 AASLD-preferred treatments of children and AASLD-nonpreferred treatments of children and adults:
adolescents46: Lamivudine (3TC) 3 mg/kg/day (max 100 mg) PO q24h for
Interferon alfa-2b for children and adolescents 52 wk for children ≥2 y (children coinfected with HIV and
1–18 y: 3 million U/m2 BSA SUBQ 3×/wk for HBV should use the approved dose for HIV) (AII). 3TC
1 wk, followed by dose escalation to approved for children ≥2 y, but antiviral resistance
6 million U/m2 BSA (max 10 million U/dose); develops during therapy in 30%; OR adefovir for children
OR entecavir for children ≥2 y (optimum ≥12 y (10 mg PO q24h for a minimum of 12 mo; optimum
duration of therapy unknown [BII]) duration of therapy unknown) (BII). There are not sufficient
Entecavir dosing IF no prior nucleoside therapy: clinical data to identify the appropriate dose for use in
≥16 y: 0.5 mg qd children.
2–15 y: Indications for treatment of chronic HBV infection, with or
10–11 kg: 0.15 mg PO soln qd without HIV coinfection, are (1) evidence of ongoing HBV
>11–14 kg: 0.2 mg PO soln qd viral replication, as indicated by serum HBV DNA
>14–17 kg: 0.25 mg PO soln qd (>20,000 IU/mL without HBeAg positivity or >2,000 IU/mL
>17–20 kg: 0.3 mg PO soln qd with HBeAg positivity) for >6 mo and persistent elevation
>20–23 kg: 0.35 mg PO soln qd of serum transaminase levels for >6 mo, or (2) evidence of
>23–26 kg: 0.4 mg PO soln qd chronic hepatitis on liver biopsy (BII). Antiviral therapy is
>26–30 kg: 0.45 mg PO soln qd not warranted in children without necroinflammatory liver
>30 kg: 0.5 mg PO soln or tab qd disease (BIII). Treatment is not recommended for children
If prior nucleoside therapy: with immunotolerant chronic HBV infection (ie, normal
Double the dosage in each weight bracket for serum transaminase levels despite detectable HBV DNA)
entecavir listed previously; OR tenofovir (BII).
dipivoxil fumarate for adolescents ≥12 y and All patients with HBV and HIV coinfection should initiate
adults: 300 mg qd. ART, regardless of CD4 count. This should include 2 drugs
NOTE: TAF is also a preferred treatment of that have HBV activity as well, specifically tenofovir
adults (25 mg daily) but has not been studied (dipivoxil fumarate or alafenamide) plus 3TC or
in children. emtricitabine.46 Patients who are already receiving
effective ART that does not include a drug with HBV
activity should have treatment changed to include
tenofovir (dipivoxil fumarate or alafenamide) plus 3TC or
emtricitabine; alternatively, entecavir is reasonable if
Hepatitis C virus (chronic)47–54 Genotypes 1–6: daily fixed-dose combination of Treatment of HCV infections in adults has been
sofosbuvir/velpatasvir (Epclusa) (<17 kg: revolutionized in recent years with the licensure of
37.5 mg velpatasvir with 150 mg sofosbuvir qd; numerous highly effective DAAs for use in adults,
17–<30 kg: 50 mg velpatasvir with 200 mg adolescents, and children as young as 3 y. Given the
sofosbuvir; ≥30 kg: 100 mg velpatasvir with efficacy of these new treatment regimens in adults (AI),55–
400 mg sofosbuvir) for patients ≥3 y with 70
treatment of children should consist only of interferon-
genotype 1–6 who are treatment naive or free regimens, and an age-appropriate antiviral should be
interferon experienced without cirrhosis or given to all HCV-infected children ≥3 y. The following
with compensated cirrhosis treatment is recommended, based on viral genotype71:
OR Sofosbuvir (Sovaldi) and sofosbuvir in a fixed-dose
Daily fixed-dose combination of glecaprevir/ combination tab with ledipasvir (Harvoni) are now
pibrentasvir (Mavyret) for patients ≥3 y with approved for patients ≥3 y; sofosbuvir/velpatasvir
genotype 1–6 who are treatment naive or (Epclusa) is now approved for patients ≥3 y; and
treatment experienced without cirrhosis or glecaprevir/pibrentasvir (Mavyret) is now approved for
with compensated cirrhosis: patients ≥3 y.
≥12 y or ≥45 kg: glecaprevir 300 mg with See www.hcvguidelines.org/unique-populations/children
pibrentasvir 120 mg qd (accessed August 15, 2024) for additional information (BI).

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

3–11 y:
<20 kg: glecaprevir 150 mg with
pibrentasvir 60 mg qd
20–<30 kg: glecaprevir 200 mg with
pibrentasvir 80 mg qd
30–<45 kg: glecaprevir 250 mg with
pibrentasvir 100 mg qd
Genotype 1: daily fixed-dose combination of
ledipasvir (90 mg)/sofosbuvir (400 mg)
(Harvoni) for patients with genotype 1 who
are treatment naive without cirrhosis or with
compensated cirrhosis or are treatment
experienced with or without cirrhosis
OR, for patients ≥12 y, elbasvir (50 mg)/
grazoprevir (100 mg) (Zepatier) qd
(Continued on next page)
 Preferred Therapy for Viral Pathogens

190 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
Hepatitis C virus (chronic)47–54 Genotype 2: daily sofosbuvir (400 mg) plus
(continued) weight-based ribavirin (as below) for patients
with genotype 2 who are treatment naive or
treatment experienced without cirrhosis or
with compensated cirrhosis
Genotype 3: daily sofosbuvir (400 mg) plus
weight-based ribavirin (as below) for patients
with genotype 3 who are treatment naive or
treatment experienced without cirrhosis or
with compensated cirrhosis
Genotype 4 in patients ≥12 y: elbasvir (50 mg)/
grazoprevir (100 mg) (Zepatier) qd
Genotype 4, 5, or 6: daily fixed-dose
combination of ledipasvir (90 mg)/sofosbuvir
(400 mg) (Harvoni) for patients with genotype
4, 5, or 6 who are treatment naive or
treatment experienced without cirrhosis or
with compensated cirrhosis
Dosing for ribavirin in combination therapy with
sofosbuvir for adolescents ≥12 y or ≥35 kg:
<47 kg: 15 mg/kg/day in 2 div doses
47–59 kg: 800 mg/day in 2 div doses
60–73 kg: 400 mg in morning and 600 mg in
evening
>73 kg: 1,200 mg/day in 2 div doses
Herpes simplex virus
– Third trimester maternal Acyclovir or valacyclovir maternal suppressive
suppressive therapy72–74 therapy in pregnant women reduces HSV
recurrences and viral shedding at the time of
delivery but does not fully prevent neonatal
HSV73 (BIII).
– Neonatal See Ch 2.
– Mucocutaneous (normal host) Acyclovir 80 mg/kg/day PO div qid (max dose Foscarnet for acyclovir-resistant strains.
800 mg) for 5–7 days, or 15 mg/kg/day IV as Immunocompromised hosts may require 10–14 days of
1- to 2-h infusion div q8h (AII). therapy.
Valacyclovir 20 mg/kg/dose (max dose 1 g) PO Topical acyclovir not efficacious and, therefore, not
bid75 for 5–7 days (BII). recommended.
Suppressive therapy for frequent recurrence (no
pediatric data): acyclovir 20 mg/kg/dose bid
or tid (max dose 400 mg) for 6–12 mo, then
reevaluate need (AIII).

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

– Genital Adult doses: acyclovir 400 mg PO tid for All 3 drugs have been used as prophylaxis to prevent
7–10 days; OR valacyclovir 1 g PO bid for recurrence.
10 days; OR famciclovir 250 mg PO tid for Topical acyclovir not efficacious and, therefore, not
7–10 days (AI) recommended.
– Encephalitis Acyclovir 60 mg/kg/day IV as 1- to 2-h infusion Safety of high-dosage acyclovir (60 mg/kg/day) not well-
div q8h; for 21 days for infants ≤4 mo. For defined beyond the neonatal period; can be used, but
older infants and children, 45 mg/kg/day IV as monitor for neurotoxicity and nephrotoxicity.
1- to 2-h infusion div q8h (AIII).
– Keratoconjunctivitis 1% trifluridine OR 0.15% ganciclovir ophthalmic Consultation with ophthalmologist required for assessment
gel (AII) and management (eg, concomitant use of topical steroids
in certain situations)
 Preferred Therapy for Viral Pathogens

192 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
HIV
Current information on HIV treatment and opportunistic infections in children76 is posted at https://clinicalinfo.hiv.gov/en/guidelines (accessed
August 15, 2024); other information on HIV programs is available at www.cdc.gov/hiv/policies/index.html (accessed August 15, 2024). Consult
with an HIV expert, if possible, for current recommendations, as treatment options are complicated and constantly evolving.
– Therapy for HIV infection
State-of-the-art therapy is rapidly Effective therapy (HAART) consists of ≥3 agents, Assess drug toxicity (based on the agents used) and
evolving with introduction of including 2 NRTIs, plus a protease inhibitor, a virologic/immunologic response to therapy (quantitative
new agents and combinations; non-NRTI, or an integrase inhibitor; many plasma HIV and CD4 count) initially monthly and then
currently there are many different combination regimens give similar q3–6mo during the maintenance phase.
individual and fixed-dose treatment outcomes; choice of agents
combination ARV agents depends on the age of the child, viral load,
approved for use by the consideration of potential viral resistance, and
FDA that have pediatric extent of immune depletion, in addition to
indications and that continue to judging the child’s ability to adhere to the
be actively used; guidelines for regimen. “Rapid initiation” of ART is
children and adolescents are recommended for all children, meaning
continually updated on the initiation within days of HIV diagnosis.
ClinicalInfo.HIV.gov and CDC
websites given previously.
– Children of any age Any child with AIDS or significant HIV-related Adherence counseling and appropriate ARV formulations are
symptoms (clinical category C and most B critical for successful implementation.
conditions) should be treated (AI). Recently, the combination of an integrase inhibitor with
Guidance from the WHO and HHS guidelines 2 NRTIs has become the preferred treatment regimen for
committees now recommends treatment of children (as well as adults). Alternative regimens may use
all children regardless of age, CD4 count, or either an NNRTI or a protease inhibitor.
clinical status.
– First 4 wk after birth HAART with ≥3 drugs is recommended for all Preferred therapy in the first 2 wk after birth is ZDV or
infants and children regardless of clinical abacavir PLUS 3TC or emtricitabine PLUS either NVP or
status or laboratory values (AI). RAL.
Preferred therapy from 2–4 wk: ZDV or abacavir PLUS 3TC or
emtricitabine PLUS either lopinavir/ritonavir (toxicity
concerns preclude its use until a PMA of 42 wk and a PNA
of at least 14 days are reached) or RAL.
– HIV-infected children 1 mo–12 y Treat all with any CD4 count (AI). Preferred regimens:
4 wk–2 y: 2 NRTIs PLUS dolutegravir (Alternatives to
dolutegravir include RAL or elvitegravir [>25 kg].)
>2 y: 2 NRTIs PLUS dolutegravir OR bictegravir (Alternatives
to dolutegravir or bictegravir include RAL OR elvitegravir
OR atazanavir/ritonavir OR darunavir/ritonavir.)
– HIV-infected youth ≥12 y Treat all regardless of CD4 count (AI). Preferred regimens comprise TAF plus emtricitabine OR
abacavir plus 3TC PLUS dolutegravir, RAL, or bictegravir.
NOTE: Cabenuva (injectable, long-acting cabotegravir plus

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

rilpivirine) has recently been approved to treat HIV
infection in 12- to 18-year-olds, which has some appeal for
youth with PO adherence challenges. It requires a PO lead-
in dosing period followed by injections q2mo (one each
for cabotegravir and rilpivirine). For this treatment
regimen, initiation by a pediatric/adult HIV specialist team
is strongly recommended.
– Antiretroviral-experienced child Consult with HIV specialist. Consider treatment history and drug resistance testing and
assess adherence.
 Preferred Therapy for Viral Pathogens

194 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
– HIV exposures, Therapy recommendations for exposures PEP remains unproven, but substantial evidence supports its
nonoccupational available on the CDC website at www.cdc. use; consider individually regarding risk, time from
gov/hiv/guidelines/preventing.html (accessed exposure, and likelihood of adherence; prophylactic
August 15, 2024) regimens administered for 4 wk.
– Negligible exposure risk (urine, Prophylaxis not recommended (BIII)
nasal secretions, saliva, sweat, or
tears—no visible blood in
secretions) OR >72 h since exposure
– Significant exposure risk (blood, Prophylaxis recommended (BIII) Consultation with a pediatric HIV specialist is advised.
semen, vaginal, or rectal Preferred regimens:
secretions from a known HIV- 4 wk–<2 y: ZDV PLUS 3TC PLUS either RAL or
infected individual) AND <72 h lopinavir/ritonavir
since exposure 2–12 y: tenofovir PLUS emtricitabine PLUS RAL
≥13 y: tenofovir PLUS emtricitabine PLUS either
RAL or dolutegravir
– Significant exposure risk PrEP Truvada (tenofovir [300 mg]/emtricitabine Daily PrEP has proven efficacy for prevention of HIV infection
[200 mg]): 1 tab daily in individuals at high risk. It is FDA approved for
adolescents/youth (13–24 y; ≥35 kg). Strategies for use
include both episodic and continuous administration.
Baseline HIV and renal function testing is indicated, and it
is recommended to evaluate HIV infection status and renal
function about q3mo while receiving PrEP.
– HIV exposure, occupational77 See guidelines on the CDC website at www.cdc.
gov/hiv/guidelines/preventing.html (accessed
August 15, 2024).
Human herpesvirus 6
– Immunocompromised children78 No prospective comparative data; ganciclovir May require high dose to control infection; safety and
10 mg/kg/day IV div q12h used in case report efficacy not defined at high doses
(AIII)
Influenza virus
Recommendations for the treatment of influenza can vary from season to season; access the AAP website (www.aap.org) and the CDC website
(www.cdc.gov/flu/hcp/antivirals/summary-clinicians.html; accessed November 26, 2024) for the most current, accurate information.
Influenza A and B
– Treatment79–81 Oseltamivir Oseltamivir is currently drug of choice for treatment of
Preterm, <38 wk of PMA: 1 mg/kg/dose PO bid79 influenza.
Preterm, 38–40 wk of PMA: 1.5 mg/kg/dose PO For patients 12–23 mo, the original FDA-approved unit dose
bid79 of 30 mg/dose may provide inadequate drug exposure;
Preterm, >40 wk of PMA: 3 mg/kg/dose PO bid 3.5 mg/kg/dose PO bid has been studied,80 but study
Full-term, birth–8 mo: 3 mg/kg/dose PO bid population sizes were small.
9–11 mo: 3.5 mg/kg/dose PO bid80 Studies of parenteral zanamivir have been completed in
12–23 mo: 30 mg/dose PO bid children.82 However, this formulation of the drug is not
2–12 y: approved in the United States and is not available for
≤15 kg: 30 mg bid compassionate use.
16–23 kg: 45 mg bid The adamantanes, amantadine and rimantadine, are

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

24–40 kg: 60 mg bid currently not effective for treatment due to near-universal
>40 kg: 75 mg bid resistance of influenza A virus.
≥13 y: 75 mg bid Resistance to baloxavir is being monitored carefully across
OR the world. Problems with resistance have limited use of
Zanamivir baloxavir in Japan.
≥7 y: 10 mg by inhalation bid for 5 days
OR
Peramivir (BII)
6 mo–<13 y: single IV dose 12 mg/kg, up to
600 mg
≥13 y: single IV dose 600 mg
OR
Baloxavir (BII)
≥5 y:
<20 kg: single dose 2 mg/kg PO
20–79 kg: single dose 40 mg PO
≥80 kg: single dose 80 mg PO
 Preferred Therapy for Viral Pathogens

196 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
– Chemoprophylaxis Oseltamivir Oseltamivir is currently drug of choice for chemoprophylaxis
3 mo–12 y: the milligram dose given for of influenza.
prophylaxis is the same as for the treatment Unless the situation is judged critical, oseltamivir
dose for all ages, but it is given qd for chemoprophylaxis is not routinely recommended for
prophylaxis rather than bid for treatment. patients <3 mo because of limited safety and efficacy data
Zanamivir in this age-group.
≥5 y: 10 mg by inhalation qd for as long as The adamantanes, amantadine and rimantadine, are
28 days (community outbreaks) or 10 days currently not effective for chemoprophylaxis due to near-
(household setting) universal resistance of influenza A virus.
Baloxavir
≥5 y:
<20 kg: single dose 2 mg/kg PO
20–79 kg: single dose 40 mg PO
≥80 kg: single dose 80 mg PO
Measles83 No prospective data on antiviral therapy. Ribavirin Immune globulin prophylaxis for exposed, unimmunized
is active against measles virus in vitro. children: 0.5 mL/kg (max 15 mL) IM
Vitamin A is beneficial in children with measles
and is recommended by the WHO for all children
with measles regardless of their country of
residence (qd dosing for 2 days): for children
≥1 y: 200,000 IU (60,000 mcg RAE); for infants
6–12 mo: 100,000 IU (30,000 mcg RAE); for
infants <6 mo: 50,000 IU (15,000 mcg RAE) (BII).
An additional (ie, a third) age-specific dose of
vitamin A should be given 2–6 wk later to
children with clinical signs and symptoms of
vitamin A deficiency. Even in countries where
measles is not usually severe, vitamin A should
be given to all children with severe measles (eg,
requiring hospitalization). Parenteral and PO
formulations are available in the United States
Mpox (monkeypox) There are no FDA-approved treatments for PrEP vaccination may be available for health care
mpox. professionals, and PEP vaccination (within 4 days from
Tecovirimat and brincidofovir are approved to date of exposure) may be available with the 2 attenuated
treat smallpox based on the FDA Animal Rule virus vaccines that are FDA approved, through the CDC
regulations, which provide a pathway for (800-CDC-INFO [800-232-4636]).
approval of certain drugs and biologic
products when it is not ethical or feasible to
conduct efficacy studies in humans. For use in
mpox, they are available only through clinical
trial(s) or under the FDA expanded access
program (www.fda.gov/emergency-
preparedness-and-response/mcm-issues/
mpox; accessed August 15, 2024).
Following consultation with the CDC, treatment
may be considered in patients experiencing
severe disease that prompts hospitalization or
in patients likely to experience severe disease

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

(ie, immunocompromised patients, children
<8 y, pregnant/breastfeeding women):
CDC-held expanded access IND protocol allows
use of VIGIV for non–variola Orthopoxvirus
infection (eg, mpox).
Respiratory syncytial virus84,85
– Therapy (severe disease in Ribavirin (6-g vial to make 20-mg/mL soln in Aerosol ribavirin provides only a small benefit and should be
compromised host) sterile water), aerosolized over 18–20 h daily considered only for use for life-threatening infection with
for 3–5 days (BII) RSV. Airway reactivity with inhalation precludes routine
use.
 Preferred Therapy for Viral Pathogens

198 — Chapter 7. Preferred Therapy for Viral Pathogens

C. PREFERRED THERAPY FOR SPECIFIC VIRAL PATHOGENS
Infection Therapy (evidence grade) Comments
– Prophylaxis (nirsevimab or Prophylaxis: Neither palivizumab nor nirsevimab provides benefit in the
palivizumab) (BI)84,85 Nirsevimab is approved and recommended over treatment of an active RSV infection.
palivizumab. Nirsevimab is recommended for all infants during their first
For infants aged <8 mo: RSV season, including well infants. Only those at high risk
Nirsevimab, 50 mg/dose (<5 kg at dose) or should receive a second dose before their second RSV
100 mg/dose (≥5 kg at dose) IM once per season.
season (a) at birth for all infants born during
October–March and (b) when entering first
RSV season and <8 mo of age for all infants
born during April–September.
For infants aged 8–19 mo, a second dose of
nirsevimab is given October–March for
children with
• Chronic lung disease who required medical
support (chronic corticosteroid therapy,
diuretic therapy, or supplemental oxygen)
anytime during the 6-mo period before the
start of the second RSV season
• Severe immunocompromise
• CF who have either manifestations of severe
lung disease (previous hospitalization for
pulmonary exacerbation in the first year after
birth or abnormalities on chest imaging that
persist when stable) or weight-for-length
<10th percentile
• American Indian or Alaska Native heritage
Varicella-zoster virus86 For prophylaxis/preemptive therapy following
exposure in an asymptomatic child, see Ch 15.
– Infection in a normal host Acyclovir 80 mg/kg/day (max single dose The sooner antiviral therapy can be started, the greater the
800 mg) PO div qid for 5 days (AI) clinical benefit.
– Severe primary chickenpox, Acyclovir 30 mg/kg/day IV as 1- to 2-h infusion PO valacyclovir, famciclovir, foscarnet also active
disseminated infection div q8h for 10 days (acyclovir doses of
(cutaneous, pneumonia, 45–60 mg/kg/day in 3 div doses IV should be
encephalitis, hepatitis); used for disseminated or CNS infection).
immunocompromised host with Dosing can also be provided as 1,500 mg/m2/
primary chickenpox or day IV div q8h. Duration in
disseminated zoster immunocompromised children: 7–14 days,
based on clinical response (AI).

2025 Nelson’s Pediatric Antimicrobial Therapy — 1

 2025 Nelson’s Pediatric Antimicrobial Therapy — 201

8. Choosing Among Antiviral Agents

As a general rule, antiviral agents are specific to certain families of viruses. That is, the
anti-herpesvirus drugs do not work against influenza, the anti–hepatitis C drugs do not
work against hepatitis B, and so on. While some antiviral agents (eg, ribavirin, remdesivir,
molnupiravir) may have cross-family coverage, an antiviral drug that is broad enough in
spectrum to cover multiple types of viruses and thus be used empirically in many situ-
ations simply does not exist at this point. It is therefore imperative that clinicians think
through what viruses need to be covered when they are selecting which specific antiviral
agent to use. For this reason, this chapter is structured by virus family.
Anti-Herpesvirus Drugs
Broadly speaking, anti-herpesvirus drugs should be considered by subfamily within the
broader Herpesviridae family. Herpes simplex virus (HSV) and varicella-zoster virus
(VZV) are in the alpha subfamily, cytomegalovirus (CMV) and human herpesvirus
6 (HHV-6) are in the beta subfamily, and Epstein-Barr virus (EBV) is in the gamma 8
subfamily.

Choosing Among Antiviral Agents

The antiviral drug of choice for the alpha herpesviruses (ie, HSV, gingivostomatitis/fever
blisters, genital infection, neonatal infection; VZV, chickenpox, shingles) is acyclovir, a
nucleoside analogue that is available intravenously (IV) or orally (PO). Orally adminis-
tered acyclovir (given in divided doses 4 or 5 times daily as tablets, capsules, or suspen-
sion) is poorly absorbed. However, the valine ester prodrug of acyclovir, valacyclovir, has
enhanced bioavailability and twice-daily dosing that makes it an attractive option if the
patient is old enough to be able to take it. Valacyclovir does not come in a liquid formula-
tion, but there is a recipe for creation of a suspension in the package insert that allows
for the compounding of a product that has a 28-day shelf life. There are data for dosing
of valacyclovir in pediatric patients, although not in very young infants. Famciclovir (the
prodrug of penciclovir), also a nucleoside analogue like acyclovir, is approved in adults for
genital HSV and shingles, but there are far less pediatric data on efficacy. Although pedi-
atric dosing recommendations are provided in the package label for infants and children,
no suspension formulation has been approved; we prefer acyclovir to famciclovir based
on much more extensive published pediatric data. Resistance to this class of antiviral may
occur with repeat treatment courses. Alternatives include cidofovir and foscarnet, but
each of these has significant toxicity issues that limit their use more widely.
For the beta herpesviruses, ganciclovir (another nucleoside analogue) is the antiviral
agent of choice for parenteral use. When PO dosing is an option, the valine ester prodrug
of ganciclovir, valganciclovir, is used. Valganciclovir has improved bioavailability relative
to PO ganciclovir. Cidofovir and foscarnet also have activity against the beta herpesvi-
ruses but, as mentioned previously, have toxicity issues that limit the use. Recently, leter-
movir, a DNA terminase complex inhibitor, and maribavir, a pUL97 kinase inhibitor, have
been approved for use in children 12 years and older (maribavir) and adults (both drugs)
in specific situations. Studies of letermovir in the pediatric population are underway.
 202 — Chapter 8. Choosing Among Antiviral Agents

There are no antiviral agents with excellent activity against the gamma herpesviruses. In
general, ganciclovir or its prodrug, valganciclovir, is used when activity is desired against
EBV. The degree of benefit that either of these drugs provides, though, is unproven.
Anti-Influenza Drugs
The drug of choice for influenza treatment in children is oseltamivir, a neuraminidase
inhibitor, which is available only as a PO formulation. Zanamivir, also a neuraminidase
inhibitor, is an active antiviral agent against most current strains of influenza but is avail-
able only in the United States as an inhalation formulation. Zanamivir is about as effective
as oseltamivir, but its inhaled delivery mechanism has limited its use. Peramivir is another
neuraminidase inhibitor given only IV as a single dose for uncomplicated outpatient
influenza for patients down to 6 months of age; starting an IV catheter and infusing pera-
mivir over 15 to 30 minutes may be difficult in many clinic settings. All the neuramini-
dase inhibitors should be given as early as possible in the influenza illness, preferably
within 48 hours of onset of illness. Influenza may mutate to develop resistance to the
8 neuraminidase inhibitors at any time, but the Centers for Disease Control and Prevention
keeps track of global resistance patterns and shares current information on its website.
Choosing Among Antiviral Agents

Baloxavir is the first approved endonuclease inhibitor drug in this class for influenza, for
use in children 5 years and older and in adults; it prevents replication of virus at a very
early stage in cell infection. It requires only a single dose for treatment of uncomplicated
outpatient influenza infection in adults, with published data in children down to 1 year of
age documenting similar efficacy. Experience with this drug is limited in the United States
at this time.
In addition to treating active infection, oseltamivir, zanamivir, and baloxavir are also
approved for prophylaxis following influenza exposure.
Anti-Hepatitis Drugs
The development of drugs that are active against hepatitis C virus (HCV) has been one
of the most remarkable aspects of antiviral drug development over the past 10 years.
There are currently 4 antiviral drugs with activity against HCV that are approved for use
in children 3 years and older: sofosbuvir/ledipasvir (Harvoni), sofosbuvir plus ribavirin,
sofosbuvir/velpatasvir (Epclusa), and glecaprevir/pibrentasvir (Mavyret). Mavyret and
Epclusa demonstrate transgenotype activity and, therefore, can be used with any genotype
of HCV. There is also 1 HCV antiviral drug approved for use in children 12 years and
older: elbasvir/grazoprevir (Zepatier). Given the pace of development, it is reasonable to
anticipate that additional antiviral drugs with HCV activity are likely to be approved in
children over the upcoming years. The American Academy of Pediatrics recommends
that all HCV-infected children 3 years and older be treated with an age-approved antiviral
regimen.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 203

Anti-Coronavirus Drugs
As of August 2024, remdesivir is the only antiviral drug with activity against coronavi-
ruses approved for use in children. In addition, nirmatrelvir/ritonavir (Paxlovid) has been
approved for use in adults and is available by Emergency Use Authorization from the US
Food and Drug Administration for adolescents 12 through 17 years of age. Paxlovid is
indicated for the treatment of mild to moderate COVID-19 disease in people 12 years and
older weighing 40 kg or more.

Choosing Among Antiviral Agents

 2025 Nelson’s Pediatric Antimicrobial Therapy — 205

9. Preferred Therapy for Specific Parasitic Pathogens

NOTES
• A list of table abbreviations and acronyms can be found at the start of this publication.
• Many of the parasitic infections listed in this chapter are not common, and current
advice from your local infectious disease/tropical medicine/global health specialist
may be invaluable. For some parasitic diseases, therapy may be available only from the
Centers for Disease Control and Prevention (CDC), as noted. The CDC also provides
up-to-date information about parasitic diseases and current treatment recommenda-
tions at www.cdc.gov/parasites. Consultation is available from the CDC for parasitic
disease diagnostic services (www.cdc.gov/dpdx), for parasitic disease diagnosis and
management (404-718-4745 or [email protected]), and for malaria (770-488-7788 or
855-856-4713 toll-free, Monday through Friday, 9:00 am to 5:00 pm [ET]; after-hours
emergency number 770-488-7100 for after hours, weekends, and holidays; or malaria@
cdc.gov). Antiparasitic drugs available from the CDC Drug Service can be reviewed
and requested at www.cdc.gov/laboratory/drugservice/formulary.html.
• Some of the drugs listed can be obtained only from the US Food and Drug Admin- 9
istration or specialized pharmacies; contact information has been provided when

Preferred Therapy for Parasitic Pathogens

available.
• Albendazole is taken with food, preferably fatty food, to enhance bioavailability but
is taken on an empty stomach when used as a luminal agent. We have noted when it
should be taken on an empty stomach; if not noted, it should be taken with food.
• Additional information about many of the organisms and diseases mentioned here,
along with treatment recommendations, can be found in the appropriate sections in
the American Academy of Pediatrics Red Book.
 Preferred Therapy for Parasitic Pathogens

9
A. SELECT COMMON PATHOGENIC PARASITES AND SUGGESTED AGENTS FOR TREATMENT
Albendazole/ Metronidazole/ Pyrantel
Mebendazole Triclabendazole Tinidazole Praziquantel Ivermectin Nitazoxanide DEC Pamoate Paromomycin TMP/SMX

Ascariasis ++ + + +
Blastocystis spp + + + +
Cryptosporidiosis + +
Cutaneous larva ++ ++
migrans
Cyclosporiasis — + ++
Cystoisospora spp + ++
Dientamoebiasis — ++ + +
Liver fluke + ++
Clonorchis/
Opisthorchis
Fasciola hepatica, ++ +
gigantica
Lung fluke — ++
Giardia spp + ++ ++ +
Hookworm ++ — +
Loiasis + ++
Mansonella ozzardi — + —
Mansonella ± — — ±
perstans
Onchocerciasis ++
Pinworm ++ ++
Schistosomiasis ++
Strongyloides spp + ++
Tapeworm ++ +
Toxocariasis ++ — +
Albendazole
preferred
Trichinellosis ++
Trichomoniasis ++
Trichuriasis ++
Wuchereria bancrofti + ++
NOTE: ++ = preferred; + = acceptable; ± = possibly effective (see text for further discussion); — = unlikely to be effective; [blank cell] = untested.
 Preferred Therapy for Parasitic Pathogens

208 — Chapter 9. Preferred Therapy for Parasitic Pathogens

B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Acanthamoeba See Amebic meningoencephalitis later in this table.
Amebiasis1–5
Entamoeba histolytica
– Asymptomatic intestinal Paromomycin 25–35 mg/kg/day PO div tid for 7 days; OR Follow-up stool examination to ensure eradication of
colonization iodoquinol 30–40 mg/kg/day (max 650 mg/dose) PO carriage; screen/treat positive close contacts.
div tid for 20 days; OR diloxanide furoate (not Entamoeba dispar and Entamoeba polecki do not require
commercially available in the United States) 20 mg/ treatment; need for treatment of Entamoeba
kg/day PO div tid (max 500 mg/dose) for 10 days (CII) moshkovskii and Entamoeba bangladeshi is uncertain.
Nitazoxanide may be an option as an alternative luminal
agent.
– Mild to moderate intestinal Metronidazole 35–50 mg/kg/day (max 500–750 mg/ Treatment options for severe and extraintestinal disease
disease dose) PO div tid for 7–10 days; OR tinidazole (age are similar to those for mild to moderate disease
>3 y) 50 mg/kg/day PO (max 2 g) qd for 3 days; OR except that the need for broad-spectrum antibiotics
nitazoxanide (age ≥12 y, 500 mg bid for 3 days; should be considered in the event of superimposed
4–11 y, 200 mg bid for 3 days; 1–3 y, 100 mg bid for bacterial infection, and the need for site-specific
3 days) FOLLOWED BY paromomycin or iodoquinol, as treatment should be considered in extraintestinal
above, to eliminate cysts (BII). infection such as liver abscess. Use of paromomycin
For mild to moderate intestinal disease, secnidazole for clearance of intestinal infection should be delayed
(FDA approved but not for this indication) 2 g once if there is concern for intestinal perforation.
PO in adults and 30 mg/kg once PO in children or Avoid antimotility drugs, steroids.
ornidazole (not approved in the United States) Tinidazole (evaluated by the FDA for children ≥3 y),
500 mg PO qd in adults and 40 mg/kg/day PO qd in when available, may be more effective with fewer
children for 3 days are alternatives. adverse events than metronidazole. Take tinidazole
with food to decrease GI side effects; pharmacists can
crush tabs and mix with syrup for those unable to take
tabs.
Avoid alcohol ingestion with nitroimidazole drugs.
– Liver abscess, extraintestinal Metronidazole 35–50 mg/kg/day IV q8h, with a switch Serologic assays >95% positive in extraintestinal
disease to PO when tolerated, for 7–10 days; OR tinidazole amebiasis.
(age >3 y) 50 mg/kg/day PO (max 2 g) qd for 5 days; Percutaneous or surgical drainage may be indicated for
OR nitazoxanide (age ≥12 y, 500 mg bid for 3 days; large liver abscesses or inadequate response to
4–11 y, 200 mg bid for 3 days; 1–3 y, 100 mg bid for medical therapy.
3 days) FOLLOWED BY paromomycin or iodoquinol, as Avoid alcohol ingestion with nitroimidazole drugs.
above, to eliminate cysts (BII) Take tinidazole with food to decrease GI side effects;
pharmacists can crush tabs and mix with syrup for
those unable to take tabs.
Amebic
meningoencephalitis6–10
Naegleria fowleri AmB 1.5 mg/kg/day IV div q12h for 3 days, then Treatment recommendations based on regimens used
1 mg/kg/day qd for 11 days; PLUS AmB intrathecally for 5 known survivors; available at www.cdc.gov/
1.5 mg qd for 2 days, then 1 mg/day qod for 8 days; naegleria/hcp/clinical-care (accessed August 9, 2024).
PLUS azithromycin 10 mg/kg/day IV or PO (max Conventional amphotericin preferred; L-AmB is less
500 mg/day) for 28 days; PLUS fluconazole 10 mg/kg/ effective in animal models.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

day IV or PO qd (max 600 mg/day) for 28 days; PLUS Treatment outcomes usually unsuccessful; early therapy
rifampin 10 mg/kg/day qd IV or PO (max 600 mg/day) (even before diagnostic confirmation if indicated) may
for 28 days; PLUS miltefosine <45 kg 50 mg PO bid; improve survival.
≥45 kg 50 mg PO tid (max 2.5 mg/kg/day) for 28 days Miltefosine is available commercially (www.impavido.
PLUS dexamethasone 0.6 mg/kg/day div qid for 4 days com); the CDC provides expertise in treatment of
patients with N fowleri infection (770-488-7100).
 Preferred Therapy for Parasitic Pathogens

210 — Chapter 9. Preferred Therapy for Parasitic Pathogens

B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Acanthamoeba Combination regimens including miltefosine, Optimal treatment regimens uncertain; combination
fluconazole, and pentamidine favored by some therapy favored.
experts; TMP/SMX, metronidazole, and a macrolide Miltefosine is available commercially (www.impavido.
may be added. Other drugs that have been used alone com).
or in combination include rifampin, other azoles, The CDC is available for consultation about
sulfadiazine, flucytosine, and caspofungin. management of these infections (770-488-7100).
Keratitis: topical therapies include PHMB (0.02%) or Keratitis should be evaluated by an ophthalmologist.
chlorhexidine, combined with propamidine Prolonged treatment often needed.
isethionate (0.1%) or hexamidine (0.1%) (topical
therapies not approved in the United States but
available at compounding pharmacies).
Balamuthia mandrillaris Combination regimens preferred. Drugs that have been Optimal treatment regimen uncertain; regimens based
used alone or in combination include pentamidine, on case reports; prolonged treatment often needed.
5-flucytosine, fluconazole, macrolides, sulfadiazine, Surgical resection of skin or CNS lesions may be
miltefosine, and itraconazole. beneficial.
The CDC is available for consultation about
management of these infections (770-488-7100).
Ancylostoma braziliense See Cutaneous larva migrans later in this table.
Ancylostoma caninum See Cutaneous larva migrans later in this table.
Ancylostoma duodenale See Hookworm later in this table.
Angiostrongyliasis11–14
Angiostrongylus cantonensis Supportive care. Most patients recover without Corticosteroids, analgesics, and repeat LP may be of
(cerebral disease) antiparasitic therapy; anthelmintic treatment alone benefit.
may provoke worsening of neurologic symptoms. Prednisolone (1–2 mg/kg/day, up to 60 mg qd, in 2 div
doses, for 2 wk) may shorten duration of headache
and reduce need for repeat LP.
Ocular disease may require surgery or laser treatment.
Angiostrongylus costaricensis Supportive care Surgery may be pursued to exclude another diagnosis,
(eosinophilic enterocolitis) such as appendicitis, or to remove inflamed intestine.
Ascariasis (Ascaris First line: albendazole 400 mg PO once OR mebendazole Follow-up stool ova and parasite examination after
lumbricoides)15 500 mg once or 100 mg bid for 3 days (BII) therapy not essential.
Pregnant women: pyrantel pamoate 11 mg/kg, Take albendazole with food (bioavailability increases
max 1 g once with food, especially fatty meals).
Alternatives: ivermectin 150–200 mcg/kg PO once (CII); Albendazole has theoretical risk of causing seizures in
nitazoxanide patients coinfected with cysticercosis.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Ages 1–3 y: 100 mg PO bid for 3 days
Ages 4–11 y: 200 mg PO bid for 3 days
Age ≥12 y: 500 mg PO bid for 3 days
 Preferred Therapy for Parasitic Pathogens

212 — Chapter 9. Preferred Therapy for Parasitic Pathogens

B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Babesiosis (Babesia spp)16–20 Mild to moderate disease: azithromycin 10 mg/kg/day Most asymptomatic infections with Babesia microti in
(max 500 mg/dose) PO on day 1; 5 mg/kg/day from immunocompetent individuals do not require
day 2 on (max 250 mg/dose) for 7–10 days PLUS treatment.
atovaquone 40 mg/kg/day (max 750 mg/dose) PO div Daily monitoring of hematocrit and percentage of
bid (this regimen preferred due to fewer adverse parasitized red blood cells (until <5%) is helpful in
events) OR clindamycin 20–40 mg/kg/day IV div tid or guiding management.
qid (max 600 mg/dose), PLUS quinine sulfate 8 mg/ Exchange blood transfusion may be of benefit for severe
kg/dose PO (max 650 mg/dose) tid for 7–10 days disease and Babesia divergens infection.
Severe disease: azithromycin 10 mg/kg/day (max Higher doses of medications and prolonged therapy
500 mg/dose) IV for 7–10 days PLUS atovaquone may be needed for asplenic or immunocompromised
40 mg/kg/day (max 750 mg/dose) PO div bid; OR individuals.
clindamycin 20–40 mg/kg/day IV div tid or qid (max Clindamycin and quinine remain the regimen of choice
600 mg/dose), PLUS quinine sulfate 8 mg/kg/dose PO for B divergens.
(max 650 mg/dose) tid for 7–10 days
Can transition from IV to PO therapy (at mild to
moderate disease doses) when symptoms improve
and parasitemia declines
Balantidium coli21 Tetracycline (patients >7 y) 40 mg/kg/day PO div qid Optimal treatment regimen uncertain. Prompt stool
for 10 days (max 2 g/day) (CII); OR metronidazole examination may increase detection of rapidly
35–50 mg/kg/day PO div tid for 5 days (max 750 mg/ degenerating trophozoites.
dose); OR iodoquinol 30–40 mg/kg/day PO (max None of these medications have been evaluated by the
650 mg/dose) div tid for 20 days FDA for this indication.
Nitazoxanide may also be effective.
Baylisascaris procyonis (raccoon Albendazole 25–50 mg/kg/day PO for 10–20 days given Therapy generally unsuccessful to prevent fatal outcome
roundworm)22–24 as soon as possible (<3 days) after exposure on an or severe neurologic sequelae once CNS disease
empty stomach (eg, used as a luminal agent for present.
proactive therapy following ingestion of raccoon feces For clinical disease, concurrent steroids are
or contaminated soil) might prevent clinical disease recommended to reduce inflammation.
(CIII). For clinical disease, administer with food,
especially fatty foods, for increased bioavailability.
Blastocystis spp25,26 Whether to treat is controversial. If symptoms are Pathogenesis debated.
significant, treatment trial is appropriate. Asymptomatic individuals do not need treatment;
Metronidazole 35–50 mg/kg/day (max 500–750 mg/ diligent search for other pathogenic parasites
dose) PO div tid for 5–10 days (CII); OR tinidazole recommended for symptomatic individuals with
50 mg/kg (max 2 g) once (age >3 y) (CII). Blastocystis spp.
Paromomycin, nitazoxanide (age ≥12 y, 500 mg PO bid;
4–11 y, 200 mg PO bid for 3 days; 1–3 y, 100 mg PO
bid for 3 days), and TMP/SMX may also be effective.
Combination therapy is another option.
Take tinidazole with food; tabs may be crushed and
mixed with flavored syrup.
Brugia malayi, timori See Filariasis later in this table.
Capillaria Mebendazole 200 mg PO bid for 20 days OR albendazole Optimal duration of therapy unknown; may treat for up
400 mg PO qd for 10 days to 30 days
Chagas disease See Trypanosomiasis later in this table.
(Trypanosoma cruzi)27–29

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Clonorchis sinensis See Flukes later in this table.
Cryptosporidiosis Nitazoxanide (ages 1–3 y, 100 mg PO bid; 4–11 y, Supportive therapy alone appropriate for
(Cryptosporidium parvum)30–33 200 mg PO bid; ≥12 y, 500 mg PO bid) for minimum immunocompetent patients unless severe or
3 days; longer courses may be needed (BII). persistent symptoms.
Paromomycin 25–35 mg/kg/day div bid–qid (CII); OR Recovery depends largely on immune status of host;
azithromycin 10 mg/kg/day for minimum 5 days (CII). medical therapy may have limited efficacy in HIV-
Combination therapy of either agent with infected patients not receiving effective ART.
azithromycin may be used for severe disease. Longer courses (>2 wk) may be needed in
immunocompromised patients.
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B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Cutaneous larva migrans Ivermectin 200 mcg/kg PO qd for 1 day (weight >15 kg) Albendazole bioavailability increased with food,
or creeping eruption34,35 (CII); OR albendazole (age >2 y) 400 mg PO qd for especially fatty meals.
(dog and cat hookworm) (A 3 days (CII) The FDA has not reviewed data on the safety and
caninum, braziliense; efficacy of ivermectin in children weighing <15 kg,
Uncinaria stenocephala) and data on albendazole in children aged <2 y are
limited. For individual children, the benefits of
treatment are likely to outweigh risks.
Cyclospora spp36–38 TMP/SMX 8–10 mg TMP/kg/day (max 1 DS tab bid) PO HIV-infected patients may require higher doses/longer
(cyanobacterium-like agent) div bid for 7–10 days (BIII) therapy.
Nitazoxanide may be an alternative for TMP/SMX-
allergic patients.
Cysticercosis39–42 (Cysticercus Neurocysticercosis Collaboration with a specialist with experience treating
cellulosae; larva of Taenia Patients with 1–2 viable parenchymal cysts: albendazole this condition is recommended.
solium) 15 mg/kg/day PO div bid (max 1,200 mg/day) for See IDSA-ASTMH guidelines.42
10–14 days PLUS steroids (prednisone 1 mg/kg/day or Imaging with both CT and MRI is recommended for
dexamethasone 0.1 mg/kg/day) begun at least 1 day classifying disease in patients newly diagnosed with
before antiparasitic therapy, continued during neurocysticercosis.
antiparasitic treatment followed by rapid taper (to Calcified cysts alone do not require antiparasitic
reduce inflammation associated with dying treatment.
organisms) Management of seizures, cerebral edema, intracranial
Patients with >2 viable parenchymal cysts: albendazole hypertension, or hydrocephalus may require
15 mg/kg/day PO div bid (max 1,200 mg/day) for antiepileptic drugs, neuroendoscopy, or surgical
10–14 days PLUS praziquantel 50 mg/kg/day PO div approaches before considering antiparasitic therapy.
tid (CII) for 10–14 days plus steroids (prednisone Optimal dose and duration of steroid therapy are
1 mg/kg/day or dexamethasone 0.1 mg/kg/day) uncertain.
begun at least 1 day before antiparasitic therapy, Screening for TB infection and Strongyloides is
continued during antiparasitic treatment followed by recommended for patients likely to require prolonged
rapid taper (to reduce inflammation associated with steroid therapy.
dying organisms) Take albendazole with food (bioavailability increases
with food, especially fatty meals).
Cystoisospora (formerly Age >2 mo: TMP/SMX 8–10 mg TMP/kg/day PO (or IV) Infection often self-limited in immunocompetent hosts;
Isospora) belli43 div bid for 7–10 days (max 160 mg TMP/800 mg SMX consider treatment if symptoms do not resolve by
bid) 5–7 days or are severe.
Immunocompromised patients should be treated;
longer courses or suppressive therapy may be needed
for severely immunocompromised patients.
Ciprofloxacin, pyrimethamine plus leucovorin, and
nitazoxanide are alternatives.
Dientamoebiasis44,45 Paromomycin 25–35 mg/kg/day PO div tid for 7 days; OR Routine treatment of asymptomatic individuals not
(Dientamoeba fragilis) metronidazole 35–50 mg/kg/day PO div tid for indicated. Treatment indicated when no other cause
10 days (max 750 mg/dose); OR tetracycline except Dientamoeba found for abdominal pain or
10 mg/kg/day PO div qid (age >7 y) (max 500 mg/ diarrhea lasting >1 wk.
dose) or doxycycline 2 mg/kg bid (max 100 mg/dose) Take paromomycin with meals.
for 10 days Tinidazole, secnidazole, ornidazole, and nitazoxanide are
potential alternatives. Albendazole and mebendazole
have no activity against Dientamoeba.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Dibothriocephalus latus See Tapeworms later in this table.
Dipylidium caninum See Tapeworms later in this table.
Echinococcosis46,47
Echinococcus granulosus Albendazole 10–15 mg/kg/day PO div bid (max Involvement with specialist with experience treating this
800 mg/day) for 1–6 mo alone (CIII) or as adjunctive condition strongly recommended.
therapy with surgery or percutaneous treatment; Surgery is the treatment of choice for management of
initiate 1–30 days before and continue for at least complicated cysts.
1 mo after surgery (duration has not been studied PAIR technique effective for appropriate cysts.
formally). Mebendazole is an alternative if albendazole is
unavailable; if used, continue for 3 mo after PAIR.
Praziquantel efficacy variable; may have a role in
combination therapy with albendazole.
Take albendazole with food (bioavailability increases
with food, especially fatty meals).
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B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Echinococcus multilocularis Surgical treatment generally the treatment of choice; Involvement with specialist with experience treating this
postoperative albendazole 10–15 mg/kg/day PO div condition recommended.
bid (max 800 mg/day) should be administered to Take albendazole with food (bioavailability increases
reduce relapse; duration uncertain (at least 2 y with with food, especially fatty meals).
long-term monitoring for relapse).
Benefit of preoperative albendazole unknown.
Entamoeba histolytica See Amebiasis earlier in this table.
Enterobius vermicularis See Pinworms later in this table.
Fasciola hepatica See Flukes later in this table.
Fasciolopsis buski See Flukes later in this table.
Eosinophilic meningitis See Angiostrongyliasis earlier in this table.
Filariasis48–51
Loa loa Symptomatic loiasis with microfilariae (MF) of L loa/mL Involvement with specialist with experience treating this
<8,000 (some experts prefer <2,500 MF/mL): DEC condition recommended.
(from the CDC) 8–10 mg/kg/day PO div tid for 21 days; Quantification of MF levels is essential before treatment.
some use a graded schedule for patients with Apheresis or albendazole may be used to reduce
microfilaremia. MF levels to <8,000 MF/mL (some experts prefer
Symptomatic loiasis, with MF/mL ≥8,000 (some experts <2,500 MF/mL) before treatment with DEC. Adverse
prefer <2,500 MF/mL): apheresis or albendazole events with DEC (due to rapid killing of MF) are more
200 mg PO bid for 21 days followed by DEC. likely when level of MF is >2,500 MF/mL.
Antihistamines and steroids may be used to limit
adverse reactions to treatment.
Do not use DEC if onchocerciasis is present.
Albendazole is an alternative after 2 failed rounds of DEC.
Mansonella ozzardi Ivermectin 150 mcg/kg PO once DEC and albendazole not effective
Mansonella perstans Combination therapy with DEC and mebendazole may Relatively resistant to DEC, ivermectin, albendazole, and
be effective. mebendazole; doxycycline 4 mg/kg/day PO (max
200 mg/day div bid) for 6 wk beneficial for clearing
microfilaria in Mali and Ghana
River blindness (Onchocerca For those in areas with ongoing transmission: ivermectin Doxycycline targets Wolbachia, the endosymbiotic
volvulus) 150 mcg/kg PO once (AII); repeat q3–6mo until bacteria associated with O volvulus.
asymptomatic. Assess for L loa coinfection before using ivermectin if
If no ongoing exposure: ivermectin 150 mcg/kg PO once exposure occurred in settings where both Onchocerca
followed 1 wk later by doxycycline 4 mg/kg/day PO and L loa are endemic. Optimal treatment of
(max 200 mg/day) for 6 wk; may continue ivermectin onchocerciasis in the setting of L loa infection is
q3–6mo for persistent symptoms. uncertain; consultation with a specialist familiar with
these diseases is recommended.
Moxidectin (8 mg PO once) was FDA approved in 2018
for adults and children ≥12 y for treatment of
onchocerciasis; not yet available commercially in the
United States. Screening for loiasis recommended

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

before use. Safety and efficacy of repeat doses have
not been studied. The FDA has not reviewed
information on safety and efficacy in children <12 y.
Wuchereria bancrofti; Brugia DEC (from the CDC) 6 mg/kg once Avoid DEC with Onchocerca and L loa coinfection.
malayi, timori; Mansonella Doxycycline (4 mg/kg/day PO, max 200 mg/day, for
streptocerca 4–6 wk) may be used concurrently with DEC or as an
alternative; effectiveness of doxycycline in
M streptocerca unknown.
Albendazole has activity against adult worms.
DEC is available from the CDC (404-639-3670).
– Tropical pulmonary DEC (from the CDC) 6 mg/kg/day PO div tid for DEC is available from the CDC Drug Service at
eosinophilia52 14–21 days; corticosteroids to reduce inflammation; 404-639-3670. Do not use DEC if onchocerciasis is
bronchodilators for bronchospasm (CII) present.
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B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Flukes
– Intestinal fluke (F buski) Praziquantel 75 mg/kg PO div tid for 1 day (BII)
– Liver flukes53 (C sinensis, Praziquantel 75 mg/kg PO div tid for 1–2 days (BII); OR Take praziquantel with liquids and food.
Opisthorchis spp) albendazole 10 mg/kg/day PO (max 400 mg bid) for Take albendazole with food (bioavailability increases
7 days (CIII). with food, especially fatty meals).
Single 30–50 mg/kg dose of praziquantel may be
effective in light infection with Opisthorchis viverrini.54
– Lung fluke55,56 (Paragonimus Praziquantel 75 mg/kg/day PO div tid for 2 days (BII) Triclabendazole should be taken with food to facilitate
westermani and other Triclabendazole 10 mg/kg/dose PO bid for 1 day absorption.
Paragonimus lung flukes) (approved for children ≥6 y for fascioliasis) A short course of corticosteroids may reduce
inflammatory response around dying flukes in
cerebral disease.
– Sheep liver fluke57 (F hepatica, Triclabendazole 10 mg/kg/dose PO bid for 1 day (FDA Responds poorly to praziquantel; albendazole and
gigantica) evaluated for age ≥6 y) (BII) OR nitazoxanide PO (take mebendazole ineffective.
with food), ages 12–47 mo, 100 mg/dose bid for Triclabendazole should be taken with food to facilitate
7 days; 4–11 y, 200 mg/dose bid for 7 days; ≥12 y, absorption.
1 tab (500 mg)/dose bid for 7 days (CII)
Giardiasis (Giardia intestinalis, Tinidazole 50 mg/kg/day (max 2 g) PO for 1 day Alternatives: metronidazole 15 mg/kg/day (max
or duodenalis [formerly (age >3 y) (BII); OR nitazoxanide PO (take with food), 250 mg/dose) PO div tid for 5–7 days (BII);
lamblia])58–60 ages 1–3 y, 100 mg/dose bid for 3 days; 4–11 y, albendazole 10–15 mg/kg/day (max 400 mg/dose) PO
200 mg/dose bid for 3 days; ≥12 y, 500 mg/dose bid for 5 days (CII) OR mebendazole 200 mg PO tid for
for 3 days (BII) 5 days; OR paromomycin 30 mg/kg/day div tid for
5–10 days; furazolidone 8 mg/kg/day (max 100 mg/
dose) in 4 doses for 7–10 days (not available in the
United States); quinacrine (refractory cases) 6 mg/kg/
day PO div tid (max 100 mg/dose) for 5 days.
 If therapy ineffective, may try a higher dose or longer
course of the same agent, or an agent in a different
class; combination therapy may be considered for
refractory cases.
Treatment of asymptomatic carriers not usually
indicated unless risk for transmission to vulnerable
individuals.
Hookworm61–63 Albendazole 400 mg once (repeat dose may be Take albendazole on an empty stomach for this
Necator americanus, necessary) (BII); OR mebendazole 100 mg PO for indication.
Ancylostoma duodenale 3 days OR 500 mg PO once; OR pyrantel pamoate
11 mg/kg (max 1 g/day) (BII) PO qd for 3 days
Hymenolepis nana See Tapeworms later in this table.
Isospora belli See Cystoisospora belli earlier in this table under
Cysticercosis.
Leishmaniasis64–72 (including Visceral: L-AmB 3 mg/kg/day on days 1–5, 14, and Consultation with a specialist familiar with managing
kala-azar) Leishmania spp 21 (AI); OR miltefosine 2.5 mg/kg/day PO (max leishmaniasis is strongly advised, especially when

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

150 mg/day) for 28 days (BII) (FDA-approved regimen treating patients with HIV coinfection. Multiple
for children ≥12 y [see IDSA-ASTMH guidelines for regimens are used globally; we have provided
these children]: 50 mg PO bid for 28 days for weight regimens approved by the FDA for use in the United
30–44 kg; 50 mg PO tid for 28 days for weight ≥45 kg); States.
other AmB products available but not evaluated by See IDSA-ASTMH guidelines for Leishmania.64
the FDA for this indication. Region where infection acquired, spp of Leishmania, skill
Cutaneous and mucosal disease: there is no generally of practitioner with some local therapies, and drugs
accepted treatment of choice; treatment decisions available in the United States affect therapeutic
should be individualized. choices.
Uncomplicated cutaneous: combination of debridement For immunocompromised patients with visceral disease,
of eschars, cryotherapy, thermotherapy, intralesional, FDA-approved dosing of liposomal amphotericin is
and topical alternative. 4 mg/kg on days 1–5, 10, 17, 24, 31, and 38, with
further therapy on an individual basis.
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B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Leishmaniasis64–72 (including Complicated cutaneous: PO or parenteral systemic See guidelines for use of pentavalent antimonial drugs
kala-azar) Leishmania spp therapy with miltefosine 2.5 mg/kg/day PO (max for visceral, mucosal, or complicated cutaneous
(continued) 150 mg/day) for 28 days (FDA-approved regimen leishmaniasis.
for children ≥12 y [see IDSA-ASTMH guidelines for Sodium stibogluconate is unavailable in the United
these children]: 50 mg PO bid for 28 days for weight States; information about acquiring meglumine
30–44 kg; 50 mg PO tid for 28 days for weight ≥45 kg) antimoniate is available here: www.astmh.org/blog/
(BII); OR pentamidine isethionate 2–4 mg/kg/day IV or instructions-for-acquiring-glucantime-(meglumine-a
IM qod for 4–7 doses; OR amphotericin (various Guideline for the Treatment of Leishmaniasis in the
regimens); OR azoles (fluconazole 200 mg PO qd for Americas (2022) is available here: www.paho.org/en/
6 wk; or ketoconazole or itraconazole); also documents/guideline-treatment-leishmaniasis-
intralesional and topical alternatives. americas-second-edition
Mucosal: AmB (Fungizone) 0.5–1 mg/kg/day IV qd or
qod for cumulative total of about 20–45 mg/kg; OR
L-AmB about 3 mg/kg/day IV qd for cumulative total
of about 20–60 mg/kg; OR miltefosine 2.5 mg/kg/day
PO (max 150 mg/day) for 28 days (FDA-evaluated
regimen for children ≥12 y [see IDSA-ASTMH
guidelines for these children]: 50 mg PO bid for 28
days for weight 30–44 kg; 50 mg PO tid for 28 days for
weight ≥45 kg).
Lice Follow manufacturer’s instructions for topical use: Launder bedding and clothing; for eyelash infestation,
Pediculosis capitis, humanus; permethrin 1% (≥2 mo) OR pyrethrin (children ≥2 y) use petrolatum; for head lice, remove nits with comb
Phthirus pubis73,74 (BII); OR ivermectin lotion 0.5% (≥6 mo) (BII); OR designed for that purpose.
spinosad topical suspension 0.9% (≥6 mo) (BII); OR Benzyl alcohol can be irritating to skin; systemic
malathion lotion 0.5% (children ≥2 y) (BIII); OR PO absorption may lead to toxicity; parasite resistance
ivermectin 200 mcg/kg PO once; repeat 7–10 days unlikely to develop.
later (children >15 kg); OR abametapir lotion 0.74% Consult specialist before re-treatment with ivermectin
(children ≥6 mo; contains benzyl alcohol) lotion; re-treatment with spinosad topical suspension
not usually needed unless live lice seen 1 wk after
treatment.
Malaria75,76
Plasmodium falciparum, vivax, CDC Malaria Hotline 770-488-7788 or 855-856-4713 toll- Consultation with a specialist familiar with management
ovale, malariae free (Monday–Friday, 9:00 am–5:00 pm [ET]) or of malaria is advised, especially for severe malaria.
emergency consultation after hours 770-488-7100; No antimalarial drug provides absolute protection
online information at www.cdc.gov/malaria/php/ against malaria; fever after return from an endemic
public-health-strategy/alternative-drug-prevention. area should prompt an immediate evaluation.
html Emphasize personal protective measures (insecticides,
bed nets, clothing, and avoidance of dusk–dawn
mosquito exposures).
Prophylaxis See wwwnc.cdc.gov/travel/yellowbook/2024/infections-
diseases/malaria#prevent for current information on
travel and prophylaxis. Other drugs not available in
the United States are used globally to prevent and
treat malaria.75
For areas with chloroquine- Atovaquone/proguanil (A/P): 5–8 kg, ½ ped tab/day; Avoid mefloquine for people with a history of seizures

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

resistant P falciparum or vivax >8–10 kg, ¾ ped tab/day; >10–20 kg, 1 ped tab or psychosis, active depression, or cardiac conduction
(62.5 mg atovaquone/25 mg proguanil); >20–30 kg, abnormalities; see black box warning.
2 ped tabs; >30–40 kg, 3 ped tabs; >40 kg, 1 adult tab Avoid A/P in severe renal impairment (CrCl <30 mL/
(250 mg atovaquone/100 mg proguanil) PO qd begun min).
1–2 days before travel, continued 7 days after last P falciparum resistance to mefloquine exists along the
exposure; for children <5 kg, data on A/P limited (BII); borders between Thailand and Myanmar and Thailand
OR mefloquine: for children <5 kg, 5 mg/kg; ≥5–9 kg, and Cambodia, Myanmar and China, and Myanmar
1/8 tab; ≥10–19 kg, ¼ tab; ≥20–30 kg, ½ tab; and Laos; isolated resistance has been reported in
≥31–45 kg, ¾ tab; ≥45 kg (adult dose), 1 tab PO once southern Vietnam.
weekly begun 1 wk before arrival in area, continued Take doxycycline with adequate fluids to avoid
for 4 wk after leaving area (BII); OR doxycycline esophageal irritation and food to avoid GI side
(patients >7 y): 2 mg/kg (max 100 mg) PO qd begun effects; use sunscreen and avoid excessive sun
1–2 days before arrival in area, continued for 4 wk exposure.
after leaving area (BIII); OR primaquine (check for
G6PD deficiency before administering): 0.5-mg/kg
base qd begun 1 day before travel, continued for
5 days after last exposure (BII)
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B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
For areas with chloroquine- Tafenoquine FDA approved August 2018 for use in
resistant P falciparum or vivax those ≥18 y; must test for G6PD deficiency before
(continued) use; pregnancy testing recommended before use.
Not evaluated by the FDA for those <18 y. LD
200 mg daily for 3 days before travel; 200 mg
weekly during travel; after return, 200 mg once
7 days after last maintenance dose; tabs must be
swallowed whole. May also be used to prevent
malaria in areas with chloroquine-resistant malaria.
For areas without chloroquine- Chloroquine phosphate 5-mg base/kg (max 300-mg
resistant P falciparum or vivax base) PO once weekly, beginning 1 wk before arrival in
area and continuing for 4 wk after leaving area
(available in suspension outside the United States and
Canada and at compounding pharmacies) (AII).
After return from heavy or prolonged (months) exposure
to infected mosquitoes: consider treatment with
primaquine (check for G6PD deficiency before
administering) 0.5-mg base/kg PO qd with final 2 wk
of chloroquine for prevention of relapse with P ovale
or vivax.
Treatment of disease See www.cdc.gov/malaria/resources/pdf/Malaria_
Treatment_Table_202306.pdf for greater detail about
treatment of malaria in the United States.
Other drugs not available in the United States are used
globally for prevention and treatment of malaria.75
– Chloroquine-resistant PO therapy: artemether/lumefantrine 6 doses over Mild disease may be treated with PO antimalarial drugs;
P falciparum, vivax 3 days at 0, 8, 24, 36, 48, and 60 h; 5–<15 kg, severe disease (impaired level of consciousness,
1 tab/dose; 15–<25 kg, 2 tabs/dose; 25–<35 kg, convulsion, hypotension, or parasitemia >5%) should
3 tabs/dose; ≥35 kg, 4 tabs/dose (BII); A/P: for children be treated parenterally.
<5 kg, data limited; 5–<8 kg, 2 ped tabs (62.5 mg Avoid mefloquine for treatment of malaria, if possible,
atovaquone/25 mg proguanil per tab) PO qd for given higher dose and increased incidence of adverse
3 days; 8–<10 kg, 3 ped tabs qd for 3 days; 10–<20 kg, events.
1 adult tab (250 mg atovaquone/100 mg proguanil) Take clindamycin and doxycycline with plenty of liquids.
qd for 3 days; 20–<30 kg, 2 adult tabs qd for 3 days; Do not use primaquine or tafenoquine during
30–<40 kg, 3 adult tabs qd for 3 days; ≥40 kg, 4 adult pregnancy.
tabs qd for 3 days (BII); OR quinine 30 mg/kg/day (max Avoid artemether/lumefantrine and mefloquine in
2 g/day) PO div tid for 3–7 days AND doxycycline patients with cardiac arrhythmias, and avoid
4 mg/kg/day div bid for 7 days OR clindamycin 30 mg/ concomitant use of drugs that prolong QT interval.
kg/day div tid (max 900 mg tid) for 7 days. Take A/P and artemether/lumefantrine with food or
Parenteral therapy: artesunate (commercially available, milk.
but if not in stock or not available within 24 h, contact Artesunate is now available commercially, but if not in
the CDC Malaria Hotline). Children >20 kg: 2.4 mg/kg/ stock or not available within 24 hours, contact the

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

dose IV at 0, 12, 24, and 48 h. Children <20 kg: 3 mg/ CDC Malaria Hotline at 770-488-7788 or 855-856-4713
kg/dose IV77 at 0, 12, 24, and 48 h (from the CDC) (BI) toll-free, Monday–Friday, 9:00 am to 5:00 pm (ET), and
AND follow artesunate by one of the following: the emergency number is 770-488-7100 for after
artemether/lumefantrine, A/P, doxycycline hours, weekends, and holidays.
(clindamycin in pregnant women), or, if no other
options, mefloquine, all dosed as above. If needed,
give interim treatment until artesunate arrives. See the
CDC website for details (www.cdc.gov/malaria/
resources/pdf/Malaria_Treatment_Table_202306.pdf).
For prevention of relapse with P vivax, ovale: primaquine
(check for G6PD deficiency before administering)
0.5-mg base/kg/day PO (max 30-mg/kg base/day) for
14 days.
 Preferred Therapy for Parasitic Pathogens

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B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
– Chloroquine-susceptible PO therapy: chloroquine 10-mg/kg base (max 600-mg Alternative if chloroquine not available:
P falciparum; chloroquine- base) PO, then 5 mg/kg at 6, 24, and 48 h after initial hydroxychloroquine 10-mg base/kg PO immediately,
susceptible P vivax, ovale, dose followed by 5-mg base/kg PO at 6, 24, and 48 h.
malariae Parenteral therapy: artesunate, as above Tafenoquine approved July 2018 for prevention of
For prevention of relapse with P vivax, ovale: primaquine relapse with P vivax malaria in those aged ≥16 y. Use
(check for G6PD deficiency before administering) only when treatment is with chloroquine or
0.5-mg base/kg/day PO (max 30-mg/kg base/day) for hydroxychloroquine. 300 mg on the first or second
14 days day of chloroquine or hydroxychloroquine for acute
malaria. Must test for G6PD deficiency before use;
pregnancy testing recommended before use. Tabs
must be swallowed whole.
Mansonella ozzardi, perstans, See Filariasis earlier in this table.
streptocerca
Naegleria See Amebic meningoencephalitis earlier in this table.
Necator americanus See Hookworm earlier in this table.
Onchocerca volvulus See Filariasis earlier in this table.
Opisthorchis spp See Flukes earlier in this table.
Paragonimus westermani See Flukes earlier in this table.
Pinworms (E vermicularis) Mebendazole 100 mg once, repeat in 2 wk; OR Treat entire household for recurrent infection (and if this
albendazole 400 mg PO on an empty stomach once; fails, consider treating close child care/school
OR pyrantel pamoate 11 mg/kg (max 1 g) PO once contacts); re-treatment of contacts after 2 wk may be
(BII); repeat in 2 wk. needed to prevent reinfection.
Children as young as 1 y may be treated; some pediatric
ID practitioners may choose to defer treatment of an
exposed but uninfected infant aged <1 y.
Launder bedding and clothing.
Plasmodium spp See Malaria earlier in this table.
Pneumocystis See Pneumocystis jirovecii pneumonia in Table 5B.
Scabies (Sarcoptes scabiei)78 Permethrin (5%) cream applied to entire body (including Launder bedding and clothing.
scalp and face of young children), left on for 8–14 h, Crotamiton treatment failure has been observed.
and then washed off—repeated in 1–2 wk (BII); OR Ivermectin should not be used in children who weigh
ivermectin 200 mcg/kg PO once weekly for 2 doses <15 kg due to lack of safety data. Itching may
(BII); OR crotamiton (10%) applied topically overnight continue for weeks after successful treatment; can be
on days 1, 2, 3, and 8 and then washed off in am (BII) managed with antihistamines.
OR spinosad (approved for children ≥4 years) applied
to skin from neck to toes, allowed to dry 10 minutes
before dressing, and left on for at least 6 h
Schistosomiasis (Schistosoma Praziquantel 40 mg/kg/day PO div bid (for Take praziquantel with food and liquids.
haematobium, intercalatum, S haematobium, S mansoni, and S intercalatum) or Oxamniquine (not available in the United States) 20 mg/
japonicum, mansoni, 60 mg/kg/day PO div tid (for S japonicum and kg PO div bid for 1 day (Brazil) or 40–60 mg/kg/day for
mekongi)79–81 S mekongi) for 1 day (AI) 2–3 days (most of Africa) (BII).
Re-treat with the same dose if eggs still present 6–12 wk
after initial treatment.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Strongyloidiasis Ivermectin 200 mcg/kg PO qd for 1–2 days (regimen Albendazole is less effective but may be adequate if
(Strongyloides stercoralis)82,83 can be repeated in 2 wk for immunocompromised longer courses used.
patients) (BI); OR albendazole 400 mg PO bid for For patients with hyperinfection syndrome, veterinary
7 days (BII) SUBQ formulations of ivermectin may be lifesaving.
Hyperinfection syndrome: optimal duration of treatment The SUBQ formulation may be used under a single-
unknown; can continue ivermectin until stool and/or patient IND protocol request to the FDA. Rectal
sputum examination findings are negative for 2 wk; administration may also be used for those unable to
may add albendazole for dual therapy tolerate PO administration.
Ivermectin should not be used in children who weigh
<15 kg due to lack of safety data.
 Preferred Therapy for Parasitic Pathogens

226 — Chapter 9. Preferred Therapy for Parasitic Pathogens

B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Tapeworms Praziquantel 5–10 mg/kg PO once (for H nana: 25 mg/kg Nitazoxanide may be effective (published clinical data
Taenia saginata, solium; once; may repeat 10 days later) (BII); OR niclosamide limited) at 500 mg PO bid for 3 days for age >11 y;
Hymenolepis nana; (not available in the United States) 50 mg/kg (max 200 mg PO bid for 3 days for 4–11 y; 100 mg PO bid
Diphyllobothrium latum; 2 g) PO once, chewed thoroughly (for H nana: weight for 3 days for 1–3 y.
Dipylidium caninum 11–34 kg: 1 g in a single dose on day 1, then 500 mg/ Albendazole (400 mg PO daily for 3 days) may be an
day PO for 6 days; weight >34 kg: 1.5 g in a single alternative.
dose on day 1, then 1 g/day PO for 6 days; adults:
2 g in a single dose for 7 days)
Toxocariasis84 (Toxocara canis Visceral larval migrans: albendazole 400 mg PO bid for Mild disease often resolves without treatment;
[dog roundworm], cati [cat 5 days (BII) eosinophilia may be prolonged.
roundworm]) Ocular larva migrans: prednisone (0.5–1 mg/kg/day with Corticosteroids may be used for severe symptoms in
slow taper) plus albendazole 400 mg PO bid for up to visceral larval migrans.
2 wk for sight-threatening inflammation Mebendazole (100–200 mg/day PO bid for 5 days) is an
alternative.
Toxoplasmosis (Toxoplasma See Ch 2 for congenital infection. Acute toxoplasmosis in immunocompetent,
gondii)85–87 Severe acute toxoplasmosis: nonpregnant individuals is typically self-limited and
Pyrimethamine 2 mg/kg/day PO div bid for 1 day (max may not require treatment.
100 mg), then 1 mg/kg/day (max 50 mg/day) PO qd Consult expert advice for treatment during pregnancy,
AND sulfadiazine 100–200 mg/kg/day PO div qid (max management of congenital infection, management of
2–4 g/day for severe disease); with supplemental chorioretinitis, and management of toxoplasmosis in
folinic acid (leucovorin) 7.5 PO qd (AI) for 2–4 wk immunocompromised individuals.
Active toxoplasmic chorioretinitis: For acute disease: clindamycin, azithromycin, or
Pyrimethamine 2 mg/kg/day PO div bid for 1 day (max atovaquone plus pyrimethamine may be effective for
100 mg), then 1 mg/kg/day (max 50 mg/day) PO qd patients intolerant of sulfa-containing drugs.
AND sulfadiazine 50 mg/kg PO bid (max 4 g/day) AND Experienced ophthalmologic consultation (retinal
folinic acid (leucovorin) 7.5 mg/day PO for 4–6 wk OR specialist with experience treating toxoplasmic
TMP/SMX 15–20 mg TMP/kg; 75–100 mg/kg SMX qd chorioretinitis) encouraged for treatment of ocular
div q6–8h for 4–6 wk. disease.
 For treatment in pregnancy, spiramycin 50–100 mg/kg/ Steroids may be given concurrently for ocular or CNS
day PO div qid (available as investigational therapy infection. Prolonged therapy if HIV positive.
through the FDA at 301-796-1400) (CII). Treatment Compounded pyrimethamine may be obtained from
with spiramycin is recommended in general when specialized pharmacies; consult your local pharmacist
infections were acquired and diagnosed before 18 wk for information on which pharmacies are approved for
of gestation and is most effective if initiated within creating these products.
8 wk of seroconversion. After 18 wk of gestation, Take pyrimethamine with food to decrease GI adverse
treatment with pyrimethamine, sulfadiazine, and effects; sulfadiazine should be taken on an empty
leucovorin can be given for new infections or if the stomach with water.
fetus is documented or suspected to have infection.
Travelers diarrhea38,88–90 Azithromycin 10 mg/kg qd for 1–3 days (AII); OR See 2017 guidelines from International Society of Travel
rifaximin 200 mg PO tid for 3 days (age ≥12 y) (BIII); Medicine: https://academic.oup.com/jtm/article/24/
OR ciprofloxacin (BII) suppl_1/S63/3782742 (accessed August 9, 2024).
Azithromycin preferable to ciprofloxacin for travelers to
Southeast Asia and India given high prevalence of
FQ-resistant Campylobacter.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Do not use rifaximin for Campylobacter, Salmonella,
Shigella, and other causes of invasive diarrhea or
bloody diarrhea that may be associated with
bacteremia.
Antibiotic regimens may be combined with loperamide
(≥2 y).
Rifamycin evaluated by the FDA in adults ≥18 y for
treatment of TD caused by noninvasive strains of
Escherichia coli (388 mg [2 tabs] bid for 3 days).
Trichinellosis (Trichinella Albendazole 400 mg PO bid for 8–14 days (BII) OR Therapy ineffective for larvae already in muscles
spiralis)91 mebendazole 200–400 mg PO tid for 3 days, then Anti-inflammatory drugs, steroids for CNS or cardiac
400–500 mg PO tid for 10 days involvement or severe symptoms
Trichomoniasis (Trichomonas Metronidazole 500 mg PO bid for 7 days for women; Treat sex partners simultaneously.
vaginalis)92 2 g PO in 1 dose for men OR tinidazole 50 mg/kg (max
2 g) PO for 1 dose (BII)
Trichuris trichiura See Whipworm later in this table.
 Preferred Therapy for Parasitic Pathogens

228 — Chapter 9. Preferred Therapy for Parasitic Pathogens

B. PREFERRED THERAPY FOR SPECIFIC PARASITIC PATHOGENS
Disease/Organism Treatment (evidence grade) Comments
Trypanosomiasis
– Chagas disease26–28 (T cruzi) Benznidazole PO: age <2 y, 5.0–7.5 mg/kg/day div bid Therapy recommended for acute and congenital
for 60 days; 2–12 y, 5–8 mg/kg/day div bid for 60 days; infection, reactivated infection, and chronic infection
≥12 y, 5–7 mg/kg/day div bid for 60 days (BIII); OR in children and teens <18 y; consider in those up to
nifurtimox PO age birth–<18 y, 2.5–<40 kg: 50 y with chronic infection without advanced
10–20 mg/kg/day, PO, in 3 div doses for 60 days; cardiomyopathy.
≥17 y, 8–10 mg/kg/day div tid for 60 days (BIII) Benznidazole has been evaluated by the FDA for use in
children aged 2–12 y (www.benznidazoletablets.com;
accessed August 9, 2024); data have not been
submitted for review in children <2 y. Some experts
use 300 mg/day for 60 days for adults regardless of
body weight.
Nifurtimox has been reviewed and approved by the FDA
for children and teens up to 17 y.
Side effects are common but occur less often in younger
patients; consultation with experts in the
management of Chagas disease and adverse drug
reactions can be helpful.
Both drugs contraindicated in pregnancy.
– Human African See CDC guidance (www.cdc.gov/sleeping-sickness/hcp/ CDC Drug Service: www.cdc.gov/laboratory/
trypanosomiasis93–98 clinical-care/index.html) or WHO interim guidance for drugservice/formulary.html
(Trypanosoma brucei treatment of gambiense HAT; consultation with an ID https://iris.who.int/bitstream/hand
gambiense [West African], or subject matter expert recommended when treating le/10665/326178/9789241550567-eng.pdf
rhodesiense [East African]) patients with HAT.
Uncinaria stenocephala See Cutaneous larva migrans earlier in this table.
Whipworm (trichuriasis) Albendazole 400 mg PO qd for 3 days; OR mebendazole Treatment can be given for 5–7 days for heavy
Trichuris trichiura 100 mg PO bid for 3 days; OR ivermectin 200 mcg/kg/ infestation.
day PO qd for 3 days (BII) Combination albendazole plus ivermectin is an
alternative.
Wuchereria bancrofti See Filariasis earlier in this table.
Yaws Azithromycin 30 mg/kg, max 2 g once (also treats bejel Alternative regimens include IM benzathine penicillin
and pinta) and second-line agents doxycycline, tetracycline, and
erythromycin.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

 2025 Nelson’s Pediatric Antimicrobial Therapy — 231

10. Choosing Among Antiparasitic Agents: Antimalarial Drugs,

Nitroimidazoles, Benzimidazoles, and Neglected Tropical Diseases
Antimalarial Drugs
Prevention of Malaria
Seven drugs are available in the United States for prevention of malaria; one (tafenoquine)
is licensed only for adults 18 years and older. Another (doxycycline) is not suitable for
children younger than 8 years due to the duration it must be taken. Two (primaquine and
tafenoquine) require testing for glucose-6-phosphate dehydrogenase (G6PD) deficiency
before use. Five of these drugs are taken weekly (chloroquine, hydroxychloroquine,
mefloquine, primaquine, and tafenoquine) and the other 2 are taken daily (atovaquone/
proguanil [A/P] and doxycycline). The first consideration in the choice of a drug for
prevention of malaria is presence of chloroquine resistance at the destination. If present,
neither chloroquine nor hydroxychloroquine can be used. The next factor to consider is
preference of caregivers about giving a medication to a child daily or weekly, as antima-
larial effectiveness depends primarily on taking the medication, not which medication is
prescribed. Potential adverse events factor into the decision families make about antima-
larials. Many parents will decline mefloquine as soon as the black box warning about the
risk of neuropsychiatric adverse reactions is explained, although taking a weekly medica-
10
tion might increase convenience and adherence, and mefloquine may be less costly. In
general, families traveling to destinations where there is chloroquine resistance will be

Choosing Among Antiparasitic Agents

choosing between A/P (daily medication, possibly more costly) and mefloquine (weekly
medication, black box warning). Primaquine is used extremely rarely in children; testing
for G6PD deficiency is required, and many clinicians are unfamiliar with the use of this
drug. Doxycycline needs to be given for a longer period than ideal for children younger
than 8 years and is limited by its adverse events profile. Tafenoquine also requires G6PD
testing and is limited to those older than 18 years.
For families traveling to areas where there is chloroquine-susceptible malaria, both chlo-
roquine and hydroxychloroquine are options. These medications may be difficult to find,
and it is prudent to be sure a family can obtain them; if not, any of the other drugs may be
prescribed.
Our preference for the best tolerated and effective agent for prophylaxis in areas of chlo-
roquine resistance is A/P; in areas of chloroquine susceptibility, chloroquine.
Treatment of Malaria
Seven drugs are available in the United States for treatment of acute malaria; choice of
drug depends on the severity of illness, location where malaria was acquired, and age of
the child. When malaria is acquired in a location without chloroquine resistance, chloro-
quine or hydroxychloroquine can be used if the patient is able to take medications orally
(PO) and it is available. When malaria is acquired in chloroquine-resistant locations, or
when it is acquired in chloroquine-susceptible areas but chloroquine or hydroxychloro-
quine is not available immediately, and when medications can be taken PO, artemether/
 232 — Chapter 10. Choosing Among Antiparasitic Agents

lumefantrine is the preferred option, with A/P (if not used for prophylaxis) also being an
option. Mefloquine and quinine (in combination with clindamycin or doxycycline) are
available but limited by adverse events profiles. When malaria is severe or the patient is
unable to take medications PO, intravenous artesunate should be used. Identification of
the species of Plasmodium may not be available at the time of choosing the antimalarial
drug; in general, treating for Plasmodium falciparum is appropriate until more informa-
tion is available.
The Centers for Disease Control and Prevention has detailed treatment decision-tree
algorithms and tables available at www.cdc.gov/malaria/hcp/clinical-guidance/index.html.
Choosing Among Nitroimidazoles (Treatment Option for Some Protozoa,
Amoebas)
The choice among nitroimidazoles (metronidazole, tinidazole, secnidazole, ornidazole,
and triclabendazole) is based primarily on spectrum of activity, availability (ornidazole is
not available in the United States), cost, convenience, and adverse events. Tinidazole has
a longer half-life and is better tolerated than metronidazole but may be more costly. Tri-
clabendazole has a narrower spectrum confined to Fasciola hepatica, Fasciola gigantica,
and paragonimiasis. Drugs in this group reportedly produce a disulfiram-like effect when
taken with alcohol; this has been called into question recently.1
10
Choosing Among Benzimidazoles (Treatment Option for Some Helminths)
Choosing Among Antiparasitic Agents

The choice between the benzimidazoles mebendazole and albendazole depends on the
specific organism, availability, and cost. Albendazole is a broader-spectrum antihelminth
than mebendazole but may be more costly. We have noted when there are data to support
recommending one agent over the other.
Need is great for effective, affordable, and easily available drugs for diseases known as
neglected tropical diseases, which include, but are not limited to, the diseases mentioned
previously and Chagas disease, leishmaniasis, lymphatic filariasis, and trypanosomiasis.
For many of these diseases, options for treatment are limited, regimens are not standard-
ized, treatment includes drugs with significant adverse events, or it includes drugs with
limited availability. Additional funding would accelerate research on drug development
and implementation of control measures for these diseases such as mass drug distribu-
tion, as it has for treatment and prevention of HIV/AIDS, malaria, and tuberculosis. Until
additional focus is put on these neglected tropical diseases, which impose large burdens
on the health primarily of those living in low-income countries, the “choosing among”
chapter in this book for antiparasitic drugs will continue to be far shorter than those for
antibacterial, antiviral, and antifungal drugs.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 233

11. How Antibiotic Dosages Are Determined by Susceptibility Data,

Pharmacodynamics, and Treatment Outcomes
Factors Involved in Dosing Recommendations
Our view of assessing the optimal dose of antimicrobials is continually changing as we
learn more about drug exposure and how antibiotics kill bacteria at the site of infection.
As the published literature and our experience with each drug increase, our recommenda-
tions for specific dosages evolve as we compare the efficacy, safety, and cost of each drug
in the context of current and previous data from adults and children. Virtually every new
antibiotic must first demonstrate some degree of efficacy and safety in adults with antibi-
otic exposures that occur at specific dosages, which are duplicated in children as closely
as possible. We keep track of pediatric pharmacokinetics (PK) in all age-groups, reported
toxicities, and unanticipated clinical failures, and on occasion, we may end up modifying
our initial recommendations for an antibiotic.
Important considerations in any recommendations we make include (1) the susceptibili-
ties of pathogens to antibiotics, which are always evolving with selective pressure from
antibiotic use in communities and hospitals and are different from region to region
and hospital to hospital; (2) the antibiotic concentrations achieved at the site of infec-
tion over a 24-hour dosing interval; (3) the mechanism of how antibiotics kill bacteria;
(4) how often the dose we select produces a clinical and microbiologic cure; (5) how
often we encounter toxicity; (6) how likely the antibiotic exposure will lead to antibiotic
11
resistance in the treated child and the general population; and (7) the effect on the child’s
microbiome.

How Antibiotic Dosages Are Determined

Susceptibility
Susceptibility data for each bacterial pathogen against a wide range of antibiotics are
available from the microbiology laboratory of virtually every hospital. This antibiogram
can help guide you in antibiotic selection for empiric therapy while you wait for specific
susceptibilities to result from cultures. Many hospitals can separate the inpatient culture
results from the outpatient results, and many can give you the data by hospital ward (eg,
pediatric ward vs neonatal intensive care unit vs adult intensive care unit). Susceptibil-
ity data are also available by region and by country from reference laboratories or public
health laboratories. The recommendations made in this book reflect overall susceptibility
patterns present in the United States. See Tables 3A and 3B for some overall guidance on
susceptibility of gram-positive and gram-negative pathogens, respectively. Wide varia-
tions may exist for certain pathogens in different regions of the United States and the
world. New techniques for rapid molecular diagnosis of a bacterial, mycobacterial, fungal,
or viral pathogen based on polymerase chain reaction or next-generation sequencing
may quickly give you the name of the pathogen, but with current molecular technology,
complete susceptibility data are not usually available.
 .

234 — Chapter 11. How Antibiotic Dosages Are Determined

Drug Concentrations at the Site of Infection

With every antibiotic, we can measure the concentration of antibiotic present in the
serum. We can also directly measure the concentrations in specific tissue sites, such as
spinal fluid or middle ear fluid. Because “free,” nonprotein-bound antibiotic is required to
inhibit and kill pathogens, it is also important to calculate the amount of free drug avail-
able at the site of infection. While traditional methods of measuring antibiotics focused
just on the peak concentrations in serum and how rapidly the drugs were excreted
(the half-life), newer models of drug distribution in both plasma and tissue sites (eg,
cerebrospinal fluid, urine, peritoneal fluid) and elimination from both plasma and tissue
compartments now exist. Antibiotic exposure to pathogens at the site of infection can be
described mathematically in many ways: (1) the percentage of time in a 24-hour dosing
interval that the antibiotic concentrations are above the minimum inhibitory concentra-
tion (MIC; the antibiotic concentration required for inhibition of growth of an organism)
at the site of infection (%T>MIC); (2) area under the curve (AUC; the mathematically
calculated area under the serum concentration-versus-time curve); and (3) the maximal
concentration of drug achieved in serum and at the tissue site (Cmax). For each of these 3
values, a ratio of that value to the MIC of the pathogen in question can be calculated and
provides more useful information on specific drug activity against a specific pathogen
than a simple look at serum concentrations or the AUC, or an MIC. It allows us to com-
pare the exposure of different antibiotics (that achieve quite different concentrations in
tissues) to a pathogen (where the MIC for each drug may be different) and to assess the
11
activity of a single antibiotic that may be used for empiric therapy against the many differ-
ent pathogens (potentially with many different MICs) that may be causing an infection at
How Antibiotic Dosages Are Determined

that tissue site.

Pharmacodynamics
Pharmacodynamic (PD) descriptions provide the clinician with information on how the
bacterial pathogens are killed (see Suggested Reading later in this chapter). β-Lactam
antibiotics tend to eradicate bacteria following prolonged exposure of relatively low
concentrations of the antibiotic to the pathogen at the site of infection, usually expressed
as the percentage of time over a dosing interval that the antibiotic is present at the site of
infection in concentrations greater than the MIC (%T>MIC). For example, amoxicillin
needs to be present at the site of a pneumococcal infection (such as the middle ear) at
a concentration above the MIC for only 40% of a 24-hour dosing interval. Remarkably,
neither higher concentrations of amoxicillin nor a more prolonged exposure will substan-
tially increase the cure rate. On the other hand, gentamicin’s activity against Escherichia
coli is based primarily on the absolute concentration of free antibiotic at the site of infec-
tion, in the context of the MIC of the pathogen (Cmax:MIC). The more antibiotic you can
deliver to the site of infection, the more rapidly you can sterilize the tissue; we are limited
only by the toxicities of gentamicin. For fluoroquinolones (FQs) such as ciprofloxa-
cin, the antibiotic exposure best linked to clinical and microbiologic success is, as with
aminoglycosides, concentration dependent. However, the best mathematical correlate to
assess microbiologic (and clinical) outcomes for FQs is the AUC:MIC, rather than the
 2025 Nelson’s Pediatric Antimicrobial Therapy — 235

Cmax:MIC. Each of the 3 PD metrics of antibiotic exposure should be linked to the MIC
of the pathogen to best understand how well the antibiotic will eradicate a particular
pathogen causing an infection.
Assessment of Clinical and Microbiologic Outcomes
In clinical trials of anti-infective agents, most adults and children will hopefully be cured,
but the therapy of a few will fail. For those few, we may note unanticipated treatment
failure that, in retrospect, is due to inadequate drug exposure (eg, more rapid drug elimi-
nation in a particular patient; the inability of a particular antibiotic to penetrate to the
site of infection) or due to a pathogen with a particularly high MIC. By analyzing the suc-
cesses and the failures based on the appropriate exposure parameters outlined previously
(%T>MIC, AUC:MIC, or Cmax:MIC), we can often observe a particular value of expo-
sure, above which we observe a higher rate of cure and below which the cure rate drops
quickly. Knowing this target value in adults (the “antibiotic exposure break point”) allows
us to calculate the dosage that should also predict treatment success in most children. We
do not evaluate antibiotics in children with study designs that have failure rates sufficient
to calculate a pediatric exposure break point, of course. It is the adult exposure value that
leads to success that we all (including the US Food and Drug Administration [FDA] and
pharmaceutical companies) subsequently share with you, a pediatric health care practitio-
ner, as one likely to cure your patient. US Food and Drug Administration–approved break
points that are reported by microbiology laboratories (S, I, and R) are now determined
by outcomes linked to drug PK and exposure, the MIC, and the PD parameter for that 11
agent. Recommendations to the FDA for break points for the United States often come

How Antibiotic Dosages Are Determined

from “break point organizations,” such as the Clinical and Laboratory Standards Institute
Subcommittee on Antimicrobial Susceptibility Testing (www.clsi.org) or the US Commit-
tee on Antimicrobial Susceptibility Testing (www.uscast.org).
Physiologic-Based Pharmacokinetic Modeling
Just to keep everyone informed about where the field of antibiotic exposure modeling is
going, the next advance has been in physiologic-based pharmacokinetic (PBPK) model-
ing. Currently, we use PK/PD modeling, in which a Monte Carlo simulation software
program uses the overall observed distribution of PK values in a specific pediatric popula-
tion (eg, neonates, infants, children, adolescents), the range of bacterial MICs observed
in the pathogen of interest, and the PD metric for inhibition of bacteria growth for the
antibiotic being evaluated to assess predicted outcomes for each antibiotic/pathogen pair.
We can find the likelihood that a certain dose will successfully treat a certain pathogen at
a certain tissue site. What PBPK adds to the equation is additional information about the
physicochemical properties of drugs (some diffuse well into adipose tissues; others, not
so well), about ongoing organ function development through childhood, and about blood
flow/organ perfusion throughout the entire body, to allow better prediction of how drugs
move through tissue compartments of the body during absorption, distribution, metabo-
lism, and excretion for each age-group in pediatrics. In that sense, PK/PD modeling can
describe by observation, but PBPK modeling can better predict how an antibiotic will
 236 — Chapter 11. How Antibiotic Dosages Are Determined

“behave” in a child for both efficacy and toxicity. The FDA is encouraging PBPK model-
ing, and the more data we have on drug behavior, the better the PBPK models become for
children. The Verscheijden review listed next gives a nice overview of PBPK modeling in
pediatrics.
Suggested Reading
Le J, et al. J Clin Pharmacol. 2018;58(suppl 10):S108–S122 PMID: 30248202
Onufrak NJ, et al. Clin Ther. 2016;38(9):1930–1947 PMID: 27449411
Trang M, et al. Curr Opin Pharmacol. 2017;36:107–113 PMID: 29128853
Verscheijden LFM, et al. Pharmacol Ther. 2020;211:107541 PMID: 32246949

11
How Antibiotic Dosages Are Determined
 2025 Nelson’s Pediatric Antimicrobial Therapy — 237

12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli

and Methicillin-Resistant Staphylococcus aureus

Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Multidrug-Resistant Gram-Negative Bacilli
Increasing antibiotic resistance in gram-negative bacilli, primarily the enteric bacilli
(eg, Escherichia coli, Klebsiella, Enterobacter, Serratia, Citrobacter), Pseudomonas
aeruginosa, and Acinetobacter species, has caused profound difficulties in treatment of
patients around the world; some of the pathogens are now resistant to all available agents.
Stenotrophomonas, with profound intrinsic antibiotic resistance, is increasing as a cause of
nosocomial infections and of infection in those with chronic recurrent disease (eg, cystic
fibrosis). At this time, only a limited number of pediatric tertiary care centers in North
America have reported outbreaks of multidrug-resistant (MDR) pathogens, but sustained
transmission of completely resistant organisms is quite uncommon in pediatric health
care institutions, likely due to the critical infection control strategies in place to identify
and prevent the spread of these pathogens. Antibiotic resistance in pathogens, particularly
the non-fermenting gram-negative rods, is not new but rather the result of more than
100 million years of exposure to antibiotics elaborated by other organisms in their
environment. Inducible enzymes to cleave antibiotics and modify binding sites, efflux
pumps, and gram-negative cell wall alterations to prevent antibiotic penetration may all
be present. Some mechanisms of resistance, if not intrinsic, can be acquired from other
bacilli. By using antibiotics, we “awaken” resistance; therefore, using antibiotics only when
appropriate limits the selection or induction of resistance for pathogens in the treated
child and for all children (see Chapter 17). Community prevalence, as well as health care
institution prevalence, of extended-spectrum β-lactamase (ESBL)–containing enteric 12
bacilli that are resistant to ceftriaxone is increasing. Carbapenemase-containing patho-
gens that are meropenem resistant are now beginning to spread in neonates, infants, and
children. Two major classes of carbapenemases exist: serine β-lactamases (SBLs), named
for a serine at the active site, and metallo–β-lactamases (MBLs), having a zinc at the active
site. Antibiotic susceptibility patterns differ for the 2 classes. The most prominent car-
bapenemases in the United States are SBLs, most often Klebsiella pneumoniae carbapen-
emase (KPC)–related enzymes and increasingly OXA-48–like enzymes. Globally, MBLs
are often the most prominent classes in circulation (eg, VIM [Verona integron-encoded
metallo–β-lactamase], NDM [New Delhi metallo–β-lactamase], IMP [imipenemase
metallo–β-lactamase]), with ongoing spread within the United States. Some SBLs and
MBLs are now being addressed by new, active antibiotics and new β-lactamase inhibi-
tors (BLIs). However, as we have found in the past, as soon as new drugs are available,
resistance develops quickly. We cannot win, but we can usually stay in the fight against
these pathogens.
In Figure 12-1, we assume that the clinician has the antibiotic susceptibility report in
hand (or at least a local antibiogram). Each tier provides increasingly broader-spectrum
activity, from the narrowest of the gram-negative agents to the broadest (and most
toxic), colistin. Tier 1 is ampicillin, safe and widely available but not active against
Klebsiella, Enterobacter, or Pseudomonas and only active against about half of E coli in
 238 — Chapter 12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

the community setting. Tier 2 contains antibiotics that have both a broader spectrum
against ampicillin-resistant strains of enteric bacilli and are very safe (trimethoprim/
sulfamethoxazole [TMP/SMX] and cephalosporins) with decades of experience. In
Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

general, use an antibiotic from tier 2 before turning to broader-spectrum agents.

More resistant organisms can be characterized by the presence of AmpC β-lactamases
(BLs) that hydrolyze first-, second-, and third-generation cephalosporins but not
cefepime, a fourth-generation cephalosporin (Tier 3). Most often the genes that encode
these BLs are chromosomal and inducible, clinically most relevant with Enterobacter
species, Klebsiella (formerly Enterobacter) aerogenes, and Citrobacter koseri (formerly
diversus). Although resistance usually develops after exposure of the pathogen to the

Figure 12-1. Enteric Bacilli: Bacilli (Enterobacterales) and Pseudomonas aeruginosa

With Known Susceptibilities and Suggested Therapy (See Text for Additional
Information)

Tier 1
Ampicillin-susceptible Escherichia coli

Ampicillin IV (amoxicillin PO)

12 Tier 2 Ampicillin-resistant E coli, all Klebsiella, Enterobacter,

Serratia, and Pseudomonas

Cephalosporin preferred (use the lowest Aminoglycoside

generation with activity): (eg, gentamicin,
• 1st: cefazolin IV (cephalexin PO) tobramycin)
• 2nd: cefuroxime IV and PO TMP/SMX (for
• 3rd: cefotaxime/ceftriaxone IV Alternative, or in enteric bacilli)
(cefdinir/cefixime PO) combination with Ciprofloxacin
• 3rd: additional Pseudomonas aminoglycoside
activity: ceftazidime IV (no PO)

Tier 3 Ceftriaxone/cefotaxime-resistant E coli, Enterobacter, Klebsiella, Serratia,

Proteus, and Citrobacter (most often due to AmpC BL)
Ceftazidime-resistant P aeruginosa

Cefepime (4th-generation Aminoglycoside

Alternative, or in
cephalosporin) (no PO) (eg, gentamicin,
combination with
tobramycin)
aminoglycoside
TMP/SMX (for
enteric bacilli)
Ciprofloxacin
 2025 Nelson’s Pediatric Antimicrobial Therapy — 239

Tier 4 ESBL ceftriaxone/cefotaxime- and cefepime-resistant Enterobacterales

(usually E coli and Klebsiella)

Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Carbapenem IV (no PO yet) Combination with BLIb
• Meropenem/imipenem IV Alternative • CAZ/AVI IV
• Ertapenem IV/IM • PIP/TAZO IV
• TOL/TAZ IV

Alternative, or in Alternative, or in
combination with combination with
aminoglycoside aminoglycoside

Aminoglycosides (eg, gentamicin, tobramycin, or amikacin)

TMP/SMX
Ciprofloxacin
Colistin or Polymyxin B

Tier 5 Carbapenem-resistant due to serine carbapenemases (KPC, OXA-48):

Enterobacterales and P aeruginosac

CAZ/AVId Colistin or Aminoglycosides

Polymyxin B TMP/SMX (for enteric bacilli)
Ciprofloxacin

Investigational: cefiderocol, IMI/REL, ± mero/vabore

Tier 6 Carbapenem-resistant and CAZ/AVI-resistant due to metallo-

carbapenemases (VIM, NDM, IMP): Enterobacterales and 12
P aeruginosac

Aztreonam + Colistin or Aminoglycosides

CAZ/AVId Polymyxin B TMP/SMX (for enteric bacilli)
Ciprofloxacin

Investigational: cefiderocol, ATM/AVI

Tier 7
Acinetobacter baumannii may demonstrate pan-antibiotic resistance;
consult a pediatric ID specialist!

ATM/AVI indicates aztreonam/avibactam; BL, β-lactamase; BLI, β-lactamase inhibitor; CAZ/AVI, ceftazidime/avibactam;
ESBL, extended-spectrum β-lactamase; ID, infectious disease; IM, intramuscularly; IMI/REL, imipenem/relebactam; IMP,
imipenemase; IV, intravenously; KPC, Klebsiella pneumoniae carbapenemase; mero/vabor, meropenem/vaborbactam;
NDM, New Delhi; PIP/TAZO, piperacillin/tazobactam; PO, orally; SMX, sulfamethoxazole; TMP, trimethoprim; TOL/TAZ,
ceftolozane/tazobactam; and VIM, Verona integron-encoded.
a
E coli, Klebsiella, Enterobacter, Serratia, Proteus, Citrobacter.
b
IMI/REL and mero/vabor are not yet approved for children (July 2024): stable to ESBLs.
c
Displays extensive variability in regional susceptibility patterns of circulating clones, with multiple mechanisms of
resistance: susceptibility testing advised.
d
Preferred due to safety consideration.
e
Cefiderocol, IMI/REL, and mero/vabor are not yet approved for children (July 2024). IMI/REL and mero/vabor are
stable to KPC, but mero/vabor is not always stable to OXA-48–like BLs.
 240 — Chapter 12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

antibiotic, in any population of pathogens some bacteria will be constantly producing

AmpC and can be selected out during antibiotic therapy with antibiotics like ceftriaxone.
Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Additional resistance occurs through ESBLs as noted earlier in this chapter. The first-
through fourth-generation cephalosporins are not reliably active against ESBL-containing
pathogens. Tier 4 is made up of very broad-spectrum antibiotics stable to most ESBLs
(carbapenems, ceftazidime/avibactam [CAZ/AVI], piperacillin/tazobactam, ceftolo-
zane/tazobactam). Ceftolozane is more active against P aeruginosa than ceftazidime or
piperacillin, and it is paired with tazobactam, allowing for some additional activity against
ESBL-producing enteric bacilli. Aminoglycosides remain active against many MDR
pathogens with resistance to β-lactams, but they demonstrate significantly more toxicity
than β-lactam agents although we have used them safely for decades. Tier 5 is represented
by a new broad-spectrum BLI, avibactam, in combination with ceftazidime (CAZ/AVI
is US Food and Drug Administration [FDA] approved for children), that demonstrates
stability to ESBL-producing enteric bacilli as well as against the KPC and OXA-48 serine
carbapenemases (associated with resistance to meropenem/imipenem) but lacks stability
against the metallo-carbapenemases present most commonly in enteric bacilli (includ-
ing E coli) worldwide.1 With substantial data on safety with widespread use, CAZ/AVI
is preferred over fluoroquinolones (FQs) for treatment of pathogens expressing serine
carbapenemases. For treatment of pathogens harboring metallo-carbapenemases, aztreo-
nam with CAZ/AVI is recommended (Tier 6). Remarkably, aztreonam is stable to current
metallo-carbapenemases but needs to be paired with avibactam to protect it from AmpC
BLs and ESBLs. Cefiderocol, under study in pediatrics, is a new siderophore cephalospo-
12
rin with stability to metallo-carbapenemases and represents an alternative to aztreonam
with CAZ/AVI. Of course, non–β-lactam antibiotics are not affected by BLs, so the clini-
cian may find other antibiotics that are effective, including aminoglycosides, FQs, TMP/
SMX, and, if all else fails, colistin. Colistin was FDA approved in 1962 with significant
toxicity and with remarkably limited prospective, controlled clinical data for children.
Some of the newer-generation tetracyclines have activity against MBL-producing enteric
bacilli (ie, tigecycline, eravacycline, omadacycline) but are not discussed in this book.
Drugs in clinical trials for adults, soon to be studied in children, are discussed next. Many
additional drugs for MDR gram-negative organisms have moved from animal models
into adult clinical trials. Stay tuned.
Investigational Agents Recently Approved for Adults and Being Studied in
Children
Cefiderocol. Represents a new class of β-lactam antibiotics as a siderophore cephalospo-
rin (eg, binding to iron) that defies the “generation” categories with respect to spectrum
of activity. The cefiderocol-iron complex allows for pathogens to actively transport the
complex across the cell wall into the periplasmic space, thus allowing the antibiotic access
to the transpeptidases not as easily achieved for antibiotics that need to diffuse the gram-
negative cell wall. It is stable to ESBLs, SBLs and MBLs, AmpC, and OXA-48 enzymes,
 2025 Nelson’s Pediatric Antimicrobial Therapy — 241

with activity that includes Pseudomonas, Acinetobacter, and Stenotrophomonas. Approved

for adults in 2019. Pediatric treatment studies are underway.

Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Imipenem and relebactam. Imipenem was the first carbapenem approved for use in
children and is now paired with relebactam, a BLI with similar structure to avibactam,
providing stability for the combination against KPC-containing enteric bacilli, thus
extending the aerobic/anaerobic broad spectrum of carbapenems that already includes
ESBLs and AmpC BLs. Approved for adults in 2019. Pediatric treatment studies are
underway.
Meropenem and vaborbactam. Meropenem, a familiar broad-spectrum aerobic/anaero-
bic coverage carbapenem that is already stable to ESBLs and AmpC BLs, is now paired
with vaborbactam, allowing for activity against the KPC serine carbapenemases but not
metallo-carbapenemases. Approved for adults in 2017. Pediatric pharmacokinetic (PK)
studies are underway.
Sulbactam and durlobactam. Targeted to Acinetobacter, including MDR strains.
Sulbactam, developed as a BLI, also has direct antibiotic activity against Acinetobacter.
However, sulbactam is degraded by many of the more broad-spectrum BLs, but when
paired with the BLI durlobactam, it is protected from ESBLs and serine carbapenemases
(SBLs) as well as AmpC enzymes. Approved for adults in 2023. Pediatric studies are being
organized.
Aztreonam and avibactam. This antibiotic is being developed to address metallo-
carbapenemases, for which avibactam and relebactam do not provide protection.
Aztreonam, a monobactam antibiotic first approved in 1986, is stable to many MBLs 12
but susceptible to cleavage from virtually all the other BLs; however, when it is paired
with avibactam, the combination becomes stable to a vast array of BLs. Pediatric PK and
efficacy studies are underway.
Fosfomycin. An older antibiotic, approved in oral (PO) form for adult women in the
United States in 1996 for uncomplicated cystitis, with intravenous (IV) formulations
approved in many countries in Europe but never approved in the United States. Interferes
with the synthesis of cell walls (inhibits linking of glycan and peptide to form peptido-
glycan cross-linked structures that form cell walls) and demonstrates stability to MBLs
carried by E coli. Clinical trials of the IV formulation are underway for adults; PK studies
are underway for children.
Plazomicin. Represents a new aminoglycoside antibiotic that is active against many of
the gentamicin-, tobramycin-, and amikacin-resistant enteric bacilli and Pseudomonas.
Approved for adults in 2018. Not currently available in the United States.
Investigational Agents Under Study in Adults
Cefepime and taniborbactam. Represents another older antibiotic, cefepime, that is now
paired with taniborbactam, a broad-spectrum, borate-based BLI, stable against ESBLs,
SBLs and MBLs, and AmpC BLs.
 242 — Chapter 12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Cefepime and enmetazobactam. Another combination with cefepime and a new broad-
spectrum BLI, a methylated tazobactam, enmetazobactam is stable against AmpC BLs
and ESBLs and SBLs but not MBLs.
Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Community-Associated Methicillin-Resistant Staphylococcus aureus

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is a
community pathogen for children (that can also spread from child to child in hospitals)
that first emerged in the United States in the mid-1990s and currently represents 10% to
30% of all community isolates in various regions of the United States (check your hospital
microbiology laboratory for your local rate); it is present in many areas of the world, with
some strain variation documented.2,3 CA-MRSA resists β-lactam antibiotics, with the
notable exception of ceftaroline and ceftobiprole, fifth-generation cephalosporin antibiot-
ics that are FDA approved for pediatrics (see Chapter 1).
There are an undetermined number of pathogenicity factors that make CA-MRSA strains,
in general, more aggressive than methicillin-susceptible Staphylococcus aureus (MSSA)
strains. Response of MRSA to therapy with non–β-lactam antibiotics (eg, vancomycin)
seems to be inferior, compared with response of MSSA to oxacillin/nafcillin or cefazolin,
but it is unknown whether poorer outcomes are due to a hardier, better-adapted, more
aggressive strain of S aureus or alternative agents are just not as effective against MRSA
as β-lactam agents are against MSSA. In children, studies using ceftaroline to treat skin
infections (many caused by MRSA) were conducted by way of a non-inferiority clinical
trial design, comparing ceftaroline with vancomycin, with the finding that ceftaroline
was equivalent to vancomycin. Guidelines for management of MRSA skin and soft tissue
12
infections have been published by the Infectious Diseases Society of America (IDSA)4 and
are available at www.idsociety.org, as well as in the AAP Red Book 2024–2027.
Antimicrobials for CA-MRSA
Ceftaroline, a fifth-generation cephalosporin antibiotic, the first FDA-approved β-lactam
antibiotic to be active against MRSA, was approved for children in June 2016. The gram-
negative coverage is similar to ceftriaxone, with no activity against Pseudomonas. Published
data are available for pediatric PK, as well as for prospective, randomized comparative
treatment trials of skin and skin-structure infections (SSSIs),5 community-acquired
pneumonia,6,7 and neonatal sepsis.8 The efficacy and toxicity profile for adults is what
one would expect from most cephalosporins. Based on these published data, ceftaroline
should be effective and possibly safer than vancomycin for treatment of MRSA infections
for all age-groups, including neonates. Just as β-lactams are preferred over vancomycin
for MSSA infections, ceftaroline may be considered by some clinicians to be the preferred
treatment of MRSA infections over vancomycin, except for central nervous system
infections/endocarditis only due to lack of clinical data for these infections. Neither renal
function nor drug levels need to be followed with ceftaroline therapy, in contrast to treat-
ment with vancomycin. Since pediatric approval in mid-2016, there have been no serious
postmarketing adverse experiences in children reported; recommendations may change
 2025 Nelson’s Pediatric Antimicrobial Therapy — 243

should unexpected clinical data on lack of efficacy or unexpected toxicity beyond what
may be expected with β-lactams be presented.

Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Ceftobiprole, another fifth-generation cephalosporin, was FDA approved in February
2024 for children down to 3 months of age. Its activity and approved indications are
similar to those of ceftaroline, with the addition of bacteremia/endocarditis.9,10 Given
the extensive experience with ceftaroline in children, we currently prefer ceftaroline
over ceftobiprole until additional safety and efficacy are available from real-world use of
ceftobiprole.
Vancomycin (IV) has been the mainstay of parenteral therapy for MRSA infections for
the past 4 decades and continues to have activity against more than 98% of strains isolated
from children. New guidelines on the use of vancomycin for MRSA infections have been
published through a collaboration among the American Society of Health-System Phar-
macists, IDSA, Pediatric Infectious Diseases Society, and Society of Infectious Diseases
Pharmacists.11 A few cases of intermediate resistance and “heteroresistance” (transient
moderately increased resistance likely to be caused by thickened staphylococcal cell walls)
have been reported, most commonly in adults who are receiving long-term therapy or
who have received multiple exposures to vancomycin. Unfortunately, the response to
therapy using standard vancomycin dosing of 40 mg/kg/day in the treatment of many
CA-MRSA strains has not been as predictably successful as in the past with MSSA. For
vancomycin efficacy, the ratio of the area under the curve (the mathematically calculated
area below the serum concentration-versus-time curve) to minimum inhibitory concen-
tration (AUC:MIC) seems to be the best exposure metric to predict a successful outcome
in adults. Better outcomes are likely to be achieved with an AUC:MIC of about 400 or 12
greater, rather than with a serum trough value in the range of 15 to 20 mcg/mL, which is
associated with greater renal toxicity (see Chapter 11 for more on the AUC:MIC). This
ratio of 400:1 is achievable for CA-MRSA strains with in vitro MIC values of 1 mcg/mL
or less but difficult to achieve for strains with values of 2 mcg/mL or greater.12 Recent data
suggest that vancomycin MICs may actually be decreasing in children for MRSA causing
bloodstream infections as they increase for MSSA.13 Strains with MIC values of 4 mcg/mL
or greater should be considered resistant to vancomycin. When using “meningitis” treat-
ment dosages of 60 mg/kg/day (or higher) to achieve a 400:1 vancomycin exposure, one
needs to follow renal function carefully for the development of toxicity and the possible
subsequent need to switch classes of antibiotics.
Dalbavancin is a glycopeptide, structurally very similar to vancomycin but with
enhanced in vitro activity against MRSA and a much longer serum half-life, allowing
once-weekly dosing, or even just a single dose, to treat skin infections. Approved for
pediatrics from birth to age 18 years in 2021, it is an important option for outpatient
parenteral therapy once-weekly IV injection, when outpatient IV therapy and PO therapy
are not feasible.
 244 — Chapter 12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Clindamycin (PO or IV) is active against about 70% to 90% of strains of either MRSA
or MSSA, with great geographic variability (again, check with your hospital laboratory).14
The dosage for moderate to severe infections is 30 to 40 mg/kg/day, in 3 divided doses,
Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

with the same milligram per kilogram dose whether PO or IV. Clindamycin is not as bac-
tericidal as vancomycin but achieves higher concentrations in abscesses (because of high
intracellular concentrations in neutrophils). Some CA-MRSA strains are susceptible to
clindamycin on testing but have inducible clindamycin resistance (methylase-mediated)
that is usually assessed by the “D-test” and can now be assessed by multi-well microti-
ter plates. Within each population of CA-MRSA organisms, a rare organism (between
1 in 1011 and 1013 organisms) will have a mutation that allows for constant, rather than
induced, resistance.15 Although still somewhat controversial, clindamycin should be
effective therapy for infections that have a relatively low organism load (eg, cellulitis,
small or drained abscesses) and are unlikely to contain a significant population of these
constitutive methylase-producing mutants that are truly resistant; in fact, staphylococ-
cal methylase is poorly induced by clindamycin. Infections with a high organism load
(empyema) may have a greater risk of failure, as a large population is more likely to have
a significant number of truly resistant organisms and clindamycin should not be used as
the preferred agent for these infections. Many laboratories do not report D-test results but
simply call the organisms “resistant,” prompting the clinician to use alternative therapy
that may not be needed.
Clindamycin is used to treat most CA-MRSA infections that are not life threatening, and
if the child responds, therapy can be switched from IV to PO (although the PO solution
12
is not very well tolerated). Clostridioides (formerly Clostridium) difficile enterocolitis is a
concern; however, despite a great increase in the use of clindamycin in children during
the past decade, recent published data do not document a clinically significant increase in
the rate of this complication in children.
Trimethoprim/sulfamethoxazole (PO, IV), Bactrim/Septra, is active against CA-MRSA
in vitro. Prospective, comparative data on treatment of SSSIs in adults and children
document efficacy equivalent to clindamycin.16 There is a lack of prospective, comparative
information in the treatment of invasive MRSA infections (eg, bacteremia, pneumonia
and osteomyelitis [in contrast to skin infections]) in children, but some experts success-
fully use TMP/SMX for the treatment of osteomyelitis.17,18
Linezolid (PO, IV), active against virtually 100% of CA-MRSA strains, is another reason-
able alternative but is considered bacteriostatic as a protein synthesis inhibitor and has
relatively frequent hematologic toxicity in adults (ie, neutropenia, thrombocytopenia) and
some infrequent neurologic toxicity (ie, peripheral neuropathy, optic neuritis), particu-
larly when used for courses of 2 weeks or longer. A complete blood cell count should be
checked every week or two in children receiving prolonged linezolid therapy. Generic
linezolid is still substantially more costly than clindamycin or vancomycin.
Daptomycin (IV) is FDA approved for adults with skin infections and bacteremia/endo-
carditis and was approved for use in children with skin infections in April 2017. It is a
 2025 Nelson’s Pediatric Antimicrobial Therapy — 245

unique class of antibiotic, a lipopeptide, and is highly bactericidal. Daptomycin became

generic in 2017 and should be considered for treatment of skin infection and bacteremia
when other, better-studied antibiotics fail. Daptomycin should not be used to treat

Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

pneumonia, as it is inactivated by pulmonary surfactant. Pediatric studies for skin infec-
tions, bacteremia, and osteomyelitis have been published,19–21 showing that daptomycin
does not differ from comparator standard-of-care antibiotics for S aureus infections
(including MRSA osteomyelitis). Some newborn animal neurologic toxicity data suggest
additional caution for the use of daptomycin in infants younger than 1 year, prompt-
ing a warning in the package label. Routine pediatric clinical trial investigations in young
infants were not pursued due to these concerns.
Tigecycline and fluoroquinolones, both of which may show in vitro activity against
MRSA, are not generally recommended for children if other agents are available and are
tolerated, due to potential toxicity issues with tetracyclines and FQs as well as emergence
of resistance with FQs.
Combination therapy for serious infections, with vancomycin and rifampin (for deep
abscesses) or vancomycin and gentamicin (for bacteremia), is often used, but no prospec-
tive, controlled human clinical data exist on improved efficacy over single antibiotic
therapy. Some experts use vancomycin and clindamycin in combination, particularly for
children with a toxic-shock clinical manifestation, considering the protein synthesis inhi-
bition properties of clindamycin. Ceftaroline has also been used in combination therapy
with other agents, including daptomycin in adults, but no prospective, controlled clinical
data exist to assess benefits (or adverse events) of combinations over single-drug therapy.
12
Investigational Gram-Positive Agents Recently Approved for Adults and Being Studied
in Children
Oritavancin. An IV glycopeptide, structurally very similar to vancomycin but with
enhanced in vitro activity against MRSA and a much longer serum half-life, allowing
once-weekly dosing. A very similar antibiotic, dalbavancin, was approved for children in
2021.
Telavancin. A glycolipopeptide with mechanisms of activity that include cell wall inhibi-
tion and cell membrane depolarization, telavancin is administered once daily. The FDA
recently waived the requirement for pediatric investigation; the pediatric PK study has
been terminated.
Tedizolid. A second-generation oxazolidinone like linezolid, tedizolid is more potent in
vitro against MRSA than linezolid, with somewhat decreased toxicity to bone marrow in
adult clinical studies; it is approved for adolescents 12 years and older.
Recommendations for Empiric Therapy for Suspected MRSA Infections
Life-threatening and serious infections. If CA-MRSA is present in your community,
empiric therapy for presumed staphylococcal infections that are life threatening, or for
infections for which any risk of failure is unacceptable, should follow the recommenda-
tions for CA-MRSA and include ceftaroline OR high-dose vancomycin, clindamycin, or
 246 — Chapter 12. Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

linezolid, in addition to nafcillin or oxacillin (β-lactam antibiotics are considered better

than vancomycin or clindamycin for MSSA).
Approach to Antibiotic Therapy for Drug-Resistant Gram-Negative Bacilli & MRSA

Moderate infections. If you live in a location with greater than 10% methicillin resistance,
consider using the CA-MRSA recommendations for hospitalized children with presumed
staphylococcal infections of any severity, and start empiric therapy with clindamycin (usu-
ally active against >80% of CA-MRSA), ceftaroline, vancomycin, or linezolid IV.
In skin and skin-structure abscess treatment, antibiotics may be unnecessary following
incision and drainage, which may, in fact, be curative.
Mild infections. For nonserious, presumed staphylococcal infections in regions with
significant CA-MRSA, topical empiric therapy with mupirocin (Bactroban) or retapamu-
lin (Altabax) ointment, or PO therapy with TMP/SMX or clindamycin, is preferred. For
older children, doxycycline and minocycline are also options based on data in adults.

12
 2025 Nelson’s Pediatric Antimicrobial Therapy — 247

13. Antibiotic Therapy for Children With Obesity

NOTE: A list of table abbreviations and acronyms can be found at the start of this
publication.
When prescribing an antimicrobial for a child with obesity or overweight, selecting a dose
based on milligrams per kilograms of total body weight (TBW) may overexpose the child
if the drug does not freely distribute into fat tissue. Conversely, underexposure can occur
when a dosage is reduced for obesity for drugs without distribution limitations.
This “distribution-centric” construct does not account for altered drug clearance due to
obesity-related pathophysiologic changes, particularly in critical illness. Further, such
changes in adults, such as glomerular hyperfiltration, nephron loss, and hepatic steatosis,
may not yet be fully developed or present in obese children, making extrapolation of
obese adult antibiotic pharmacokinetic (PK) data to children problematic.

Antibiotic Therapy for Children With Obesity

In addition to empiric dose adjustment for obesity, we also recommend therapeutic drug
monitoring (TDM) of serum or plasma antibiotic concentrations of certain antibiotics to
achieve both safe and effective doses for these children.
Table 13-1 lists major antimicrobial classes and our suggestions on appropriate empiric
dosing. The evidence to support these recommendations is Level II to III (PK studies in

TABLE 13-1. DOSING RECOMMENDATIONS

Drug Class By EBWa By Adjusted Body Weight By TBWb
Antibacterials
β-Lactams
Aminopenicillins X (2 g ampicillin/dose max) 13
Piperacillin/tazobactam X (4 g PIP/dose max)
Cephalosporins X
Meropenem X (2 g/dose max)
Ertapenem X
Clindamycin X (no max)
Vancomycin 1,500–2,000 mg/m2/day 20 mg/kg LD, then 60 mg/
kg/day div q6–8h
Aminoglycosides 0.7 × TBW
Fluoroquinolones EBW + 0.45 (TBW−EBW)
Miscellaneous
TMP/SMX X
Metronidazole X
Linezolid X
Daptomycin X (See max doses in
comments.)
 248 — Chapter 13. Antibiotic Therapy for Children With Obesity

TABLE 13-1.(continued
DOSING RECOMMENDATIONS
)
Drug Class By EBWa By Adjusted Body Weight By TBWb
Antifungals
Amphotericin B X (max 150 mg for AmB-D,
max 500 mg for L-AmB)
Fluconazole X (max 1,600 mg LD,
max 1,200 mg/day)
Flucytosine X
Anidulafungin X (max 250 mg LD,
max 125 mg/day)
Caspofungin X (max 150 mg/day)
Micafungin X (max 300 mg/day)
Antibiotic Therapy for Children With Obesity

Voriconazole X
Antivirals (Non-HIV)
Nucleoside analogues X
(acyclovir, ganciclovir)
Antimycobacterials
Isoniazid X
Rifampin X
Pyrazinamide X
Ethambutol X
a 2
13 EBW (kg) = BMI 50th percentile for age × actual height (in meters) ; from Le Grange D, et al. Pediatrics.
2012;129(2):e438–e446 PMID: 22218841.
b
Dose up to adult max (see Ch 18) if not otherwise specified.

children, extrapolations from adult studies, and expert opinion). Maximum doses for
TBW dosing are given, and, for individual agents, are also found in Chapter 18. For each
antibiotic, recommendations for dosing are based on one of the following: expected body
weight, the actual or total body weight (ie, TBW), or adjusted body weight.
For tobramycin and other aminoglycosides, use the child’s fat-free mass, which is an
approximate 30% reduction in TBW. Closely following serum or plasma concentrations.
Vancomycin is traditionally dosed based on TBW in adults with obesity due to increases
in kidney size and glomerular filtration rate. In children with obesity, weight-adjusted
distribution volume and clearance are slightly lower than in their counterparts without
 2025 Nelson’s Pediatric Antimicrobial Therapy — 249

obesity. An empiric maximum dose of 60 mg/kg/day based on TBW, or dosing

using body surface area, may be more appropriate. Closely follow serum or plasma
concentrations.
In the setting of cefazolin for surgical prophylaxis (see Chapter 15), adult studies of
patients with obesity have generally shown that distribution to the subcutaneous fat
tissue target can be subtherapeutic when standard doses are used. Higher single doses are
recommended in adults with obesity (eg, 2 g instead of the standard 1 g) with re-dosing
at 4-hour intervals for longer cases. In children with obesity, we recommend dosing
cefazolin for surgical prophylaxis based on TBW up to the adult maximum of 2 g. For
treatment of skin infections, dose by TBW up to a maximum of 3 g every 8 hours. The US
Food and Drug Administration–approved maximum dose for life-threatening infections
is 3 g every 6 hours.
In critically ill adults with obesity treated with ceftazidime, cefepime, carbapenems,

Antibiotic Therapy for Children With Obesity

or piperacillin/tazobactam, extended infusion times (over 2–4 hours, instead of
30 minutes) should increase the likelihood of achieving therapeutic bloodstream antibi-
otic exposures, particularly against bacteria with higher minimum inhibitory concen-
trations (MICs). Some hospital laboratories perform serum or plasma concentration
testing of β-lactam antibiotics in-house, while most offer the service as a send-out.
Daptomycin can be dosed by using TBW, but the maximum dose should be 500 mg
for skin infections and 750 mg for bloodstream infections. Bolus administration over
2 minutes can improve the likelihood of achieving target concentrations when the maxi-
mum dose is less than the calculated dose in an adolescent with obesity. Serum or plasma
concentration testing is not routinely available for daptomycin.
Adult maximum doses of linezolid may be inadequate to achieve target plasma concen- 13
trations to treat susceptible methicillin-resistant Staphylococcus aureus infections with
high MICs. Higher doses should be attempted only with the aid of TDM to avoid hemato-
logic toxicity if serum or plasma concentration testing is available.
Bibliography
Camaione L, et al. Pharmacotherapy. 2013;33(12):1278–1287 PMID: 24019205
Castro-Balado A, et al. Antimicrob Agents Chemother. 2024;68(5):e0171923 PMID:
38526051
Donoso FA, et al. Arch Argent Pediatr. 2019;117(2):e121–e130 PMID: 30869490
Gorham J, et al. Antibiotics. 2023;12(7):1099 PMID: 37508195
Hall RG. Curr Pharm Des. 2015;21(32):4748–4751 PMID: 26112269
Harskamp-van Ginkel MW, et al. JAMA Pediatr. 2015;169(7):678–685 PMID: 25961828
Maharaj AR, et al. Paediatr Drugs. 2021;23(5):499–513 PMID: 34302290
 250 — Chapter 13. Antibiotic Therapy for Children With Obesity

Meng L, et al. Pharmacotherapy. 2023;43(3):226–246 PMID: 36703246

Moffett BS, et al. Ther Drug Monit. 2018;40(3):322–329 PMID: 29521784
Natale S, et al. Pharmacotherapy. 2017;37(3):361–378 PMID: 28079262
Pai MP. Clin Ther. 2016;38(9):2032–2044 PMID: 27524636
Pai MP, et al. Antimicrob Agents Chemother. 2011;55(12):5640–5645 PMID: 21930881
Payne KD, et al. Expert Rev Anti Infect Ther. 2016;14(2):257–267 PMID: 26641135
Smith MJ, et al. Antimicrob Agents Chemother. 2017;61(4):e02014-16 PMID: 28137820
Xie F, et al. J Antimicrob Chemother. 2019;74(3):667–674 PMID: 30535122
Antibiotic Therapy for Children With Obesity

13
 2025 Nelson’s Pediatric Antimicrobial Therapy — 251

14. Sequential Parenteral-Oral Antibiotic Therapy (Oral Step-Down

Therapy) for Serious Infections
The concept of oral step-down or “oral switch” therapy is well established, initially
published by Nelson and colleagues more than 40 years ago in the Journal of Pediatrics.1,2
Bone and joint infections,3–5 complicated bacterial pneumonia with empyema,6 deep-
tissue abscesses, and appendicitis,7,8 as well as cellulitis or pyelonephritis,9 may require
initial parenteral therapy and surgical drainage if necessary to control the growth and
spread of pathogens and minimize injury to tissues. Recent data in adults document the
effectiveness of early switch to oral (PO) therapy in uncomplicated gram-negative bacte-

Sequential Parenteral-Oral Antibiotic Therapy for Serious Infections

remia.10,11 When the signs and symptoms of infection begin to resolve, often within just a
few days, with no residual abscess or necrotic tissue noted, intravenous (IV) therapy may
no longer be required. A normal host neutrophil response is also capable of clearing the
infection as the pathogen load drops below a certain critical density, as has been demon-
strated in an animal model.12 It is likely that the good outcomes seen with PO step-down
therapy in normal hosts are based on contributions from both antibiotic and host.
In addition to following the clinical response before PO switch, following objective labo-
ratory markers, such as C-reactive protein (CRP) or procalcitonin (PCT), during the hos-
pitalization may also help the clinician better assess the response to antibacterial therapy,
particularly in the infant or child who is difficult to examine.13,14 The benefits of PO step-
down therapy over prolonged parenteral therapy are substantial and well-documented in
the treatment of acute osteomyelitis, including a decrease in both emergency department
visits and rehospitalizations, with equivalent treatment success outcomes (including for
those children with Staphylococcus aureus bacteremia).15,16
For children with intra-abdominal abscesses who recover quickly after surgical drainage
and initial antibiotic therapy, either short-course PO therapy (7 days total) or no addi-
tional antibiotic treatment following clinical and laboratory recovery may be appropri-
14
ate.17 But differentiating between those who may require ongoing PO step-down therapy
and those who will not can be difficult, as the extent of an intra-abdominal abscess, the
adequacy of source control (surgical drainage), and the susceptibility of pathogen(s)
involved are not always known.18
For the β-lactam class of antibiotics, absorption of PO administered antibiotics in
standard dosages usually studied by pharmaceutical companies for US Food and Drug
Administration (FDA) approval for mild to moderate respiratory tract, skin, or urinary
tract infections provides peak serum concentrations that are routinely only 5% to 20% of
those achieved with IV or intramuscular administration. High-dose PO β-lactam therapy,
however, provides the tissue antibiotic exposure closer to that achieved with parenteral
therapy that is thought to be helpful to eradicate the remaining pathogens at the infection
site as the tissue perfusion and antibiotic exposure there improve. For most PO antibiot-
ics, prospectively collected data on safety and efficacy at higher dosages have not been
systematically collected and presented by companies or investigators to the FDA for
 252 — Chapter 14. Sequential Parenteral-Oral Antibiotic Therapy for ­Serious Infections

approval; most of the data to support high-dose PO β-lactam often come from retrospec-
tively reviewed data or small prospective studies.
High-dose PO β-lactam antibiotic therapy for osteoarticular infections has been associ-
ated with treatment success since 1978.3 For β-lactams, begin with a dosage 2 to 3 times
the normal dosage (eg, 75–100 mg/kg/day of amoxicillin or 100 mg/kg/day of cephalexin)
supported by recent pharmacokinetic/pharmacodynamic assessment.19 High-quality
retrospective cohort data have recently confirmed similar outcomes achieved in those
treated with PO step-down therapy compared with those treated with IV therapy.15 High-
dose, prolonged PO β-lactam therapy may be associated with reversible neutropenia;
checking for hematologic toxicity every few weeks during therapy is suggested.20
Sequential Parenteral-Oral Antibiotic Therapy for Serious Infections

Clindamycin and many antibiotics of the fluoroquinolone class (eg, ciprofloxacin,

levofloxacin) and oxazolidinone class (eg, linezolid, tedizolid) have excellent absorption
of their PO formulations and provide virtually the same tissue antibiotic exposure at a
particular milligram per kilogram dose, compared with that dose given IV; therefore, for
these antibiotic classes, higher dosages are not needed for PO therapy. Trimethoprim/sul-
famethoxazole and metronidazole are also very well absorbed and should be effective for
PO step-down therapy if appropriate for the pathogen, infection site, and child.
One must also assume that the parent and child are adherent to the administration of
each antibiotic dose, that the PO antibiotic will be absorbed from the gastrointestinal
tract into the systemic circulation (no vomiting or diarrhea), and that the parent will seek
medical care if the clinical course does not continue to improve for their child.
Monitor the child clinically for a continued response during PO therapy; follow CRP or
PCT after the switch to PO therapy, and if there are concerns about continued response,
make sure the antibiotic and dosage you selected are appropriate and the family is adher-
ent. As John Nelson has pointed out, in one of the first published series of PO step-down
14 therapy for osteoarticular infection from Dallas in 1988, a reported failure of PO therapy
was caused by presumed nonadherence.21
 2025 Nelson’s Pediatric Antimicrobial Therapy — 253

15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

NOTE: A list of table abbreviations and acronyms can be found at the start of this
publication.
This chapter summarizes recommendations for prophylaxis of infections, defined as
antibiotic therapy before the onset of clinical signs or symptoms of infection in children
exposed or at high risk for exposure. Prophylaxis can be considered in several clinical
scenarios.
A. Postexposure Antimicrobial Prophylaxis to Prevent Symptomatic New Infection
Given for a relatively short, specified period (days) after a single exposure to spe-
cific pathogens/organisms, where the risks of acquiring the infection are felt to justify
antimicrobial treatment to prevent symptomatic infection or eradicate a colonizing

Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

pathogen when the child (healthy or with increased susceptibility to infection) is likely
to have been inoculated/exposed (eg, a child closely exposed to meningococcus; a
neonate born to a mother with active genital herpes simplex virus [HSV]) but not yet
showing signs or symptoms of infection.
B. Long-Term Antimicrobial Prophylaxis to Prevent Symptomatic New Infection
Given to a particular, defined population of children with relatively high risk of acquir-
ing a severe infection from a single exposure or multiple exposures (eg, a child post-
splenectomy; a child with documented rheumatic heart disease to prevent subsequent
streptococcal infection), with prophylaxis provided during the period of risk, poten-
tially for months or years.
C. Prophylaxis of Symptomatic Disease in Children Who Have Asymptomatic
Infection/Latent Infection
Where a child has a documented infection but is asymptomatic. Targeted antimicrobi-
als are given to prevent the development of symptomatic disease (eg, latent tuberculosis
[TB] infection or therapy of a stem cell transplant patient with documented cytomega-
15
lovirus viremia but no symptoms of infection or rejection; to prevent reactivation of
HSV). Treatment period is usually defined, particularly when the latent infection can
be cured (TB, requiring 6 months of therapy), but other circumstances, such as preven-
tion of reactivation of latent HSV, may require months or years of prophylaxis.
D. Surgical/Procedure Prophylaxis
A child receives a surgical/invasive catheter procedure, planned or unplanned, in
which the risk for infection postoperatively or post-procedure may justify prophylaxis
to prevent an infection from occurring (eg, prophylaxis to prevent infection following
spinal rod placement). Treatment is usually short-term (hours), beginning just before
the procedure and ending at the conclusion of the procedure, or within 24 hours.
 254 — Chapter 15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

E. Travel-Related Exposure Prophylaxis

Not discussed in this chapter; refer to information on specific disease entities (eg,
travelers diarrhea, Chapters 1 and 9) or specific pathogens (eg, malaria, Chapter 9).
Constantly updated, current information for travelers about prophylaxis (often starting
just before travel and continuing until return) and current worldwide infection risks
can be found on the Centers for Disease Control and Prevention website at www.cdc.
gov/travel (accessed October 21, 2024).
Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

15
A. POSTEXPOSURE ANTIMICROBIAL PROPHYLAXIS TO PREVENT INFECTION
Prophylaxis Category Therapy (evidence grade) Comments
Bacterial
Bites, animal and Amox/clav 45 mg/kg/day PO div tid (amox/clav 7:1; Recommended for children who (1) have moderate to
human1–5 (Pasteurella see Aminopenicillins in Ch 4 for amox/clav ratio severe injuries, especially to the hand or face; (2) are
multocida; Staphylococcus descriptions) for 3–5 days (AII) OR ampicillin and immunocompromised; (3) are asplenic; or (4) have inju-
aureus, including CA-MRSA; clindamycin OR ceftriaxone and clindamycin (BII), ries that may have penetrated the periosteum or joint
Streptococcus spp, anaer- OR, for IV: amp/sul. For penicillin allergy, consider capsule (AII).3
obes; Capnocytophaga ciprofloxacin (for Pasteurella) plus clindamycin Consider rabies prophylaxis for at-risk animal bites through
canimorsus, particularly in (BIII). state and local rabies consultation contacts (AI)6; consider
asplenic hosts) tetanus prophylaxis.7
Human bites have a very high rate of infection (do not
close open wounds routinely).
Cat bites have a higher rate of infection than dog bites.
S aureus coverage is only fair with amox/clav and amp/sul,

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

and it provides no coverage for MRSA.
Endocarditis prophylaxis8,9: Given that (1) endocarditis is rarely caused by dental/GI procedures and (2) prophylaxis for procedures prevents an
exceedingly small number of cases, the risks of antibiotics most often outweigh benefits. However, some “highest-risk” conditions are currently
recommended for prophylaxis: (1) prosthetic heart valve (or prosthetic material used to repair a valve); (2) previous endocarditis; (3) cyanotic
congenital heart disease that is unrepaired (or palliatively repaired with shunts and conduits); (4) congenital heart disease that is repaired but
with defects at the site of repair adjacent to prosthetic material; (5) completely repaired congenital heart disease by using prosthetic material, for
the first 6 mo after repair; or (6) cardiac transplant patients with valvulopathy. Routine prophylaxis has not been required for children with native
valve abnormalities since updated guidelines were published in 2015.9 Follow-up data in children suggest that following these new guidelines,
no increase in endocarditis has been detected.10–13
– In highest-risk patients: den- Amoxicillin 50 mg/kg (max 2 g) PO 1 h before pro- If penicillin allergy: clindamycin 20 mg/kg PO (1 h before)
tal procedures that involve cedure OR ampicillin or ceftriaxone or cefazolin, or IV (30 min before) OR azithromycin 15 mg/kg or cla­
manipulation of the gingival all at 50 mg/kg IM/IV 30–60 min before rithromycin 15 mg/kg (1 h before)
or periodontal region of procedure
teeth
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A. POSTEXPOSURE ANTIMICROBIAL PROPHYLAXIS TO PREVENT INFECTION
Prophylaxis Category Therapy (evidence grade) Comments
– Genitourinary and GI None No longer recommended
procedures
Lyme disease (Borrelia Doxycycline 4.4 mg/kg (max 200 mg), once. Dental ONLY for those in highly Lyme-endemic areas AND the tick
burgdorferi)14 staining should not occur with a single dose of has been attached for >36 h (and is engorged) AND pro-
doxycycline. Amoxicillin prophylaxis is not well phylaxis started within 72 h of tick removal.
studied, and experts recommend a full 14-day
course if amoxicillin is used.
Meningococcus (Neisseria For prophylaxis of close contacts, including house- A single dose of ciprofloxacin should not present a signifi-
meningitidis)15,16 hold members, child care center contacts, and cant risk of cartilage damage, but no prospective data
anyone directly exposed to the child’s oral secre- exist in children for prophylaxis of meningococcal dis-
tions (eg, through kissing, mouth-to-mouth ease. For a child, an exposure for ciprofloxacin equivalent
resuscitation, endotracheal intubation/manage- to that in adults would be 15–20 mg/kg as a single dose
ment) in the 7 days before symptom onset (max 500 mg).
Rifampin A few ciprofloxacin-resistant strains have been reported.
Infants <1 mo: 5 mg/kg PO q12h for 4 doses Azithromycin is not recommended routinely, but when
Children ≥1 mo: 10 mg/kg PO q12h for 4 doses used, give 10 mg/kg as a single dose.
(max 600 mg/dose) OR Meningococcal vaccines that target the specific serogroup
Ceftriaxone may also be recommended in case of an outbreak.
Children <15 y: 125 mg IM once
Children ≥15 y: 250 mg IM once OR
Ciprofloxacin
Children ≥1 mo: 20 mg/kg PO (max 500 mg) once
Pertussis17,18 PEP uses the same regimen as for treatment of per- Prophylaxis to family members regardless of immunization
tussis (see Ch 1) per the AAP17: azithromycin status; contacts defined by the CDC: persons within
10 mg/kg/day qd for 5 days through age 5 mo; 21 days of exposure to infectious pertussis, who are at
then, for those ≥6 mo, 10 mg/kg/day (max high risk for severe illness or will have close contact with
500 mg) on day 1, followed by 5 mg/kg/day (max a person at high risk for severe illness (including infants,
250 mg) for days 2–5 OR clarithromycin (for pregnant women in their third trimester, immunocom-
infants >1 mo) 15 mg/kg/day div bid for 7 days promised persons, and those who have close contact
 Alternative for infants >2 mo: Community-wide prophylaxis is not recommended as the
TMP/SMX 8 mg TMP/kg/day div bid for 14 days CDC attempts to limit unnecessary antibiotic use.
(BIII) Azithromycin and clarithromycin are better tolerated than
erythromycin (see Ch 2); azithromycin is preferred in
exposed very young infants to reduce pyloric stenosis
risk.
Tetanus
Need for Tetanus Vaccine or TIGa
(Clostridium tetani)7,19
Clean Wound Contaminated Wound
Number of past tetanus Need for Need for Need for Need for
vaccine doses tetanus vaccine TIG 500 U IMa tetanus vaccine TIG 500 U IMa
<3 doses Yes No Yes Yes
≥3 doses No (if <10 yb) No No (if <5 yb) No
Yes (if ≥10 yb) Yes (if ≥5 yb)
a
IV immune globulin should be used when TIG is not available.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

b
Years since last tetanus-containing vaccine dose.
For deep, contaminated wounds, wound debridement is essential. Antimicrobial prophylaxis has not been
shown to prevent tetanus, but randomized, controlled studies would be difficult to perform.
 15
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A. POSTEXPOSURE ANTIMICROBIAL PROPHYLAXIS TO PREVENT INFECTION
Prophylaxis Category Therapy (evidence grade) Comments
Tuberculosis Scenario 1: Previously uninfected child at high risk If PPD or IGRA remains negative at 2–3 mo and child
(Mycobacterium for serious infection and dissemination becomes remains well, consider stopping empiric therapy.
tuberculosis) exposed to a person with active disease. However, tests at 2–3 mo may not be reliable in
“Window prophylaxis” of Exposed children <4 y, or immunocompromised immunocompromised patients.
exposed children <4 y, or patient (high risk for dissemination): rifampin
immunocompromised 15–20 mg/kg/dose PO qd OR INH 10–20 mg/kg
patient (high risk for dis- PO qd; for at least 2–3 mo (AIII), at which time
semination) to prevent cellular immunity is established and PPD/IGRA
infection after exposure, may be more accurately assessed. If positive,
rather than to treat latent treatment for latent TB should continue.
asymptomatic infection20,21 Children ≥4 y may also begin prophylaxis postex-
For treatment of latent TB posure, but if exposure is questionable, can wait
infection,21,22 see 2–3 mo after exposure to assess for infection; if
Tuberculosis in Table 15C. not given prophylaxis, and PPD/IGRA at 2–3 mo
is positive and child remains asymptomatic at
that time, see Scenario 2 below.
Scenario 2: An asymptomatic child is found to have
a positive skin test/IGRA for TB, documenting
latent TB infection; see Tuberculosis in Table 15C.
Treat with at least 4 mo of rifampin OR 6 mo of
INH, OR 3 mo of combination INH and rifampin,
OR, for those ≥2 y, INH and rifapentine.
Viral
Herpes simplex virus
– During pregnancy For women with recurrent genital herpes, follow Neonatal HSV disease after unsuccessful maternal suppres-
ACOG guidelines23: acyclovir 400 mg PO tid; vala- sion has been documented.24
cyclovir 500 mg PO bid from 36 wk of gestation
until delivery (CII).
– Neonatal: primary or Asymptomatic, exposed neonate: at 24 h after AAP Red Book 2024–202725 provides a management algo-
nonprimary first clinical birth, sample mucosal sites for HSV culture (and rithm that determines the type of maternal infection and,
episode of maternal PCR if possible) (see Comments), obtain CSF and thus, the appropriate evaluation and preemptive therapy
infection, neonate whole-blood PCR for HSV DNA, obtain ALT, and of the neonate.
exposed at delivery25 start preemptive therapeutic acyclovir IV Mucosal sites for culture: conjunctivae, mouth, nasophar-
(60 mg/kg/day div q8h) for 10 days (AII). ynx, rectum.
Some experts would evaluate at birth for exposure Infants treated with 10 days of preemptive IV therapy
following presumed maternal primary infection should not subsequently receive PO acyclovir suppres-
and start preemptive therapy rather than wait sion, because their HSV exposure never progressed to
24 h. infection or disease.
Any symptomatic baby, at any time, requires a full evalua-
tion for invasive infection and IV acyclovir therapy for
14–21 days, depending on extent of disease.
– Neonatal: recurrent Asymptomatic, exposed neonate: at 24 h after AAP Red Book 2024–202725 provides a management algo-
maternal infection, birth, sample mucosal sites for HSV culture (and rithm that determines the type of maternal infection and,
neonate exposed at PCR if desired) (see Comments) and obtain thus, the appropriate evaluation and preemptive therapy

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

delivery25 whole-blood PCR for HSV DNA. Hold on therapy of the neonate.
unless cultures or PCRs are positive, at which Mucosal sites for culture: conjunctivae, mouth, nasophar-
time the diagnostic evaluation should be ynx, rectum.
completed (CSF PCR for HSV DNA, serum ALT) Infants treated with 10 days of preemptive IV therapy
and preemptive therapeutic IV acyclovir should not subsequently receive PO acyclovir suppres-
(60 mg/kg/day div q8h) should be administered sion, because their HSV exposure never progressed to
for 10 days (AIII). infection or disease.
Any symptomatic baby, at any time, requires a full evalua-
tion for invasive infection and IV acyclovir therapy for
14–21 days, depending on extent of disease.
– Neonatal: following symp- See Neonatal in Table 15C under Herpes simplex
tomatic disease, to prevent virus.
recurrence
– Keratitis (ocular) in other- See Keratitis in Table 15C under Herpes simplex
wise healthy children virus.
 15
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A. POSTEXPOSURE ANTIMICROBIAL PROPHYLAXIS TO PREVENT INFECTION
Prophylaxis Category Therapy (evidence grade) Comments
Influenza virus (A or B) 26
Oseltamivir prophylaxis (AI) Not routinely recommended for infants 0–≤3 mo unless
3–≤8 mo: 3 mg/kg/dose qd for 10 days; 9–11 mo: exposure judged substantial (single event or ongoing
3.5 mg/kg/dose PO qd for 10 days27; based on [eg, breastfeeding mother with active influenza]),
body weight for children ≥12 mo: ≤15 kg: because of limited reported data on safety/efficacy and
30 mg qd for 10 days; >15–23 kg: 45 mg qd for variability of drug exposure in this age-group
10 days; >23–40 kg: 60 mg qd for 10 days;
>40 kg: 75 mg qd for 10 days
Zanamivir prophylaxis (AI)
≥5 y: 10 mg (two 5-mg inhalations) qd for as long
as 28 days (community outbreaks) or 10 days
(household settings)
Baloxavir prophylaxis (AI)
≥5 y:
<20 kg: single dose PO of 2 mg/kg
20–79 kg: single dose PO of 40 mg
≥80 kg: single dose PO of 80 mg
Rabies virus28 RIG, 20 IU/kg, infiltrated around wound, with For dog, cat, or ferret bite from symptomatic animal,
remaining volume injected IM (AII) immediate RIG and immunization; otherwise, can wait
PLUS 10 days for observation of animal, if possible, before RIG
Rabies immunization (AII). or vaccine.
State and local public health departments and the PLEASE evaluate the context of the bite. A provoked bite
CDC can provide advice on risk and management from a threatened or annoyed dog (especially a known
(www.cdc.gov/rabies/hcp/prep-pep/index.html; dog) is not an indication for rabies prophylaxis.
June 20, 2024; accessed October 21, 2024). Bites of squirrels, hamsters, guinea pigs, gerbils, chipmunks,
rats, mice and other rodents, rabbits, hares, and pikas
almost never require anti-rabies prophylaxis.
 If vaccine is not available immediately, RIG should For bites of bats, skunks, raccoons, foxes, most other carni-
be administered alone, and vaccination should vores, and woodchucks, immediate RIG and immuniza-
be started as soon as possible. If RIG is not avail- tion (regard as rabid unless geographic area is known to
able immediately, vaccine should be adminis- be free of rabies or until animal’s condition is proven neg-
tered, and RIG should be administered ative by laboratory tests).
subsequently if obtained within 7 days after initi-
ating vaccination. If administration of both vac-
cine and RIG is delayed, both should be used
regardless of the interval between exposure and
treatment.
Varicella-zoster virus29 Varicella vaccine, administered ideally within Preemptive VZIG or antiviral therapy in those who have
3 days but up to 5 days after exposure for those been exposed to varicella, during the incubation period,
without immunity to prevent symptomatic infection: for immunocompro-
VZIG mised patients without evidence of immunity from past
Acyclovir 20 mg/kg/dose PO qid (max daily dose infection or vaccine or for immunocompetent, suscepti-
3,200 mg) or valacyclovir 20 mg/kg/dose PO tid ble patients for whom varicella may be severe (eg, preg-
(max daily dose 3,000 mg) beginning 7 days after nancy, neonates without significant transplacental

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

exposure and continuing for 7–10 days varicella antibody, adolescents)
 15
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B. LONG-TERM ANTIMICROBIAL PROPHYLAXIS TO PREVENT SYMPTOMATIC NEW INFECTION
Prophylaxis
Category Therapy (evidence grade) Comments
Bacterial otitis Amoxicillin or other antibiotics can be used in The AAP and American Academy of Family Physicians recommend
media30,31 half the therapeutic dose qd or bid to prevent that clinicians not prescribe antibiotics for prophylaxis of AOM in
infections if the benefits outweigh the risks of children aged 6 mo–12 y. However, the guidance does not apply to
(1) emergence/selection of resistant organisms children with anatomic abnormalities or genetic conditions that
for that child (and contacts) and (2) antibiotic may affect the ears or children with cochlear implants or
side effects. immunodeficiencies.
True, recurrent acute bacterial otitis is far less common in the era of
conjugate pneumococcal immunization.
To prevent recurrent infections, as an alternative to antibiotic prophy-
laxis, also consider the risks and benefits of placing tympanostomy
tubes to improve middle ear ventilation.31
Studies have demonstrated that amoxicillin, sulfisoxazole, and TMP/
SMX are effective. However, antimicrobial prophylaxis may alter the
nasopharyngeal flora and foster colonization with resistant organ-
isms, compromising long-term efficacy of the prophylactic drug.
Continuous PO administered antimicrobial prophylaxis should be
reserved for control of recurrent AOM, only when defined as
≥3 distinct and well-documented episodes during a period of 6 mo
or ≥4 episodes during a period of 12 mo, which is now uncommon
in the era of pneumococcal conjugate vaccines.
Impaired splenic Penicillin V Use of antibiotic prophylaxis is generally favored for asplenic and
function <3 y: 125 mg bid hyposplenic patients who are at highest risk of severe infection
(including ≥3 y: 250 mg bid OR (eg, immunocompromised, those in first year post-splenectomy).
splenectomy) Amoxicillin 10 mg/kg bid (max 250 mg/dose). Patient age, immune status, history of infections with encapsulated
Alternative agents: cephalexin 25 mg/kg bid organisms, risk of adverse drug reactions, local prevalence of
(max 250 mg/dose) OR resistant organisms, and other factors are used to determine the
Azithromycin 5 mg/kg daily (max 250 mg/dose) need for daily prophylaxis and its duration for individual patients.
For most children with anatomic or functional asplenia, daily
antibiotic prophylaxis is recommended until age 5 y.
 For children with additional immunocompromising conditions (eg,
hematologic malignancy, HIV, transplant), antibiotic prophylaxis is
recommended until at least age 18 y and often for life or total dura-
tion of immunocompromise.
Rheumatic fever For >27.3 kg (>60 lb): 1.2 million U penicillin G AHA policy statement at www.ahajournals.org/doi/epub/10.1161/
benzathine, q4wk (q3wk for high-risk children) CirculationAHA.109.191959 (accessed October 21, 2024).
For ≤27.3 kg: 600,000 U penicillin G benzathine, Doses studied many years ago, with no new data; ARF is an uncom-
q4wk (q3wk for high-risk children) mon disease currently in the United States, as “rheumatogenic”
OR strains are apparently not circulating widely at this time.
Penicillin V (phenoxymethyl), 250 mg PO bid Alternatives to penicillin include amoxicillin, sulfisoxazole, or mac-
rolides, including erythromycin, azithromycin, and clarithromycin.
Urinary tract TMP/SMX 3 mg/kg/dose of TMP PO qhs OR TMP Amoxicillin is an alternative (although >50% of community-acquired
infection, alone, 2 mg/kg/dose (max 100 mg) PO qhs, OR Escherichia coli isolates are resistant).
recurrent32–38 nitrofurantoin 1–2 mg/kg PO qhs; more rapid Only used for those with grade III–V reflux or recurrent febrile UTI:
resistance may develop by using β-lactams prophylaxis no longer recommended for patients with grade I–II
(BII). (some also exclude grade III) reflux. Prophylaxis prevents infection

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

but may not prevent scarring. Early treatment of new infections is
recommended for children not given prophylaxis.
Resistance eventually develops to every antibiotic; follow resistance
patterns for each patient.
Cranberries can, in fact, prevent UTI.32
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B. LONG-TERM ANTIMICROBIAL PROPHYLAXIS TO PREVENT SYMPTOMATIC NEW INFECTION
Prophylaxis
Category Therapy (evidence grade) Comments
Fungal: For detailed information on prevention of candidiasis in the neonate, see Ch 2; for detailed information on prevention of fungal infection
(Candida, Aspergillus, or Rhizopus spp) in children undergoing chemotherapy, see Ch 5.
Pneumocystis jirovecii Non-HIV infection regimens (stem cell trans- Prophylaxis in specific populations based on degree of immunosup-
(formerly plants, solid-organ transplants, many malig- pression. For children with HIV, see ClinicalInfo.HIV.gov for informa-
carinii)39–42 nancies, and T-cell immunodeficiencies tion on pediatric opportunistic infections: https://clinicalinfo.hiv.
[congenital or secondary to treatment]). gov/en/guidelines/hiv-clinical-guidelines-pediatric-opportunistic-
Duration of prophylaxis depends on the under- infections/pneumocycstis-jirovecii-pneumonia (updated November
lying condition. 6, 2013; accessed October 21, 2024).
TMP/SMX 5–10 mg/kg/day of TMP PO, in 2 div Inhaled pentamidine only for those who cannot tolerate the regimens
doses, q12h, either qd or 2×/wk or 3×/wk, on noted above.
consecutive days or alternating days (AI); OR
TMP/SMX 5–10 mg/kg/day of TMP PO as a
single dose, qd, given daily, 7 days per week
(AI) (once-weekly regimens have also been
successful); OR dapsone 2 mg/kg (max
100 mg) PO qd, or 4 mg/kg (max 200 mg)
once weekly; OR atovaquone 30 mg/kg/day
for infants 1–3 mo; 45 mg/kg/day for infants/
children 4–24 mo; and 30 mg/kg/day for
children ≥24 mo.
C. PROPHYLAXIS OF SYMPTOMATIC DISEASE IN CHILDREN WHO HAVE ASYMPTOMATIC INFECTION/LATENT
INFECTION
Prophylaxis Category Therapy (evidence grade) Comments
Herpes simplex virus
Neonatal: following symptomatic Acyclovir 300 mg/m2/dose PO tid for Neonates who recover from early infection may experience
disease, to prevent recurrence 6 mo, following cessation of IV acy- relapse and are likely to still be at risk for disseminated infec-
clovir treatment of acute disease tion until out of the neonatal period of immunocompromise.
(AIII) No prospective studies to examine potential benefits of pro-
phylaxis until age 2–3 mo.
Follow absolute neutrophil counts at 2 and 4 wk, then monthly
during prophylactic/suppressive therapy.
Keratitis (ocular) in otherwise healthy Suppressive acyclovir therapy for fre- Decisions to continue suppressive therapy should be assessed
children quent recurrence (no pediatric data): annually. The frequency of dosing may need to be increased
long-term suppression (≥1 y) of to qid or the drug may need to be changed to valacyclovir, if
recurrent infection with PO acyclovir breakthrough ocular infection occurs. Potential risks must

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

80 mg/kg/day in 3 div doses (max balance potential benefits to vision (BIII).
dose 800 mg) (AIII) Check for acyclovir resistance for those who relapse during
appropriate therapy.
Suppression oftentimes required for many years.
Watch for severe recurrence at conclusion of suppression.
Tuberculosis20–22 (latent TB infection Rifampin 15–20 mg/kg/dose qd, pref- Alternative regimens:
[asymptomatic, true infection], erably the entire daily dose given qd INH 10–20 mg/kg PO qd AND rifampin 15–20 mg/kg/dose daily
defined by a positive skin test or (max 600 mg) for 4 mo, OR (max 600 mg) for 3 mo, OR
IGRA, with no clinical or radio- For children ≥2 y, once-weekly DOT for INH 10–20 mg/kg PO qd for 6 to 9 mo, OR
graphic evidence of active disease), 12 wk using BOTH INH 15 mg/kg/ INH 20–40 mg/kg PO DOT twice weekly for 6–9 mo
currently called “TB infection” in con- dose (max 900 mg) AND rifapentine: For exposure to drug-resistant strains, consult with TB specialist.
trast to active, symptomatic infec- 10.0–14.0 kg: 300 mg; 14.1–25.0 kg:
tion that is now called “TB disease” 450 mg; 25.1–32.0 kg: 600 mg;
32.1–49.9 kg: 750 mg; ≥50.0 kg:
900 mg (max)
 15
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266 — Chapter 15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

D. SURGICAL/PROCEDURE PROPHYLAXIS43–48
The CDC National Healthcare Safety Network uses a classification of surgical procedure-related wound infections based on an estimation of the
load of bacterial contamination: Class I, clean; Class II, clean-contaminated; Class III, contaminated; and Class IV, dirty/infected.44,48 Other major
factors creating risk for postoperative surgical site infection include the duration of surgery (a longer-duration operation, defined as one that
exceeded the 75th percentile for a given procedure) and the medical comorbidities of the patient, as determined by an American Society of
Anesthesiologists score of III, IV, or V (presence of severe systemic disease that results in functional limitations, is life threatening, or is expected
to preclude survival from the operation). The virulence/pathogenicity of bacteria inoculated and the presence of foreign debris/devitalized tis-
sue/surgical material in the wound are also considered risk factors for infection.
For all categories of surgical prophylaxis, dosing recommendations are derived from (1) choosing agents based on the organisms likely to be
responsible for inoculation of the surgical site; (2) giving the agents at an optimal time (<60 min for cefazolin, or <60–120 min for vancomycin
and ciprofloxacin) before starting the operation to achieve appropriate serum and tissue exposures at the time of incision; (3) providing addi-
tional doses during the procedure at times based on the standard dosing guideline for that agent (or excessive blood loss during surgery); and
(4) stopping the agents at the end of the procedure, even if drains remain.48 Optimal duration of prophylaxis after delayed sternal or abdominal
closure is not well-defined in adults or children.
Topical perioperative use of chlorhexidine or povidone-iodine decreases the risk of surgical site infection.49,50
Intraoperative Re-Dosing
Interval (h) for Prolonged
Procedure/Operation Recommended Agents Preoperative Dose Surgery
Cardiovascular
Cardiac48,51 Cefazolin 30–40 mg/kg 4
Staphylococcus epidermidis, Vancomycin, if MRSA likely 15 mg/kg 8
Staphylococcus aureus,
Corynebacterium spp Amp/sul if enteric GNB a concern 50 mg/kg ampicillin 3
Other options: cefuroxime, clindamycin
Cardiac with CPB45,52 Cefazolin 30–40 mg/kg 15 mg/kg at CPB start and
also at rewarming. Begin
postoperative prophylaxis
30–40 mg/kg 8 h after
intraoperative rewarming
dose.
Other antibiotics may be used but should be dosed based on patient’s anticipated antibiotic elimination during
Vascular Cefazolin, OR 30–40 mg/kg 4
Staphylococcus epidermidis,
Staphylococcus aureus, Vancomycin, if MRSA likely 15 mg/kg 8
Corynebacterium spp, enteric
Other option: clindamycin 10 mg/kg
GNB, particularly for proce-
dures in the groin
Thoracic (noncardiac)
Lobectomy, video-assisted tho- Cefazolin, OR 30–40 mg/kg 4
racoscopic surgery, thoracot-
omy (but no prophylaxis Amp/sul if enteric GNB a concern 50 mg/kg ampicillin 3
needed for simple chest tube Vancomycin or clindamycin if drug 15 mg/kg vancomycin 8
placement for pneumothorax) allergy or MRSA likely
10 mg/kg clindamycin 6
Gastrointestinal
Gastroduodenal Cefazolin 30–40 mg/kg 4

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Enteric GNB, respiratory tract
gram-positive cocci
Biliary procedure, open Cefazolin, OR 30–40 mg/kg 4
Enteric GNB, enterococci,
Clostridia Cefoxitin, OR 40 mg/kg 2
Amp/sul 50 mg/kg ampicillin 3
Appendectomy, non- Cefoxitin, OR 40 mg/kg 2
perforated (no prophylaxis
needed postoperatively if Cefazolin and metronidazole 30–40 mg/kg cefazolin, 10 mg/kg 4 for cefazolin
appendix is intact)48,53 metronidazole 8 for metronidazole
 15
Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

268 — Chapter 15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

D. SURGICAL/PROCEDURE PROPHYLAXIS43–48
Complicated appendicitis or Cefazolin and metronidazole, OR 30–40 mg/kg cefazolin, 10 mg/kg 4 for cefazolin
other ruptured colorectal metronidazole 8 for metronidazole
viscus54
Enteric GNB, enterococci, Cefoxitin, OR 40 mg/kg 2
anaerobes Ceftriaxone and metronidazole, OR 50 mg/kg ceftriaxone, 10 mg/kg 12 for ceftriaxone
For complicated appendicitis, metronidazole 8 for metronidazole
antibiotics provided to treat
ongoing infection, rather than Meropenem, OR 20 mg/kg 4
prophylaxis Imipenem 20 mg/kg 4
Genitourinary
Cystoscopy (requires prophy- Cefazolin, OR 30–40 mg/kg 4
laxis only for children with sus-
pected active UTI or those TMP/SMX (if low local resistance), 4–5 mg/kg NA
having foreign material OR
placed) Select a 2nd- (cefuroxime) or 3rd-
Enteric GNB, enterococci generation cephalosporin (ceftriax-
one) or FQ (ciprofloxacin) if the child
is known or suspected to be colonized
with cefazolin-resistant, TMP/
SMX-resistant strains.
Open or laparoscopic Cefazolin 30–40 mg/kg 4
surgery
Enteric GNB, enterococci
Head and neck surgery
Assuming incision through respi- Clindamycin, OR 10 mg/kg 6
ratory tract mucosa (eg,
contaminated) Cefazolin and metronidazole, OR 30–40 mg/kg cefazolin, 10 mg/kg 4 for cefazolin
Anaerobes, enteric GNB, metronidazole 8 for metronidazole
Staphylococcus aureus Amp/sul if enteric GNB a concern 50 mg/kg ampicillin 3
Neurosurgery
Craniotomy, ventricular shunt Cefazolin, OR 30–40 mg/kg 4
placement
Staphylococcus epidermidis, Vancomycin or clindamycin, if MRSA 15 mg/kg vancomycin 8
Staphylococcus aureus likely
10 mg/kg clindamycin 6
Orthopedic
Internal fixation of fractures, spi- Cefazolin, OR 30–40 mg/kg 4
nal rod placement, prosthetic

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

joints Vancomycin or clindamycin, if MRSA 15 mg/kg vancomycin 8
Staphylococcus epidermidis, likely
10 mg/kg clindamycin 6
Staphylococcus aureus
 15
Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

270 — Chapter 15. Antimicrobial Prophylaxis/Prevention of Symptomatic Infection

D. SURGICAL/PROCEDURE PROPHYLAXIS43–48
Trauma
Exceptionally varied; no prospec- Cefazolin (for skin), OR 30–40 mg/kg 4
tive, comparative data in chil-
dren; agents should focus on Vancomycin or clindamycin (for skin), if 15 mg/kg vancomycin 8
skin flora (S epidermidis, MRSA likely, OR
10 mg/kg clindamycin 6
S aureus) as well as flora inocu-
lated into the wound, based Meropenem OR imipenem (for anaer- 20 mg/kg for either 4
on the trauma exposure, that obes, including Clostridium spp, and
may include enteric GNB, non-fermenting GNB), OR
anaerobes (including Gentamicin and metronidazole (for non- 2.5 mg/kg gentamicin, 10 mg/kg 6 for gentamicin
Clostridium spp), and fungi. fermenting GNB and anaerobes, includ- metronidazole 8 for metronidazole
Cultures at wound exploration ing Clostridium spp), OR
are critical to focus therapy for
potential pathogens inocu- PIP/TAZO 100 mg/kg PIP component 2
lated into the wound.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 271

16. Approach to Antibiotic Allergies

NOTE: A list of table abbreviations and acronyms can be found at the start of this
publication.
Introduction
Antibiotics are a common cause of drug reactions. β-Lactam antibiotics are most com-
monly implicated, with about 10% of the US population reporting a history of penicillin
allergy. However, antibiotic allergies are frequently mislabeled and, even if present, may
not persist throughout childhood and into adolescence. In such cases, unnecessary use
of alternative broad-spectrum antibiotics may result in suboptimal therapy, medication-
related side effects, the development of antibiotic resistance, and increased health care
costs. More than 90% of those who report a history of an antibiotic allergy are ultimately
able to safely tolerate the antibiotic. Thus, it is important to use a systematic approach to
children with reported antibiotic allergies, including the routine evaluation of reported
penicillin allergy.
American Academy of Allergy, Asthma and Immunology (AAAAI); American College of
Allergy, Asthma, and Immunology; and Joint Council of Allergy, Asthma and Immunol-
ogy practice parameters provide an excellent overview of drug allergies; the following
information summarizes recommendations with respect to antibiotic allergies from these
guidelines and other resources listed in Suggested Reading later in this chapter.
Classification of Antibiotic Allergies
Antibiotic allergies are immune-mediated reactions to a drug that occur in a previously

Approach to Antibiotic Allergies

sensitized child. More commonly, adverse drug reactions are not immune mediated
and do not represent a true antibiotic allergy (but are often mislabeled as such). It is
important to distinguish between clinically relevant categories of adverse antibiotic reac-
tions (Table 16-1).

16
 16
Approach to Antibiotic Allergies

272 — Chapter 16. Approach to Antibiotic Allergies

TABLE 16-1. CLASSIFICATION OF ADVERSE ANTIBIOTIC REACTIONS
Classification Mechanism Characteristics Examples Future Use of Antibiotic
Immediate hyper- Type I Anaphylactic Immediate urticaria If β-lactam, consider repeat
sensitivity IgE mediated May be life threatening Angioedema skin testing 5–10 y after
reactions Occur within minutes to <6 h of Laryngeal edema/stridor positive skin test or ana-
exposure to the antibiotic Bronchospasm/wheezing phylactic reaction.1
Uncommon Cardiorespiratory symptoms If no alternative antibiotic,
administer through
desensitization protocol
(Table 16-3).
Delayed drug- Type IV Nonanaphylactic Delayed maculopapular rash Future use of antibiotic may
induced Cell mediated Not life threatening (typically fixed/nonmobile, be considered.
exanthems Typically occur after several days non-pruritic)
of antibiotic exposure Delayed urticaria
More common
Severe cutaneous Type IV Severe delayed hypersensitivity EM major Future use of antibiotic con-
adverse reactions T-cell mediated reactions SJS/TEN traindicated for all cases of
May be life threatening DRESS SJS, TEN, DRESS, or AGEP.
Rare AGEP Some allergists may con-
sider supervised PO chal-
lenge for children with EM
minor due to possibility of
infection-induced rash
(eg, HSV, Mycoplasma).
Serum sickness Type III Delayed reaction at 1–3 wk after Classic symptoms: fever, rash, Future use of antibiotic
Immune-complex exposure polyarthralgia, or contraindicated.
mediated (drug- May occur earlier if preformed polyarthritis
antibody complex) antibody present May also have urticaria and
Uncommon lymphadenopathy

Serum sickness– SSLR immunopathol- Some allergists may recom-

like reaction ogy unclear mend PO challenge for
children with a history of
SSLR to β-lactam therapy,
given the possibility of
infectious (typically viral)
etiology.2,3
Nonimmune drug Nonallergic response Multiple types; examples include Drug intolerance Future use of antibiotic can
reaction to a drug • Drug intolerance • GI symptoms be considered by using
• Pseudoallergic reaction • Headache prevention/management

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Do not require prior sensitization • Diaper rash/yeast infection strategies.
or testing • Pseudoallergic reaction
Common, frequently mislabeled • Vancomycin glycopeptide
as allergy flushing syndrome
 16
Approach to Antibiotic Allergies
General Approach

274 — Chapter 16. Approach to Antibiotic Allergies

Table 16-2 describes a modified stepwise approach to the workup and management of potential antibiotic allergies.

TABLE 16-2. STEPWISE APPROACH TO REPORTED ANTIBIOTIC ALLERGIES

Steps Components Notes
Step 1 Perform a thorough history and physical Attempt to classify the reaction.
examination; review available clinical • Timing and duration of symptoms in relation to antibiotic administration
data. • Evaluation for evidence of tolerance of drug in question since adverse reaction, with
review of previous antibiotic administration history and other medications
• Review of associated signs and symptoms
• Physical manifestations (examination and/or review of photos, if available)
• Review of imaging/laboratory results (if available)
NOTE: While the PEN-FAST score has been shown to accurately predict low-risk penicillin
allergies among adults, a recent study showed that use of this score was not helpful in
predicting low-risk penicillin allergies among children aged <12 y.4
Step 2 Determine if the adverse reaction is likely If yes, determine type of suspected reaction (eg, immediate hypersensitivity reaction vs
due to antibiotic. delayed drug-induced exanthem vs nonimmune adverse drug reaction).
If no, consider removing antibiotic allergy label.
Step 3 If possible immediate hypersensitivity Testing typically performed ≥4–6 wk after symptom resolution.
reaction It is recommended that patients with nonanaphylaxis undergo a direct amoxicillin chal-
• Perform confirmatory testing (if available); lenge (without skin testing).
consider referral to allergist. Penicillin skin testing can be used to test for IgE-mediated penicillin allergy.
Although not standardized, most allergy clinics will also perform ampicillin skin testing.
If suspected delayed drug-induced exan- Depending on type of suspected reaction
them (not SCAR) or nonimmune drug • Consider management/prevention strategies if nonimmune.
reaction • May consider skin testing.
• Consider strategies for evaluation and/or • May consider observed challenge.
de-labeling. • May be able to remove antibiotic allergy label.
 Step 4 Review available results. Confirmed not allergic
• OK to give antibiotic.
• Remove antibiotic allergy label and counsel families to remove in other health care
entities.
Confirmed allergic
• Choose alternative antibiotic.
• Consider repeat penicillin skin testing in 5–8 y to determine if child has outgrown
allergy.
• Perform desensitization procedure if need to give antibiotic.
Possibly allergic
• Choose alternative antibiotic.
• Perform observed challenge before giving antibiotic.
Adapted from Khan DA, et al. Drug allergy: a 2022 practice parameter update. J Allergy Clin Immunol. 2022;150(6):1333–1393 PMID: 36122788 and The Joint Task Force on
Practice Parameters; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma, and Immunology; Joint Council of Allergy, Asthma and
Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol. 2010;105(4):259–273 PMID: 20934625.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

 276 — Chapter 16. Approach to Antibiotic Allergies

Table 16-3 details protocols.

TABLE 16-3. OBSERVED CHALLENGE AND DESENSITIZATION PROTOCOLS

Protocol Details Notes
Observed Test dosing of antibiotic. Used when low likelihood of IgE-
challenge Perform controlled administration of single mediated allergy
dose or divided increasing doses (graded Can verify child will not have
challenge) until full dose reached. immediate hypersensitivity
Example graded challenge: give 10%–25% reaction
of therapeutic dose and observe for Does not alter immune response or
15–30 min (about 75% will react within induce tolerance
20 min), then give rest of dose and
observe for another 30–60 min (up to
2 h; about 100% will react within 2 h).
Desensitization Rapid induction of antibiotic tolerance Used when high likelihood of IgE-
procedure Administration of incremental doses mediated allergy and no alterna-
Performed under the guidance of an aller- tive antibiotics available
gist in a controlled setting Alters immune response by provid-
ing temporary tolerance (will
need to repeat desensitization
protocol if >24 h has elapsed
since drug exposure)
Adapted from Khan DA, et al. Drug allergy: a 2022 practice parameter update. J Allergy Clin Immunol. 2022;150(6):1333–
1393 PMID: 36122788 and The Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and
Immunology; American College of Allergy, Asthma, and Immunology; Joint Council of Allergy, Asthma and
Approach to Antibiotic Allergies

Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol. 2010;105(4):259–273 PMID:
20934625.

Specific Antibiotic Allergies and Allergic Cross-Reactivity

β-Lactam Antibiotics
Penicillin
Although the AAAAI position statement continues to recommend penicillin skin testing
for children with a history of anaphylaxis or recent immediate-onset urticaria following
16 exposure to a penicillin, children with a history of nonserious reactions should forgo
penicillin skin testing and instead receive a supervised oral (PO) amoxicillin challenge to
test for allergy. For those who require skin testing, the penicillin skin test has a negative
predictive value near 100%. If skin testing is negative, the child should then receive a
supervised PO challenge to confirm tolerance, ideally in a same-day visit.5 The positive
predictive value of penicillin skin testing appears to be high. If positive, penicillin should
be avoided for at least 5 to 8 years; however, repeat testing after this time is recommended,
as up to 80% of children will ultimately outgrow penicillin allergy within 10 years.6 If
use of penicillin is indicated before this time (if no acceptable alternatives are available),
desensitization should be performed under the care of an allergy specialist. Of note,
in vitro serum testing for penicillin-specific IgE has an undefined predictive value and
should not be used in lieu of skin testing and/or an observed PO challenge.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 277

Penicillin allergic cross-reactivity: The rate of allergic cross-reactivity between penicillin

and cephalosporins was traditionally reported to be about 10%, although more recent
studies suggest a rate of less than 2%. Cross-reactivity is more common with some PO
first-generation cephalosporins (as these antibiotics may have similar R-group side
chains; see Cephalosporins discussed next), principally if the reaction to penicillin was
anaphylaxis. Most children with a history of penicillin allergy tolerate cephalosporins,
particularly if the reaction was not severe. For patients with a history of an unverified
nonanaphylactic penicillin allergy, any cephalosporin can be administered routinely with-
out testing or additional precautions. Of children who have a positive penicillin skin test
result, about 2% will react to some cephalosporins. Table 16-4 details various approaches
to cephalosporin administration in children with a reported history of penicillin allergy.

TABLE 16-4. APPROACHES TO CEPHALOSPORIN ADMINISTRATION IN

CHILDREN WITH REPORTED HISTORY OF PENICILLIN ALLERGY
Skin Test Options for Cephalosporin Administration
Penicillin skin test Negative result
• OK to give
Positive result
• Choose alternative (non–β-lactam) antibiotic.
• Administer via observed challenge or desensitization (depending
on severity of prior reaction).
Cephalosporin skin test (not Negative result
standardized) • Administer via observed challenge.

Approach to Antibiotic Allergies

Positive result
• Choose alternative (non–β-lactam) antibiotic.
• Choose alternative cephalosporin (with dissimilar R-group side
chain) and administer via cautious observed challenge or desensi-
tization (depending on severity of prior reaction).
• Administer via desensitization if no alternative antibiotic.
Skin testing unavailable Administer via cautious observed challenge or desensitization
(depending on severity of prior reaction).
Adapted from Khan DA, et al. Drug allergy: a 2022 practice parameter update. J Allergy Clin Immunol. 2022;150(6):1333–
1393 PMID: 36122788 and The Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and 16
Immunology; American College of Allergy, Asthma, and Immunology; Joint Council of Allergy, Asthma and
Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol. 2010;105(4):259–273 PMID:
20934625.

Cephalosporins
The rate of allergic reactions to cephalosporins is significantly lower than for penicillin.
Cephalosporin skin testing is not standardized, although many allergists will perform
cefazolin skin testing by using a nonirritating concentration of the antibiotic. While a
positive skin test result suggests the presence of specific IgE antibodies, a negative skin
test result does not definitively rule out an allergy, and an observed challenge should be
considered before administration.
 278 — Chapter 16. Approach to Antibiotic Allergies

Cephalosporin allergic cross-reactivity: Most immediate hypersensitivity reactions with

cephalosporins are directed at the R-group side chains (rather than the core β-lactam
ring). Tables are available that detail the β-lactam antibiotics that share similar R-group
side chains (see Suggested Reading later in this chapter and Table 16-5). If there is a his-
tory of an immediate hypersensitivity reaction to a given cephalosporin, β-lactams with
similar R-group side chains should be avoided. For those patients with a nonanaphylactic
cephalosporin allergy, a direct challenge should be performed to determine tolerance. In
contrast, for administration of cephalosporins with similar side chains and for the less
common anaphylactic reaction history, a negative cephalosporin skin test to a paren-
teral cephalosporin should be performed before the challenge to determine tolerance.
For patients with a history of a nonanaphylactic cephalosporin allergy, a penicillin can
be administered without testing or additional precautions. For example, those with a
prior history of skin reactions, including urticaria, to cephalexin can receive amoxicillin
without prior testing. But for patients with a history of anaphylaxis to a cephalosporin,
penicillin skin testing and a drug challenge should be performed before administration of
a penicillin.1

TABLE 16-5. CLINICALLY RELEVANT β-LACTAM ANTIBIOTICS WITH SIMILAR

R-GROUP SIDE CHAINS
Antibiotics in italics are in different classes and/or generations.
Antibiotic β-Lactam Antibiotics Sharing Similar R-Group Side Chains
Penicillins Penicillin G, penicillin V (PO phenoxymethyl penicillin)
Approach to Antibiotic Allergies

Aminopenicillins Amoxicillin, cefadroxil, cefprozil

Ampicillin, cefaclor, cephalexin
First-generation Cefaclor, cefadroxil, cephalexin, cefprozil, amoxicillin, ampicillin
cephalosporins Cephalothin, cefoxitin
NOTE: Cefazolin has unique R-group side chains.
Second-generation Cefoxitin, cephalothin
cephalosporins Cefuroxime, cefoxitin
Cefprozil, cefaclor, cefadroxil, cephalexin, amoxicillin, ampicillin
16 NOTE: Cefotetan and cefamandole have unique R-group side
chains.
Third-, fourth-, and Ceftriaxone, cefotaxime, cefepime
fifth-generation Cefdinir, cefixime
cephalosporins Ceftaroline, ceftobiprole, ceftolozane
Cefditoren, cefpodoxime
Ceftazidime, aztreonam
Monobactams Aztreonam, ceftazidime
Adapted from Norton AE, et al. Antibiotic allergy in pediatrics. Pediatrics. 2018;141(5):e20172497 PMID: 29700201.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 279

Aminopenicillins
Immediate hypersensitivity reactions to amoxicillin or ampicillin are less common than
with penicillin. Skin testing with aminopenicillins is not as standardized as penicillin,
although many allergists will perform testing by using a nonirritating concentration of
ampicillin along with the major determinants for penicillin. It should be noted that the
negative predictive value is unknown, so an observed challenge is recommended in the
setting of negative aminopenicillin skin testing results. Children with low-risk histo-
ries (eg, nonanaphylactic reactions) may bypass skin testing and proceed directly to an
observed challenge with PO amoxicillin.
Delayed drug-induced, non-urticarial exanthems are relatively common with amino­
penicillin use in children. The reaction is hypothesized to occur in the setting of a con-
comitant viral illness, with the classic example being an amoxicillin-induced rash in the
setting of a child with acute Epstein-Barr virus infection (occurs in nearly 100%). In such
cases, an observed challenge may be conducted before a future course is given.
Aminopenicillin allergic cross-reactivity: Immediate hypersensitivity reactions to amino-
penicillins may be directed at either the core penicillin determinants or the R-group side
chains. If the reaction is due to IgE antibodies versus the R-group side chains, children
will have a negative penicillin skin test result and will be able to tolerate other penicil-
lins. If there is a history of an immediate hypersensitivity reaction to an aminopenicillin,
β-lactams with the same R-group side chains should be avoided (see Table 16-5). If there
is no alternative antibiotic, desensitization should be performed.
Monobactams

Approach to Antibiotic Allergies

Allergic reactions to aztreonam are much less common than those to other β-lactam
antibiotics.
Monobactam allergic cross-reactivity: Monobactams do not exhibit allergic cross-reactivity
with other β-lactams, which can be given without prior testing, except for ceftazidime,
which shares an R-group side chain with aztreonam.
Carbapenems
Immediate hypersensitivity reactions to carbapenems appear to be rare. Carbapenem skin
testing is not standardized and has unknown predictive value. 16

Carbapenem allergic cross-reactivity: Allergic cross-reactivity between other β-lactams

and carbapenems is extremely low (<1%). Current recommendations are to administer a
carbapenem without testing or additional precautions regardless of whether the previous
penicillin or cephalosporin reaction was anaphylactic.
Non–β-Lactam Antibiotics
Immediate hypersensitivity reactions to non–β-lactam antibiotics are uncommon (Table
16-6). There are no validated tests to evaluate IgE-mediated reactions for these antibiotic
classes (eg, skin testing is not standardized and lacks adequate predictive value). If the
 280 — Chapter 16. Approach to Antibiotic Allergies

prior reaction to a non–β-lactam antibiotic is consistent with an immediate hypersensitiv-

ity reaction, that antibiotic should be used only if there is no alternative agent and then
only via desensitization.

TABLE 16-6. NON–β-LACTAM ANTIBIOTIC REACTIONS

Frequency of Immediate
Hypersensitivity
Antibiotic Class Reactions Other Antibiotic Reaction Notes
Aminoglycoside Rare None
Glycopeptide Rare Vancomycin frequently causes non–IgE-mediated
histamine release (pseudoallergic reaction),
often related to the rapidity of infusion, which is
now called “vancomycin glycopeptide flushing
syndrome.”
This syndrome is not a contraindication; premedi-
cate with antihistamines and slow the infusion
rate.
Lincosamide Rare None
Macrolide Rare Delayed drug-induced exanthems more common
Quinolone Increasingly reported with Delayed drug-induced exanthems in about 2%
expanded use
Sulfonamide Rare Delayed drug-induced exanthems more common
Severe cutaneous adverse reactions possible
Approach to Antibiotic Allergies

Tetracyclines Rare None

Non–β-lactam antibiotics allergic cross-reactivity: Importantly, there is no reported allergic

cross-reactivity with β-lactam antibiotics (or with alternative classes of non–β-lactam
antibiotics). There may be allergic cross-reactivity within the same antibiotic class (eg,
some quinolone or macrolide groups).
Alternative Antibiotic Options for Common Infections
16
As detailed previously, it is important to identify children who are mislabeled or who
have outgrown a reported allergy and can safely receive the antibiotic. For children with
confirmed allergies, alternative antibiotic selection should be as narrow in spectrum as
possible while balancing the effectiveness, rate of resistance, side effects, and potential
allergic cross-reactivity of the medication. Table 16-7 details alternative antibiotic options
for select common infections. Consider the susceptibilities of the pathogens for each
infection category, as all alternatives may not cover the required antibacterial spectrum
equally well.
 2025 Nelson’s Pediatric Antimicrobial Therapy — 281

TABLE 16-7. ALTERNATIVE ANTIBIOTIC OPTIONS FOR SELECT COMMON

INFECTIONS
Infection Category
(Antibiotic Allergy) Alternative Antibiotic Options
Acute otitis media Third-generation cephalosporin (IV: ceftriaxone, cefotaxime; PO:
(Amoxicillin allergy) cefdinir, cefixime, cefpodoxime)
Clindamycin (does not cover Haemophilus influenzae or Moraxella)
Levofloxacin
Group A streptococcus Cephalexin if nonanaphylactic reaction
pharyngitis Clindamycin, although the CDC has now documented up to
(Penicillin/amoxicillin allergy) 20% resistance to clindamycin
Macrolides (eg, azithromycin, erythromycin), although rates of
macrolide resistance are increasing globally
NOTE: TMP/SMX is not recommended, as it does not reliably prevent
rheumatic fever.
Community-acquired Cephalosporins active against pneumococcus (IV: ceftriaxone,
pneumonia cefotaxime, ceftaroline; PO: cefdinir, cefixime, cefpodoxime)
(Amoxicillin/ampicillin Clindamycin IV or PO (does not cover H influenzae or Moraxella)
allergy) Levofloxacin IV or PO
Linezolid IV or PO (does not cover H influenzae or Moraxella)
Vancomycin IV (does not cover H influenzae or Moraxella)
Atypical pneumonia Doxycycline IV or PO
(Macrolide allergy) Levofloxacin IV or PO

Approach to Antibiotic Allergies

Skin and soft tissue/osteoar- Clindamycin IV or PO
ticular infections TMP/SMX (skin) IV or PO
(Staphylococcus aureus) Linezolid IV or PO
(β-Lactam allergy) Vancomycin IV
Daptomycin IV

Suggested Reading
Blumenthal KG, et al. Lancet. 2019;393(10167):183–198 PMID: 30558872
Broyles AD, et al. J Allergy Clin Immunol Pract. 2020;8(9)(suppl):S16–116 PMID: 33039007
Collins C. J Pediatr. 2019;212:216–223 PMID: 31253408 16
Collins CA, et al. Ann Allergy Asthma Immunol. 2019;122(6):663–665 PMID: 30878624
Joint Task Force on Practice Parameters, et al. Ann Allergy Asthma Immunol. 2010;105(4):259–273 PMID:
20934625
Khan DA, et al. Drug allergy: a 2022 practice parameter update. J Allergy Clin Immunol. 2022;150(6):1333–
1393 PMID: 36122788
Norton AE, et al. Pediatrics. 2018;141(5):e20172497 PMID: 29700201
Penicillin Allergy in Antibiotic Resistance Workgroup. J Allergy Clin Immunol Pract. 2017;5(2):333–334
PMID: 28283158
 2025 Nelson’s Pediatric Antimicrobial Therapy — 283

17. Antibiotic Stewardship

NOTE: A list of table abbreviations and acronyms can be found at the start of this publication.
Antibiotic therapy is one of the most important advances in health care, along with the
development of vaccines and the improvements in environmental health at the beginning
of the 20th century. Appropriate use of antibiotics can be lifesaving. However, the use
of antibiotics is also associated with increased microbial resistance, toxicity to the child,
and cost. Therefore, antibiotic prescribing should be done carefully and responsibly to
maximize benefit while minimizing adverse or unintended consequences. It is this need
for balance on which the term antibiotic stewardship is based. Merriam-Webster defines
stewardship as “the careful and responsible management of something entrusted to one’s
care.”1 It is not the purpose of antibiotic stewardship to drive antibiotic use inexora-
bly toward a hypothetical zero, denying the benefit of treatment to those in need. It is,
instead, the role of the steward to ensure that the right drug, at the right dose, for the right
duration, is administered the right way to the right host for a particular infection caused
by the “right” pathogen. In so doing, the steward maximizes the effect of the antibiotic
while ensuring its continued availability and efficacy for the patients who follow.
To optimize use, there are 7 principles that should be followed (Table 17-1). These include
infection prevention, diagnostic stewardship, effective empiric therapy for suspected
infections, narrowing or stopping of therapy as additional information becomes available
and the infection resolves, avoidance of unnecessary therapy by treating only infections,
optimization of administration, and multidisciplinary accountability.
Infection Prevention
Infection prevention is a key component of antibiotic stewardship. Put simply, each
infection that does not occur is one less that will require antibiotic treatment. Effective
infection prevention strategies vary by site and by pathogen, and a full discussion of

Antibiotic Stewardship
infection prevention is beyond the scope of this book. We direct the interested reader to
the Centers for Disease Control and Prevention library.2 The single most effective strategy
for infection prevention remains adherence to hand hygiene. Effective hand hygiene
can reduce person-to-person spread of pathogens that are spread by contact and droplet
transmission, and studies have shown that infection rates correlate closely with hand
hygiene performance regardless of other strategies that may be in place.
17
Diagnostic Stewardship
As discussed later in this chapter, selecting an appropriate antibiotic regimen for a patient
depends largely on obtaining the proper test results for infection. Samples for culture or
molecular diagnostic tests should be obtained before antibiotic therapy whenever possible,
and the samples should be collected in a manner that will maximize the likelihood ratio
of a positive or negative test result. For example, it matters if a urine culture that yields
Escherichia coli was obtained via catheterization or by bag collection, just as it matters if a
sterile urine culture was obtained before administering antibiotics or 48 hours after admin-
istration. Culture of non-sterile sites, such as the skin, mucous membranes, and trachea,
 284 — Chapter 17. Antibiotic Stewardship

TABLE 17-1. OPTIMIZING ANTIBIOTIC USE

Facets of
Stewardship Examples for Implementation
Infection • Effective infection control and prevention
prevention • Close attention to hand hygiene
Diagnostic • Obtain appropriate cultures before antibiotic therapy.
stewardship • Avoid culturing non-sterile sites, and interpret cultures from those sites carefully.
• Consider molecular diagnostics when appropriate.
• Use ancillary laboratory tests for infection, but remember that positive pre-
dictive value may be poor.
Empiric therapy • Use the narrowest-spectrum agents that cover the likely pathogens to
achieve the necessary cure rate for your patient, infection site, severity of
infection, and underlying comorbid conditions.
• Use an antibiotic that penetrates the infected compartment (eg, achieves
effective exposure at the site of infection) (see Ch 11).
• Use local epidemiology (including antibiogram) and previous patient cul-
tures to guide therapy.
Reevaluation of • Discontinue empiric antibiotics when infection is no longer suspected.
therapy • For proven infection, adjust antibiotics once speciation and susceptibilities
are available.
• Treat for the shortest effective duration, and follow up to ensure a successful
outcome.
Treatment of • Avoid treating
infections – Colonization
only – Contaminants
– Noninfectious conditions
Optimization of • Closely collaborate with pharmacists.
administration • Use protocols that maximize PD of agent.
Antibiotic Stewardship

• Perform therapeutic drug monitoring where appropriate.

Accountability • Multidisciplinary team
• Prospective audit and feedback
• Guarantee of representation and buy-in by including “champions”

17 may be useful in specific scenarios, but positive culture results from non-sterile sites must
be interpreted with caution in the context of the pretest probability of infection. Simi-
larly, molecular diagnostic test results from nucleic acid amplification or next-generation
sequencing (usually obtained from blood or infected tissue sites) are frequently positive
even after antibiotic administration, when sensitivity of cultures decreases quickly.3 Next-
generation sequencing has not been well studied in children; it is likely to pick up a low
signal by colonization of commensal organisms that may not represent invasive infection.
Those with mucositis may have DNA from multiple organisms detected, which does not
necessarily indicate invasive infection by all detected bacteria. Finally, abnormal values of
ancillary tests, such as white blood cell count, C-reactive protein (CRP), and procalcitonin,
 2025 Nelson’s Pediatric Antimicrobial Therapy — 285

may lead to unnecessary antibiotic use when the likelihood of infection is low. A careful
diagnostic approach is needed to optimize antibiotic use.
Empiric Therapy
Appropriate therapy for a suspected infection should be administered once the appropri-
ate diagnostic tests have been obtained. This empiric therapy should be based on a variety
of factors, including the organisms most likely to cause the suspected infection, the body
compartment(s) infected, host characteristics including renal and hepatic clearance,
drug-drug interactions, and local antibiotic susceptibilities. Ideally, empiric therapy is the
narrowest-possible regimen that penetrates the infected space and covers the most likely
organisms. These parameters may change over time; for example, in the setting of a local
methicillin-resistant Staphylococcus aureus (MRSA) outbreak, clinicians might consider
different empiric therapy for skin and soft tissue infection than they would otherwise.
Similarly, prior antibiotic susceptibilities of a recurrent infection should be used to
guide empiric treatment. For example, therapy for a child with a first occurrence of
E coli pyelonephritis will be guided by local rates of susceptibility, but past susceptibility
information should guide empiric therapy in the same child experiencing a recurrence.
It is also important to assess the need to achieve a certain level of success in selecting
empiric antimicrobial therapy. For the child with mild impetigo, perhaps using drugs
that provide 70% coverage of the suspected pathogens is acceptable, and the clinician can
follow the treatment progress to see if changes need to be made. On the other hand, for
the child who has leukemia and neutropenia, with bacterial meningitis associated with
gram-negative bacilli on stains of cerebrospinal fluid, we strive to start empiric therapy
with antibiotic(s) as close to covering 100% of suspected pathogens as possible, quickly
reevaluating therapy (see Reevaluation of Therapy discussed next). Clinicians should
assess their willingness to accept some degree of treatment failure for any given infection,
acknowledging that 100% coverage is not required for less severe infections.

Antibiotic Stewardship
Reevaluation of Therapy
Empiric therapy is just that, and it should change once additional information is avail-
able. In most cases, this means stopping therapy if infection is no longer suspected (eg, if
cultures are sterile after 36–48 hours; if molecular tests for pathogens show no significant
pathogen signal) or narrowing therapy if an organism is identified (eg, narrowing from
ceftriaxone to ampicillin for susceptible E coli recovered from urine). However, therapy
17
should also be reevaluated and possibly broadened if the clinical situation dictates (eg,
if a child’s condition becomes clinically unstable; if new physical examination findings
or radiographic changes are seen; if a culture yields an organism that is unlikely to be
covered by the empiric antimicrobials).
Treatment of Infections Only
Antibiotics are powerful tools, but they treat only fever and other local and systemic
signs and symptoms of infection if those findings are caused by bacteria, fungi, or
mycobacteria. If a stable patient has fever and a careful, systematic evaluation and diag-
nostic workup have not identified a treatable organism, it is reasonable in many cases to
 286 — Chapter 17. Antibiotic Stewardship

continue to evaluate that patient without prolonged antibiotic therapy. Many noninfec-
tious diseases can develop with signs and symptoms that are consistent with infection,
including numerous rheumatologic and oncologic conditions. Anchoring to a diagnosis
of infection in the absence of evidence for infection may not only drive unnecessary anti-
biotic use but also delay time to diagnosis of another significant health condition. Simi-
larly, clinicians should strive to avoid treating organisms that are colonizing commensals
or contaminants. For example, prolonged vancomycin therapy for a Corynebacterium
species recovered from blood culture after 58 hours of incubation is not an appropriate
use of antibiotics. Cultures from non-sterile sites are particularly challenging to inter-
pret in this context, and those cultures should be obtained only when the likelihood
of infection at those sites is high. Often, tests for inflammation are elevated when true,
invasive infection is present. A normal CRP level after 3 to 4 days of high fever suggests a
diagnosis other than bacterial infection, particularly when supported by negative culture
and negative molecular test results. Next-generation sequencing tests do not require prior
knowledge of a specific pathogen to make a diagnosis; they assess the presence of nucleic
acid sequences from any of a thousand pathogens in a gene library.
Optimization of Administration
The dose, route, and frequency of antibiotics can be manipulated to optimize their
pharmacodynamics (PD) and efficacy and minimize toxicity. Close collaboration with
pharmacology is critical to ensure that dosing is optimal. Examples of strategies include
continuous infusion of β-lactam antibiotics to maximize time above minimum inhibitory
concentration (MIC) for a resistant Pseudomonas aeruginosa infection in a child with
cystic fibrosis, vancomycin clearance calculations to ensure adequate area under the curve
(the mathematically calculated area under the serum concentration-versus-time curve)
to MIC ratio for a complex MRSA infection, or therapeutic drug monitoring to mini-
mize toxicity of aminoglycosides or voriconazole. Dosing strategies can be protocolized,
but such strategies should be reviewed periodically, as approaches designed to optimize
Antibiotic Stewardship

pharmacokinetics and PD are constantly evolving.

Accountability
Effective antibiotic stewardship cannot be accomplished in a vacuum. Effective stew-
ardship programs require multidisciplinary buy-in and support as well as effective and
continuous closed-loop communication. At a minimum, these teams usually consist of
17
pharmacists, physicians including infectious disease (ID) specialists, designated clinicians
for representative service lines (eg, a “unit champion”), nurses and nursing leadership,
and hospital administrators. Clinical microbiologists, infection control and prevention
specialists, information technology specialists, and hospital epidemiologists are key
resources even if they do not participate directly in stewardship activities. Antibiotic
stewardship programs have myriad tools available (Table 17-2), including prospective
audit and feedback, prior authorization, clinical practice guidelines, electronic decision
support, antibiotic time-outs, electronic hard stops, and intravenous-to-oral conversion.
Use of some or all of these interventions must be coupled to education and reporting to
staff to demonstrate the utility of the program.
TABLE 17-2. ANTIBIOTIC STEWARDSHIP INTERVENTIONS
Intervention Description Advantages and Disadvantages
Prospective audit and Antibiotic use is monitored prospectively, and Staple of stewardship
feedback information about use is shared with clinicians Can be time consuming if not automated
via continuous or intermittent reports. Specific Should be combined with education to maximize effect
areas of antibiotic misuse and overuse are tar-
geted for education and feedback.
Prior authorization Specific antibiotics are restricted without prior Extremely effective in curtailing specific antibiotic usage but can
approval of ID team or stewardship team. be unpopular; clinicians may develop work-arounds to circum-
vent restrictions.
Clinical practice Antibiotic use for a given clinical scenario is built Can reduce time to effective therapy, but may not allow flexibility
guidelines into a protocol or guideline. if certain aspects of case are different from usual (eg, if patient
has a history of ESBL-producing Escherichia coli infection but gets
ceftriaxone because of UTI guideline)

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Electronic decision Language built into EMRs to recognize specific Can increase awareness of specific conditions, but may contribute
support conditions (eg, suspected sepsis) and trigger to “alert fatigue”
decision support
Antibiotic time-outs Scheduled reevaluation of empiric therapy at a set Important role in ensuring that empiric therapy is reevaluated as
time point, usually 48 or 72 h after initiation new information comes in. Timing may differ based on clinical
scenario.
Electronic hard stops More automated time-out in which antibiotic ther- Very effective in limiting empiric therapy, but must be imple-
apy is automatically discontinued at a set time mented and monitored carefully to ensure antibiotic therapy is
point not inadvertently discontinued without notice
Intravenous-to-oral Periodic or automated review by stewardship team Particularly useful at hospital discharge to avoid unnecessary out-
conversion to determine if antibiotics can be changed to patient parenteral antibiotic therapy. John Nelson first docu-
PO administration mented success approximately 50 years ago for osteomyelitis.
 288 — Chapter 17. Antibiotic Stewardship

Historically, many of us opposed antibiotic stewardship programs that reported outcomes

only in reduced antibiotic costs and volume and did not consider the adverse effects of the
inappropriate use of inexpensive narrow-spectrum antibiotics for serious infection (eg,
empiric ampicillin treatment of severe pyelonephritis). However, clinicians are generally
more concerned with the outcome of their patients than they are on abstract purchasing
data. As a result, stewardship programs have moved toward reporting more patient-
centered outcomes, including adverse drug reactions, antibiotic resistance rates, length
of stay, and failure of initial therapy. Clinicians are also more inclined to participate in
and adhere to stewardship program interventions if they have a seat at the table and can
contribute to shared decision-making. This is the role of the unit champion. For example,
neonatologists, pulmonologists, and ambulatory pediatricians might each designate a fac-
ulty member to attend monthly stewardship meetings to ensure that their perspectives are
considered. Finally, pediatricians should consider including parents or family members in
shared decision-making about antibiotic use.
In conclusion, antibiotics are critically important for treatment of infections. However,
overuse or misuse of antibiotics will drive antimicrobial resistance and adverse patient
outcomes. We have learned that there is no “new antibiotic” against which bacteria do
not develop resistance. It is the role of the antibiotic steward to maximize the benefit of
antibiotics, minimize their toxicity, and preserve their use for subsequent children. There
are many resources available to achieve these goals—for example, antibiotic stewardship
programs, pharmacists, ID physicians, and prescribing guides such as this book. However,
at the end of the day, every health care worker who cares for children is also charged
with being a steward of antibiotics—to optimize their use for the patient at hand, while
safeguarding their efficacy for all the children yet to come.
Antibiotic Stewardship

17
 2025 Nelson’s Pediatric Antimicrobial Therapy — 289

18. Systemic and Topical Antimicrobial Dosing and Dose Forms

NOTES
• A list of table abbreviations and acronyms can be found at the start of this publication.
• Higher dosages in a dose range are generally indicated for more serious infections.
• Maximum dosages for adult-sized children (≥40 kg) are based on US Food and Drug
Administration (FDA)–approved product labeling or postmarketing data.
• See Chapter 7 for HIV and SARS-CoV-2 antiviral agents not listed in this chapter.
• Antiviral monoclonal antibodies and immunomodulators are not listed.
• Dose Levels of Evidence:
Level I: FDA or European Medicines Agency–approved pediatric dosing, or based on
randomized clinical trials
Level II: data from noncomparative trials or small comparative trials
Level III: expert or consensus opinion or case reports
• If no oral liquid form is available, round the child’s dose to a combination of available
solid dosage forms. Consult a pediatric pharmacist for recommendations on the avail-
ability of extemporaneously compounded liquid formulations.
• Cost estimates are in US dollars per course, or per month for maintenance regimens.

Systemic & Topical Antimicrobial Dosing & Dose Forms

Estimates are based on wholesale acquisition costs at the editor’s institution. These
may differ from those of the reader. Legend: $ = <$100, $$ = $100–$400, $$$ = $401–
$1,000, $$$$ = >$1,000, $$$$$ = >$10,000.
• There are some agents that we do not recommend even though they may be
available. We believe they are significantly inferior to those we do recommend in
Chapters 1 through 12 and could possibly lead to poor outcomes if used. Such agents
are not listed.

18
 18
Systemic & Topical Antimicrobial Dosing & Dose Forms

290 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Acyclovir,a Zovirax 500-, 1,000-mg vials ($) IV 15–45 mg/kg/day (I) (See Chs 2 and 7.) q8h
See also Valacyclovir later in Max 1,500 mg/m2/day (II) (See Ch 13.)
this table. 200-mg/5-mL susp ($) PO 900 mg/m2/day (I) q8h
200-mg cap ($) 60–80 mg/kg/day, max 3,200 mg/day (I) q6–8h
400-, 800-mg tab ($) Adult max 4 g/day for VZV (I)
See Chs 2 and 7.
Albendazole,a Albenza 200-mg tab ($–$$$) PO 15 mg/kg/day for cysticercosis or echinococcosis (I) q12h
See Ch 9 for other indications.
Amikacin,a,b Amikin 500-mg/2-mL, 1,000-mg/4-mL IV, IM 15–22.5 mg/kg/day (I) (See Ch 4.) q8–24h
vials ($) 30–35 mg/kg/day for CF (II)
IVesic 50–100 mL of 0.5 mg/mL in NS (III) q12h
Amoxicillin,a Amoxil 125-, 200-, 250-, 400-mg/5-mL PO Standard dosage: 40–45 mg/kg/day (I) q8–12h
susp ($) High dosage: 80–90 mg/kg/day (I) q12h
125-, 250-mg chew tab ($) 150 mg/kg/day for pen-R Streptococcus pneumoniae q8h
250-, 500-mg cap ($) otitis media (III)
500-, 875-mg tab ($) Max 4,000 mg/day (III)
Amoxicillin/clavulanate,a 14:1 Augmentin ES: PO 14:1 formulation q12h
Augmentin 600/42.9-mg/5-mL susp ($) ≥3 mo, <40 kg: 90 mg amox/kg/day for AOM (I),
NOTE: Only forms likely to max 4,000 mg amox/day (III)
be used in children are ≥40 kg: 90 mg amox/kg/day for AOM or sinusitis
listed. div q12h, or aspiration pneumonia div q8h (II)
7:1 Augmentin ($): PO 7:1 formulation q12h
875/125-mg tab ≥3 mo, <40 kg: 25 or 45 mg amox/kg/day
200/28.5-, 400/57-mg chew tab ≥40 kg and adults: 1,750 mg amox/day (I)
200/28.5-, 400/57-mg/5-mL susp
4:1 Augmentin: PO 4:1 formulation q12h
250/62.5-mg/5-mL susp ($) <3 mo: 30 mg amox/kg/day (I)
125/31.25-mg/5-mL susp ($$$) See Ch 2.
Amphotericin B 50-mg vial ($$) IV 1–1.5 mg/kg (I), max 150 mg (II) q24h
deoxycholate,a Fungizone 0.5 mg/kg for Candida esophagitis or cystitis (II)
IVesic 50–100 mcg/mL in sterile water × 50–100 mL (III) q8h

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Amphotericin B, lipid com- 100-mg/20-mL vial ($$$) IV 5 mg/kg (I), up to 10 mg/kg or 500 mg for CNS q24h
plex, Abelcet invasive mold disease (II)
Amphotericin B, liposomal,a 50-mg vial ($$$) IV 5 mg/kg (I), up to 10 mg/kg or 500 mg for CNS q24h
AmBisome invasive mold disease (II)
Ampicillin sodiuma 125-, 250-, 500-mg vial ($) IV, IM 50–200 mg/kg/day, max 8 g/day (I) q6h
1-, 2-, 10-g vial ($) 300–400 mg/kg/day, max 12 g/day endocarditis/ q4–6h
meningitis (III)
Ampicillin trihydratea 500-mg cap ($) PO 50–100 mg/kg/day if <20 kg (I) q6h
PO susp not available in the ≥20 kg and adults: 1–2 g/day (I)
United States
Ampicillin/sulbactam,a 1/0.5-, 2/1-, 10/5-g vial ($–$$) IV, IM 200-mg amp/kg/day (I) q6h
Unasyn ≥40 kg and adults: 4–max 8 g/day (I)
Anidulafungin, Eraxis 100-mg vial ($$$) IV 3 mg/kg LD, then 1.5 mg/kg (I) q24h
Max 250-mg LD, then 125-mg (not per kg) if
obesity (II)
 18
Systemic & Topical Antimicrobial Dosing & Dose Forms

292 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Artemether and 20/120-mg tab ($) PO 5–<15 kg: 1 tab 6 doses over
lumefantrine, Coartem ≥15–<25 kg: 2 tabs 3 days at 0,
≥25–<35 kg: 3 tabs 8, 24, 36, 48,
≥35 kg: 4 tabs (I) 60 h
See Malaria in Table 9B.
Artesunate 110-mg vial ($$$$$) IV 2.4 mg/kg (I) q12h × 3, then
See Malaria in Table 9B. q24h
Atovaquone,a Mepron 750-mg/5-mL susp ($$–$$$) PO 30 mg/kg/day if 1–3 mo or >24 mo (I) q12h
45 mg/kg/day if >3–24 mo (I) q24h for
Max 1,500 mg/day (I) prophylaxis
Atovaquone/proguanil,a 62.5/25-mg ped tab ($–$$) PO Prophylaxis (I): q24h
Malarone 250/100-mg adult tab ($) 5–8 kg: ½ ped tab
See Malaria in Table 9B. >8–10 kg: ¾ ped tab
>10–20 kg: 1 ped tab
>20–30 kg: 2 ped tabs
>30–40 kg: 3 ped tabs
>40 kg: 1 adult tab
Treatment (I):
5–8 kg: 2 ped tabs
>8–10 kg: 3 ped tabs
>10–20 kg: 1 adult tab
>20–30 kg: 2 adult tabs
>30–40 kg: 3 adult tabs
>40 kg: 4 adult tabs
Azithromycin,a Zithromax 250-, 500-, 600-mg tab ($) PO Otitis: 10 mg/kg/day for 1 day, then 5 mg/kg for q24h
100-, 200-mg/5-mL susp ($) 4 days; or 10 mg/kg/day for 3 days; or 30 mg/kg
1-g packet for susp ($) once (I)
Pharyngitis: 12 mg/kg/day for 5 days, max 2,500-
mg total dose (I)
Sinusitis: 10 mg/kg/day for 3 days, max 1.5-g total
dose (I)
CABP: 10 mg/kg for 1 day, then 5 mg/kg/day for
4 days (max 1.5-g total dose), or 60 mg/kg once
of ER (Zmax) susp, max 2 g (I)
MAC prophylaxis: 20 mg/kg, max 1.2 g weekly (III)
Adult dosing for RTI: 500 mg day 1, then 250 mg
daily for 4 days or 500 mg for 3 days
Adult and adolescent dosing for STI:
Non-gonorrhea: 1 g once
Gonorrhea: 2 g once
For other indications, see Chs 1, 3, and 9.

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

500-mg vial ($) IV 10 mg/kg, max 500 mg (II) q24h
Aztreonam,a Azactam 1-, 2-g vial ($$–$$$) IV, IM 90–120 mg/kg/day, max 8 g/day (I) q6–8h
Baloxavir, Xofluza 40-, 80-mg tab ($$) PO ≥5 y, <20 kg: 2 mg/kg (I) Once
40-mg/20-mL susp ($$) 20–79 kg: 40 mg (I)
≥80 kg: 80 mg (I)
Bedaquiline, Sirturo 20-mg dispersible tab, 100-mg PO ≥5 y, ≥15 kg: 200 mg (not per kg), then 100 mg (I) q24h for 2 wk,
tab ≥30 kg: 400 mg, then 200 mg (I); in combination then the
Available from Metro Medical with other agents for MDR TB lower dose
specialty distributor: 855-691- See Table 1F. 3×/wk
0963
Benznidazole 12.5-, 100-mg tab PO 2–12 y: 5–8 mg/kg/day (I) q12h
Contact: 877-303-7181 or See Trypanosomiasis in Table 9B.
[email protected]
 18
Systemic & Topical Antimicrobial Dosing & Dose Forms

294 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Bezlotoxumab, Zinplava 1-g vial ($$$$) IV Adults: 10 mg/kg (I)c One time
Caspofungin,a Cancidas 50-, 70-mg vial ($$) IV 70 mg/m2 LD once, then 50 mg/m2, max 70 mg (I), q24h
max 150 mg if obesity (II)
Cefaclor,a Ceclor 250-, 500-mg cap ($) PO 20–40 mg/kg/day, max 1 g/day (I) q12h
500-mg ER tab ($)
Cefadroxil,a Duricef 250-, 500-mg/5-mL susp ($) PO 30 mg/kg/day, max 2 g/day (I) q12–24h
500-mg cap ($)
1-g tab ($)
Cefazolin,a Ancef 0.5-, 1-, 10-g vial ($) IV, IM 25–100 mg/kg/day (I) q8h
100–150 mg/kg/day for serious infections (III), q6h
max 12 g/day
Cefdinir,a Omnicef 125-, 250-mg/5-mL susp ($) PO 14 mg/kg/day, max 600 mg/day (I) q12–24h
300-mg cap ($)
Cefepime,a Maxipime 1-, 2-g vial ($) IV, IM 100 mg/kg/day, max 4 g/day (I) q12h
1-g/50-mL IVPB ($$)
150 mg/kg/day empiric therapy for fever with q8h
neutropenia, max 6 g/day (I)
Cefiderocol, Fetroja 1-g vial ($$$$) IV Adults: 2 g/day (I)c q8h
Cefixime, Suprax
a
100-, 200-mg/5-mL susp ($) PO 8 mg/kg/day, max 400 mg/day (I) q24h
400-mg cap ($$)
For convalescent PO therapy for serious infections, q12h
up to 20 mg/kg/day (III)
Cefotaxime,a Claforan 0.5-, 1-, 2-, 10-g vial IV, IM 150–180 mg/kg/day, max 8 g/day (I) q8h
Not currently manufactured in 200–225 mg/kg/day for meningitis, max 12 g/day q6h
the United States (I)
Cefotetan,a Cefotan 1-, 2-g vial ($$) IV, IM 60–100 mg/kg/day (II), max 6 g/day (I) q12h
Cefoxitin,a Mefoxin 1-, 2-, 10-g vial ($) IV, IM 80–160 mg/kg/day, max 12 g/day (I) q6–8h
40 mg/kg for surgical prophylaxis (I), no max (II) See Ch 15.
Cefpodoxime,a Vantin 100-mg/5-mL susp ($) PO 10 mg/kg/day, max 400 mg/day (I) q12h
100-, 200-mg tab ($)
Cefprozil,a Cefzil 125-, 250-mg/5-mL susp ($) PO 15–30 mg/kg/day, max 1 g/d (I) q12h
250-, 500-mg tab ($)
Ceftaroline, Teflaro 400-, 600-mg vial ($$$$) IV 0–<2 mo: 18 mg/kg/day (I) q8h
≥2 mo–<2 y: 24 mg/kg/day (I) q8h
≥2 y: 36 mg/kg/day (I) q8h
>33 kg: 1.2 g/day (I) q12h
Adults: 1.2 g/day (I) q12h
45–60 mg/kg/day, max 3 g/day ± prolonged q8h
infusion for CF (II)

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

Ceftazidimea; Tazicef, Fortaz 0.5-, 1-, 2-, 6-g vial ($) IV, IM 90–150 mg/kg/day, max 6 g/day (I), max 8 g/day q8h
div q6h in children with obesity (II)
IV 200–300 mg/kg/day for serious Pseudomonas q8h
infection, max 12 g/day (II)
Ceftazidime/avibactam, 2-g/0.5-g vial ($$$$) IV 3–<6 mo: 120 mg ceftazidime/kg/day (I) q8h infused
Avycaz ≥6 mo: 150 mg ceftazidime/kg/day, max 6 g/day (I) over 2 h
Ceftolozane/tazobactam, 1.5-g (1-g/0.5-g) vial ($$$$) IV 60 mg ceftolozane/kg/day, max 3 g ceftolozane/ q8h
Zerbaxa day (I)
Ceftriaxone,a Rocephin 0.25-, 0.5-, 1-, 2-, 10-g vial ($) IV, IM 50–75 mg/kg/day, max 2 g/day (I) q24h
Meningitis: 100 mg/kg/day, max 4 g/day (I) q12h
AOM: 50 mg/kg, max 1 g, 1–3 doses (II) q24h
Cefuroxime,a Ceftin 250-, 500-mg tab ($) PO 20–30 mg/kg/day, max 1 g/day (I) q12h
For bone and joint infections, up to 100 mg/kg/day, q8h
max 3 g/day (III)
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A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Cefuroxime,a Zinacef 0.75-, 1.5-g vial ($) IV, IM 100–150 mg/kg/day, max 6 g/day (I) q8h
Cephalexin,a Keflex 125-, 250-mg/5-mL susp ($) PO 25–50 mg/kg/day (I) q12h
250-, 500-mg cap, tab ($)
750-mg cap ($-$$)
75–100 mg/kg/day for bone and joint, or severe, q6–8h
infections (II); max 4 g/day (I)
Chloroquine phosphate,a 250-, 500-mg (150-, 300-mg base) PO 5 mg/kg, max 300 mg for prophylaxis (I) Weekly
Aralen tabs ($) See Malaria in Table 9B.
Dosed by base content
10 mg/kg, max 600 mg for treatment (I) One time, then
See Malaria in Table 9B. 5 mg/kg at
6, 24, and
36 h later
Cidofovir,a Vistide 375-mg vial ($$$) IV 5 mg/kg (III) Weekly
See Adenovirus in Table 7C.
Ciprofloxacin,a Cipro 250-, 500-mg/5-mL susp ($$) PO 20–40 mg/kg/day, max 1.5 g/day (I). q12h
250-, 500-, 750-mg tab ($) Do not administer susp via feeding tubes.
100-mg tab ($) PO Adults: 200 mg/day for 3 days (I)
200-mg/100-mL, 400-mg/200-mL IV 20–30 mg/kg/day, max 1.2 g/day (I) q12h
IVPB ($)
Clarithromycin,a Biaxin 125-, 250-mg/5-mL susp ($–$$) PO 15 mg/kg/day, max 1 g/day (I) q12h
250-, 500-mg tab ($)
Clarithromycin ER,a Biaxin 500-mg ER tab ($) PO Adults: 1 g (I) q24h
XL
Clindamycin,a Cleocin 75-mg/5-mL soln ($) PO 10–25 mg/kg/day, max 1.8 g/day (I) q8h
75-, 150-, 300-mg cap ($) 30–40 mg/kg/day for CA-MRSA or AOM (III)
150-mg/mL vial in 2-, 4-, 6-, and IV, IM 20–40 mg/kg/day, max 2.7 g/day (I). q8h
60-mL sizes ($) Convert 1:1 when switching to PO.
0.3-, 0.6-, 0.9-g/50-mL IVPB ($$)
Clotrimazole,a Mycelex 10-mg lozenge ($) PO ≥3 y: dissolve lozenge in mouth (I). 5 times daily
Colistimethate,a 150-mg (colistin base) vial ($). IV, IM 2.5- to 5-mg base/kg/day (I) q8h
Coly-Mycin M 1-mg base = 2.7 mg Max 360 mg/dayb (III)
colistimethate = 30,000 IU.
Cycloserine, Seromycin 250-mg cap ($$$$) PO 10–20 mg/kg/day (III) q12h
Adults: max 1 g/day (I)
Dalbavancin, Dalvance 500-mg vial ($$$$) IV Birth–<6 y: 22.5 mg/kg (I) One time
≥6 y: 18 mg/kg, max 1,500 mg (I)
Dapsonea 25-, 100-mg tab ($) PO 2 mg/kg, max 100 mg (I) q24h

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

4 mg/kg, max 200 mg (I) Once weekly
Daptomycin, Cubicin
a
350-, 500-mg vial ($$) IV For SSSI (I): 1–2 y: 10 mg/kg, 2–6 y: 9 mg/kg, q24h
7–11 y: 7 mg/kg, 12–17 y: 5 mg/kg.
For Staphylococcus aureus bacteremia (I): 1–6 y:
12 mg/kg, 7–11 y: 9 mg/kg, 12–17 y: 7 mg/kg.
For other indications, see Ch 1.
Adults: 4–6 mg/kg TBW (I).
Delafloxacin, Baxdela 450-mg tab ($$$$) PO Adults: 450 mg (I) q12h
300-mg vial ($$$) IV Adults: 300 mg (I) q12h
Demeclocycline,a 150-, 300-mg tab ($) PO ≥8 y: 7–13 mg/kg/day, max 600 mg/day (I). q6–12h
Declomycin Dosage differs for SIADH.
Dicloxacillin,a Dynapen 250-, 500-mg cap ($) PO 12–25 mg/kg/day (adults: 0.5–1 g/day) (I) q6h
For bone and joint infections, up to 100 mg/kg/day,
max 2 g/day (III)
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298 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Doxycycline, Vibramycin 25-mg/5-mL suspa ($) PO 4.4 mg/kg/day LD day 1, then 2.2–4.4 mg/kg/day, q12–24h
50-mg/5-mL syrup ($$) max 200 mg/day (I)
20-, 40-, 50-, 75-, 100-, 150-mg See also Malaria in Table 9B.
tab/capa ($–$$)
200-mg taba ($$$)
100-mg viala ($$) IV
Elbasvir/grazoprevir, 50-mg/100-mg tab ($$$$) PO Aged ≥12 y or weighing ≥30 kg: 1 tab (I) q24h
Zepatier
Entecavir, Baraclude 0.05-mg/mL soln ($$$) PO 2–<16 y (I) (double the following doses if previous q24h
See Hepatitis B virus in 0.5-, 1-mg taba ($) 3TC exposure):
Ch 7. 10–11 kg: 0.15 mg
>11–14 kg: 0.2 mg
>14–17 kg: 0.25 mg
>17–20 kg: 0.3 mg
>20–23 kg: 0.35 mg
>23–26 kg: 0.4 mg
>26–30 kg: 0.45 mg
>30 kg: 0.5 mg
≥16 y: 0.5 mg (I)
Eravacycline, Xerava 50-mg vial ($$$) IV ≥18 y: 1 mg/kg q12h
Ertapenem,a Invanz 1-g vial ($$) IV, IM 30 mg/kg/day, max 1 g/day (I) q12h
≥13 y and adults: 1 g/day (I) q24h
Erythromycin basea 250-, 500-mg tab ($–$$) PO 50 mg/kg/day, max 4 g/day (I) q6–8h
250-mg DR cap ($) 12–40 mg/kg/day for GI motility, max 250 mg/dose
250-, 333-, 500-mg DR tab (II)
(Ery-Tab) ($$)
Erythromycin ethylsucci- 200-, 400-mg/5-mL susp ($$–$$$) PO 50 mg/kg/day, max 4 g/day (I) q6–8h
natea; EES, EryPed 400-mg tab ($$)
Erythromycin lactobionate, 0.5-g vial ($$–$$$) IV 20 mg/kg/day, max 4 g/day (I) q6h
Erythrocin
Ethambutol,a Myambutol 100-, 400-mg tab ($) PO 15–25 mg/kg, max 2.5 g (I) q24h
Ethionamide, Trecator 250-mg tab ($$) PO 15–20 mg/kg/day, max 1 g/day (I) q12–24h
Famciclovir,a Famvir 125-, 250-, 500-mg tab ($) PO Adults: 0.5–2 g/day (I) q8–12h
Fexinidazole 600-mg tab available from the PO ≥6 y, ≥20 kg: 2 tabs, then 1 tab (I) q24h for
WHO: neglected.diseases@who. ≥35 kg: 3 tabs, then 2 tabs (I) 4 days, then
int See Trypanosomiasis in Table 9B. the lower
dose q24h
for 6 days
Fidaxomicin, Dificid 200-mg tab ($$$$) PO ≥6 mo (I) (per dose, not per kg): q12h
200-mg/5-mL susp ($$$$) 4–<7 kg: 80 mg

2025 Nelson’s Pediatric Antimicrobial Therapy — 2

7–<9 kg: 120 mg
9–<12.5 kg: 160 mg
≥12.5 kg: 200 mg
Adults: 200 mg (I)
Fluconazole,a Diflucan 50-, 100-, 150-, 200-mg tab ($) PO 6–12 mg/kg, max 800 mg (I). q24h
50-, 200-mg/5-mL susp ($) 800–1,000 mg/day may be used for some CNS
fungal infections (see Ch 5).
See Ch 2 for neonatal dosing.
100-mg/50-mL, 200-mg/100-mL, IV
400-mg/200-mL IVPB ($)
Flucytosine,a Ancobon 250-, 500-mg cap ($$$$) PO 100 mg/kg/day (I)b q6h
Foscarnet, Foscavir 6-g/250-mL vial ($$$$) IV CMV/VZV: 180 mg/kg/day (I) q8–12h
CMV suppression: 90–120 mg/kg (I) q24h
HSV: 120 mg/kg/day (I) q8–12h
F f i M l 3 l ($) PO Ad lt 3 (I) O
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A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Ganciclovir,a Cytovene 500-mg vial ($$) IV CMV treatment: q12h
Non-congenital: 10 mg/kg/day (I).
Congenital: See Ch 2.
CMV suppression: 5 mg/kg (I) q24h
VZV treatment: 10 mg/kg/day (III) q12h
Gentamicina 10-mg/mL vial ($) IV, IM 3–7.5 mg/kg/day (I), CF and oncology 7–10 mg/kg/ q8–24h
40-mg/mL vial ($) day (II)b
See Ch 4 for q24h dosing.
IVesic 0.5 mg/mL in NS × 50–100 mL (III) q12h
Glecaprevir/pibrentasvir, 50-mg/20-mg pellet packet PO ≥3 y (I), dosing not in mg/kg q24h
Mavyret ($$$$) <20 kg: 150 mg
Doses given in glecaprevir 100-mg/40-mg tab ($$$$$) 20–<30 kg: 200 mg
30–<45 kg: 250 mg
≥45 kg: 300 mg
Griseofulvin microsize,a 125-mg/5-mL susp ($) PO 20–25 mg/kg (II), max 1 g (I) q24h
Grifulvin V 500-mg tab ($$)
Griseofulvin ultramicrosize,a 125-, 250-mg tab ($$) PO 10–15 mg/kg (II), max 750 mg (I) q24h
Gris-PEG
Hydroxychloroquine sulfate, 100-, 200-, 300-, 400-mg tab ($). PO 10-mg base/kg, max 800-mg base (I) One time, then
Plaquenila 200 mg = 155-mg hydroxychloro- See Malaria in Table 9B. 5 mg/kg at
quine base. 6, 24, and
48 h later
Ibrexafungerp, Brexafemme 150-mg tab ($$$) PO Post-menarchal females 300 mg/day (not per kg) (I) q12h × 2
doses
Imipenem/cilastatin,a 250/250-, 500/500-mg vial ($) IV, IM 60–100 mg/kg/day, max 4 g/day (I) q6h
Primaxin IM form not approved for <12 y
Imipenem/cilastatin/ 500/500/250-mg vial ($$$$) IV Adults: 2 g/day of imipenem (I)c q6h
relebactam, Recarbrio
Interferon-PEG alfa-2a, All ($$$$) SUBQ See Hepatitis B virus and Hepatitis C virus in Ch 7. Weekly
Pegasys 180-mcg vials, prefilled
Isavuconazonium sulfate, 74.5-mg cap (40-mg base) ($$$$) PO 16–<18 kg: 80 mg/dose (I) q8h × 6 doses,
Cresemba 186-mg cap (100-mg base) ($$$$) 18–<25 kg: 120 mg/dose (I) then q24h
Dosing in isavuconazole 25–<32 kg: 160 mg/dose (I)
base ≥32 kg: 200 mg/dose (I)
372-mg vial (200-mg base) ($$$$) IV 1–<3 y: 15 mg/kg/dose (I) q8h × 6 doses,
≥3 y: 10 mg/kg/dose (I) then q24h
≥37 kg: 200 mg (not per kg) per dose (I)
Isoniazid,a Nydrazid 50-mg/5-mL soln ($$) PO 10–15 mg/kg/day, max 300 mg/day (I) q12–24h
100-, 300-mg tab ($) IV, IM
1,000-mg vial ($$)
With biweekly DOT, dosage is 20–30 mg/kg, max Twice weekly

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

900 mg/dose (I).
In combination with rifapentine (see Rifapentine Once weekly
later in this table):
≥12 y: 15 mg/kg rounded up to the nearest 50 or
100 mg; 900 mg max
2–<12 y: 25 mg/kg; 900 mg max
Itraconazole,a Sporanox 50-mg/5-mL soln ($$) (preferred PO 10 mg/kg/day (II), max 200 mg/dayb q12h
over caps; see Ch 5).
100-mg cap ($).
5 mg/kg/day for chronic mucocutaneous Candida q24h
(II)
Itraconazole, Tolsura 65-mg cap ($$$$) PO Adults: 130 mg/dose (I) q12h–q24h
Ivermectin,a Stromectol 3-mg tab ($) PO 0.15–0.2 mg/kg, no max (I) 1 dose
Ketoconazole,a Nizoral 200-mg tab ($) PO ≥2 y: 3.3–6.6 mg/kg, max 400 mg (I) q24h
 18
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A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Lefamulin, Xenleta 150-mg vial ($$$) IV Adults (I): q12h
600-mg tab ($$$$) PO 300 mg/day IV
1,200 mg/day PO
Letermovir, Prevymis 240-, 480-mg tab ($$$$) PO, IV Adults: 480 mg, 240 mg if concomitant q24h
240-, 480-mg vial ($$$$) cyclosporine therapy (I)
See Cytomegalovirus in Ch 7.
Levofloxacin,a Levaquin 125-mg/5-mL soln ($) PO, IV For postexposure anthrax prophylaxis (I):
250-, 500-, 750-mg tab ($) <50 kg: 16 mg/kg/day, max 500 mg/day q12h
500-, 750-mg vial ($) ≥50 kg: 500 mg q24h
250-mg/50-mL, 500-mg/100-mL, For respiratory infections: <5 y: 20 mg/kg/day (II), q12h
750-mg/150-mL IVPB ($) ≥5 y: 10 mg/kg/day; max 500 mg/day (II), up to q24h
1,000 mg/dose in children with obesity (III)
Linezolid,a Zyvox 100-mg/5-mL susp ($$$) PO, IV Birth–11 y (I): 30 mg/kg/day; 45 mg/kg/day for MIC q8h
600-mg tab ($) 2 (II)
600-mg/300-mL IVPB ($) >11 y (I): 1.2 g/day q12h
Maribavir, Livtencity 200-mg tab PO ≥12 y: 400 mg (not per kg) (I) q12h
Available through
www.livtencity.com
Mebendazole, Emverm 100-mg chew tab ($$$–$$$$) PO ≥2 y: 100 mg (not per kg) (I) Varies based
See parasitic nematodes and helminths (worms) on indication
and other indications in Ch 9. See Ch 9.
Mefloquine,a Lariam 250-mg tab ($) PO 5 mg/kg (I) Weekly
See Malaria in Table 9B.
Meropenem,a Merrem 0.5-, 1-g vial ($) IV 60 mg/kg/day, max 3 g/day (I) q8h
2-g vial ($$$) 120 mg/kg/day meningitis (I) or PICU sepsis with
suspected ARC (II), max 6 g/day
Meropenem/vaborbactam, 2-g vial (contains 1-g each mero IV Adults: 6 g mero/day (I)c q8h
Vabomere + vabor) ($$$$)
Methenamine hippurate,a 1-g tab ($) PO 6–12 y: 1–2 g/day (I) q12h
Hiprex >12 y: 2 g/day (I)
Methenamine mandelatea 0.5-, 1-g tab ($) PO <6 y: 75 mg/kg/day (I) q6h
6–12 y: 2 g/day (I)
>12 y: 4 g/day (I)
Metronidazole,a Flagyl, 250-, 500-mg tab ($) PO 30–50 mg/kg/day, max 2,250 mg/day (I) q8h
Likmez (susp) 500-mg/5-mL susp ($$)
375-mg cap ($$)
500-mg/100-mL IVPB ($) IV 22.5–40 mg/kg/day (II), max 4 g/day (I) q6–8h
Micafungin,a Mycamine 50-, 100-mg vial ($$) IV Neonates: 10 mg/kg (II) (See Ch 2.) q24h
50-mg/50-mL IVPB ($$) 1–<4 mo (I): 4 mg/kg
100-mg/100-mL IVPB ≥4 mo (I): 2 mg/kg, max 100 mg (I)
150-mg/150-mL IVPB Esophageal candidiasis ≥4 mo (I):

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

≤30 kg: 3 mg/kg
>30 kg: 2.5 mg/kg, max 150 mg/day; up to
300 mg/day if obesity (II)
Prophylaxis: 1 mg/kg q24h (I) or 3 mg/kg q48h (II)
Miltefosine, Impavido 50-mg cap PO <12 y: 2.5 mg/kg/day (II) bid
Available from www.impavido.com ≥12 y (I):
30–44 kg: 50 mg (not per kg) bid
≥45 kg: 50 mg (not per kg) tid
See Leishmaniasis and Amebic
meningoencephalitis in Table 9B.
Minocycline, Minocin 50-, 75-, 100-mg capa ($) PO, IV ≥8 y: 4 mg/kg/day, max 200 mg/day (I) q12h
50-, 75-, 100-mg taba ($)
100-mg vial ($$$$)
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A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Minocycline ER; Solodyn,a 45-, 55-, 65-, 80-, 90-, 105-, 115-, PO ≥12 y: 1 mg/kg/day for acne (I). q24h
Ximino 135-mg ER taba ($–$$) Round dose to nearest strength tab or cap.
45-, 90-, 135-mg ER cap ($$$)
Moxidectin 2-mg tab PO ≥12 y: 8 mg (I)c Once
Available from info@medicines- See River Blindness in Table 9B under Filariasis.
development.com
Moxifloxacin,a Avelox 400-mg tab ($) PO, IV Adults: 400 mg/day (I) q24h
400-mg/250-mL IVPB ($$)
IV Studied in but not FDA approved for children (II): q12h
3 mo–<2 y: 12 mg/kg/day
2–<6 y: 10 mg/kg/day
≥6–<12 y: 8 mg/kg/day, max 400 mg/day
≥12–<18 y (weight <45 kg): 8 mg/kg/day
PO, IV ≥12–<18 y (weight >45 kg): 400 mg q24h
Nafcillin,a Nallpen 1-, 2-, 10-g vial ($–$$) IV, IM 150–200 mg/kg/day (II) q6h
Adults: 6 g/day, max 12 g/day (I) q4h
Neomycina 500-mg tab ($) PO 50–100 mg/kg/day (II) q6–8h
Adults: 4–12 g/day (I)
Nifurtimox, Lampit 30-, 120-mg tab ($$) PO <40 kg: 10–20 mg/kg/day (I) q8h
≥40 kg: 8–10 mg/kg/day (I)
Nirmatrelvir/ritonavir, 150-mg/100-mg dose pack PO ≥12 y and ≥40 kg: 300 mg nirmatrelvir with q12h
Paxlovid Distributed by ASPR (https:// 100 mg ritonavir
covid-19-therapeutics-locator-
dhhs.hub.arcgis.com)
Nirsevimab 50 mg/0.5 mL in 0.5-mL syringe IM 50 mg/dose (<5 kg) or 100 mg/dose (≥5 kg) once 1 dose for a
($$$) per season (a) at birth for all infants born during 5-mo RSV
100 mg/1.0 mL in 1.0-mL syringe October–March and (b) when entering first RSV season
($$$) season and <8 mo of age for all infants born
during April–September
200 mg/dose for infants at high risk during their
second RSV season
Nitazoxanide, Alinia 100-mg/5-mL susp ($$$) PO 1–3 y: 200 mg/day (I) q12h
500-mg taba ($$) 4–11 y: 400 mg/day (I)
12 y–adults: 1 g/day (I)
See Giardiasis in Table 9B.
Nitrofurantoin,a Furadantin 25-mg/5-mL susp ($$$$) PO 5–7 mg/kg/day, max 400 mg/day (I) q6h
1–2 mg/kg for UTI prophylaxis (I) q24h
Nitrofurantoin 25-, 50-, 100-mg cap ($) PO Same as susp
macrocrystals,a

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

Macrodantin
Nitrofurantoin 100-mg cap ($) PO >12 y: 200 mg/day (I) q12h
monohydrate and
macrocrystalline,a
Macrobid
Nystatin,a Mycostatin 500,000-U/5-mL susp ($) PO Infants 2 mL/dose, children 4–6 mL/dose; to coat q6h
500,000-U tabs ($) PO mucosa (I)
Tabs: 3–6 tabs/day
Obiltoxaximab, Anthim 600-mg/6-mL vial IV ≤15 kg: 32 mg/kg (I) Once
Available from the Strategic >15–40 kg: 24 mg/kg (I)
National Stockpile >40 kg and adults: 16 mg/kg (I)
Omadacycline, Nuzyra 150-mg tab ($$$$) PO Adults: 450 mg qd for 2 days, then 300 mg (not per q24h
kg) (I)
100-mg vial ($$$$) IV Adults: 200 mg once, then 100 mg (not per kg) (I) q24h
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306 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Oritavancin, Orbactiv 400-mg vial ($$$$) IV Adults: 1.2 g/day (I)c One time
Oseltamivir,a Tamiflu 30-mg/5-mL susp ($) PO Preterm <38 wk PMA: 2 mg/kg/day q12h
See Influenza in Chs 2 30-, 45-, 75-mg cap ($) Preterm 38–40 wk PMA: 3 mg/kg/day
and 7. Preterm >40 wk PMA, and full-term, birth–8 mo (I):
6 mg/kg/day
9–11 mo (II): 7 mg/kg/day
≥12 mo (I), dosing by weight bracket:
≤15 kg: 60 mg/day
>15–23 kg: 90 mg/day
>23–40 kg: 120 mg/day
>40 kg: 150 mg/day (I)
Prophylaxis: Give half the daily dose (I). Not q24h
recommended for infants aged <3 mo.
Oxacillin,a Bactocill 1-, 2-, 10-g vial ($–$$) IV, IM 100 mg/kg/day, max 12 g/day (I) q4–6h
150–200 mg/kg/day for meningitis (III)
Penicillin G IM
– Penicillin G benzathine, 600,000 U/mL in 1-, 2-, 4-mL IM Infants: 50,000 U/kg (I) 1 dose
Bicillin L-A prefilled syringes ($$) Children (I): <60 lb: 300,000–600,000 U; ≥60 lb:
900,000 U (not per kg)
(FDA approved in 1952 for dosing by pounds)
Adults: 1.2–2.4 million U (I)
See also Syphilis in Chs 1 and 2.
– Penicillin G procaine 600,000 U/mL in 1-, 2-mL prefilled IM Infants: 50,000 U/kg (I) q24h
syringes ($$) See also Syphilis in Ch 2.
Children (I): <60 lb: 300,000 U (not per kg); ≥60 lb
or >12 y: 600,000 U
Penicillin G IV
– Penicillin G potassium,a 5-, 20-million U vial ($) IV, IM 100,000–300,000 U/kg/day (I) q4–6h
Pfizerpen Max daily dose 24 million U
– Penicillin G sodiuma 5-million U vial ($–$$) IV, IM 100,000–300,000 U/kg/day (I) q4–6h
Max daily dose 24 million U
Penicillin V PO
– Penicillin V potassiuma 125-, 250-mg/5-mL soln ($) PO 25–50 mg/kg/day, max 2 g/day (I) q6h
250-, 500-mg tab ($)
Pentamidine; Pentam, 300-mg viala ($$$) IV, IM 4 mg/kg/day (I), max 300 mg q24h
Nebupent 300-mg vial ($) Inhaled 300 mg for prophylaxis (I) Monthly

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

Peramivir, Rapivab 200-mg vial IV ≥6 mo: 12 mg/kg, max 600 mg (I) One time
Available from 833-964-2956
Piperacillin/tazobactam,a 2/0.25-, 3/0.375-, 4/0.5-, 12/1.5-, IV 2–9 mo: 240 or 320 mg PIP/kg/day (I) q8h for IAI
Zosyn 36/4.5-g vial ($) >9 mo: 300 or 400 mg PIP/kg/day, max 16 g PIP/ q6h for HAP
day (I)
Higher dose for HAP
Plazomicin, Zemdri 500-mg vial ($$$$) IV Adults: 15 mg/kg (I) q24h
Polymyxin Ba 500,000-U vial ($). IV 2.5 mg/kg/day (I) q12h
1 mg = 10,000 U. Based on TBW, no max (II)
 18
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308 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Posaconazole,b Noxafil 300-mg DR susp packet ($$$$) PO Candida or Aspergillus prophylaxis ≥2 y (I), not in q12h × 1 day,
mg/kg: then q24h
10–<12 kg: 90 mg
12–<17 kg: 120 mg
17–<21 kg: 150 mg
21–<26 kg: 180 mg
26–<36 kg: 210 mg
36–40 kg: 240 mg
200-mg/5-mL suspa ($$$) PO ≥13 y (I): not per kg
Candida or Aspergillus prophylaxis: 600 mg/day q8h
OPC treatment: 100 mg/day q12h × 1 day,
then q24h
Refractory OPC: 800 mg/day q12h
100-mg DR taba ($$) PO, IV Candida or Aspergillus prophylaxis ≥2 y (I): q12h × 1 day,
≤40 kg IV: 6 mg/kg then q24h
>40 kg IV or DR tab (I): 300 mg (not per kg)
300-mg/16.7-mL viala ($$$$) IV
Praziquantel,a Biltricide 600-mg tab ($$) PO 20–25 mg/kg/dose, no max (I). q4–6h for
Round dose to nearest 200 mg (1/3 tab). 3 doses
Pretomanid 200-mg tab ($$) PO Adults: 200 mg (I) q24h
In combination with other agents for MDR TB
Primaquine phosphatea 15-mg base tab ($) (26.3-mg PO 0.5 mg (base)/kg, max 30 mg (III) q24h
primaquine phosphate) See Malaria in Table 9B.
Pyrantel pamoatea 250-mg base/5-mL susp ($) PO 11 mg (base)/kg, max 1 g (I) Once
(720-mg pyrantel pamoate/5-mL)
Pyrazinamidea 500-mg tab ($) PO 30 mg/kg/day, max 2 g/day (I) q24h
Biweekly DOT, 50 mg/kg (I), no max Twice weekly
Raxibacumab 1,700-mg/35-mL vial IV ≤15 kg: 80 mg/kg (I) Once
Available from the Strategic >15–50 kg: 60 mg/kg (I)
National Stockpile >50 kg: 40 mg/kg (I)
Remdesivir, Veklury 100-mg and 100-mg/20-mL vial IV <28 days of age and ≥1.5 kg OR ≥28 days of age q24h
($$$$) and 1.5–<3 kg: 2.5 mg/kg LD, then 1.25 mg/kg (I)
≥28 days of age and ≥3 kg: 5 mg/kg LD, then
2.5 mg/kg (I)
≥40 kg and adults: 200 mg LD, then 100 mg (not
per kg) (I)
Rezafungin, Rezzayo 200-mg vial ($$$$) IV Adults: 400 mg LD, then 200 mg (I) Weekly
Ribavirin,a Rebetol 200-mg cap/tab ($) PO <47 kg: 15 mg/kg/day (I) q12h
12–17 y (not per kg) (I):
47–59 kg: 800 mg/day

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

60–73 kg: 1,000 mg/day
74–105 kg: 1,200 mg/day
>105 kg: 1,400 mg/day
Given as combination therapy with other agents
(See Hepatitis C virus in Ch 7.)
Ribavirin,a Virazole 6-g vial ($$$$$) Inhaled 1 vial by SPAG-2 q24h
See Respiratory syncytial virus in Table 7C.
Rifabutin,a Mycobutin 150-mg cap ($$) PO 5 mg/kg for MAC prophylaxis (II) q24h
10–20 mg/kg for MAC or TB treatment (I)
Max 300 mg/day
 18
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310 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Rifampin,a Rifadin 150-, 300-mg cap ($) PO, IV 15–20 mg/kg, max 600 mg for active TB (in combi- q24h
600-mg vial ($$–$$$) nation) (I) or as single-drug therapy for latent TB.
Also for non-TB infections (see Ch 3) (II).
With biweekly DOT, dosage is still 15–20 mg/kg/ Twice weekly
dose, max 600 mg.
20 mg/kg/day for 2 days for meningococcus q12h
prophylaxis, max 1.2 g/day (I)
Rifampin/isoniazid/ 75-/50-/150-mg dispersible tab PO 4–7 kg: 1 tab q24h
pyrazinamide available from the Stop TB 8–11 kg: 2 tab
Partnership global drug facility 12–15 kg: 3 tabs
(www.stoptb.org/buyers; 16–24 kg: 4 tab
accessed August 15, 2024)
Rifamycin, Aemcolo 194-mg tab ($$) PO Adults: 2 tabs for TD (I) q12h for 3
days
Rifapentine, Priftin 150-mg tab ($$) PO ≥12 y and adults: 600 mg/dose (I) Twice weekly
>2 y, with INH for treatment of latent TB (I): Once weekly
10–14 kg: 300 mg
14.1–25 kg: 450 mg
25.1–32 kg: 600 mg
32.1–50 kg: 750 mg
>50 kg: 900 mg max
Rifaximin, Xifaxan 200-mg tab ($) PO 20–30 mg/kg/day (II) q8h
550-mg tab ($$$$) used for adults ≥12 y and adults: 600 mg/day (I) for TD
with IBS-D
Sarecycline, Seysara 60-, 100-, 150-mg tabs ($$$) PO For acne (I): q24h
≥9 y: 60 mg (not per kg)
55–84 kg: 100 mg
>84 kg: 150 mg
Secnidazole, Solosec 2-g granules ($$) PO ≥12 y: 2 g (I) Once
≥2 y: 30 mg/kg (III)
Sofosbuvir, Sovaldi 150-, 200-mg pellet packet PO Children ≥3 y (I): q24h
See Hepatitis C virus in 200-, 400-mg tab ($$$$$) <17 kg: 150 mg
Ch 7. 17–<35 kg: 200 mg
≥35 kg or ≥12 y: 400 mg
Sofosbuvir/ledipasvir,a 150-/33.75-mg pellet packet PO Children ≥3 y (I): q24h
Harvoni 200-/45-mg pellet packet <17 kg: 37.5 mg ledipasvir with 150 mg
Doses given in sofosbuvir 200-/45-mg tab sofosbuvir qd
400-/90-mg tab 17–<35 kg: 200 mg
All forms ($$$$) ≥35 kg: 400 mg (See Hepatitis C virus in Ch 7.)

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

Sofosbuvir/velpatasvir,a 150-/37.5-mg, 200-/50-mg pellet PO Children ≥3 y (I): q24h
Epclusa packets ($$$$$) <17 kg: 150 mg
Doses given in sofosbuvir 200-/50-mg tab ($$$$) 17–<30 kg: 200 mg
400-/100-mg tab ($$$$) ≥30 kg: 400 mg
See Hepatitis C virus in Ch 7.
Sofosbuvir/velpatasvir/ 400-/100-/100-mg tab ($$$$$) PO Adults: 1 tab (I) q24h
voxilaprevir, Vosevi See Hepatitis C virus in Ch 7.
Streptomycina,b 1-g vial ($$) IM, IV 20–40 mg/kg/day, max 1 g/day (I) q12–24h
Sulbactam/durlobactam, 1-g sulbactam/1-g durlobactam IV ≥18 y: 4 g/day (I) q6h
Xacduro vial (not yet commercially avail-
able as of May 25, 2023)
Sulfadiazinea 500-mg tab ($$$) PO 120–150 mg/kg/day, max 4–6 g/day (I) q6h
See Ch 9.
Rheumatic fever secondary prophylaxis: 500 mg qd q24h
if ≤27 kg, 1,000 mg qd if >27 kg (II)
 18
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312 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Tafenoquine, Arakoda 100-mg tab ($$) PO Adults: 200 mg (I) q24h for 3 days,
then weekly
Tafenoquine, Krintafel 150-mg tab ($) PO ≥16 y: 300 mg (I) Once
See Malaria in Table 9B.
Tecovirimat, Tpoxx 200-mg vial, cap IV <35 kg: 12 mg/kg/day (I) q12h infused
Available from the Strategic 35–<120 kg: 400 mg/day (I) over 6 h
National Stockpile (www.cdc. ≥120 kg: 600 mg/day (I)
gov/poxvirus/mpox/clinicians/
Tecovirimat.html; 770-488-7100)
PO <6 kg: 100 mg/day (I) q12h
6–<13 kg: 200 mg/day (I)
13–<25 kg: 400 mg/day (I)
25–<40 kg: 800 mg/day (I)
40–<120 kg: 1,200 mg/day (I)
≥120 kg: 1,800 mg/day (I) q8h
Tedizolid, Sivextro 200-mg tab, vial ($$$$) PO, IV ≥12 y and adults: 200 mg (I)c q24h
Telavancin, Vibativ 250-, 750-mg vial ($$$$) IV Adults: 10 mg/kg (I)c q24h
Tenofovir alafenamide, 25-mg tab ($$$$) PO ≥12 y: 25 mg (I) for chronic HBV q24h
Vemlidy
Tenofovir disoproxil 40 mg per scoop pwd for mixing PO ≥2 y, PO pwd: 8 mg/kg (rounded to nearest 20 mg q24h
fumarate, Viread with soft food ($$$) [½ scoop]) (I)
150-, 200-, 250-mg tab ($$$$) Tab (I):
300-mg taba ($) 17–<22 kg: 150 mg (not per kg)
22–<28 kg: 200 mg
28–<35 kg: 250 mg
≥35 kg: 300 mg
See Ch 7 for HBV and HIV-HBV coinfection use.
Terbinafine,a Lamisil 250-mg tab ($) PO Adults: 250 mg (I) q24h
Tetracyclinea 250-, 500-mg cap ($) PO ≥8 y: 25–50 mg/kg/day (I) q6h
Tinidazole,a Tindamax 250-, 500-mg tab ($) PO 50 mg/kg, max 2 g (I) q24h
See Giardiasis in Table 9B.
Tobramycin,a Nebcin 10-mg/mL vial ($) IV, IM 3–7.5 mg/kg/day (CF 7–10 mg/kg/day)b q8–24h
40-mg/mL vial ($)
Tobramycin inhalationa; 300-mg ampule ($$$$) Inhaled ≥6 y: 600 mg/day (I) q12h
Tobi, Bethkis
Tobi Podhaler 28-mg cap for inhalation ($$$$) Inhaled ≥6 y: 224 mg/day via Podhaler device (I) q12h
Triclabendazole, Egaten 250-mg scored tab available from PO ≥6 y (I): 20 mg/kg/day, given as 2 doses in 1 day q12h
the WHO fascioliasis partner- See Flukes in Table 9B.
ship ([email protected])
Trimethoprim/ 80-mg TMP/400-mg SMX tab PO, IV 8 mg TMP/kg/day (I) q12h
sulfamethoxazolea; (single-strength) ($) Adults: 2 DS tabs/day (I)

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

Bactrim, Septra 160-mg TMP/800-mg SMX tab 12 mg TMP/kg/day for bacterial MIC 1, max 640 mg
(DS) ($) TMP/day (II)
40-mg TMP/200-mg SMX per
5-mL PO susp ($)
16-mg TMP/80-mg SMX per mL
injection soln in 5-, 10-, 30-mL
vial ($$)
2 mg TMP/kg/day for UTI prophylaxis (I) q24h
15–20 mg TMP/kg/day for PCP treatment (I), no q6–8h
max
150 mg TMP/m2/day for PCP prophylaxis, max q24h OR q12h
320 mg TMP/day (I) 3×/wk
 18
Systemic & Topical Antimicrobial Dosing & Dose Forms

314 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
A. SYSTEMIC ANTIMICROBIALS WITH DOSAGE FORMS AND USUAL DOSAGES
Dosage Form
Generic and Trade Names (cost estimate) Route Dose (evidence level) Interval
Valacyclovir,a Valtrex 500-mg, 1-g tab ($) PO VZV: ≥3 mo: 60 mg/kg/day (I, II) q8h
Recipe for preparing susp HSV: ≥3 mo: 40 mg/kg/day (II) q12h
formulation provided in Max single dose 1 g (I)
product labeling
Valganciclovir,a Valcyte 250-mg/5-mL soln ($$) PO Congenital CMV treatment: 32 mg/kg/day (II) (See q12h
450-mg tab ($$) Ch 2.)
CMV prophylaxis (in mg, not mg/kg): 7 mg × BSA q24h
(m2) × CrCl (mL/min/1.73 m2 with the modified
Schwartz formula), max 900 mg (I) (See also Ch 7.)
Vancomycin, Vancocin 125-, 250-mg/5-mL susp ($–$$) PO 40 mg/kg/day (I), max 500 mg/day (III) q6h
125-, 250-mg capa ($–$$)
0.5-, 0.75-, 1-, 5-, 10-g viala ($) IV 30–45 mg/kg/day (I) q6–8h
1.25-, 1.5-g vial ($–$$) For invasive MRSA infection, 60–80 mg/kg/day
0.5-, 0.75-, 1-, 1.25-, 1.5-, 1.75-, adjusted to achieve AUC:MIC 400, max 3,600 mg/
2-g IVPB ($$) day
Voriconazole,a,b Vfend 200-mg/5-mL susp ($$$) PO ≥2 y and <50 kg: 18 mg/kg/day, max 700 mg/day q12h
See Aspergillosis in 50-, 200-mg tab ($) (I)
Table 5B. ≥50 kg: 400–600 mg/day (I)
200-mg vial ($$) IV ≥2 y and <50 kg: 18 mg/kg/day LD for 1 day, then q12h
16 mg/kg/day (I)
≥50 kg: 12 mg/kg/day LD for 1 day, then 8 mg/kg/
day (I)
Zanamivir, Relenza 5-mg blister cap for inhalation ($) Inhaled Prophylaxis: ≥5 y: 10 mg/day (I) q24h
Treatment: ≥7 y: 20 mg/day (I) q12h
a
Available in a generic formulation.
b
Monitor serum or plasma concentrations.
c
Also currently under investigation in children younger than the age given for the listed dosages
 B. TOPICAL ANTIMICROBIALS (SKIN, EYE, EAR, MUCOSA)
Generic and Trade Names Dosage Form Route Dose Interval
Acyclovir, Sitavig 50-mg tab Buccal Adults: 50 mg, for herpes labialis One time
Azithromycin, AzaSite 1% ophth soln Ophth 1 drop bid for 2 days, then qd
for 5 days
Bacitracina Ophth oint Ophth Apply to affected eye. q3–4h
Ointb Top Apply to affected area. bid–qid
Benzyl alcohol, Ulesfia 5% lotion Top Apply to scalp and hair. Once; repeat in 7 days.
Berdazimer, Zelsuvmi 10.3% gel Top Apply to lesion. Daily
Besifloxacin, Besivance 0.6% ophth susp Ophth ≥1 y: 1 drop to affected eye tid
Butenafine; Mentax, Lotrimin-Ultra 1% cream Top ≥12 y: apply to affected area. qd
Butoconazole, Gynazole-1 2% prefilled cream Vag Adults: 1 applicatorful One time

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

Ciclopiroxa; Loprox, Penlac 0.77% cream, gel, lotion Top ≥10 y: apply to affected area. bid
1% shampoo ≥16 y: apply to scalp. Twice weekly
8% nail lacquer ≥12 y: apply to infected nail. qd
Ciprofloxacin,a Cetraxal 0.2% otic soln Otic ≥1 y: apply 3 drops to affected ear. bid for 7 days
Ciprofloxacin, Ciloxan 0.3% ophth solna Ophth Apply to affected eye. q2h for 2 days, then
q4h for 5 days
0.3% ophth oint q8h for 2 days, then
q12h for 5 days
Ciprofloxacin, Otiprio 6% otic susp Otic ≥6 mo: 0.1 mL each ear intratympan- One time
ic, 0.2 mL to external ear canal for
otitis externa
Ciprofloxacin + dexamethasone, Ciprodex 0.3% + 0.1% otic soln Otic ≥6 mo: apply 4 drops to affected ear. bid for 7 days
Ciprofloxacin + fluocinolone, Otovel 0.3% + 0.025% otic soln Otic ≥6 mo: instill 0.25 mL to affected ear. bid for 7 days
 18
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316 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
B. TOPICAL ANTIMICROBIALS (SKIN, EYE, EAR, MUCOSA)
Generic and Trade Names Dosage Form Route Dose Interval
Ciprofloxacin + hydrocortisone, Cipro HC 0.2% + 1% otic soln Otic ≥1 y: apply 3 drops to affected ear. bid for 7 days
Clindamycin
– Cleocin 100-mg ovule Vag 1 ovule qhs for 3 days
2% vag creama 1 applicatorful qhs for 3–7 days
– Cleocin-Ta 1% soln, gel, lotion Top Apply to affected area. qd–bid
– Clindesse 2% cream Vag Adolescents and adults: One time
– Evoclina 1% foam 1 applicatorful qd
– Xaciato 2% gel One time
Clindamycin + adapalene benzoyl 1.2%, 0.15% gel Top ≥12 y: apply to affected area. qd
peroxide, Cabtreo
Clindamycin + benzoyl peroxide, BenzaClin 1% gela Top ≥12 y: apply to affected area. bid
– Acanya 1.2% gel Apply small amount to face. q24h
Clindamycin + tretinoin; Ziana, Veltin 1.2% gel Top Apply small amount to face. hs
Clotrimazole,a,b Lotrimin 1% cream, lotion, soln Top Apply to affected area. bid
– Gyne-Lotrimin-3a,b 2% cream Vag ≥12 y: 1 applicatorful qhs for 7–14 days
– Gyne-Lotrimin-7a,b 1% cream qhs for 3 days
Clotrimazole + betamethasone,a Lotrisone 1% + 0.05% cream, lotion Top ≥12 y: apply to affected area. bid
Colistin + neomycin + hydrocortisone; 0.3% otic susp Otic Apply 3–4 drops to affected ear canal; q6–8h
Coly-Mycin S, Cortisporin TC otic may use with wick.
Cortisporin; bacitracin + neomycin + Oint Top Apply to affected area. bid–qid
polymyxin B + hydrocortisone
Cortisporin; neomycin + polymyxin B + Otic solna Otic 3 drops to affected ear bid–qid
hydrocortisone Cream Top Apply to affected area bid–qid
Dapsone,a Aczone 5% gel Top ≥9 y: apply to affected area. bid
7.5% gel qd
Econazole,a Spectazole 1% cream Top Apply to affected area. qd–bid
Efinaconazole, Jublia 10% soln Top Apply to toenail. qd for 48 wk
Erythromycin a
0.5% ophth oint Ophth Apply to affected eye. q4h
– Akne-Mycin 2% oint Top Apply to affected area. bid
– Ery Pads 2% pledgetsa
– Eryderm,a Erygela 2% soln, gel
Erythromycin + benzoyl peroxide,a 3% gel Top ≥12 y: apply to affected area. qd–bid
Benzamycin
Ganciclovir, Zirgan 0.15% ophth gel Ophth ≥2 y: 1 drop in affected eye q3h while awake
(5 times daily) until
healed, then tid for

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

7 days
Gatifloxacin, Zymar 0.3% ophth soln Ophth 1 drop in affected eye q2h for 2 days, then
q6h
Gatifloxacin,a Zymaxid 0.5% ophth soln Ophth ≥1 y: 1 drop in affected eye q2h for 1 day, then q6h
Gentamicin, Garamycin
a
0.1% cream, oint Top Apply to affected area. tid–qid
0.3% ophth soln, oint Ophth Apply to affected eye. q1–4h (soln)
q4–8h (oint)
Gentamicin + prednisolone, Pred-G 0.3% ophth soln, oint Ophth Adults: apply to affected eye. q1–4h (soln)
qd–tid (oint)
Imiquimod,a Aldara 5% cream Top ≥12 y: to perianal or external genital 3×/wk
warts
 18
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318 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
B. TOPICAL ANTIMICROBIALS (SKIN, EYE, EAR, MUCOSA)
Generic and Trade Names Dosage Form Route Dose Interval
Ivermectin, Sklice 0.5% lotion Top ≥6 mo: thoroughly coat hair and Once
scalp; rinse after 10 minutes.
Ivermectin,a Soolantra 1% cream Top Adults: apply to face. qd
Ketoconazole,a Nizoral 2% shampoo Top ≥12 y: apply to affected area. qd
2% cream qd–bid
– Extina, Xolegel 2% foam, gel bid
– Nizoral A-D 1% shampoo bid
Levofloxacina; Quixin, Iquix 0.5%, 1.5% ophth soln Ophth Apply to affected eye. q1–4h
Luliconazole, Luzu 1% cream Top ≥12 y: apply to affected area. q24h for 1–2 wk
Mafenide, Sulfamylon 8.5% cream Top Apply to burn. qd–bid
5-g pwd for reconstitution To keep burn dressing wet q4–8h as needed
Malathion,a Ovide 0.5% soln Top ≥6 y: apply to hair and scalp. Once
Maxitrola; neomycin + polymyxin + Susp, oint Ophth Apply to affected eye. q1–4h (susp)
dexamethasone q4h (oint)
Metronidazolea 0.75% cream, gel, lotion Top Adults: apply to affected area. bid
0.75% vag gel Vag Adults: 1 applicatorful qd–bid
1% gel Top Adults: apply to affected area. qd
Noritate 1% cream Top Adults: apply to affected area. qd
Nuvessa 1.3% vag gel Vag ≥12 y: 1 applicatorful Once
Miconazole
– Fungoida,b 2% tincture Top Apply to affected area. bid
– Micatina,b and others 2% cream, pwd, oint, spray, Top Apply to affected area. qd–bid
lotion, gel
– Monistat-1a,b 1.2-g ovule + 2% cream Vag ≥12 y: insert one ovule (plus cream to Once
– Monistat-3a,b 200-mg ovule, 4% cream external vulva bid as needed). qhs for 3 days
– Monistat-7a,b 100-mg ovule, 2% cream qhs for 7 days
– Vusion 0.25% oint Top To diaper dermatitis Each diaper change for
7 days
Minocycline, Amzeeq 4% foam Top ≥9 y: apply to acne. qd
Moxifloxacin, Vigamox 0.5% ophth soln Ophth Apply to affected eye. tid
Mupirocin,a Bactroban 2% oint, cream Top Apply to infected skin. tid
Naftifine,a Naftin 1%, 2% cream, gel Top Apply to affected area. qd
Natamycin, Natacyn 5% ophth soln Ophth Adults: apply to affected eye. q1–4h
Neosporina

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

– bacitracin + neomycin + polymyxin B Ophth oint Ophth Apply to affected eye. q4h
Ointa,b Top Apply to affected area. bid–qid
– gramicidin + neomycin + polymyxin B Ophth soln Ophth Apply to affected eye. q4h
Nystatin,a Mycostatin 100,000 U/g cream, oint, Top Apply to affected area. bid–qid
pwd
Nystatin + triamcinolone,a Mycolog II 100,000 U/g + 0.1% cream, Top Apply to affected area. bid
oint
Ofloxacina; Floxin Otic, Ocuflox 0.3% otic soln Otic 5–10 drops to affected ear qd–bid
0.3% ophth soln Ophth Apply to affected eye. q1–6h
Oxiconazole, Oxistat 1% cream, lotion
a
Top Apply to affected area. qd–bid
Ozenoxacin, Xepi 1% cream Top Apply to affected area. bid for 5 days
 18
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320 — Chapter 18. Systemic & Topical Antimicrobial Dosing & Dose Forms
B. TOPICAL ANTIMICROBIALS (SKIN, EYE, EAR, MUCOSA)
Generic and Trade Names Dosage Form Route Dose Interval
Permethrin, Nixa,b 1% cream Top Apply to hair/scalp. Once for 10 min
– Elimitea 5% cream Apply to all skin surfaces. Once for 8–14 h
Piperonyl butoxide + pyrethrins,a,b Rid 4% + 0.3% shampoo, gel Top Apply to affected area. Once for 10 min
Polysporin,a polymyxin B + bacitracin Ophth oint Ophth Apply to affected eye. qd–tid
Ointb Top Apply to affected area.
Polytrim, polymyxin B + trimethoprim
a
Ophth soln Ophth Apply to affected eye. q3–4h
Retapamulin, Altabax 1% oint Top Apply thin layer to affected area. bid for 5 days
Selenium sulfide,a Selsun 2.5% lotion Top Lather into scalp or affected area. Twice weekly, then
2.25% shampoo q1–2wk
– Selsun Bluea,b 1% shampoo qd
Sertaconazole, Ertaczo 2% cream Top ≥12 y: apply to affected area. bid
Silver sulfadiazine,a Silvadene 1% cream Top Apply to affected area. qd–bid
Spinosad,a Natroba 0.9% susp Top Apply to scalp and hair. Once; may repeat in
7 days
Sulconazole, Exelderm 1% soln, cream Top Adults: apply to affected area. qd–bid
Sulfacetamide sodiuma 10% soln Ophth Apply to affected eye. q1–3h
10% ophth oint q4–6h
10% lotion, wash, cream Top ≥12 y: apply to affected area. bid–qid
Sulfacetamide sodium + prednisolone, a
10% ophth oint, soln Ophth Apply to affected eye. tid–qid
Blephamide
Tavaborole, Kerydin 5% soln Top Adults: apply to toenail. qd for 48 wk
Terbinafine,b Lamisil-AT 1% cream,a spray, gel Top Apply to affected area. qd–bid
Terconazole,a Terazol 0.4% cream Vag Adults: qhs for 7 days
0.8% cream 1 applicatorful or qhs for 3 days
80-mg suppository 1 suppository

Tioconazolea,b 6.5% oint Vag ≥12 y: 1 applicatorful One time

Tobramycin, Tobrex 0.3% soln, oint
a
Ophth Apply to affected eye. q1–4h (soln)
q4–8h (oint)
Tobramycin + dexamethasone, Tobradex 0.3% soln,a oint Ophth Apply to affected eye. q2–6h (soln)
q6–8h (oint)
Tobramycin + loteprednol, Zylet 0.3% + 0.5% ophth susp Ophth Adults: apply to affected eye. q4–6h
Tolnaftate,a,b Tinactin 1% cream, soln, pwd, spray Top Apply to affected area. bid
Trifluridine,a Viroptic 1% ophth soln Ophth 1 drop (max 9 drops/day) q2h
a
Generic available.
b
Over the counter.

2025 Nelson’s Pediatric Antimicrobial Therapy — 3

 Nomogram for Determining Body Surface Area — 323

Appendix
Nomogram for Determining Body Surface Area
Based on the nomogram shown below, a straight line joining the patient’s height and
weight will intersect the center column at the calculated body surface area (BSA). For
children of normal height for weight, the child’s weight in pounds is used, and then the
examiner reads across to the corresponding BSA in meters. Alternatively, the Mosteller
formula can be used.

Nomogram
Height For children of SA Weight
cm in normal height m2 lb kg
for weight 180 80
90 160 70
1.30
2.0 140
80 1.20 1.9 130 60
240 70 1.10 1.8 120
1.7 110 50
220 85 1.00 1.6 100
60 1.5
80 90 40
200 .90 1.4
190 75 50 80
1.3
180 70 .80 1.2 70
30
170 40 1.1 60
Surface area in square meters

65 .70
160 1.0 25
60 50
150 0.9
30 .60 45 20
140 55
.55 40
0.8
Weight in pounds

130 50 .50 35
0.7 15
120 30

Appendix: Nomogram for Determining Body Surface Area

20 .45
45
110 0.6 25
.40
100 40 10
15 .35 0.5 20 9.0
90 18 8.0
35
16 7.0
.30 0.4
80 14
6.0
30 10
12
28 9 .25 5.0
70
8 10
26 0.3 9 4.0
24 7 8
60
6 .20 7
22 3.0
6
20 5 2.5
50 0.2
19 5
18 4 .15 2.0
17 4
40 16
3 1.5
15
3
14
13
.10 1.0
30 12 2 0.1

Alternative (Mosteller formula):

Surface area (m2) = Height (cm) × Weight (kg)
3600
Nomogram and equation to determine body surface area.
From Engorn B, Flerlage J, eds. The Harriet Lane Handbook. 20th ed. Elsevier Mosby; 2015. Reproduced with permission
from Elsevier.
 References — 325

References

Chapter 1
1. Hultén KG, et al. Pediatr Infect Dis J. 2018;37(3):235–241 PMID: 28859018
2. Prochaska EC, et al. Antimicrob Steward Healthc Epidemiol. 2023;3(1):e12 PMID: 36714287
3. Stevens DL, et al. Clin Infect Dis. 2014;59(2):147–159 PMID: 24947530
4. Liu C, et al. Clin Infect Dis. 2011;52(3):e18–e55 PMID: 21208910
5. Brown NM, et al. JAC Antimicrob Resist. 2021;3(1):dlaa114 PMID: 34223066
6. AAP. Staphylococcus aureus. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:767–782
7. AAP. Group A streptococcal infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:785–798
8. Klotz SA, et al. Am Fam Physician. 2011;83(2):152–155 PMID: 21243990
9. Hatzenbuehler LA, et al. Pediatr Infect Dis J. 2014;33(1):89–91 PMID: 24346597
10. Muñoz-Egea MC, et al. Expert Opin Pharmacother. 2020;21(8):969–981 PMID: 32200657
11. Zimmermann P, et al. J Infect. 2017;74(suppl 1):S136–S142 PMID: 28646953
12. Tebruegge M, et al. PLoS One. 2016;11(1):e0147513 PMID: 26812154
13. Aliano D, et al. Pediatr Infect Dis J. 2020;39(8):671–677 PMID: 32235244
14. Neven Q, et al. Eur Arch Otorhinolaryngol. 2020;277(6):1785–1792 PMID: 32144570
15. Nolt D, et al. Pediatrics. 2021;148(6):e2021054663 PMID: 34851422
16. AAP. Tuberculosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:888–920
17. Bradley JS, et al. Pediatrics. 2014;133(5):e1411–e1436 PMID: 24777226
18. Oehler RL, et al. Lancet Infect Dis. 2009;9(7):439–447 PMID: 19555903
19. Thomas N, et al. Expert Rev Anti Infect Ther. 2011;9(2):215–226 PMID: 21342069
20. Bula-Rudas FJ, et al. Pediatr Rev. 2018;39(10):490–500 PMID: 30275032
21. AAP. Bite wounds. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:202–206
22. Talan DA, et al. N Engl J Med. 1999;340(2):85–92 PMID: 9887159
23. Goldstein EJ, et al. Antimicrob Agents Chemother. 2012;56(12):6319–6323 PMID: 23027193
24. AAP. Rabies. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:702–711
25. Talan DA, et al. Clin Infect Dis. 2003;37(11):1481–1489 PMID: 14614671
26. Miller LG, et al. N Engl J Med. 2015;372(12):1093–1103 PMID: 25785967
27. Talan DA, et al. N Engl J Med. 2016;374(9):823–832 PMID: 26962903
28. Moran GJ, et al. JAMA. 2017;317(20):2088–2096 PMID: 28535235
29. Bradley J, et al. Pediatrics. 2017;139(3):e20162477 PMID: 28202770
30. AAP. Haemophilus influenzae infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of
the Committee on Infectious Diseases. 33rd ed. 2024:400–409
31. Brindle R, et al. JAMA Dermatol. 2019;155(9):1033–1040 PMID: 31188407
32. Koning S, et al. Cochrane Database Syst Rev. 2012;(1):CD003261 PMID: 22258953
33. Bridwell R, et al. Am J Emerg Med. 2021;41:1–5 PMID: 33383265
34. Vij N, et al. J Pediatr Orthop. 2021;41(9):e849–e854 PMID: 34411048
35. Hedetoft M, et al. BMJ Open. 2023;13(2):e066117 PMID: 36813488
36. Schröder A, et al. BMC Infect Dis. 2019;19(1):317 PMID: 30975101
References

37. Zundel S, et al. Eur J Pediatr Surg. 2017;27(2):127–137 PMID: 27380058

38. Totapally BR. Pediatr Infect Dis J. 2017;36(7):641–644 PMID: 28005689
39. Levett D, et al. Cochrane Database Syst Rev. 2015;(1):CD007937 PMID: 25879088
40. Stevens DL, et al. Infect Dis Clin North Am. 2021;35(1):135–155 PMID: 33303335
41. Daum RS. N Engl J Med. 2007;357(4):380–390 PMID: 17652653
42. Sharara SL, et al. Infect Dis Clin North Am. 2021;35(1):107–133 PMID: 33303331
43. Elliott SP. Clin Microbiol Rev. 2007;20(1):13–22 PMID: 17223620
 326 — References

44. AAP. Rat-bite fever. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:711–713
45. Braunstein I, et al. Pediatr Dermatol. 2014;31(3):305–308 PMID: 24033633
46. Liy-Wong C, et al. Pediatr Dermatol. 2021;38(1):149–153 PMID: 33283348
47. Woods CR, et al. J Pediatric Infect Dis Soc. 2021:10(8):801–844 PMID: 34350458
48. Woods CR, et al. J Pediatric Infect Dis Soc. 2024:13(1):1–59 PMID: 37941444
49. Saavedra-Lozano J, et al. Pediatr Infect Dis J. 2017;36(8):788–799 PMID: 28708801
50. Keren R, et al. JAMA Pediatr. 2015;169(2):120–128 PMID: 25506733
51. McNeil JC, et al. Pediatr Infect Dis J. 2017;36(6):572–577 PMID: 28027279
52. Pääkkönen M. Pediatric Health Med Ther. 2017;8:65–68 PMID: 29388627
53. Arnold JC, et al. Pediatrics. 2012;130(4):e821–e828 PMID: 22966033
54. Chou AC, et al. J Pediatr Orthop. 2016;36(2):173–177 PMID: 25929777
55. Delgado-Noguera MF, et al. Cochrane Database Syst Rev. 2018;(11):CD012125 PMID: 30480764
56. Workowski KA, et al. Clin Infect Dis. 2022;74(suppl 2):S89–S94 PMID: 35416966
57. McDaniel LM, et al. J Pediatr Infect Dis Soc. 2023;12(1):534–539 PMID: 37757866
58. McNeil JC, et al. Pediatr Infect Dis J. 2021;40(6):518–524 PMID: 33902075
59. Workowski KA, et al. MMWR Recomm Rep. 2021;70(4):1–187 PMID: 34292926
60. AAP. Gonococcal infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:394–399
61. Peltola H, et al. N Engl J Med. 2014;370(4):352–360 PMID: 24450893
62. Funk SS, et al. Orthop Clin North Am. 2017;48(2):199–208 PMID: 28336042
63. Messina AF, et al. Pediatr Infect Dis J. 2011;30(12):1019–1021 PMID: 21817950
64. Howard-Jones AR, et al. J Paediatr Child Health. 2013;49(9):760–768 PMID: 23745943
65. De Marco G, et al. Front Pediatr. 2022;10:1043251 PMID: 36601031
66. Chen CJ, et al. Pediatr Infect Dis J. 2007;26(11):985–988 PMID: 17984803
67. Volk A, et al. Pediatr Emerg Care. 2017;33(11):724–729 PMID: 26785095
68. Kornelsen E, et al. Cochrane Database Syst Rev. 2021;(4):CD013535 PMID: 33908631
69. McKenna D, et al. Clin Case Rep. 2019;7(3):593–594 PMID: 30899507
70. Seltz LB, et al. Pediatrics. 2011;127(3):e566–e572 PMID: 21321025
71. Anosike BI, et al. J Pediatric Infect Dis Soc. 2022;11(5):214–220 PMID: 35438766
72. Saltagi MZ, et al. Allergy Rhinol (Providence). 2022;13:21526575221097311 PMID: 35496892
73. McDermott SM, et al. Otolaryngol Head Neck Surg. 2020;163(4):814–821 PMID: 32396416
74. Murphy DC, et al. J Paediatr Child Health. 2021;57(2):227–233 PMID: 32987452
75. Williams KJ, et al. Curr Opin Ophthalmol. 2019;30(5):349–355 PMID: 31261188
76. Chen YY, et al. Cochrane Database Syst Rev. 2023;(3):CD001211 PMID: 36912752
77. Johnson D, et al. JAMA. 2022;327(22):2231–2237 PMID: 35699701
78. Wilhelmus KR. Cochrane Database Syst Rev. 2015;(1):CD002898 PMID: 25879115
79. Sibley D, et al. Eye (Lond). 2020;34(12):2219–2226 PMID: 32843744
80. Wilhelmus KR, et al. Ophthalmology. 2020;127(4)(suppl):S5–S18 PMID: 32200827
81. Ali MJ. Ophthalmic Plast Reconstr Surg. 2015;31(5):341–347 PMID: 25856337
82. Khan S, et al. J Pediatr Ophthalmol Strabismus. 2014;51(3):140–153 PMID: 24877526
83. Slean GR, et al. Clin Exp Ophthalmol. 2017;45(5):481–488 PMID: 28013528
84. Birnbaum F, et al. EyeNet Magazine. 2016:33–35
85. Pappas PG, et al. Clin Infect Dis. 2016;62(4):e1–e50 PMID: 26679628
86. Bragg KJ, et al. Hordeolum. In: StatPearls. StatPearls Publishing; 2023 PMID: 28723014
References

87. Munro M, et al. Microorganisms. 2019;8(1):55 PMID: 31905656

88. Groth A, et al. Int J Pediatr Otorhinolaryngol. 2012;76(10):1494–1500 PMID: 22832239
89. Loh R, et al. J Laryngol Otol. 2018;132(2):96–104 PMID: 28879826
90. Laulajainen-Hongisto A, et al. Int J Pediatr Otorhinolaryngol. 2014;78(12):2072–2078 PMID: 25281339
91. Chong LY, et al. Cochrane Database Syst Rev. 2021;(2):CD013053 PMID: 33561891
92. Hussain SZM, et al. Cureus. 2022;14(12):e32780 PMID: 36686080
93. Khatri H, et al. Emerg Med Australas. 2021;33(6):961–965 PMID: 34569162
94. Rosenfeld RM, et al. Otolaryngol Head Neck Surg. 2014;150(1)(suppl):S1–S24 PMID: 24491310
95. Izurieta P, et al. Hum Vaccin Immunother. 2022;18(1):2013693 PMID: 35020530
 References — 327

96. Vadlamudi NK, et al. J Antimicrob Chemother. 2021;76(9):2419–2427 PMID: 34021757

97. Wald ER, et al. Pediatr Infect Dis J. 2018;37(12):1255–1257 PMID: 29570583
98. Lieberthal AS, et al. Pediatrics. 2013;131(3):e964–e999 PMID: 23439909
99. Venekamp RP, et al. Cochrane Database Syst Rev. 2015;(6):CD000219 PMID: 26099233
100. Shaikh N, et al. J Pediatr. 2017;189:54–60.e3 PMID: 28666536
101. Suzuki HG, et al. BMJ Open. 2020;10(5):e035343 PMID: 32371515
102. Van Dyke MK, et al. Pediatr Infect Dis J. 2017;36(3):274–281 PMID: 27918383
103. Frost HM, et al. J Pediatr. 2022;251:98–104.e5 PMID: 35944719
104. Sader HS, et al. Open Forum Infect Dis. 2019;6(suppl 1):S14–S23 PMID: 30895211
105. Gregory J, et al. JAMA Netw Open. 2021;4(3):e212713 PMID: 33755168
106. Wald ER, et al. Pediatrics. 2013;132(1):e262–e280 PMID: 23796742
107. Shaikh N, et al. Cochrane Database Syst Rev. 2014;(10):CD007909 PMID: 25347280
108. Chow AW, et al. Clin Infect Dis. 2012;54(8):e72–e112 PMID: 22438350
109. Ogle OE. Dent Clin North Am. 2017;61(2):235–252 PMID: 28317564
110. Cooper L, et al. Evid Based Dent. Published online September 7, 2022 PMID: 36071280
111. AAP. Diphtheria. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:357–361
112. Tibballs J, et al. J Paediatr Child Health. 2011;47(3):77–82 PMID: 21091577
113. Sobol SE, et al. Otolaryngol Clin North Am. 2008;41(3):551–566 PMID: 18435998
114. Nasser M, et al. Cochrane Database Syst Rev. 2008;(4):CD006700 PMID: 18843726
115. Amir J, et al. BMJ. 1997;314(7097):1800–1803 PMID: 9224082
116. Kimberlin DW, et al. Clin Infect Dis. 2010;50(2):221–228 PMID: 20014952
117. Riordan T. Clin Microbiol Rev. 2007;20(4):622–659 PMID: 17934077
118. Correia MS, et al. J Emerg Med. 2019;56(6):709–712 PMID: 31229258
119. Ridgway JM, et al. Am J Otolaryngol. 2010;31(1):38–45 PMID: 19944898
120. Lee WS, et al. J Microbiol Immunol Infect. 2020;53(4):513–517 PMID: 32303484
121. Valerio L, et al. J Intern Med. 2021;289(3):325–339 PMID: 32445216
122. Esposito S, et al. Children (Basel). 2022;9(5):618 PMID: 35626793
123. Hur K, et al. Laryngoscope. 2018;128(1):72–77 PMID: 28561258
124. Shulman ST, et al. Clin Infect Dis. 2012;55(10):e86–e102 PMID: 22965026
125. van Driel ML, et al. Cochrane Database Syst Rev. 2021;(3):CD004406 PMID: 33728634
126. Skoog Ståhlgren G, et al. BMJ. 2019;367:15337 PMID: 31585944
127. Altamimi S, et al. Cochrane Database Syst Rev. 2012;(8):CD004872 PMID: 22895944
128. Abdel-Haq N, et al. Pediatr Infect Dis J. 2012;31(7):696–699 PMID: 22481424
129. Cheng J, et al. Otolaryngol Head Neck Surg. 2013;148(6):1037–1042 PMID: 23520072
130. Casazza G, et al. Otolaryngol Head Neck Surg. 2019;160(3):546–549 PMID: 30348058
131. de Benedictis FM, et al. Lancet. 2020;396(10253):786–798 PMID: 32919518
132. Ramgopal S, et al. Pediatr Emerg Care. 2017;33(2):112–115 PMID: 26785088
133. Brook I. J Chemother. 2016;28(3):143–150 PMID: 26365224
134. Wardlaw AJ, et al. J Asthma Allergy. 2021;14:557–573 PMID: 34079294
135. Mathew JL, et al. Indian J Pediatr. 2023;90(7):708–717 PMID: 37264275
136. Agarwal R, et al. Chest. 2018;153(3):656–664 PMID: 29331473
137. Meissner HC. N Engl J Med. 2016;374(1):62–72 PMID: 26735994
138. Magréault S, et al. Clin Pharmacokinet. 2021;60(4):409–445 PMID: 33486720
139. Hahn A, et al. J Pediatr Pharmacol Ther. 2018;23(5):379–389 PMID: 30429692
References

140. Chmiel JF, et al. Ann Am Thorac Soc. 2014;11(7):1120–1129 PMID: 25102221
141. Flume PA, et al. Am J Respir Crit Care Med. 2009;180(9):802–808 PMID: 19729669
142. Saint GL, et al. Arch Dis Child. 2022;107(5):479–485 PMID: 34740877
143. Milinic T, et al. Semin Respir Crit Care Med. 2023;44(2):225–241 PMID: 36746183
144. Chmiel JF, et al. Ann Am Thorac Soc. 2014;11(8):1298–1306 PMID: 25167882
145. Waters V, et al. Cochrane Database Syst Rev. 2020;(6):CD010004 PMID: 32521055
146. Cogen JD, et al. Ann Am Thorac Soc. 2020;17(12):1590–1598 PMID: 32726564
147. Smith S, et al. Cochrane Database Syst Rev. 2020;(5):CD006961 PMID: 32412092
148. Langton Hewer SC, et al. Cochrane Database Syst Rev. 2023;(6):CD004197 PMID: 37268599
 328 — References

149. Smith S, et al. Cochrane Database Syst Rev. 2022;(11):CD001021 PMID: 36373968
150. Flume PA, et al. J Cyst Fibros. 2016;15(6):809–815 PMID: 27233377
151. Mogayzel PJ Jr, et al. Am J Respir Crit Care Med. 2013;187(7):680–689 PMID: 23540878
152. Southern KW, et al. Cochrane Database Syst Rev. 2012;(11):CD002203 PMID: 23152214
153. Li D, et al. Antibiotics (Basel). 2023;12(3):484 PMID: 36978351
154. Nichols DP, et al. Thorax. 2022;77(6):581–588 PMID: 34706982
155. AAP. Pertussis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:656–667
156. Kilgore PE, et al. Clin Microbiol Rev. 2016;29(3):449–486 PMID: 27029594
157. Wang K, et al. Cochrane Database Syst Rev. 2014;(9):CD003257 PMID: 25243777
158. Jain S, et al. N Engl J Med. 2015;372(9):835–845 PMID: 25714161
159. Bradley JS, et al. Clin Infect Dis. 2011;53(7):e25–e76 PMID: 21880587
160. Blumer JL, et al. Pediatr Infect Dis J. 2016;35(7):760–766 PMID: 27078119
161. Ambroggio L, et al. Pediatr Pulmonol. 2016;51(5):541–548 PMID: 26367389
162. Williams DJ, et al. JAMA Pediatr. 2017;171(12):1184–1191 PMID: 29084336
163. Bielicki JA, et al. JAMA. 2021;326(17):1713–1724 PMID: 34726708
164. Same RG, et al. J Pediatric Infect Dis Soc. 2021;10(3):267–273 PMID: 32525203
165. Dorman RM, et al. J Pediatr Surg. 2016;51(6):885–890 PMID: 27032611
166. Islam S, et al. J Pediatr Surg. 2012;47(11):2101–2110 PMID: 23164006
167. Redden MD, et al. Cochrane Database Syst Rev. 2017;(3):CD010651 PMID: 28304084
168. Pacilli M, et al. Paediatr Resp Rev. 2019;30:42–48 PMID: 31130425
169. Derderian SC, et al. J Pediatr Surg. 2020;55(11):2356–2361 PMID: 31973927
170. Dworsky ZD, et al. Hosp Pediatr. 2022;12(4):377–384 PMID: 35233619
171. Randolph AG, et al. Clin Infect Dis. 2019;68(3):365–372 PMID: 29893805
172. Bradley JS, et al. Pediatr Infect Dis J. 2007;26(10):868–878 PMID: 17901791
173. Hidron AI, et al. Lancet Infect Dis. 2009;9(6):384–392 PMID: 19467478
174. Frush JM, et al. J Hosp Med. 2018;13(12):848–852 PMID: 30379141
175. Wunderink RG, et al. Clin Infect Dis. 2012;54(5):621–629 PMID: 22247123
176. Lehrnbecher T, et al. J Clin Oncol. 2023;41(9):1774–1785 PMID: 36689694
177. Kalil AC, et al. Clin Infect Dis. 2016;63(5):e61–e111 PMID: 27418577
178. Chang I, et al. Paediatr Respir Rev. 2016;20:10–16 PMID: 26527358
179. Sweeney DA, et al. Clin Microbiol Infect. 2019;25(10):1195–1199 PMID: 31035015
180. AAP. Chlamydial infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:298–308
181. AAP. Cytomegalovirus infection. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:344–352
182. Balani SS, et al. Front Pediatr. 2023;11:1098434 PMID: 36891229
183. Limaye AP, et al. Clin Microbiol Rev. 2020;34(1):e00043-19 PMID: 33115722
184. Danziger-Isakov L, et al. J Pediatric Infect Dis Soc. 2018;7(suppl 2):S72–S74 PMID: 30590625
185. AAP. Tularemia. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:929–932
186. Galgiani JN, et al. Clin Infect Dis. 2016;63(6):e112–e146 PMID: 27470238
187. AAP. Coccidioidomycosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:320–324
188. AAP. Histoplasmosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
References

Infectious Diseases. 33rd ed. 2024:478–482

189. Barros N, et al. J Fungi (Basel). 2023;9(2):236 PMID: 36836350
190. Arrieta AC, et al. Infect Dis Ther. 2023;12(6):1465–1485 PMID: 37209297
191. Salmanton-García J, et al. J Antimicrob Chemother. 2019;74(11):3315–3327 PMID: 31393591
192. Uyeki TM, et al. Clin Infect Dis. 2019;68(6):895–902 PMID: 30834445
193. AAP Committee on Infectious Disease. Pediatrics. 2022;150(4):e2022059274 PMID: 36065749
194. Kimberlin DW, et al. J Infect Dis. 2013;207(5):709–720 PMID: 23230059
195. Stewart AG, et al. Open Forum Infect Dis. 2021;8(8):ofab387 PMID: 34395716
196. Lu B, et al. J Antimicrob Chemother. 2023;78(4):1009–1014 PMID: 36879495
 References — 329

197. Daley CL, et al. Clin Infect Dis. 2020;71(4):905–913 PMID: 32797222
198. Gardiner SJ. Cochrane Database Syst Rev. 2015;(1):CD004875 PMID: 25566754
199. Lee H, et al. Expert Rev Anti Infect Ther. 2018;16(1):23–34 PMID: 29212389
200. Panel on Opportunistic Infections in Children With and Exposed to HIV. Guidelines for the prevention
and treatment of opportunistic infections in children with and exposed to HIV. Pneumocystis jirovecii
pneumonia. Updated November 6, 2013. Accessed October 29, 2024. https://clinicalinfo.hiv.gov/
en/guidelines/hiv-clinical-guidelines-pediatric-opportunistic-infections/pneumocycstis-jirovecii-
pneumonia
201. Caselli D, et al. J Pediatr. 2014;164(2):389–392.e1 PMID: 24252793
202. Karruli A, et al. Antibiotics (Basel). 2023;12(2):399 PMID: 36830309
203. Reynolds D, et al. Drugs. 2021;81(18):2117–2131 PMID: 34743315
204. AAP. Respiratory syncytial virus. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:713–721
205. Nahid P, et al. Am J Respir Crit Care Med. 2019;200(10):e93–e142 PMID: 31729908
206. Jaganath D, et al. Infect Dis Clin North Am. 2022;36(1):49–71 PMID: 35168714
207. Sterling TR, et al. MMWR Recomm Rep. 2020;69(1):1–11 PMID: 32053584
208. Pantell RH, et al. Pediatrics. 2021;148(2):e2021052228 PMID: 34281996
209. Aronson PL, et al. Pediatrics. 2018;142(6):e20181879 PMID: 30425130
210. Aronson PL, et al. Pediatrics. 2019;144(1):e20183604 PMID: 31167938
211. Greenhow TL, et al. Pediatrics. 2017;139(4):e20162098 PMID: 28283611
212. Yaeger JP, et al. J Hosp Med. 2022;17(11):893–900 PMID: 36036211
213. Kuppermann N, et al. JAMA Pediatr. 2019;173(4):342–351 PMID: 30776077
214. McMullan BJ, et al. JAMA Pediatr. 2016;170(10):979–986 PMID: 27533601
215. Ruiz J, et al. Minerva Pediatr (Torino). 22;74(5):525–529 PMID: 29651827
216. Russell CD, et al. J Med Microbiol. 2014;63(pt 6):841–848 PMID: 24623637
217. Ligon J, et al. Pediatr Infect Dis J. 2014;33(5):e132–e134 PMID: 24732394
218. Arrieta AC, et al. Pediatr Infect Dis J. 2018;37(9):893–900 PMID: 29406465
219. Baddour LM, et al. Circulation. 2015;132(15):1435–1486 PMID: 26373316
220. Baltimore RS, et al. Circulation. 2015;132(15):1487–1515 PMID: 26373317
221. Eleyan L, et al. Eur J Pediatr. 2021;180(10):3089–3100 PMID: 33852085
222. Abdelghani M, et al. J Am Heart Assoc. 2018;7(13):e008163 PMID: 29934419
223. Dixon G, et al. Curr Opin Infect Dis. 2017;30(3):257–267 PMID: 28319472
224. Wilson WR, et al. Circulation. 2021;143(20):e963–e978 PMID: 33853363
225. Williams ML, et al. Ther Adv Cardiovasc Dis. 2021;15:17539447211002687 PMID: 33784909
226. Radovanovic M, et al. J Cardiovasc Dev Dis. 2022;9(4):103 PMID: 35448079
227. Abdel-Haq N, et al. Int J Pediatr. 2018;2018:5450697 PMID: 30532791
228. Shane AL, et al. Clin Infect Dis. 2017;65(12):1963–1973 PMID: 29194529
229. Denno DM, et al. Clin Infect Dis. 2012;55(7):897–904 PMID: 22700832
230. Freedman SB, et al. Clin Infect Dis. 2016;62(10):1251–1258 PMID: 26917812
231. Bennish ML, et al. Clin Infect Dis. 2006;42(3):356–362 PMID: 16392080
232. Smith KE, et al. Pediatr Infect Dis J. 2012;31(1):37–41 PMID: 21892124
233. Imdad A, et al. Cochrane Database Syst Rev. 2021;(7):CD012997 PMID: 34219224
234. Florez ID, et al. Curr Infect Dis Rep. 2020;22(2):4 PMID: 31993758
235. Ashkenazi S, et al. Pediatr Infect Dis J. 2016;35(6):698–700 PMID: 26986771
236. Taylor DN, et al. J Travel Med. 2017;24(suppl 1):S17–S22 PMID: 28520998
References

237. Riddle MS, et al. J Travel Med. 2017;24(suppl 1):S57–S74 PMID: 28521004
238. Williams PCM, et al. Paediatr Int Child Health. 2018;38(suppl 1):S50–S65 PMID: 29790845
239. Med Lett Drugs Ther. 2019;61(1582):153–160 PMID: 31599872
240. Adler AV, et al. J Travel Med. 2022;29(1):taab099 PMID: 34230966
241. Kantele A, et al. Clin Infect Dis. 2015;60(6):837–846 PMID: 25613287
242. Riddle MS, et al. Clin Infect Dis. 2008;47(8):1007–1014 PMID: 18781873
243. Janda JM, et al. Clin Microbiol Rev. 2010;23(1):35–73 PMID: 20065325
244. AAP. Campylobacter infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:283–286
 330 — References

245. Same RG, et al. Pediatr Rev. 2018;39(11):533–541 PMID: 30385582

246. Kanungo S, et al. Lancet. 2022;399(10333):1429–1440 PMID: 35397865
247. Connor BA, et al. J Travel Med. 2019;26(8):taz085 PMID: 31804684
248. AAP. Clostridioides difficile (formerly Clostridium difficile). In: Kimberlin DW, et al, eds. Red Book:
2024–2027 Report of the Committee on Infectious Diseases. 33rd ed. 2024:313–319
249. McDonald LC, et al. Clin Infect Dis. 2018;66(7):987–994 PMID: 29562266
250. Adams DJ, et al. J Pediatric Infect Dis Soc. 2021;10(suppl 3):S22–S26 PMID: 34791398
251. O’Gorman MA, et al. J Pediatric Infect Dis Soc. 2018;7(3):210–218 PMID: 28575523
252. Weng MK, et al. Epidemiol Infect. 2019;147:e172 PMID: 31063097
253. Mühlen S, et al. Antimicrob Agents Chemother. 2020;64(4):e02159-19 PMID: 32015030
254. Jones NL, et al. J Pediatr Gastroenterol Nutr. 2017;64(6):991–1003 PMID: 28541262
255. Crowe SE. N Engl J Med. 2019;380(12):1158–1165 PMID: 30893536
256. AAP. Helicobacter pylori infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:412–417
257. Helmbold L, et al. Pathogens. 2022;11(2):178 PMID: 35215122
258. AAP. Giardia duodenalis (formerly Giardia lamblia and Giardia intestinalis) infections. In: Kimberlin
DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious Diseases. 33rd ed.
2024:390–393
259. Ordóñez-Mena JM, et al. J Antimicrob Chemother. 2018;73(3):596–606 PMID: 29186570
260. Leinert JL, et al. Antibiotics (Basel). 2021;10(10):1187 PMID: 34680768
261. AAP. Salmonella infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:742–750
262. Frenck RW Jr, et al. Clin Infect Dis. 2004;38(7):951–957 PMID: 15034826
263. Trivedi NA, et al. J Postgrad Med. 2012;58(2):112–118 PMID: 22718054
264. Kuehn R, et al. Cochrane Database Syst Rev. 2022;(11):CD010452 PMID: 36420914
265. Begum B, et al. Mymensingh Med J. 2014;23(3):441–448 PMID: 25178594
266. Akram J, et al. Biomed Res Int. 2020;2020:6432580 PMID: 32462008
267. CDC. National Antimicrobial Resistance Monitoring System for Enteric Bacteria (NARMS). Accessed
October 29, 2024. www.cdc.gov/narms/data/index.html
268. Kotloff KL, et al. Lancet. 2018;391(10122):801–812 PMID: 29254859
269. AAP. Shigella infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:756–760
270. Abdel-Haq NM, et al. Pediatr Infect Dis J. 2000;19(10):954–958 PMID: 11055595
271. Abdel-Haq NM, et al. Int J Antimicrob Agents. 2006;27(5):449–452 PMID: 16621458
272. El Qouqa IA, et al. Int J Infect Dis. 2011;15(1):e48–e53 PMID: 21131221
273. Yousef Y, et al. J Pediatr Surg. 2018;53(2):250–255 PMID: 29223673
274. Marino NE, et al. Surg Infect (Larchmt). 2017;18(8):894–903 PMID: 29064344
275. Anandalwar SP, et al. JAMA Surg. 2018;153(11):1021–1027 PMID: 30046808
276. Solomkin JS, et al. Clin Infect Dis. 2010;50(2):133–164 PMID: 20034345
277. Sawyer RG, et al. N Engl J Med. 2015;372(21):1996–2005 PMID: 25992746
278. Felber J, et al. Front Cell Infect Microbiol. 2023;13:1027769 PMID: 37228669
279. Kronman MP, et al. Pediatrics. 2016;138(1):e20154547 PMID: 27354453
280. Bradley JS, et al. Pediatr Infect Dis J. 2019;38(8):816–824 PMID: 31306396
281. Hurst AL, et al. J Pediatric Infect Dis Soc. 2017;6(1):57–64 PMID: 26703242
282. Theodorou CM. J Pediatr Surg. 2021;56(10):1826–1830 PMID: 33223225
References

283. Hamdy RF, et al. Surg Infect (Larchmt). 2019;20(5):399–405 PMID: 30874482
284. Wang C, et al. BMC Pediatr. 2019;19(1):407 PMID: 31684906
285. Scott C, et al. Clin Infect Dis. 2016;63(5):594–601 PMID: 27298329
286. Sartoris G, et al. J Pediatric Infect Dis Soc. 2020;9(2):218–227 PMID: 31909804
287. Soni H, et al. Infection. 2019;47(3):387–394 PMID: 30324229
288. Lin CA, et al. J Pediatr Surg. 2023;58(7):1274–1280 PMID: 36894443
289. Sethna CB, et al. Clin J Am Soc Nephrol. 2016;11(9):1590–1596 PMID: 27340282
290. Warady BA, et al. Perit Dial Int. 2012;32(suppl 2):S32–S86 PMID: 22851742
291. Preece ER, et al. ANZ J Surg. 2012;82(4):283–284 PMID: 22510192
 References — 331

292. Gkentzis A, et al. Ann R Coll Surg Engl. 2014;96(3):181–183 PMID: 24780779
293. George CRR, et al. PloS One. 2019;14(4):e0213312 PMID: 30943199
294. Radovanovic M, et al. Pathogens. 2022;11(11):1230 PMID: 36364980
295. Hammad WAB, et al. Eur J Obstet Gynecol Reprod Biol. 2021;259:38–45 PMID: 33581405
296. Obstet Gynecol. 2020;135(5):e193–e202 PMID: 32332414
297. Savaris RF, et al. Sex Transm Infect. 2019;95(1):21–27 PMID: 30341232
298. Peeling RW, et al. Nat Rev Dis Primers. 2017;3:17073 PMID: 29022569
299. Jordan SJ, et al. Sex Transm Infect. 2020;96(4):306–311 PMID: 31515293
300. Abbe C, et al. Front Reprod Health. 2023;5:1100029 PMID: 37325243
301. Matheson A, et al. Aust N Z J Obstet Gynaecol. 2017;57(2):139–145 PMID: 28299777
302. Baka S, et al. Eur J Pediatr. 2022;181(12):4149–4155 PMID: 36163515
303. Beyitler İ, et al. World J Pediatr. 2017;13(2):101–105 PMID: 28083751
304. Hansen MT, et al. J Pediatr Adolesc Gynecol. 2007;20(5):315–317 PMID: 17868900
305. Brouwer MC, et al. N Engl J Med. 2014;371(5):447–456 PMID: 25075836
306. Mameli C, et al. Childs Nerv Syst. 2019;35(7):1117–1128 PMID: 31062139
307. Boucher A, et al. Med Mal Infect. 2017;47(3):221–235 PMID: 28341533
308. Dalmau J, et al. N Engl J Med. 2018;378(9):840–851 PMID: 29490181
309. Abzug MJ, et al. J Pediatric Infect Dis Soc. 2016;5(1):53–62 PMID: 26407253
310. Cheng H, et al. BMC Infect Dis. 2020;20(1):886 PMID: 33238935
311. Matthews E, et al. Curr Trop Med Rep. 2022;9(3):92–100 PMID: 36186545
312. Ajibowo AO, et al. Cureus. 2021;13(4):e14579 PMID: 34036000
313. Iro MA, et al. Cochrane Database Syst Rev. 2017;(10):CD011367 PMID: 28967695
314. Brouwer MC, et al. Cochrane Database Syst Rev. 2015;(9):CD004405 PMID: 26362566
315. Tunkel AR, et al. Clin Infect Dis. 2017;64(6):e34–e65 PMID: 28203777
316. Jhaveri R. J Pediatric Infect Dis Soc. 2019;8(1):92–93 PMID: 30380088
317. Bradley JS, et al. Pediatr Infect Dis J. 1991;10(11):871–873 PMID: 1749702
318. Prasad K, et al. Cochrane Database Syst Rev. 2016;(4):CD002244 PMID: 27121755
319. Konrad E, et al. Arch Dis Child. 2022;108(9):693–697 PMID: 36450441
320. Cies JJ, et al. J Pediatr Pharmacol Ther. 2020;25(4):336–339 PMID: 32461749
321. Bradley JS. Pediatrics. 2022;150(1):e2022056219 PMID: 35734947
322. National Institute for Health and Care Excellence. Urinary tract infection in under 16s: diagnosis and
management. July 27, 2022. Accessed October 29, 2024. www.nice.org.uk/guidance/ng224
323. Tullus K, et al. Lancet. 2020;395(10237):1659–1668 PMID: 32446408
324. Meesters K, et al. Antimicrob Agents Chemother. 2018;62(9):e00517-18 PMID: 29987142
325. Chen WL, et al. Pediatr Neonatal. 2015;56(3):176–182 PMID: 25459491
326. Fujita Y, et al. Pediatr Infect Dis J. 2021;40(7):e278–e280 PMID: 34097665
327. Strohmeier Y, et al. Cochrane Database Syst Rev. 2014;(7):CD003772 PMID: 25066627
328. Fox MT, et al. JAMA Netw Open. 2020;3(5):e203951 PMID: 32364593
329. Tamma PD, et al. Clin Infect Dis. 2015;60(9):1319–1325 PMID: 25586681
330. National Institute for Health and Care Excellence. Urinary tract infection (recurrent): antimicrobial
prescribing; treatment for children and young people under 16 years with recurrent UTI.
October 31, 2018. Accessed October 29, 2024. www.nice.org.uk/guidance/ng112/chapter/
Recommendations#treatment-for-children-and-young-people-under-16-years-with-recurrent-uti
331. AAP Subcommittee on Urinary Tract Infection and Steering Committee on Quality Improvement and
Management. Pediatrics. 2011;128(3):595–610 PMID: 21873693
References

332. Williams G, et al. Cochrane Database Syst Rev. 2019;(4):CD001534 PMID: 30932167
333. Williams G, et al. Cochrane Database Syst Rev. 2023;(4):CD001321 PMID: 37068952
334. Hoberman A, et al. N Engl J Med. 2014;370(25):2367–2376 PMID: 24795142
335. Craig JC. J Pediatr. 2015;166(3):778 PMID: 25722276
336. Hewitt IK, et al. Pediatrics. 2017;139(5):e20163145 PMID: 28557737
337. AAP. Actinomycosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:221–222
338. Chew SJ, et al. J Paediatr Child Health. 2023;59(6):833–839 PMID: 37017147
339. Wacharachaisurapol N, et al. Pediatr Infect Dis J. 2017;36(3):e76–e79 PMID: 27870811
 332 — References

340. Biggs HM, et al. MMWR Recomm Rep. 2016;65(2):1–44 PMID: 27172113
341. Dixon DM, et al. Ticks Tick Borne Dis. 2021;12(6):101823 PMID: 34517150
342. AAP. Brucellosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:277–280
343. Bukhari EE. Saudi Med J. 2018;39(4):336–341 PMID: 29619483
344. Shorbatli LA, et al. Int J Clin Pharm. 2018;40(6):1458–1461 PMID: 30446895
345. Zangwill KM. Adv Exp Med Biol. 2013;764:159–166 PMID: 23654065
346. Chang CC, et al. Paediatr Int Child Health. 2016;36(3):232–234 PMID: 25940800
347. Mogg M, et al. Vector Borne Zoonotic Dis. 2020;20(7):547–550 PMID: 32077809
348. Mukkada S, et al. Infect Dis Clin North Am. 2015;29(3):539–555 PMID: 26188606
349. Ruhayel SD, et al. Pediatr Infect Dis J. 2021;40(9):832–834 PMID: 34285167
350. Taplitz RA, et al. J Clin Oncol. 2018;36(14):1443–1453 PMID: 29461916
351. Alali M, et al. J Pediatr Hematol Oncol. 2020;42(6):e445–e451 PMID: 32404688
352. Haeusler GM, et al. EClinicalMedicine. 2020;23:100394 PMID: 32637894
353. Miedema KG, et al. Eur J Cancer. 2016;53:16–24 PMID: 26700076
354. Payne JR, et al. J Pediatr. 2018;193:172–177 PMID: 29229452
355. Son MBF, et al. Pediatr Rev. 2018;39(2):78–90 PMID: 29437127
356. Green J, et al. Cochrane Database Syst Rev. 2022;(5):CD011188 PMID: 35622534
357. Friedman KG, et al. Arch Dis Child. 2021;106(3):247–252 PMID: 32943389
358. McCrindle BW, et al. Circulation. 2017;135(17):e927–e999 PMID: 28356445
359. Broderick C, et al. Cochrane Database Syst Rev. 2023;(1):CD014884 PMID: 36695415
360. Yang J, et al. J Pediatr. 2022;243:173–180.e8 PMID: 34953816
361. AAP. Leprosy. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:539–532
362. Haake DA, et al. Curr Top Microbiol Immunol. 2015;387:65–97 PMID: 25388133
363. AAP. Leptospirosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:542–545
364. AAP. Lyme disease. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:549–556
365. Nguyen CT, et al. JAMA. 2022;327(8):772–773 PMID: 35191942
366. Wiersinga WJ, et al. Nat Rev Dis Primers. 2018;4:17107 PMID: 29388572
367. Chetchotisakd P, et al. Lancet. 2014;383(9919):807–814 PMID: 24284287
368. Haworth CS, et al. BMJ Open Respir Res. 2017;4(1):e000242 PMID: 29449949
369. Griffith DE, et al. Chest. 2022;161(1):64–75 PMID: 34314673
370. Pasipanodya JG, et al. Antimicrob Agents Chemother. 2017;61(11):e01206-17 PMID: 28807911
371. Traxler RM, et al. Clin Microbiol Rev. 2022;35(4):e0002721 PMID: 36314911
372. AAP. Nocardiosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:620–622
373. Kugeler KJ, et al. Clin Infect Dis. 2020;70(suppl 1):S20–S26 PMID: 32435801
374. Barbieri R, et al. Clin Microbiol Rev. 2020;34(1):e00044-19 PMID: 33298527
375. Apangu T, et al. Emerg Infect Dis. 2017;23(3):553–555 PMID: 28125398
376. Cherry CC, et al. Curr Infect Dis Rep. 2020;22(4) PMID: 34135692
377. Anderson A, et al. MMWR Recomm Rep. 2013;62(RR-03):1–30 PMID: 23535757
378. AAP. Rocky Mountain spotted fever. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:727–730
References

379. Jay R, et al. J Vector Borne Dis. 2020;57(2):114–120 PMID: 34290155

380. AAP. Tetanus. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:848–854
381. CDC. Clinical overview of tetanus. August 15, 2024. Accessed October 29, 2024. www.cdc.gov/tetanus/
hcp/clinical-overview/index.html
382. Gaensbauer JT, et al. Pediatr Infect Dis J. 2018;37(12):1223–1226 PMID: 29601458
383. Cook A, et al. Emerg Infect Dis. 2020;26(6):1077–1083 PMID: 32442091
384. Harik NS. Pediatr Ann. 2013;42(7):288–292 PMID: 23805970
 References — 333

Chapter 2
1. Allegaert K, et al. Acta Clin Belg. 2019;74(3):157–163 PMID: 29745792
2. Keij FM, et al. BMJ Open. 2019;9(7):e026688 PMID: 31289068
3. Gifford A, et al. Arch Dis Child. 2024;109(8):681–687 PMID: 38307705
4. Arnold CJ, et al. Pediatr Infect Dis J. 2015;34(9):964–968 PMID: 26376308
5. Martin E, et al. Eur J Pediatr. 1993;152(6):530–534 PMID: 8335024
6. Hile GB, et al. J Pediatr Pharmacol Ther. 2021;26(1):99–103 PMID: 33424507
7. Bradley JS, et al. Pediatrics. 2009;123(4):e609–e613 PMID: 19289450
8. Zikic A, et al. J Pediatric Infect Dis Soc. 2018;7(3):e107–e115 PMID: 30007329
9. AAP. Chlamydial infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:298–308
10. Honein MA, et al. Lancet. 1999;354(9196):2101–2105 PMID: 10609814
11. Hammerschlag MR, et al. Pediatr Infect Dis J. 1998;17(11):1049–1050 PMID: 9849993
12. Abdellatif M, et al. Eur J Pediatr. 2019;178(3):301–314 PMID: 30470884
13. Laga M, et al. N Engl J Med. 1986;315(22):1382–1385 PMID: 3095641
14. Workowski KA, et al. MMWR Recomm Rep. 2015;64(RR-3):1–137 PMID: 26042815
15. Newman LM, et al. Clin Infect Dis. 2007;44(suppl 3):S84–S101 PMID: 17342672
16. MacDonald N, et al. Adv Exp Med Biol. 2008;609:108–130 PMID: 18193661
17. AAP. Gonococcal infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:394–399
18. Cimolai N. Am J Ophthalmol. 2006;142(1):183–184 PMID: 16815280
19. Marangon FB, et al. Am J Ophthalmol. 2004;137(3):453–458 PMID: 15013867
20. AAP. Coagulase-negative staphylococcal infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027
Report of the Committee on Infectious Diseases. 33rd ed. 2024:782–785
21. Brito DV, et al. Braz J Infect Dis. 2003;7(4):234–235 PMID: 14533982
22. Chen CJ, et al. Am J Ophthalmol. 2008;145(6):966–970 PMID: 18378213
23. Shah SS, et al. J Perinatol. 1999;19(6, pt 1):462–465 PMID: 10685281
24. Kimberlin DW, et al. J Pediatr. 2003;143(1):16–25 PMID: 12915819
25. Kimberlin DW, et al. J Infect Dis. 2008;197(6):836–845 PMID: 18279073
26. AAP. Cytomegalovirus infection. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:344–352
27. Kimberlin DW, et al. N Engl J Med. 2015;372(10):933–943 PMID: 25738669
28. Kimberlin DW, et al. J Pediatr. 2024;268:113934 PMID: 38309519
29. Marsico C, et al. J Infect Dis. 2019;219(9):1398–1406 PMID: 30535363
30. Chung PK, et al. J Pediatr. 2024;268:113945 PMID: 38336204
31. AAP. Candidiasis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:286–293
32. Hundalani S, et al. Expert Rev Anti Infect Ther. 2013;11(7):709–721 PMID: 23829639
33. Saez-Llorens X, et al. Antimicrob Agents Chemother. 2009;53(3):869–875 PMID: 19075070
34. Ericson JE, et al. Clin Infect Dis. 2016;63(5):604–610 PMID: 27298330
35. Smith PB, et al. Pediatr Infect Dis J. 2009;28(5):412–415 PMID: 19319022
36. Wurthwein G, et al. Antimicrob Agents Chemother. 2005;49(12):5092–5098 PMID: 16304177
37. Heresi GP, et al. Pediatr Infect Dis J. 2006;25(12):1110–1115 PMID: 17133155
38. Kawaguchi C, et al. Pediatr Int. 2009;51(2):220–224 PMID: 19405920
39. Hsieh E, et al. Early Hum Dev. 2012;88(suppl 2):S6–S10 PMID: 22633516
References

40. Pappas PG, et al. Clin Infect Dis. 2016;62(4):e1–e50 PMID: 26679628
41. Hwang MF, et al. Antimicrob Agents Chemother. 2017;61(12):e01352-17 PMID: 28893774
42. Watt KM, et al. Antimicrob Agents Chemother. 2015;59(7):3935–3943 PMID: 25896706
43. Ascher SB, et al. Pediatr Infect Dis J. 2012;31(5):439–443 PMID: 22189522
44. Swanson JR, et al. Pediatr Infect Dis J. 2016;35(5):519–523 PMID: 26835970
45. Santos RP, et al. Pediatr Infect Dis J. 2007;26(4):364–366 PMID: 17414408
46. Frankenbusch K, et al. J Perinatol. 2006;26(8):511–514 PMID: 16871222
47. Thomas L, et al. Expert Rev Anti Infect Ther. 2009;7(4):461–472 PMID: 19400765
 334 — References

48. Mehler K, et al. Pediatr Infect Dis J. 2022;41(4):352–357 PMID: 34817413

49. Fatemizadeh R, et al. Pediatr Infect Dis J. 2020;39(4):310–312 PMID: 32084112
50. Verweij PE, et al. Drug Resist Updat. 2015;21–22:30–40 PMID: 26282594
51. Shah D, et al. Cochrane Database Syst Rev. 2012;(8):CD007448 PMID: 22895960
52. Cohen-Wolkowiez M, et al. Clin Infect Dis. 2012;55(11):1495–1502 PMID: 22955430
53. Knell J, et al. Curr Probl Surg. 2019;56(1):11–38 PMID: 30691547
54. Smith MJ, et al. Pediatr Infect Dis J. 2021;40(6):550–555 PMID: 33902072
55. Commander SJ, et al. Pediatr Infect Dis J. 2020;39(9):e245–e248 PMID: 32453198
56. Blakely ML, et al. Ann Surg. 2021;274(4):e370–e380 PMID: 34506326
57. Morgan RL, et al. Gastroenterology. 2020;159(2):467–480 PMID: 32592699
58. Gray KD, et al. J Pediatr. 2020;222:59–64.e1 PMID: 32418818
59. AAP. Salmonella infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:742–750
60. Pinninti SG, et al. Pediatr Clin North Am. 2013;60(2):351–365 PMID: 23481105
61. AAP. Herpes simplex. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:467–478
62. Jones CA, et al. Cochrane Database Syst Rev. 2009;(3):CD004206 PMID: 19588350
63. Downes KJ, et al. J Pediatr. 2020;219:126–132 PMID: 32037154
64. Kimberlin DW, et al. N Engl J Med. 2011;365(14):1284–1292 PMID: 21991950
65. Grondin A, et al. Neuropediatrics. 2020;51(3):221–224 PMID: 31887772
66. Sampson MR, et al. Pediatr Infect Dis J. 2014;33(1):42–49 PMID: 24346595
67. Panel on Antiretroviral Therapy and Medical Management of Children Living with HIV. Guidelines for
the use of antiretroviral agents in pediatric HIV infection. What’s new in the guidelines? Updated June
27, 2024. Accessed October 29, 2024. https://clinicalinfo.hiv.gov/en/guidelines/pediatric-arv/whats-new
68. Panel on Treatment of HIV During Pregnancy and Prevention of Perinatal Transmission.
Recommendations for the use of antiretroviral drugs in pregnant women with HIV infection and
interventions to reduce perinatal HIV transmission in the United States. Updated January 31, 2024.
Accessed October 29, 2024. https://clinicalinfo.hiv.gov/en/guidelines/perinatal/whats-new
69. Luzuriaga K, et al. N Engl J Med. 2015;372(8):786–788 PMID: 25693029
70. AAP Committee on Infectious Diseases. Pediatrics. 2019;144(4):e20192478 PMID: 31477606
71. Acosta EP, et al. J Infect Dis. 2010;202(4):563–566 PMID: 20594104
72. McPherson C, et al. J Infect Dis. 2012;206(6):847–850 PMID: 22807525
73. Kamal MA, et al. Clin Pharmacol Ther. 2014;96(3):380–389 PMID: 24865390
74. Kimberlin DW, et al. J Infect Dis. 2013;207(5):709–720 PMID: 23230059
75. Bradley JS, et al. Pediatrics. 2017;140(5):e20162727 PMID: 29051331
76. Hayden FG, et al. N Engl J Med. 2018;379(10):913–923 PMID: 30184455
77. Fraser N, et al. Acta Paediatr. 2006;95(5):519–522 PMID: 16825129
78. Ulloa-Gutierrez R, et al. Pediatr Emerg Care. 2005;21(9):600–602 PMID: 16160666
79. Sawardekar KP. Pediatr Infect Dis J. 2004;23(1):22–26 PMID: 14743041
80. Bingol-Kologlu M, et al. J Pediatr Surg. 2007;42(11):1892–1897 PMID: 18022442
81. Brook I. J Perinat Med. 2002;30(3):197–208 PMID: 12122901
82. Kaplan SL. Adv Exp Med Biol. 2009;634:111–120 PMID: 19280853
83. Korakaki E, et al. Jpn J Infect Dis. 2007;60(2–3):129–131 PMID: 17515648
84. Dessi A, et al. J Chemother. 2008;20(5):542–550 PMID: 19028615
85. Berkun Y, et al. Arch Dis Child. 2008;93(8):690–694 PMID: 18337275
References

86. Greenberg D, et al. Paediatr Drugs. 2008;10(2):75–83 PMID: 18345717

87. Ismail EA, et al. Pediatr Int. 2013;55(1):60–64 PMID: 23039834
88. Megged O, et al. J Pediatr. 2018;196:319 PMID: 29428272
89. Engle WD, et al. J Perinatol. 2000;20(7):421–426 PMID: 11076325
90. Brook I. Microbes Infect. 2002;4(12):1271–1280 PMID: 12467770
91. Darville T. Semin Pediatr Infect Dis. 2005;16(4):235–244 PMID: 16210104
92. Eberly MD, et al. Pediatrics. 2015;135(3):483–488 PMID: 25687145
93. Waites KB, et al. Semin Fetal Neonatal Med. 2009;14(4):190–199 PMID: 19109084
 References — 335

94. Morrison W. Pediatr Infect Dis J. 2007;26(2):186–188 PMID: 17259889

95. AAP. Pertussis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:656–667
96. Foca MD. Semin Perinatol. 2002;26(5):332–339 PMID: 12452505
97. AAP Committee on Infectious Diseases and Bronchiolitis Guidelines Committee. Pediatrics.
2014;134(2):e620–e638 PMID: 25070304
98. Banerji A, et al. CMAJ Open. 2016;4(4):E623–E633 PMID: 28443266
99. Borse RH, et al. J Pediatric Infect Dis Soc. 2014;3(3):201–212 PMID: 26625383
100. Vergnano S, et al. Pediatr Infect Dis J. 2011;30(10):850–854 PMID: 21654546
101. Nelson MU, et al. Semin Perinatol. 2012;36(6):424–430 PMID: 23177801
102. Lyseng-Williamson KA, et al. Paediatr Drugs. 2003;5(6):419–431 PMID: 12765493
103. AAP. Group B streptococcal infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:799–806
104. Schrag S, et al. MMWR Recomm Rep. 2002;51(RR-11):1–22 PMID: 12211284
105. AAP. Ureaplasma urealyticum and Ureaplasma parvum infections. In: Kimberlin DW, et al, eds. Red
Book: 2024–2027 Report of the Committee on Infectious Diseases. 33rd ed. 2024:936–938
106. Merchan LM, et al. Antimicrob Agents Chemother. 2015;59(1):570–578 PMID: 25385115
107. Viscardi RM, et al. Arch Dis Child Fetal Neonatal Ed. 2020;105(6):615–622 PMID: 32170033
108. Viscardi RM, et al. Pediatr Res. 2022;91(1):178–187 PMID: 33658655
109. AAP. Escherichia coli diarrhea. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:376–382
110. Venkatesh MP, et al. Expert Rev Anti Infect Ther. 2008;6(6):929–938 PMID: 19053905
111. Aguilera-Alonso D, et al. Antimicrob Agents Chemother. 2020;64(3):e02183-19 PMID: 31844014
112. Nakwan N, et al. Pediatr Infect Dis J. 2019;38(11):1107–1112 PMID: 31469781
113. Abzug MJ, et al. J Pediatric Infect Dis Soc. 2016;5(1):53–62 PMID: 26407253
114. AAP. Listeria monocytogenes infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:545–549
115. Workowski KA, et al. MMWR Recomm Rep. 2021;70(4):1–187 PMID: 34292926
116. van der Lugt NM, et al. BMC Pediatr. 2010;10:84 PMID: 21092087
117. Fortunov RM, et al. Pediatrics. 2006;118(3):874–881 PMID: 16950976
118. Fortunov RM, et al. Pediatrics. 2007;120(5):937–945 PMID: 17974729
119. Riccobene TA, et al. J Clin Pharmacol. 2017;57(3):345–355 PMID: 27510635
120. Stauffer WM, et al. Pediatr Emerg Care. 2003;19(3):165–166 PMID: 12813301
121. Kaufman DA, et al. Clin Infect Dis. 2017;64(10):1387–1395 PMID: 28158439
122. Dehority W, et al. Pediatr Infect Dis J. 2006;25(11):1080–1081 PMID: 17072137
123. AAP. Syphilis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:825–841
124. AAP. Tetanus. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:848–854
125. AAP. Toxoplasma gondii infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:867–875
126. Petersen E. Semin Fetal Neonatal Med. 2007;12(3):214–223 PMID: 17321812
127. Beetz R. Curr Opin Pediatr. 2012;24(2):205–211 PMID: 22227782
128. RIVUR Trial Investigators, et al. N Engl J Med. 2014;370(25):2367–2376 PMID: 24795142
129. Williams G, et al. Cochrane Database Syst Rev. 2019;(4):CD001534 PMID: 30932167
References

130. van Donge T, et al. Antimicrob Agents Chemother. 2018;62(4):e02004-17 PMID: 29358294
131. Sahin L, et al. Clin Pharmacol Ther. 2016;100(1):23–25 PMID: 27082701
132. Roberts SW, et al. Placental transmission of antibiotics. In: Glob Libr Women’s Med. Updated June 2008.
Accessed October 29, 2024. www.glowm.com/section_view/heading/Placental%20Transmission%20
of%20Antibiotics/item/174
133. Zhang Z, et al. Drug Metab Dispos. 2017;45(8):939–946 PMID: 28049636
134. Pacifici GM. Int J Clin Pharmacol Ther. 2006;44(2):57–63 PMID: 16502764
135. Sachs HC, et al. Pediatrics. 2013;132(3):e796–e809 PMID: 23979084
 336 — References

136. Hale TW. Medication and Mothers’ Milk 2021: A Manual of Lactational Pharmacology. 19th ed. 2021
137. Briggs GG, et al. Briggs Drugs in Pregnancy and Lactation. 12th ed. 2021
138. Ito S, et al. Am J Obstet Gynecol. 1993;168(5):1393–1399 PMID: 8498418

Chapter 3
1. Shields RK, et al. Clin Infect Dis. 2023;76(suppl 2):S179–S193 PMID: 37125467
2. Watkins RR, et al. Clin Infect Dis. 2023;76(suppl 2):S163–S165 PMID: 37125465
3. Viale P, et al. Ann Intensive Care. 2023;13(1):52 PMID: 37322293
4. Chiotos K, et al. J Pediatric Infect Dis Soc. 2020;9(1):56–66 PMID: 31872226
5. Aguilera-Alonso D, et al. Antimicrob Agents Chemother. 2020;64(3):e02183-19 PMID: 31844014
6. Mantzana P, et al. Antibiotics (Basel). 2023;12(1):93 PMID: 36671295
7. Mohd Sazlly Lim S, et al. Int J Antimicrob Agents. 2019;53(6):726–745 PMID: 30831234
8. Wacharachaisurapol N, et al. Pediatr Infect Dis J. 2017;36(3):e76–e79 PMID: 27870811
9. Gandhi K, et al. Ann Otol Rhinol Laryngol. 2021:34894211021273 PMID: 34060325
10. Pessoa RBG, et al. Front Microbiol. 2022;13:868890 PMID: 35711774
11. Sharma K, et al. Ann Clin Microbiol Antimicrob. 2017;16(1):12 PMID: 28288638
12. Maraki S, et al. J Microbiol Immunol Infect. 2016;49(1):119–122 PMID: 24529567
13. Sigurjonsdottir VK, et al. Diagn Microbiol Infect Dis. 2017;89(3):230–234 PMID: 29050793
14. Dixon DM, et al. Ticks Tick Borne Dis. 2021;12(6):101823 PMID: 34517150
15. Alrwashdeh AM, et al. IDCases. 2022;31:e01645 PMID: 36579145
16. Bradley JS, et al. Pediatrics. 2014;133(5):e1411–e1436 PMID: 24777226
17. AAP. Bacillus cereus infections and intoxications. In: Kimberlin DW, et al, eds. Red Book: 2024–2027
Report of the Committee on Infectious Diseases. 33rd ed. 2024:256–258
18. Lotte R, et al. Clin Microbiol Rev. 2022;35(2):e0008821 PMID: 35138121
19. Zafar H, et al. Gut Microbes. 2021;13(1):1–20 PMID: 33535896
20. Snydman DR, et al. Anaerobe. 2017;43:21–26 PMID: 27867083
21. Shorbatli LA, et al. Int J Clin Pharm. 2018;40(6):1458–1461 PMID: 30446895
22. Zangwill KM. Adv Exp Med Biol. 2013;764:159–166 PMID: 23654065
23. Angelakis E, et al. Int J Antimicrob Agents. 2014;44(1):16–25 PMID: 24933445
24. Kilgore PE, et al. Clin Microbiol Rev. 2016;29(3):449–486 PMID: 27029594
25. AAP. Pertussis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:656–667
26. Nguyen CT, et al. JAMA. 2022;327(8):772–773 PMID: 35191942
27. AAP. Lyme disease. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:549–556
28. AAP. Borrelia infections other than Lyme disease. In: Kimberlin DW, et al, eds. Red Book: 2024–2027
Report of the Committee on Infectious Diseases. 33rd ed. 2024:274–277
29. Rodino KG, et al. Infect Dis Clin North Am. 2022;36(3):689–701 PMID: 36116843
30. AAP. Brucellosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:277–280
31. Bukhari EE. Saudi Med J. 2018;39(4):336–341 PMID: 29619483
32. Yagupsky P. Adv Exp Med Biol. 2011;719:123–132 PMID: 22125040
33. AAP. Burkholderia infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:280–283
34. Massip C, et al. J Antimicrob Chemother. 2019;74(2):525–528 PMID: 30312409
References

35. Mazer DM, et al. Antimicrob Agents Chemother. 2017;61(9):e00766-17 PMID: 28674053
36. Lord R, et al. Cochrane Database Syst Rev. 2020;(4):CD009529 PMID: 32239690
37. Wiersinga WJ, et al. N Engl J Med. 2012;367(11):1035–1044 PMID: 22970946
38. Wiersinga WJ, et al. Nat Rev Dis Primers. 2018;4:17107 PMID: 29388572
39. Chetchotisakd P, et al. Lancet. 2014;383(9919):807–814 PMID: 24284287
40. Same RG, et al. Pediatr Rev. 2018;39(11):533–541 PMID: 30385582
41. Wagenaar JA, et al. Clin Infect Dis. 2014;58(11):1579–1586 PMID: 24550377
 References — 337

42. AAP. Campylobacter infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:283–286
43. Schiaffino F, et al. Antimicrob Agents Chemother. 2019;63(2):e01911-18 PMID: 30420482
44. Bula-Rudas FJ, et al. Pediatr Rev. 2018;39(10):490–500 PMID: 30275032
45. Butler T. Eur J Clin Microbiol Infect Dis. 2015;34(7):1271–1280 PMID: 25828064
46. Wang HK, et al. J Clin Microbiol. 2007;45(2):645–647 PMID: 17135428
47. Alhifany AA, et al. Am J Case Rep. 2017;18:674–667 PMID: 28620153
48. Rivero M, et al. BMC Infect Dis. 2019;19(1):816 PMID: 31533642
49. Kohlhoff SA, et al. Expert Opin Pharmacother. 2015;16(2):205–212 PMID: 25579069
50. AAP. Chlamydial infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:298–308
51. Workowski KA, et al. Clin Infect Dis. 2022;74(suppl 2):S89–S94 PMID: 35416966
52. Blasi F, et al. Clin Microbiol Infect. 2009;15(1):29–35 PMID: 19220337
53. Hogerwerf L, et al. Epidemiol Infect. 2017;145(15):3096–3105 PMID: 28946931
54. Campbell JI, et al. BMC Infect Dis. 2013;13:4 PMID: 23286235
55. Alisjahbana B, et al. Int J Gen Med. 2021;14:3259–3270 PMID: 34267544
56. Richard KR, et al. Am J Case Rep. 2015;16:740–744 PMID: 26477750
57. Paterson DL, et al. Curr Opin Infect Dis. 2020;33(2):214–223 PMID: 32068644
58. Harris PN, et al. J Antimicrob Chemother. 2016;71(2):296–306 PMID: 26542304
59. National Institute for Health and Care Excellence. Clostridioides difficile infection: antimicrobial
prescribing. July 23, 2021. Accessed October 29, 2024. www.nice.org.uk/guidance/ng199
60. AAP. Clostridioides difficile (formerly Clostridium difficile). In: Kimberlin DW, et al, eds. Red Book:
2024–2027 Report of the Committee on Infectious Diseases. 33rd ed. 2024:313–319
61. McDonald LC, et al. Clin Infect Dis. 2018;66(7):987–994 PMID: 29562266
62. O’Gorman MA, et al. J Pediatric Infect Dis Soc. 2018;7(3):210–218 PMID: 28575523
63. Carrillo-Marquez MA. Pediatr Rev. 2016;37(5):183–192 PMID: 27139326
64. AAP. Botulism and infant botulism. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:308–312
65. Hill SE, et al. Ann Pharmacother. 2013;47(2):e12 PMID: 23362041
66. AAP. Clostridial myonecrosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:312–313
67. AAP. Clostridium perfringens foodborne illness. In: Kimberlin DW, et al, eds. Red Book: 2024–2027
Report of the Committee on Infectious Diseases. 33rd ed. 2024:319–320
68. AAP. Tetanus. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:848–854
69. Yen LM, et al. Lancet. 2019;393(10181):1657–1668 PMID: 30935736
70. Rhinesmith E, et al. Pediatr Rev. 2018;39(8):430–432 PMID: 30068747
71. AAP. Diphtheria. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:357–361
72. Fernandez-Roblas R, et al. Int J Antimicrob Agents. 2009;33(5):453–455 PMID: 19153032
73. Gupta R, et al. Cardiol Rev. 2021;29(5):259–262 PMID: 32976125
74. Forouzan P, et al. Cureus. 2020;12(9):e10733 PMID: 33145138
75. Dalal A, et al. J Infect. 2008;56(1):77–79 PMID: 18036665
76. Eldin C, et al. Clin Microbiol Rev. 2017;30(1):115–190 PMID: 27856520
77. Cherry CC, et al. Curr Infect Dis Rep. 2020;22(4):10.1007/s11908-020-0719-0 PMID: 34135692
References

78. Mayslich C, et al. Microorganisms. 2021;9(2):303 PMID: 33540667

79. Lin ZX, et al. Orthopedics. 2020;43(1):52–61 PMID: 31958341
80. Dixon DM, et al. Ticks Tick Borne Dis. 2021;12(6):101823 PMID: 34517150
81. Xu G, et al. Emerg Infect Dis. 2018;24(6):1143–1144 PMID: 29774863
82. Paul K, et al. Clin Infect Dis. 2001;33(1):54–61 PMID: 11389495
83. Tricard T, et al. Arch Pediatr. 2016;23(11):1146–1149 PMID: 27663465
84. Huang YC, et al. Int J Antimicrob Agents. 2018;51(1):47–51 PMID: 28668676
 338 — References

85. Dziuban EJ, et al. Clin Infect Dis. 2018;67(1):144–149 PMID: 29211821
86. Siedner MJ, et al. Clin Infect Dis. 2014;58(11):1554–1563 PMID: 24647022
87. Tamma PD, et al. Clin Infect Dis. 2013;57(6):781–788 PMID: 23759352
88. Tamma PD, et al. IDSA 2024 guidance on the treatment of antimicrobial resistant gram-negative
infections. Infectious Diseases Society of America. June 12, 2024. Accessed October 29, 2024. www.
idsociety.org/practice-guideline/amr-guidance
89. Iovleva A, et al. Clin Lab Med. 2017;37(2):303–315 PMID: 2845735290
90. Arias CA, et al. Nat Rev Microbiol. 2012;10(4):266–278 PMID: 22421879
91. Yim J, et al. Pharmacotherapy. 2017;37(5):579–592 PMID: 28273381
92. Beganovic M, et al. Clin Infect Dis. 2018;67(2):303–309 PMID: 29390132
93. Shah NH, et al. Open Forum Infect Dis. 2021;8(4):ofab102 PMID: 34805443
94. Principe L, et al. Infect Dis Rep. 2016;8(1):6368 PMID: 27103974
95. AAP. Tularemia. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:929–932
96. Mittal S, et al. Pediatr Rev. 2019;40(4):197–201 PMID: 30936402
97. Van TT, et al. J Clin Microbiol. 2018;56(12):e00487-18 PMID: 30482869
98. Riordan T. Clin Microbiol Rev. 2007;20(4):622–659 PMID: 17934077
99. Valerio L, et al. J Intern Med. 2021;289(3):325–339 PMID: 32445216
100. Abou Chacra L, et al. Front Cell Infect Microbiol. 2022;11:672429 PMID: 35118003
101. Butler DF, et al. Infect Dis Clin North Am. 2018;32(1):119–128 PMID: 29233576
102. AAP. Helicobacter pylori infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:412–417
103. Jones NL, et al. J Pediatr Gastroenterol Nutr. 2017;64(6):991–1003 PMID: 28541262
104. Crowe SE. N Engl J Med. 2019;380(12):1158–1165 PMID: 30893536
105. Yagupsky P. Clin Microbiol Rev. 2015;28(1):54–79 PMID: 25567222
106. Gouveia C, et al. Pediatr Infect Dis J. 2021;40(7):623–627 PMID: 33657599
107. Livermore DM, et al. Clin Infect Dis. 2020;71(7):1776–1782 PMID: 32025698
108. Mesini A, et al. Clin Infect Dis. 2018;66(5):808–809 PMID: 29020309
109. Bradley JS, et al. Pediatr Infect Dis J. 2019;38(9):920–928 PMID: 31335570
110. van Duin D, et al. Clin Infect Dis. 2018;66(2):163–171 PMID: 29020404
111. Viasus D, et al. Infect Dis Ther. 2022;11(3):973–986 PMID: 35505000
112. Jiménez JIS, et al. J Crit Care. 2018;43:361–365 PMID: 29129539
113. Janow G, et al. Am J Perinatol. 2009;26(1):89–91 PMID: 19031357
114. Schlech WF. Microbiol Spectr. 2019;7(3) PMID: 31837132
115. Dickstein Y, et al. Eur J Clin Microbiol Infect Dis. 2019;38(12):2243–2251 PMID: 31399915
116. Murphy TF, et al. Clin Infect Dis. 2009;49(1):124–131 PMID: 19480579
117. Shi H, et al. J Clin Lab Anal. 2022;36(5):e24399 PMID: 35349730
118. Milligan KL, et al. Clin Pediatr (Phila). 2013;52(5):462–464 PMID: 22267858
119. AAP. Nontuberculous mycobacteria. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:920–929
120. Daley CL, et al. Clin Infect Dis. 2020;71(4):905–913 PMID: 32797222
121. Koh WJ, et al. Clin Infect Dis. 2017;64(3):309–316 PMID: 28011608
122. Waters V, et al. Cochrane Database Syst Rev. 2020;(6):CD010004 PMID: 32521055
123. Haworth CS, et al. BMJ Open Respir Res. 2017;4(1):e000242 PMID: 29449949
124. Adelman MH, et al. Curr Opin Pulm Med. 2018;24(3):212–219 PMID: 29470253
References

125. Griffith DE, et al. Chest. 2022;161(1):64–75 PMID: 34314673

126. Muñoz-Egea MC. Expert Opin Pharmacother. 2020;21(8):969–981 PMID: 32200657
127. AAP. Tuberculosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:888–920
128. Scott C, et al. Clin Infect Dis. 2016;63(5):594–601 PMID: 27298329
129. Sartoris G, et al. J Pediatric Infect Dis Soc. 2020;9(2):218–227 PMID: 31909804129
130. Brown-Elliott BA, et al. J Clin Microbiol. 2016;54(6):1586–1592 PMID: 27053677
131. CDC. Clinical overview of Hansen’s disease (leprosy). May 8, 2024. Accessed November 18, 2024. www.
cdc.gov/leprosy/hcp/clinical-overview
 References — 339

132. Johnson MG, et al. Infection. 2015;43(6):655–662 PMID: 25869820

133. Jaganath D, et al. Infect Dis Clin North Am. 2022;36(1):49–71 PMID: 35168714
134. Scaggs Huang FA, et al. Pediatr Infect Dis J. 2019;38(7):749–751 PMID: 30985508
135. Watt KM, et al. Pediatr Infect Dis J. 2012;31(2):197–199 PMID: 22016080
136. Waites KB, et al. Clin Microbiol Rev. 2017;30(3):747–809 PMID: 28539503
137. Gardiner SJ, et al. Cochrane Database Syst Rev. 2015;(1):CD004875 PMID: 25566754
138. Oishi T, et al. J Clin Med. 2022;11(7):1782 PMID: 35407390
139. St Cyr S, et al. MMWR Morb Mortal Wkly Rep. 2020;69(50):1911–1916 PMID: 33332296
140. Brady RC. Adv Pediatr. 2020;67:29–46 PMID: 32591062
141. Nadel S, et al. Front Pediatr. 2018;6:321 PMID: 30474022
142. Traxler RM, et al. Clin Microbiol Rev. 2022;35(4):e0002721 PMID: 36314911
143. AAP. Nocardiosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:620–622
144. Wilson BA, et al. Clin Microbiol Rev. 2013;26(3):631–655 PMID: 23824375
145. Mogilner L, et al. Pediatr Rev. 2019;40(2):90–92 PMID: 30709978
146. Badri M, et al. Clin Microbiol Infect. 2019;25(6):760.e1–760.e6 PMID: 30217761
147. Ozdemir O, et al. J Microbiol Immunol Infect. 2010;43(4):344–346 PMID: 20688296
148. Janda JM, et al. Clin Microbiol Rev. 2016;29(2):349–374 PMID: 26960939
149. Brook I, et al. Clin Microbiol Rev. 2013;26(3):526–546 PMID: 23824372
150. Schaffer JN, et al. Microbiol Spectr. 2015;3(5) PMID: 26542036
151. Abdallah M, et al. New Microbes New Infect. 2018;25:16–23 PMID: 29983987
152. Kunz Coyne AJ, et al. Infect Dis Ther. 2022;11(2):661–682 PMID: 35150435
153. Kalil AC, et al. Clin Infect Dis. 2016;63(5):e61–e111 PMID: 27418577
154. Alali M, et al. J Pediatr Hematol Oncol. 2020;42(6):e445–e451 PMID: 32404688
155. Jiao Y, et al. Antimicrob Agents Chemother. 2019;63(7):e00425-19 PMID: 30988147
156. McCarthy KL, et al. Infect Dis (Lond). 2018;50(5):403–406 PMID: 29205079
157. Kim HS, et al. BMC Infect Dis. 2017;17(1):500 PMID: 28716109
158. Milinic T, et al. Semin Respir Crit Care Med. 2023;44(2):225–241 PMID: 36746183
159. Epps QJ, et al. Pediatr Pulmonol. 2021;56(6):1784–1788 PMID: 33524241
160. Langton Hewer SC, et al. Cochrane Database Syst Rev. 2023;(6):CD004197 PMID: 37268599
161. Mogayzel PJ Jr, et al. Ann Am Thorac Soc. 2014;11(10):1640–1650 PMID: 25549030
162. Ryan MP, et al. Eur J Clin Microbiol Infect Dis. 2014;33(3):291–304 PMID: 24057141
163. Lin WV, et al. Clin Microbiol Infect. 2019;25(3):310–315 PMID: 29777923
164. AAP. Rickettsial diseases. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:723–725
165. Blanton LS. Infect Dis Clin North Am. 2019;33(1):213–229 PMID: 30712763
166. AAP. Salmonella infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee
on Infectious Diseases. 33rd ed. 2024:742–750
167. Leinert JL, et al. Antibiotics (Basel). 2021;10(10):1187 PMID: 34680768
168. Onwuezobe IA, et al. Cochrane Database Syst Rev. 2012;(11):CD001167 PMID: 23152205
169. Karkey A, et al. Curr Opin Gastroenterol. 2018;34(1):25–30 PMID: 29059070
170. Manesh A, et al. J Travel Med. 2021;28(3):taab012 PMID: 33550411
171. Yousfi K, et al. Eur J Clin Microbiol Infect Dis. 2017;36(8):1353–1362 PMID: 28299457
172. Janda JM, et al. Crit Rev Microbiol. 2014;40(4):293–312 PMID: 23043419
173. Baker S, et al. Nat Rev Microbiol. 2023;21(7):409–410 PMID: 37188805
References

174. AAP. Shigella infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:756–760
175. Kotloff KL, et al. Lancet. 2018;391(10122):801–812 PMID: 29254859
176. CDC. NARMS Now: Human Data. Accessed October 29, 2024. https://wwwn.cdc.gov/narmsnow
177. Rognrud K, et al. Case Rep Infect Dis. 2020;2020:7185834 PMID: 33101743
178. El Beaino M, et al. Int J Infect Dis. 2018;77:68–73 PMID: 30267938
179. AAP. Rat-bite fever. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:711–713
180. Stevens DL, et al. Clin Infect Dis. 2014;59(2):e10–e52 PMID: 24973422
 340 — References

181. Sharma R, et al. Curr Infect Dis Rep. 2019;21(10):37 PMID: 31486979
182. Korczowski B, et al. Pediatr Infect Dis J. 2016;35(8):e239–e247 PMID: 27164462
183. Bradley J, et al. Pediatrics. 2017;139(3):e20162477 PMID: 28202770
184. Rybak MJ, et al. Am J Health Syst Pharm. 2020;77(11):835–864 PMID: 32191793
185. Arrieta AC, et al. Pediatr Infect Dis J. 2018;37(9):893–900 PMID: 29406465
186. Becker K, et al. Expert Rev Anti Infect Ther. 2020;18(4):349–366 PMID: 32056452
187. Sader HS, et al. Diagn Microbiol Infect Dis. 2016;85(1):80–84 PMID: 26971182
188. Mojica MF, et al. JAC Antimicrob Resist. 2022;4(3):dlac040 PMID: 35529051
189. Anđelković MV, et al. J Chemother. 2019;31(6):297–306 PMID: 31130079
190. Delgado-Valverde M, et al. J Antimicrob Chemother. 2020;75(7):1840–1849 PMID: 32277821
191. Edholm A, et al. Clin Pract Cases Emerg Med. 2021;5(4):407–411 PMID: 34813430
192. Gerber MA, et al. Circulation. 2009;119(11):1541–1551 PMID: 19246689
193. AAP. Group B streptococcal infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:799–806
194. Faden H, et al. Pediatr Infect Dis J. 2017;36(11):1099–1100 PMID: 28640003
195. Furuichi M, et al. J Infect Chemother. 2018;24(2):99–102 PMID: 29050796
196. Faden HS. Pediatr Infect Dis J. 2016;35(9):1047–1048 PMID: 27294306
197. Otto WR, et al. J Pediatric Infect Dis Soc. 2021;10(3):309–316 PMID: 32955086
198. Baltimore RS, et al. Circulation. 2015;132(15):1487–1515 PMID: 26373317
199. Bradley JS, et al. Clin Infect Dis. 2011;53(7):e25–e76 PMID: 21880587
200. Mendes RE, et al. Diagn Microbiol Infect Dis. 2014;80(1):19–25 PMID: 24974272
201. Kaplan SL, et al. Pediatrics. 2019;144(3):e20190567 PMID: 31420369
202. AAP. Syphilis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:825–841
203. Viscardi RM, et al. Arch Dis Child Fetal Neonatal Ed. 2020;105(6):615–622 PMID: 32170033
204. CDC. Treating cholera. April 12, 2024. Accessed October 29, 2024. www.cdc.gov/cholera/treatment
205. Kanungo S, et al. Lancet. 2022;399(10333):1429–1440 PMID: 35397865
206. Trinh SA, et al. Antimicrob Agents Chemother. 2017;61(12):e01106-17 PMID: 28971862
207. Coerdt KM, et al. Cutis. 2021;107(2):E12–E17 PMID: 33891847
208. Leng F, et al. Eur J Clin Microbiol Infect Dis. 2019;38(11):1999–2004 PMID: 31325061
209. AAP. Yersinia enterocolitica and Yersinia pseudotuberculosis infections. In: Kimberlin DW, et al, eds. Red
Book: 2024–2027 Report of the Committee on Infectious Diseases. 33rd ed. 2024:960–963
210. Kato H, et al. Medicine (Baltimore). 2016;95(26):e3988 PMID: 27368001
211. Yang R. J Clin Microbiol. 2017;56(1):e01519-17 PMID: 29070654
212. Barbieri R, et al. Clin Microbiol Rev. 2020;34(1):e00044-19 PMID: 33298527
213. CDC. Clinical care of plague. May 15, 2024. Accessed November 18, 2023. www.cdc.gov/plague/hcp/
clinical-care
214. Somova LM, et al. Pathogens. 2020;9(6):436 PMID: 32498317

Chapter 4
1. Bosheva M, et al. Pediatr Infect Dis J. 2021;40(6):e222–e229 PMID: 33480665
2. Cannavino CR, et al. Pediatr Infect Dis J. 2016;35(7):752–759 PMID: 27093162
3. Bhatt J, et al. Cochrane Database Syst Rev. 2019;(9):CD002009 PMID: 31483853
4. Kaye KS, et al. Infect Dis Ther. 2023(3):777–806 PMID: 36847998
5. Schmid H, et al. Pediatr Infect Dis J. 2024;43(8):772–776 PMID: 38564757
References

6. Chang CK, et al. Front Pharmacol. 2022;13:814333 PMID: 35387340

7. Wirth S, et al. Pediatr Infect Dis J. 2018;37(8):e207–e213 PMID: 29356761
8. Jackson MA, et al. Pediatrics. 2016;138(5):e20162706 PMID: 27940800
9. Bradley JS, et al. Pediatrics. 2014;134(1):e146–e153 PMID: 24918220

Chapter 5
1. Groll AH, et al. Lancet Oncol. 2014;15(8):e327–e340 PMID: 24988936
2. Wingard JR, et al. Blood. 2010;116(24):5111–5118 PMID: 20826719
3. Van Burik JA, et al. Clin Infect Dis. 2004;39(10):1407–1416 PMID: 15546073
 References — 341

4. Cornely OA, et al. N Engl J Med. 2007;356(4):348–359 PMID: 17251531

5. Kung HC, et al. Cancer Med. 2014;3(3):667–673 PMID: 24644249
6. Science M, et al. Pediatr Blood Cancer. 2014;61(3):393–400 PMID: 24424789
7. Bow EJ, et al. BMC Infect Dis. 2015;15:128 PMID: 25887385
8. Tacke D, et al. Ann Hematol. 2014;93(9):1449–1456 PMID: 24951122
9. Almyroudis NG, et al. Curr Opin Infect Dis. 2009;22(4):385–393 PMID: 19506476
10. Maschmeyer G. J Antimicrob Chemother. 2009;63(suppl 1):i27–i30 PMID: 19372178
11. Freifeld AG, et al. Clin Infect Dis. 2011;52(4):e56–e93 PMID: 21258094
12. Fisher BT. JAMA. 2019;322(17):1673–1681 PMID: 31688884
13. Dvorak CC, et al. J Pediatric Infect Dis Soc. 2021;10(4):417–425 PMID: 33136159
14. Kim BK, et al. Children (Basel). 2022;9(3):372 PMID: 35327744
15. De Pauw BE, et al. N Engl J Med. 2007;356(4):409–411 PMID: 17251538
16. Salavert M. Int J Antimicrob Agents. 2008;32(suppl 2):S149–S153 PMID: 19013340
17. Eschenauer GA, et al. Liver Transpl. 2009;15(8):842–858 PMID: 19642130
18. Winston DJ, et al. Am J Transplant. 2014;14(12):2758–2764 PMID: 25376267
19. Sun HY, et al. Transplantation. 2013;96(6):573–578 PMID: 23842191
20. Radack KP, et al. Curr Infect Dis Rep. 2009;11(6):427–434 PMID: 19857381
21. Patterson TF, et al. Clin Infect Dis. 2016;63(4):e1–e60 PMID: 27365388
22. Thomas L, et al. Expert Rev Anti Infect Ther. 2009;7(4):461–472 PMID: 19400765
23. Friberg LE, et al. Antimicrob Agents Chemother. 2012;56(6):3032–3042 PMID: 22430956
24. Burgos A, et al. Pediatrics. 2008;121(5):e1286–e1294 PMID: 18450871
25. Herbrecht R, et al. N Engl J Med. 2002;347(6):408–415 PMID: 12167683
26. Mousset S, et al. Ann Hematol. 2014;93(1):13–32 PMID: 24026426
27. Blyth CC, et al. Intern Med J. 2014;44(12b):1333–1349 PMID: 25482744
28. Denning DW, et al. Eur Respir J. 2016;47(1):45–68 PMID: 26699723
29. Cornely OA, et al. Clin Infect Dis. 2007;44(10):1289–1297 PMID: 17443465
30. Maertens JA, et al. Lancet. 2016;387(10020):760–769 PMID: 26684607
31. Tissot F, et al. Haematologica. 2017;102(3):433–444 PMID: 28011902
32. Ullmann AJ, et al. Clin Microbiol Infect. 2018;24(suppl 1):e1–e38 PMID: 29544767
33. Walsh TJ, et al. Antimicrob Agents Chemother. 2010;54(10):4116–4123 PMID: 20660687
34. Arrieta AC, et al. Antimicrob Agents Chemother. 2021;65(8):e0029021 PMID: 34031051
35. Maertens JA, et al. Lancet. 2021;397(10273):499–509 PMID: 33549194
36. Bartelink IH, et al. Antimicrob Agents Chemother. 2013;57(1):235–240 PMID: 23114771
37. Slavin MA, et al. J Antimicrob Chemother. 2022;77(1):16–23 PMID: 34508633
38. Marr KA, et al. Ann Intern Med. 2015;162(2):81–89 PMID: 25599346
39. Verweij PE, et al. Drug Resist Updat. 2015;21–22:30–40 PMID: 26282594
40. Kohno S, et al. Eur J Clin Microbiol Infect Dis. 2013;32(3):387–397 PMID: 23052987
41. Naggie S, et al. Clin Chest Med. 2009;30(2):337–353 PMID: 19375639
42. Revankar SG, et al. Clin Microbiol Rev. 2010;23(4):884–928 PMID: 20930077
43. Wong EH, et al. Infect Dis Clin North Am. 2016;30(1):165–178 PMID: 26897066
44. Revankar SG, et al. Clin Infect Dis. 2004;38(2):206–216 PMID: 14699452
45. Li DM, et al. Lancet Infect Dis. 2009;9(6):376–383 PMID: 19467477
46. Chowdhary A, et al. Clin Microbiol Infect. 2014;20(suppl 3):47–75 PMID: 24483780
47. McCarty TP, et al. Med Mycol. 2015;53(5):440–446 PMID: 25908651
48. Schieffelin JS, et al. Transplant Infect Dis. 2014;16(2):270–278 PMID: 24628809
References

49. Chapman SW, et al. Clin Infect Dis. 2008;46(12):1801–1812 PMID: 18462107
50. McKinnell JA, et al. Clin Chest Med. 2009;30(2):227–239 PMID: 19375630
51. Walsh CM, et al. Pediatr Infect Dis J. 2006;25(7):656–658 PMID: 16804444
52. Fanella S, et al. Med Mycol. 2011;49(6):627–632 PMID: 21208027
53. Smith JA, et al. Proc Am Thorac Soc. 2010;7(3):173–180 PMID: 20463245
54. Bariola JR, et al. Clin Infect Dis. 2010;50(6):797–804 PMID: 20166817
55. Limper AH, et al. Am J Respir Crit Care Med. 2011;183(1):96–128 PMID: 21193785
56. Thompson GR, et al. Lancet Infect Dis. 2021;21(12):e364–e374 PMID: 34364529
57. Pappas PG, et al. Clin Infect Dis. 2016;62(4):e1–e50 PMID: 26679628
 342 — References

58. Lortholary O, et al. Clin Microbiol Infect. 2012;18(suppl 7):68–77 PMID: 23137138
59. Ullman AJ, et al. Clin Microbiol Infect. 2012;18(suppl 7):53–67 PMID: 23137137
60. Hope WW, et al. Clin Microbiol Infect. 2012;18(suppl 7):38–52 PMID: 23137136
61. Cornely OA, et al. Clin Microbiol Infect. 2012;18(suppl 7):19–37 PMID: 23137135
62. Hope WW, et al. Antimicrob Agents Chemother. 2015;59(2):905–913 PMID: 25421470
63. Piper L, et al. Pediatr Infect Dis J. 2011;30(5):375–378 PMID: 21085048
64. Watt KM, et al. Antimicrob Agents Chemother. 2015;59(7):3935–3943 PMID: 25896706
65. Ascher SB, et al. Pediatr Infect Dis J. 2012;31(5):439–443 PMID: 22189522
66. Sobel JD. Lancet. 2007;369(9577):1961–1971 PMID: 17560449
67. Kim J, et al. J Antimicrob Chemother. 2020;75(1):215–220 PMID: 31586424
68. Almangour TA, et al. Saudi Pharm J. 2021;29(4):315–323 PMID: 33994826
69. Barnes KN, et al. Ann Pharmacother. 2023;57(1):99–106 PMID: 35502451
70. Martinez RL, et al. Clin Dermatol. 2007;25(2):188–194 PMID: 17350498
71. Ameen M. Clin Exp Dermatol. 2009;34(8):849–854 PMID: 19575735
72. Chowdhary A, et al. Clin Microbiol Infect. 2014;20(suppl 3):47–75 PMID: 24483780
73. Queiroz-Telles F. Rev Inst Med Trop Sao Paulo. 2015;57(suppl 19):46–50 PMID: 26465369
74. Queiroz-Telles F, et al. Clin Microbiol Rev. 2017;30(1):233–276 PMID: 27856522
75. Galgiani JN, et al. Clin Infect Dis. 2016;63(6):717–722 PMID: 27559032
76. Anstead GM, et al. Infect Dis Clin North Am. 2006;20(3):621–643 PMID: 16984872
77. Williams PL. Ann N Y Acad Sci. 2007;1111:377–384 PMID: 17363442
78. Homans JD, et al. Pediatr Infect Dis J. 2010;29(1):65–67 PMID: 19884875
79. Kauffman CA, et al. Transplant Infectious Diseases. 2014;16(2):213–224 PMID: 24589027
80. McCarty JM, et al. Clin Infect Dis. 2013;56(11):1579–1585 PMID: 23463637
81. Bravo R, et al. J Pediatr Hematol Oncol. 2012;34(5):389–394 PMID: 22510771
82. Catanzaro A, et al. Clin Infect Dis. 2007;45(5):562–568 PMID: 17682989
83. Thompson GR, et al. Clin Infect Dis. 2016;63(3):356–362 PMID: 27169478
84. Thompson GR III, et al. Clin Infect Dis. 2017;65(2):338–341 PMID: 28419259
85. Chayakulkeeree M, et al. Infect Dis Clin North Am. 2006;20(3):507–544 PMID: 16984867
86. Jarvis JN, et al. Semin Respir Crit Care Med. 2008;29(2):141–150 PMID: 18365996
87. Perfect JR, et al. Clin Infect Dis. 2010;50(3):291–322 PMID: 20047480
88. Joshi NS, et al. Pediatr Infect Dis J. 2010;29(12):e91–e95 PMID: 20935590
89. Day JN, et al. N Engl J Med. 2013;368(14):1291–1302 PMID: 23550668
90. Chang CC, et al. Lancet Infect Dis. 2024;24(8):e495–e512 PMID: 38346436
91. Jarvis JN, et al. N Engl J Med. 2022;386(12):1109–1120 PMID: 3532064
92. Cortez KJ, et al. Clin Microbiol Rev. 2008;21(1):157–197 PMID: 18202441
93. Tortorano AM, et al. Clin Microbiol Infect. 2014;20(suppl 3):27–46 PMID: 24548001
94. Horn DL, et al. Mycoses. 2014;57(11):652–658 PMID: 24943384
95. Muhammed M, et al. Medicine (Baltimore). 2013;92(6):305–316 PMID: 24145697
96. Rodriguez-Tudela JL, et al. Med Mycol. 2009;47(4):359–370 PMID: 19031336
97. Wheat LJ, et al. Clin Infect Dis. 2007;45(7):807–825 PMID: 17806045
98. Myint T, et al. Medicine (Baltimore). 2014;93(1):11–18 PMID: 24378739
99. Assi M, et al. Clin Infect Dis. 2013;57(11):1542–1549 PMID: 24046304
100. Chayakulkeeree M, et al. Eur J Clin Microbiol Infect Dis. 2006;25(4):215–229 PMID: 16568297
101. Spellberg B, et al. Clin Infect Dis. 2009;48(12):1743–1751 PMID: 19435437
102. Reed C, et al. Clin Infect Dis. 2008;47(3):364–371 PMID: 18558882
References

103. Cornely OA, et al. Clin Microbiol Infect. 2014;20(suppl 3):5–26 PMID: 24479848
104. Spellberg B, et al. Clin Infect Dis. 2012;54(suppl 1):S73–S78 PMID: 22247449
105. Chitasombat MN, et al. Curr Opin Infect Dis. 2016;29(4):340–345 PMID: 27191199
106. Pana ZD, et al. BMC Infect Dis. 2016;16(1):667 PMID: 27832748
107. Pagano L, et al. Haematologica. 2013;98(10):e127–e130 PMID: 23716556
108. Kyvernitakis A, et al. Clin Microbiol Infect. 2016;22(9):811.e1–811.e8 PMID: 27085727
109. Marty FM, et al. Lancet Infect Dis. 2016;16(7):828–837 PMID: 26969258
110. Cornely OA. Lancet Infect Dis. 2019;19(12):e405–e421 PMID: 31699664
111. Queiroz-Telles F, et al. Clin Infect Dis. 2007;45(11):1462–1469 PMID: 17990229
 References — 343

112. Menezes VM, et al. Cochrane Database Syst Rev. 2006;(2):CD004967 PMID: 16625617
113. Marques SA. An Bras Dermatol. 2013;88(5):700–711 PMID: 24173174
114. Borges SR, et al. Med Mycol. 2014;52(3):303–310 PMID: 24577007
115. Panel on Opportunistic Infections in Children With and Exposed to HIV. Guidelines for the prevention
and treatment of opportunistic infections in children with and exposed to HIV. What’s new in the
guidelines? Updated July 3, 2024. Accessed October 29, 2024. https://clinicalinfo.hiv.gov/en/guidelines/
hiv-clinical-guidelines-pediatric-opportunistic-infections/whats-new
116. Siberry GK, et al. Pediatr Infect Dis J. 2013;32(suppl 2):i–KK4 PMID: 24569199
117. Maschmeyer G, et al. J Antimicrob Chemother. 2016;71(9):2405–2413 PMID: 27550993
118. Kauffman CA, et al. Clin Infect Dis. 2007;45(10):1255–1265 PMID: 17968818
119. Aung AK, et al. Med Mycol. 2013;51(5):534–544 PMID: 23286352
120. Ali S, et al. Pediatr Emerg Care. 2007;23(9):662–668 PMID: 17876261
121. Shy R. Pediatr Rev. 2007;28(5):164–174 PMID: 17473121
122. Andrews MD, et al. Am Fam Physician. 2008;77(10):1415–1420 PMID: 18533375
123. Kakourou T, et al. Pediatr Dermatol. 2010;27(3):226–228 PMID: 20609140
124. Gupta AK, et al. Pediatr Dermatol. 2013;30(1):1–6 PMID: 22994156
125. Chen X, et al. J Am Acad Dermatol. 2017;76(2):368–374 PMID: 27816294
126. Gupta AK, et al. Pediatr Dermatol. 2020;37(6):1014–1022 PMID: 32897584
127. de Berker D. N Engl J Med. 2009;360(20):2108–2116 PMID: 19439745
128. Ameen M, et al. Br J Dermatol. 2014;171(5):937–958 PMID: 25409999
129. Gupta AK. J Eur Acad Dermatol Venereol. 2020;34(3):580–588 PMID: 31746067
130. Sprenger AB. J Fungi (Basel). 2019;5(3):82 PMID: 31487828
131. Pantazidou A, et al. Arch Dis Child. 2007;92(11):1040–1042 PMID: 17954488
132. Gupta AK, et al. J Cutan Med Surg. 2014;18(2):79–90 PMID: 24636433

Chapter 6
1. Cavassin FB, et al. Paediatr Drugs. 2022;24(5):513–528 PMID: 35849282
2. Cornely OA, et al. Clin Infect Dis. 2007;44(10):1289–1297 PMID: 17443465
3. Lestner JM, et al. Antimicrob Agents Chemother. 2016;60(12):7340–7346 PMID: 27697762
4. Seibel NL, et al. Antimicrob Agents Chemother. 2017;61(2):e01477-16 PMID: 27855062
5. Azoulay E, et al. PLoS One. 2017;12(5):e0177093 PMID: 28531175
6. Ascher SB, et al. Pediatr Infect Dis J. 2012;31(5):439–443 PMID: 22189522
7. Piper L, et al. Pediatr Infect Dis J. 2011;30(5):375–378 PMID: 21085048
8. Gerhart JG, et al. CPT Pharmacometrics Syst Pharmacol. 2019;8(7):500–510 PMID: 31087536
9. Watt KM, et al. Antimicrob Agents Chemother. 2015;59(7):3935–3943 PMID: 25896706
10. Watt KM, et al. CPT Pharmacometrics Syst Pharmacol. 2018;7(10):629–637 PMID: 30033691
11. Mathew JL, et al. Indian J Pediatr. 2023;90(7):708–717 PMID: 37264275
12. Agarwal R, et al. Eur Respir J. 2024;63(4):2400061 PMID: 38423624
13. Friberg LE, et al. Antimicrob Agents Chemother. 2012;56(6):3032–3042 PMID: 22430956
14. Schweiger JA, et al. J Pediatr Hematol Oncol. 2024;46(6):e419–e425 PMID: 38934583
15. Zembles TN, et al. J Pediatr Pharmacol Ther. 2023;28(3):247–254 PMID: 37303767
16. Zembles TN, et al. Pharmacotherapy. 2016;36(10):1102–1108 PMID: 27548272
17. Moriyama B, et al. Clin Pharmacol Ther. 2017;102(1):45–51 PMID: 27981572
18. McCann S, et al. Clin Pharmacokinet. 2023;62(7):997–1009 PMID: 37179512
19. Kane Z, et al. Antimicrob Agents Chemother. 2023;67(7):e0007723 PMID: 37260401
References

20. Arrieta AC, et al. PLoS One. 2019;14(3):e0212837 PMID: 30913226

21. Groll AH, et al. Int J Antimicrob Agents. 2020;56(3):106084 PMID: 32682946
22. Winchell G, et al. Antimicrob Agents Chemother. 2024;68(4):e0119723 PMID: 38376229
23. Bernardo V, et al. Pediatr Transplant. 2020;24(6):e13777 PMID: 32639095
24. Maertens JA, et al. Lancet. 2016;387(10020):760–769 PMID: 26684607
25. Marty FM, et al. Lancet Infect Dis. 2016;16(7):828–837 PMID: 26969258
26. Cornely OA, et al. Lancet Infect Dis. 2019;19(12):e405–e421 PMID: 31699664
27. Arrieta AC, et al. Antimicrob Agents Chemother. 2021;65(8):e0029021 PMID: 34031051
28. Furfaro E, et al. J Antimicrob Chemother. 2019;74(8):2341–2346 PMID: 31119272
 344 — References

29. Fisher BT, et al. JAMA. 2019;322(17):1673–1681 PMID: 31688884

30. Dvorak CC, et al. J Pediatric Infect Dis Soc. 2021;10(4):417–425 PMID: 33136159
31. Niu CH, et al. Front Pharmacol. 2020;11:184 PMID: 32194415
32. Du B, et al. J Antimicrob Chemother. 2024;79(10):2678–2687 PMID: 39119901
33. Smith PB, et al. Pediatr Infect Dis J. 2009;28(5):412–415 PMID: 19319022
34. Hope WW, et al. Antimicrob Agents Chemother. 2010;54(6):2633–2637 PMID: 20308367
35. Benjamin DK Jr, et al. Clin Pharmacol Ther. 2010;87(1):93–99 PMID: 19890251
36. Auriti C, et al. Antimicrob Agents Chemother. 2021;65(4):e02494-20 PMID: 33558294
37. Bury D, et al. Int J Antimicrob Agents. 2024;63(1):107058 PMID: 38081549
38. Kim BK, et al. Children (Basel). 2022;9(3):372 PMID: 35327744
39. Cohen-Wolkowiez M, et al. Clin Pharmacol Ther. 2011;89(5):702–707 PMID: 21412233
40. Roilides E, et al. Pediatr Infect Dis J. 2019;38(3):275–279 PMID: 30418357
41. Roilides E, et al. Pediatr Infect Dis J. 2020;39(4):305–309 PMID: 32032174
42. Thompson GR, et al. Lancet. 2023;401(10370):49–59 PMID: 36442484
43. Spec A, et al. J Antimicrob Chemother. 2019;74(10):3056–3062 PMID: 31304536

Chapter 7
1. Lenaerts L, et al. Rev Med Virol. 2008;18(6):357–374 PMID: 18655013
2. Michaels MG. Expert Rev Anti Infect Ther. 2007;5(3):441–448 PMID: 17547508
3. Biron KK. Antiviral Res. 2006;71(2–3):154–163 PMID: 16765457
4. Boeckh M, et al. Blood. 2009;113(23):5711–5719 PMID: 19299333
5. Vaudry W, et al. Am J Transplant. 2009;9(3):636–643 PMID: 19260840
6. Emanuel D, et al. Ann Intern Med. 1988;109(10):777–782 PMID: 2847609
7. Reed EC, et al. Ann Intern Med. 1988;109(10):783–788 PMID: 2847610
8. Studies of Ocular Complications of AIDS Research Group in collaboration with the AIDS Clinical
Trials Group. Ophthalmology. 1994;101(7):1250–1261 PMID: 8035989
9. Singh N, et al. JAMA. 2020;323(14):1378–1387 PMID: 32286644
10. Martin DF, et al. N Engl J Med. 2002;346(15):1119–1126 PMID: 11948271
11. Kempen JH, et al. Arch Ophthalmol. 2003;121(4):466–476 PMID: 12695243
12. Studies of Ocular Complications of AIDS Research Group. The AIDS Clinical Trials Group. Am J
Ophthalmol. 2001;131(4):457–467 PMID: 11292409
13. Dieterich DT, et al. J Infect Dis. 1993;167(2):278–282 PMID: 8380610
14. Gerna G, et al. Antiviral Res. 1997;34(1):39–50 PMID: 9107384
15. Markham A, et al. Drugs. 1994;48(3):455–484 PMID: 7527763
16. Kimberlin DW, et al. J Infect Dis. 2008;197(6):836–845 PMID: 18279073
17. Kimberlin DW, et al. N Engl J Med. 2015;372(10):933–943 PMID: 25738669
18. Griffiths P, et al. Herpes. 2008;15(1):4–12 PMID: 18983762
19. Panel on Opportunistic Infections in Children With and Exposed to HIV. Guidelines for the prevention
and treatment of opportunistic infections in children with and exposed to HIV. What’s new in the
guidelines? Updated July 3, 2024. Accessed October 29, 2024. https://clinicalinfo.hiv.gov/en/guidelines/
hiv-clinical-guidelines-pediatric-opportunistic-infections/whats-new
20. Marty FM, et al. N Engl J Med. 2017;377(25):2433–2444 PMID: 29211658
21. Abzug MJ, et al. J Pediatric Infect Dis Soc. 2016;5(1):53–62 PMID: 26407253
22. Biebl A, et al. Nat Clin Pract Neurol. 2009;5(3):171–174 PMID: 19262593
23. Chadaide Z, et al. J Med Virol. 2008;80(11):1930–1932 PMID: 18814244
References

24. AAP. Epstein-Barr virus infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:372–376
25. Gross TG. Herpes. 2009;15(3):64–67 PMID: 19306606
26. Styczynski J, et al. Bone Marrow Transplant. 2009;43(10):757–770 PMID: 19043458
27. Jonas MM, et al. Hepatology. 2016;63(2):377–387 PMID: 26223345
28. Marcellin P, et al. Gastroenterology. 2016;150(1):134–144.e10 PMID: 26453773
29. Chen HL, et al. Hepatology. 2015;62(2):375–386 PMID: 25851052
30. Wu Q, et al. Clin Gastroenterol Hepatol. 2015;13(6):1170–1176 PMID: 25251571
 References — 345

31. Hou JL, et al. J Viral Hepat. 2015;22(2):85–93 PMID: 25243325

32. Kurbegov AC, et al. Expert Rev Gastroenterol Hepatol. 2009;3(1):39–49 PMID: 19210112
33. Jonas MM, et al. Hepatology. 2008;47(6):1863–1871 PMID: 18433023
34. Lai CL, et al. Gastroenterology. 2002;123(6):1831–1838 PMID: 12454840
35. Honkoop P, et al. Expert Opin Investig Drugs. 2003;12(4):683–688 PMID: 12665423
36. Shaw T, et al. Expert Rev Anti Infect Ther. 2004;2(6):853–871 PMID: 15566330
37. Elisofon SA, et al. Clin Liver Dis. 2006;10(1):133–148 PMID: 16376798
38. Jonas MM, et al. Hepatology. 2010;52(6):2192–2205 PMID: 20890947
39. Haber BA, et al. Pediatrics. 2009;124(5):e1007–e1013 PMID: 19805457
40. Shneider BL, et al. Hepatology. 2006;44(5):1344–1354 PMID: 17058223
41. Jain MK, et al. J Viral Hepat. 2007;14(3):176–182 PMID: 17305883
42. Sokal EM, et al. Gastroenterology. 1998;114(5):988–995 PMID: 9558288
43. Jonas MM, et al. N Engl J Med. 2002;346(22):1706–1713 PMID: 12037150
44. Chang TT, et al. N Engl J Med. 2006;354(10):1001–1010 PMID: 16525137
45. Liaw YF, et al. Gastroenterology. 2009;136(2):486–495 PMID: 19027013
46. Terrault NA, et al. Hepatology. 2018;67(4):1560–1599 PMID: 29405329
47. Keam SJ, et al. Drugs. 2008;68(9):1273–1317 PMID: 18547135
48. Marcellin P, et al. Gastroenterology. 2011;140(2):459–468 PMID: 21034744
49. Poordad F, et al. N Engl J Med. 2011;364(13):1195–1206 PMID: 21449783
50. Schwarz KB, et al. Gastroenterology. 2011;140(2):450–458 PMID: 21036173
51. Nelson DR. Liver Int. 2011;31(suppl 1):53–57 PMID: 21205138
52. Strader DB, et al. Hepatology. 2004;39(4):1147–1171 PMID: 15057920
53. Soriano V, et al. AIDS. 2007;21(9):1073–1089 PMID: 17502718
54. Murray KF, et al. Hepatology. 2018;68(6):2158–2166 PMID: 30070726
55. Feld JJ, et al. N Engl J Med. 2014;370(17):1594–1603 PMID: 24720703
56. Zeuzem S, et al. N Engl J Med. 2014;370(17):1604–1614 PMID: 24720679
57. Andreone P, et al. Gastroenterology. 2014;147(2):359–365.e1 PMID: 24818763
58. Ferenci P, et al. N Engl J Med. 2014;370(21):1983–1992 PMID: 24795200
59. Poordad F, et al. N Engl J Med. 2014;370(21):1973–1982 PMID: 24725237
60. Jacobson IM, et al. Lancet. 2014;384(9941):403–413 PMID: 24907225
61. Manns M, et al. Lancet. 2014;384(9941):414–426 PMID: 24907224
62. Forns X, et al. Gastroenterology. 2014;146(7):1669–1679.e3 PMID: 24602923
63. Zeuzem S, et al. Gastroenterology. 2014;146(2):430–441.e6 PMID: 24184810
64. Lawitz E, et al. Lancet. 2014;384(9956):1756–1765 PMID: 25078309
65. Afdhal N, et al. N Engl J Med. 2014;370(20):1889–1898 PMID: 24725239
66. Afdhal N, et al. N Engl J Med. 2014;370(16):1483–1493 PMID: 24725238
67. Kowdley KV, et al. N Engl J Med. 2014;370(20):1879–1888 PMID: 24720702
68. Lawitz E, et al. N Engl J Med. 2013;368(20):1878–1887 PMID: 23607594
69. Jacobson IM, et al. N Engl J Med. 2013;368(20):1867–1877 PMID: 23607593
70. Zeuzem S, et al. N Engl J Med. 2014;370(21):1993–2001 PMID: 24795201
71. American Association for the Study of Liver Diseases, Infectious Diseases Society of America. HCV
in children. Updated October 24, 2022. Accessed October 29, 2024. www.hcvguidelines.org/unique-
populations/children
72. Hollier LM, et al. Cochrane Database Syst Rev. 2008;(1):CD004946 PMID: 18254066
73. Pinninti SG, et al. J Pediatr. 2012;161(1):134–138 PMID: 22336576
References

74. ACOG. Obstet Gynecol. 2020;135(5):e193–e202 PMID: 32332414

75. Kimberlin DW, et al. Clin Infect Dis. 2010;50(2):221–228 PMID: 20014952
76. Mofenson LM, et al. MMWR Recomm Rep. 2009;58(RR-11):1–166 PMID: 19730409
77. Kuhar DT, et al. Infect Control Hosp Epidemiol. 2013;34(9):875–892 PMID: 23917901
78. Abdel Massih RC, et al. World J Gastroenterol. 2009;15(21):2561–2569 PMID: 19496184
79. Acosta EP, et al. J Infect Dis. 2010;202(4):563–566 PMID: 20594104
80. Kimberlin DW, et al. J Infect Dis. 2013;207(5):709–720 PMID: 23230059
81. McPherson C, et al. J Infect Dis. 2012;206(6):847–850 PMID: 22807525
 346 — References

82. Bradley JS, et al. Pediatrics. 2017;140(5):e20162727 PMID: 29051331

83. AAP. Measles. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:570–585
84. AAP Committee on Infectious Diseases and Bronchiolitis Guidelines Committee. Pediatrics.
2014;134(2):415–420 PMID: 25070315
85. AAP Committee on Infectious Diseases and Bronchiolitis Guidelines Committee. Pediatrics.
2014;134(2):e620–e638 PMID: 25070304
86. Whitley RJ. Adv Exp Med Biol. 2008;609:216–232 PMID: 18193668

Chapter 9
1. Gonzales MLM, et al. Cochrane Database Syst Rev. 2019;(1):CD006085 PMID: 30624763
2. Haque R, et al. N Engl J Med. 2003;348(16):1565–1573 PMID: 1270037
3. Rossignol JF, et al. Trans R Soc Trop Med Hyg. 2007;101(10):1025–1031 PMID: 17658567
4. Mackey-Lawrence NM, et al. BMJ Clin Evid. 2011;2011:0918 PMID: 21477391
5. Fox LM, et al. Clin Infect Dis. 2005;40(8):1173–1180 PMID: 15791519
6. Cope JR, et al. Clin Infect Dis. 2016;62(6):774–776 PMID: 26679626
7. Vargas-Zepeda J, et al. Arch Med Res. 2005;36(1):83–86 PMID: 15900627
8. Linam WM, et al. Pediatrics. 2015;135(3):e744–e748 PMID: 25667249
9. Visvesvara GS, et al. FEMS Immunol Med Microbiol. 2007;50(1):1–26 PMID: 17428307
10. Martínez DY, et al. Clin Infect Dis. 2010;51(2):e7–e11 PMID: 20550438
11. Chotmongkol V, et al. Am J Trop Med Hyg. 2009;81(3):443–445 PMID: 19706911
12. Lo Re V III, et al. Am J Med. 2003;114(3):217–223 PMID: 12637136
13. Jitpimolmard S, et al. Parasitol Res. 2007;100(6):1293–1296 PMID: 17177056
14. Checkley AM, et al. J Infect. 2010;60(1):1–20 PMID: 19931558
15. Bethony J, et al. Lancet. 2006;367(9521):1521–1532 PMID: 16679166
16. Krause PJ, et al. N Engl J Med. 2000;343(20):1454–1458 PMID: 11078770
17. Vannier E, et al. Infect Dis Clin North Am. 2008;22(3):469–488 PMID: 18755385
18. Krause PJ, et al. Clin Infect Dis. 2021;72(2):185–189 PMID: 33501959
19. Sanchez E, et al. JAMA. 2016;315(16):1767–1777 PMID: 27115378
20. Kletsova EA, et al. Ann Clin Microbiol Antimicrob. 2017;16(1):26 PMID: 28399851
21. Schuster FL, et al. Clin Microbiol Rev. 2008;21(4):626–638 PMID: 18854484
22. Murray WJ, et al. Clin Infect Dis. 2004;39(10):1484–1492 PMID: 15546085
23. Sircar AD, et al. MMWR Morb Mortal Wkly Rep. 2016;65(35):930–933 PMID: 27608169
24. Malik K, et al. Albendazole. In: StatPearls. StatPearls Publishing; 2024 PMID: 31971723
25. Rossignol JF, et al. Clin Gastroenterol Hepatol. 2005;3(10):987–991 PMID: 16234044
26. Nigro L, et al. J Travel Med. 2003;10(2):128–130 PMID: 12650658
27. Bern C, et al. JAMA. 2007;298(18):2171–2181 PMID: 18000201
28. Salvador F, et al. Clin Infect Dis. 2015;61(11):1688–1694 PMID: 26265500
29. Miller DA, et al. Clin Infect Dis. 2015;60(8):1237–1240 PMID: 25601454
30. Smith HV, et al. Curr Opin Infect Dis. 2004;17(6):557–564 PMID: 15640710
31. Davies AP, et al. BMJ. 2009;339:b4168 PMID: 19841008
32. Krause I, et al. Pediatr Infect Dis J. 2012;31(11):1135–1138 PMID: 22810017
33. Abubakar I, et al. Cochrane Database Syst Rev. 2007;(1):CD004932 PMID: 17253532
34. Jelinek T, et al. Clin Infect Dis. 1994;19(6):1062–1066 PMID: 7534125
35. Schuster A, et al. Clin Infect Dis. 2013;57(8):1155–1157 PMID: 23811416
References

36. Hoge CW, et al. Lancet. 1995;345(8951):691–693 PMID: 7885125

37. Ortega YR, et al. Clin Microbiol Rev. 2010;23(1):218–234 PMID: 20065331
38. Steffen R, et al. J Travel Med. 2018;25(1):tay116 PMID: 30462260
39. Nash TE, et al. Neurology. 2006;67(7):1120–1127 PMID: 17030744
40. Garcia HH, et al. Lancet Neurol. 2014;13(12):1202–1215 PMID: 25453460
41. Lillie P, et al. J Infect. 2010;60(5):403–404 PMID: 20153773
42. White AC Jr, et al. Clin Infect Dis. 2018;66(8):1159–1163 PMID: 29617787
43. Verdier RI, et al. Ann Intern Med. 2000;132(11):885–888 PMID: 10836915
 References — 347

44. Stark DJ, et al. Trends Parasitol. 2006;22(2):92–96 PMID: 16380293

45. Röser D, et al. Clin Infect Dis. 2014;58(12):1692–1699 PMID: 24647023
46. Smego RA Jr, et al. Clin Infect Dis. 2003;37(8):1073–1083 PMID: 14523772
47. Brunetti E, et al. Acta Trop. 2010;114(1):1–16 PMID: 19931502
48. Fernando SD, et al. J Trop Med. 2011;2011:175941 PMID: 21234244
49. Walker M, et al. Clin Infect Dis. 2015;60(8):1199–2017 PMID: 25537873
50. Debrah AY, et al. Clin Infect Dis. 2015;61(4):517–526 PMID: 25948064
51. Mand S, et al. Clin Infect Dis. 2012;55(5):621–630 PMID: 22610930
52. Ottesen EA, et al. Annu Rev Med. 1992;43:417–424 PMID: 1580599
53. Jong EC, et al. J Infect Dis. 1985;152(3):637–640 PMID: 3897401
54. Sayasone S, et al. Clin Infect Dis. 2017;64(4):451–458 PMID: 28174906
55. Calvopina M, et al. Trans R Soc Trop Med Hyg. 1998;92(5):566–569 PMID: 9861383
56. Johnson RJ, et al. Rev Infect Dis. 1985;7(2):200–206 PMID: 4001715
57. Graham CS, et al. Clin Infect Dis. 2001;33(1):1–5 PMID: 11389487
58. Granados CE, et al. Cochrane Database Syst Rev. 2012;(12):CD007787 PMID: 23235648
59. Ross AG, et al. N Engl J Med. 2013;368(19):1817–1825 PMID: 23656647
60. Requena-Mendez A, et al. J Infect Dis. 2017;215(6):946–953 PMID: 28453841
61. Hotez PJ, et al. N Engl J Med. 2004;351(8):799–807 PMID: 15317893
62. Keiser J, et al. JAMA. 2008;299(16):1937–1948 PMID: 18430913
63. Steinmann P, et al. PLoS One. 2011;6(9):e25003 PMID: 21980373
64. Aronson N, et al. Clin Infect Dis. 2016;63(12):e202–e264 PMID: 27941151
65. Control of the leishmaniases: report of a meeting of the WHO Expert Committee on the Control of
Leishmaniases, Geneva, 22–26 March 2010. 2010. Accessed October 29, 2024. https://apps.who.int/iris/
handle/10665/44412
66. Alrajhi AA, et al. N Engl J Med. 2002;346(12):891–895 PMID: 11907288
67. Bern C, et al. Clin Infect Dis. 2006;43(7):917–924 PMID: 16941377
68. Ritmeijer K, et al. Clin Infect Dis. 2006;43(3):357–364 PMID: 16804852
69. Monge-Maillo B, et al. Clin Infect Dis. 2015;60(9):1398–1404 PMID: 25601455
70. Sundar S, et al. N Engl J Med. 2002;347(22):1739–1746 PMID: 12456849
71. Sundar S, et al. N Engl J Med. 2007;356(25):2571–2581 PMID: 17582067
72. Pinart M, et al. Cochrane Database Syst Rev. 2020;(8):CD004834 PMID: 32853410
73. Drugs for head lice. JAMA. 2017;317(19):2010–2011 PMID: 28510677
74. Nolt D, et al. Pediatrics. 2022;150(4):e2022059282 PMID: 36156158
75. Ashley EA, et al. Lancet Child Adolesc Health. 2020;4(10):775–789 PMID: 32946831
76. CDC Yellow Book: Health Information for International Travel. 2024. Reviewed August 14, 2023.
Accessed November 18, 2024. https://wwwnc.cdc.gov/travel/page/yellowbook-home
77. Haghiri A, et al. Clin Pharmacol Ther. 2023;114(6):1304–1312 PMID: 37666798
78. Usha V, et al. J Am Acad Dermatol. 2000;42(2, pt 1):236–240 PMID: 10642678
79. Brodine SK, et al. Am J Trop Med Hyg. 2009;80(3):425–430 PMID: 19270293
80. Doenhoff MJ, et al. Expert Rev Anti Infect Ther. 2006;4(2):199–210 PMID: 16597202
81. Fenwick A, et al. Curr Opin Infect Dis. 2006;19(6):577–582 PMID: 17075334
82. Marti H, et al. Am J Trop Med Hyg. 1996;55(5):477–481 PMID: 8940976
83. Segarra-Newnham M. Ann Pharmacother. 2007;41(12):1992–2001 PMID: 17940124
84. Barisani-Asenbauer T, et al. J Ocul Pharmacol Ther. 2001;17(3):287–294 PMID: 11436948
85. McAuley JB. Pediatr Infect Dis J. 2008;27(2):161–162 PMID: 18227714
References

86. Maldonado YA, et al. Pediatrics. 2017;139(2):e20163860 PMID: 28138010

87. de-la-Torre A, et al. Ocul Immunol Inflamm. 2011;19(5):314–320 PMID: 21970662
88. Shane AL, et al. Clin Infect Dis. 2017;65(12):e45–e80 PMID: 29053792
89. DuPont HL. Clin Infect Dis. 2007;45(suppl 1):S78–S84 PMID: 17582576
90. Riddle MS, et al. J Travel Med. 2017;24(suppl 1):S57–S74 PMID: 28521004
91. Gottstein B, et al. Clin Microbiol Rev. 2009;22(1):127–145 PMID: 19136437
92. Workowski KA, et al. MMWR Recomm Rep. 2015;64(RR-03):1–137 PMID: 26042815
93. Fairlamb AH. Trends Parasitol. 2003;19(11):488–494 PMID: 14580959
 348 — References

94. Schmid C, et al. Lancet. 2004;364(9436):789–790 PMID: 15337407

95. Bisser S, et al. J Infect Dis. 2007;195(3):322–329 PMID: 17205469
96. Priotto G, et al. Lancet. 2009;374(9683):56–64 PMID: 19559476
97. Buscher P, et al. Lancet. 2017;390(10110):2397–2409 PMID: 28673422
98. Control and surveillance of human African trypanosomiasis: report of a WHO expert committee.
2013. Accessed October 29, 2024. https://apps.who.int/iris/handle/10665/95732

Chapter 10
1. Mergenhagen KA, et al. Antimicrob Agents Chemother. 2020;64(3):e02167-19 PMID: 31871085

Chapter 12
1. Wu W, et al. Clin Microbiol Rev. 2019;32(2):e00115-18 PMID: 30700432
2. Hultén KG, et al. Pediatr Infect Dis J. 2018;37(3):235–241 PMID: 28859018
3. Acree ME, et al. Infect Control Hosp Epidemiol. 2017;38(10):1226–1234 PMID: 28903801
4. Liu C, et al. Clin Infect Dis. 2011;52(3):e18–e55 PMID: 21208910
5. Korczowski B, et al. Pediatr Infect Dis J. 2016;35(8):e239–e247 PMID: 27164462
6. Cannavino CR, et al. Pediatr Infect Dis J. 2016;35(7):752–759 PMID: 27093162
7. Blumer JL, et al. Pediatr Infect Dis J. 2016;35(7):760–766 PMID: 27078119
8. Bradley JS. Pediatr Infect Dis J. 2020;39(5):411–418 PMID: 32091493
9. Rybak MJ. Am J Health Syst Pharm. 2020;77(11):835–864 PMID: 32191793
10. Le J, et al. Pediatr Infect Dis J. 2013;32(4):e155–e163 PMID: 23340565
11. McNeil JC, et al. Pediatr Infect Dis J. 2016;35(3):263–268 PMID: 26646549
12. Sader HS, et al. Antimicrob Agents Chemother. 2017;61(9):e01043-17 PMID: 28630196
13. Depardieu F, et al. Clin Microbiol Rev. 2007;20(1):79–114 PMID: 17223624
14. Miller LG, et al. N Engl J Med. 2015;372(12):1093–1103 PMID: 25785967
15. Bradley J, et al. Pediatrics. 2017;139(3):e20162477 PMID: 28202770
16. Arrieta AC, et al. Pediatr Infect Dis J. 2018;37(9):890–900 PMID: 29406465
17. Bradley JS, et al. Pediatr Infect Dis J. 2020;39(9):814–823 PMID: 32639465
18. Huang JT, et al. Pediatrics. 2009;123(5):e808–e814 PMID: 19403473
19. Finnell SM, et al. Clin Pediatr (Phila). 2015;54(5):445–450 PMID: 25385929
20. Kaplan SL, et al. Clin Infect Dis. 2014;58(5):679–682 PMID: 24265356
21. McNeil JC, et al. Curr Infect Dis Rep. 2019;21(4):12 PMID: 30859379

Chapter 14
1. Nelson JD. J Pediatr. 1978;92(1):175–176 PMID: 619073
2. Nelson JD, et al. J Pediatr. 1978;92(1):131–134 PMID: 619055
3. Tetzlaff TR, et al. J Pediatr. 1978;92(3):485–490 PMID: 632997
4. Ballock RT, et al. J Pediatr Orthop. 2009;29(6):636–642 PMID: 19700997
5. Peltola H, et al. N Engl J Med. 2014;370(4):352–360 PMID: 24450893
6. Bradley JS, et al. Pediatrics. 2011;128(4):e1034–e1045 PMID: 21949152
7. Rice HE, et al. Arch Surg. 2001;136(12):1391–1395 PMID: 11735866
8. Fraser JD, et al. J Pediatr Surg. 2010;45(6):1198–1202 PMID: 20620320
9. Strohmeier Y, et al. Cochrane Database Syst Rev. 2014;(7):CD003772 PMID: 25066627
10. Tingsgård S, et al. JAMA Netw Open. 2024;7(1):e2352314 PMID: 38261322
11. Omrani AS, et al. Clin Microbiol Infect. 2024;30(4):492–498 PMID: 37858867
References

12. Drusano GL, et al. J Infect Dis. 2014;210(8):1319–1324 PMID: 24760199

13. Arnold JC, et al. Pediatrics. 2012;130(4):e821–e828 PMID: 22966033
14. Zaoutis T, et al. Pediatrics. 2009;123(2):636–642 PMID: 19171632
15. Keren R, et al. JAMA Pediatr. 2015;169(2):120–128 PMID: 25506733
16. Gunter SG, et al. Pharmacy (Basel). 2022;10(1):16 PMID: 35076616
17. Desai AA, et al. J Pediatr Surg. 2015;50(6):912–914 PMID: 25812441
18. Marino NE, et al. Surg Infect (Larchmt). 2017;18(8):894–903 PMID: 29064344
19. Haynes AS, et al. Antimicrob Agents Chemother. 2024;68(5):e0018224 PMID: 38597672
 References — 349

20. Liu C, et al. Clin Infect Dis. 2011;52(3):e18–e55 PMID: 21208910

21. Syrogiannopoulos GA, et al. Lancet. 1988;1(8575–8576):37–40 PMID: 2891899

Chapter 15
1. Oehler RL, et al. Lancet Infect Dis. 2009;9(7):439–447 PMID: 19555903
2. Bula-Rudas FJ, et al. Pediatr Rev. 2018;39(10):490–500 PMID: 30275032
3. Elcock KL, et al. Injury. 2022;53(2):227–236 PMID: 34838260
4. Talan DA, et al. Clin Infect Dis. 2003;37(11):1481–1489 PMID: 14614671
5. Aziz H, et al. J Trauma Acute Care Surg. 2015;78(3):641–648 PMID: 25710440
6. CDC. Clinical overview of rabies. June 20, 2024. Accessed November 18, 2024. www.cdc.gov/rabies/
hcp/clinical-overview
7. AAP. Tetanus. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:848–854
8. Wilson WR, et al. Circulation. 2021;143(20):e963–e978 PMID: 33853363
9. Baltimore RS, et al. Circulation. 2015;132(15):1487–1515 PMID: 26373317
10. Williams ML, et al. Ther Adv Cardiovasc Dis. 2021;15:17539447211002687 PMID: 33784909
11. Gupta S, et al. Congenit Heart Dis. 2017;12(2):196–201 PMID: 27885814
12. Cahill TJ, et al. Heart. 2017;103(12):937–944 PMID: 28213367
13. Dayer M, et al. J Infect Chemother. 2018;24(1):18–24 PMID: 29107651
14. AAP. Lyme disease. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:549–556
15. McNamara LA, et al. Meningococcal disease. In: Manual for the Surveillance of Vaccine-Preventable
Diseases. 2019. October 30, 2024. Accessed November 18, 2024. www.cdc.gov/surv-manual/php/table-
of-contents/chapter-8-meningococcal-disease.html
16. McNamara LA, et al. Lancet Infect Dis. 2018;18(9):e272–e281 PMID: 29858150
17. AAP. Pertussis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:656–667
18. CDC. Whooping cough (pertussis). Postexposure antimicrobial prophylaxis. April 2, 2024. Accessed
October 29, 2024. www.cdc.gov/pertussis/php/postexposure-prophylaxis
19. CDC. Clinical overview of tetanus. August 15, 2024. Accessed October 29, 2024. www.cdc.gov/tetanus/
hcp/clinical-overview
20. CDC. Tuberculosis (TB). Treatment regimens for latent TB infection. Reviewed February 13, 2020.
Accessed October 29, 2024. www.cdc.gov/tb/topic/treatment/ltbi.htm
21. AAP. Tuberculosis. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:888–920
22. Sterling TR, et al. MMWR Recomm Rep. 2020;69(1):1–11 PMID: 32053584
23. ACOG. Obstet Gynecol. 2020;135(5):e193–e202 PMID: 32332414
24. Pinninti SG, et al. Semin Perinatol. 2018;42(3):168–175 PMID: 29544668
25. AAP. Herpes simplex. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on
Infectious Diseases. 33rd ed. 2024:467–478
26. AAP Committee on Infectious Diseases. Pediatrics. 2020;146(4):e2020024588 PMID: 32900875
27. Kimberlin DW, et al. J Infect Dis. 2013;207(5):709–720 PMID: 23230059
28. AAP. Rabies. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the Committee on Infectious
Diseases. 33rd ed. 2024:702–711
29. AAP. Varicella-zoster virus infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
References

Committee on Infectious Diseases. 33rd ed. 2024:938–951

30. Leach AJ, et al. Cochrane Database Syst Rev. 2006;(4):CD004401 PMID: 17054203
31. Lieberthal AS, et al. Pediatrics. 2013;131(3):e964–e999 PMID: 23439909
32. Williams G, et al. Cochrane Database Syst Rev. 2023;(4):CD001321 PMID: 37068952
33. Marsh MC, et al. Pediatr Rev. 2024;45(5):260–270 PMID: 38689106
34. RIVUR Trial Investigators, et al. N Engl J Med. 2014;370(25):2367–2376 PMID: 24795142
35. AAP Subcommittee on Urinary Tract Infection and Steering Committee on Quality Improvement and
Management. Pediatrics. 2011;128(3):595–610 PMID: 21873693
 350 — References

36. Craig JC. J Pediatr. 2015;166(3):778 PMID: 25722276

37. National Institute for Health and Care Excellence. Urinary tract infection (recurrent): antimicrobial
prescribing; treatment for children and young people under 16 years with recurrent UTI.
October 31, 2018. Accessed October 29, 2024. www.nice.org.uk/guidance/ng112/chapter/
Recommendations#treatment-for-children-and-young-people-under-16-years-with-recurrent-uti
38. Williams G, et al. Cochrane Database Syst Rev. 2019;(4):CD001534 PMID: 30932167
39. AAP. Pneumocystis jirovecii infections. In: Kimberlin DW, et al, eds. Red Book: 2024–2027 Report of the
Committee on Infectious Diseases. 33rd ed. 2024:676–682
40. Caselli D, et al. J Pediatr. 2014;164(2):389–392.e1 PMID: 24252793
41. Proudfoot R, et al. J Pediatr Hematol Oncol. 2017;39(3):194–202 PMID: 28267082
42. Stern A, et al. Cochrane Database Syst Rev. 2014;(10):CD005590 PMID: 25269391
43. Delaplain PT, et al. Surg Infect (Larchmt). 2022;23(3):232–247 PMID: 35196154
44. UpToDate. Antimicrobial prophylaxis for prevention of surgical site infection in adults. Updated
October 18, 2022. Accessed October 29, 2024. www.uptodate.com/contents/antimicrobial-prophylaxis-
for-prevention-of-surgical-site-infection-in-adults#H852308389
45. Paruk F, et al. Int J Antimicrob Agents. 2017;49(4):395–402 PMID: 28254373
46. Branch-Elliman W, et al. JAMA Surg. 2019;154(7):590–598 PMID: 31017647
47. Berríos-Torres SI, et al. JAMA Surg. 2017;152(8):784–791 PMID: 28467526
48. Calderwood MS, et al. Infect Control Hosp Epidemiol. 2023;44(5):695–720 PMID: 37137483
49. PREP-IT Investigators, et al. N Engl J Med. 2024;390(5):409–420 PMID: 38294973
50. Darouiche RO, et al. N Engl J Med. 2010;362(1):18–26 PMID: 20054046
51. de Tymowski C, et al. Antibiotics (Basel). 2023;12(1):85 PMID: 36671286
52. De Cock PA, et al. J Antimicrob Chemother. 2017;72(3):791–800 PMID: 27999040
53. Marino NE, et al. Surg Infect (Larchmt). 2017;18(8):894–903 PMID: 29064344
54. Andersen BR, et al. Cochrane Database Syst Rev. 2005;(3):CD001439 PMID: 16034862

Chapter 16
1. Broyles AD, et al. J Allergy Clin Immunol Pract. 2020;8(9)(suppl):S16–S116 PMID: 33039007
2. Bergmann MM, et al. Pediatr Allergy Immunol. 2023;34(12):e14058 PMID: 38146108
3. Delli Colli L, et al. J Allergy Clin Immunol Pract. 2021;9(2):916–921 PMID: 32898711
4. Copaescu AM, et al. JAMA Netw Open. 2022;5(9):e2233703 PMID: 36121658
5. Khan DA, et al. J Allergy Clin Immunol. 2022;150(6):1333–1393 PMID: 36122788
6. Ponvert C, et al. Allergy. 2007;62(1):42–46 PMID: 17156340

Chapter 17
1. Merriam-Webster. Stewardship. Accessed October 29, 2024. www.merriam-webster.com/dictionary/
stewardship
2. CDC. Infection control. Guidelines and guidance library. April 8, 2024. Accessed November 18, 2024.
www.cdc.gov/infection-control/hcp/guidance/index.html
3. Farnaes L, et al. Diagn Microbiol Infect Dis. 2019;94(2):188–191 PMID: 30819624
References
 Index — 351

Index

A
Abdominal actinomycosis, 114 Actinomycosis, 66
Abelcet, 172, 291 Actinomyces israelii, 114
ABLC. See Amphotericin B lipid complex Acute conjunctivitis, 14
(ABLC) Acute cystitis, 64
Abscesses Acute mastoiditis, 17
Bacteroides fragilis, 115 Acute osteomyelitis, 11
Bacteroides spp, 116 Acute otitis media (AOM), 19–20
brain, 58–59 alternative antibiotic options for, 281
Aggregatibacter Acute SARS-CoV-2 infection. See
actinomycetemcomitans, 115 Coronavirus (SARS-CoV-2)
Aggregatibacter aphrophilus, 115 Acute sinusitis, 20
Nocardia asteroides, brasiliensis, 130 Acyclovir, 182, 201
Streptococcus milleri/anginosus for children with obesity, 248
group, 137 dosage form/usual dosage, 290, 315
Capnocytophaga ochracea, 117 neonates, 100
Chromobacterium violaceum, 118 susceptibility of non-HIV, non–hepatitis
dental, 21 B or C viral pathogens to,
Prevotella spp, melaninogenica, 131 182
Eikenella corrodens, 121 Aczone, 317
Enterococcus spp, 122 Adenitis
epidural, 137 acute bacterial, 3
Erysipelothrix rhusiopathiae, 122 group A streptococcus, 137
liver, 209 mycobacteria, nontuberculous, 71
lung, 24 Mycobacterium avium complex, 128
Mycobacterium chelonae, 128 Mycobacterium tuberculosis, 129
Mycobacterium marinum, balnei, 129 nontuberculous mycobacterial, 4
Nocardia asteroides, brasiliensis, 130 tuberculous, 4
Pasteurella multocida, 130 Yersinia pseudotuberculosis, 139
perirectal, 53 Adenovirus, 184
peritonsillar, 22 Aemcolo, 310
pyoderma, cutaneous, 8 Aerobes
retropharyngeal; parapharyngeal; lateral abscess, lung, 24
pharyngeal, 23 aspiration pneumonia, 24
Acanthamoeba, 59, 208, 210 dental abscess, 21
Acanya, 316 Ludwig angina, 7
Accountability, antibiotic stewardship, 286– necrotizing fasciitis, 8
288 retropharyngeal; parapharyngeal; lateral
Acinetobacter baumannii, 114 pharyngeal cellulitis or
Acinetobacter spp, susceptibility to abscess, 23
antibiotics, 110–111 Aeromonas hydrophila, 48, 114
Acne Aeromonas spp, necrotizing fasciitis, 8
Index

Cutibacterium acnes, 121 Aggregatibacter actinomycetemcomitans, 115

Propionbacterium acnes, 131 Aggregatibacter aphrophilus, 115
Actinomyces israelii, 114 Akne-Mycin, 317
 352 — Index

Albendazole, 206–207, 232 neonates, 100

dosage form/usual dosage, 290 susceptibility of fungal pathogens to,
Albenza, 290 150–151
Aldara, 317 Amphotericin B deoxycholate (AmB-D),
Alinia, 305 171–173
Allergic bronchopulmonary aspergillosis, 24 neonates, 100
Allergies, antibiotic. See Antibiotic allergies Amphotericin B lipid complex (ABLC)
Altabax, 320 dosage form/usual dosage, 291
AmB-D. See Amphotericin B deoxycholate neonates, 100
(AmB-D) Amphotericin B liposomal (AmBisome)
AmBisome. See Amphotericin B liposomal dosage form/usual dosage, 291
(AmBisome) neonates, 100
Amebiasis, 208–209 Ampicillin
Amebic encephalitis, 59 alternative antibiotic options for allergies
Amebic meningoencephalitis, 209–210 to, 281
Amikacin endocarditis, 41
dosage form/usual dosage, 290 neonates, 100
neonates, 104 susceptibility of anaerobes to, 112
Amikin, 290 susceptibility of gram-negative bacterial
Aminoglycosides, 146–147 pathogens to, 110
for children with obesity, 247 susceptibility of gram-positive bacterial
neonates, 104 pathogens to, 108
Aminopenicillins, 144–145 Ampicillin sodium, 291
allergies to, 279 Ampicillin/sulbactam, 291
for children with obesity, 247 Ampicillin trihydrate, 291
Amoebas, 232 Amzeeq, 319
Amoxicillin Anaerobes
alternative antibiotic options for allergies abscess, lung, 24
to, 281 aspiration pneumonia, 24
dosage form/usual dosage, 290 bites
neonates, 100 dog and cat, 5
susceptibility of anaerobes to, 112 human, 5
susceptibility of gram-negative bacterial dental abscess, 21
pathogens to, 110 head and neck surgery prophylaxis, 269
susceptibility of gram-positive bacterial Ludwig angina, 7
pathogens to, 108 mastoiditis, chronic, 18
Amoxicillin/clavulanate necrotizing fasciitis, 8
dosage form/usual dosage, 291 omphalitis and funisitis, 87
neonates, 100 pelvic inflammatory disease, 56
susceptibility of anaerobes to, 112 perirectal abscess, 53
susceptibility of gram-negative bacterial peritonsillar cellulitis and abscess, 22
pathogens to, 110 postexposure antimicrobial prophylaxis,
susceptibility of gram-positive bacterial 255
pathogens to, 108 surgical/procedure prophylaxis, 268
Amoxil, 290 susceptibility to antibiotics, 112–113
Index

Amphotec, 172 Anaerobic streptococci, 112

Amphotericin B, 171–173 Anaplasma phagocytophilum, 66, 115
for children with obesity, 248 Anaplasmosis, 66
dosage form/usual dosage, 291 Rickettsia rickettsii, 133
 Index — 353

Ancef, 294 physiologic-based pharmacokinetic

Ancobon, 299 modeling of, 235–236
Ancylostoma braziliense, 210, 214 preferred therapy, 107, 114–139
Ancylostoma caninum, 210, 214 sequential parenteral-oral antibiotic
Ancylostoma duodenale, 210, 219 therapy, 251–252
Angiostrongyliasis, 211 susceptibility data on, 233
Angiostrongylus cantonensis, 211 susceptibility of anaerobes to, 112–113
Angiostrongylus costaricensis, 211 susceptibility of gram-negative bacilli to,
Anidulafungin, 180 110–111
for children with obesity, 248 susceptibility of gram-positive bacilli to,
dosage form/usual dosage, 291 108–109
susceptibility of fungal pathogens to, Antibiotic stewardship, 283–288
150–151 accountability, 286–288
Animal bites diagnostic stewardship, 283–285
Pasteurella multocida, 130 empiric therapy, 285
postexposure antimicrobial prophylaxis, infection prevention, 283
255 optimization of administration, 286
Anthim, 305 reevaluation of therapy, 285
Anthrax treatment of infections only, 285–286
Bacillus anthracis, 115 Anti-coronavirus drugs, 203
cutaneous, 4 Antifungal agents, 171–180. See also Fungal
sepsis/pneumonia, community vs pathogens
bioterror exposure, 67 azoles, 173–178
Antibiotic allergies, 271–281 for children with obesity, 248
allergic cross-reactivity and specific, 276– echinocandins, 178–180
280 polyenes, 171–173
alternative antibiotic options for common prophylaxis of invasive fungal infection
infections, 280–281 in patients with
β-Lactam antibiotics, 276–279 hematologic malignancies,
classification, 271–273 152
introduction, 271 prophylaxis of invasive fungal infection
observed challenge and desensitization in patients with solid-organ
protocols, 276 transplants, 152
stepwise approach to reported, 274–275 susceptibility of fungal pathogens to,
Antibiotic-associated colitis, 119 150–151
Antibiotics, 141–148. See also Antimicrobials; Anti-hepatitis drugs, 202
Bacterial and mycobacterial Anti-herpesvirus drugs, 201–202
pathogens Anti-influenza drugs, 202
aminoglycosides, 146–147 Antimalarial drugs, 231–232
β-Lactam, 142–146 Antimicrobials. See also Antibiotics;
β-Lactam/β-lactamase inhibitor (BLI) Bacterial and mycobacterial
combinations, 141–142 pathogens
dosing for children with obesity, 47–249 assessment of clinical and microbiologic
drug concentrations at site of infection, outcomes of, 235
234 for children with obesity, 247–249
Index

fluoroquinolones, 147–148 for community-associated methicillin-

macrolides, 146 resistant Staphylococcus
for multidrug-resistant gram-negative aureus (CA-MRSA)
bacilli, 237–240 infections, 242–245
 354 — Index

Antimicrobials (continued) Haemophilus influenzae, 124

dosing, 233–234 Kingella kingae, 124
forms and usual dosages, 290–314 Lyme disease, 70
topical, 315–321 Neisseria gonorrhoeae, 130
neonates, 75–76 reactive
during pregnancy or breastfeeding, 105– Yersinia enterocolitica, 139
106 Yersinia pseudotuberculosis, 139
prophylaxis/prevention of symptomatic Streptococcus milleri/anginosus group,
infection, 253–270 137
therapy according to clinical syndromes, Streptococcus pneumoniae, 138
1–2 Ascariasis, 206, 211
Antimycobacterials for children with Ascaris lumbricoides, 211
obesity, 248 Aspergillosis, 153–155
Antiparasitic agents, 231–232 Aspergillus
albendazole/mebendazole, 206–207 neonates, 82–83
antimalarial drugs, 231–232 pneumonia, 32
benzimidazoles, 232 Aspergillus calidoustus, 150
ivermectin, 206–207 Aspergillus fumigatus, 150
metronidazole/tinidazole, 206–207 Aspergillus terreus, 150
nitazoxanide, 206–207 Aspiration, lung abscess secondary to, 24
nitroimidazoles, 232 Aspiration pneumonia, 24
preferred therapy, 205, 208–229 neonates, 90
triclabendazole, 206–207 Asymptomatic infection, 253
triterpenoid, 180 Atovaquone, 292
Antipseudomonal and anti-enteric gram- Atovaquone/proguanil, 292
negative β-lactams, 144 Augmentin, 291
Antiviral agents, 201–203. See also Viral Avelox, 304
pathogens Avibactam, 241
anti-coronavirus drugs, 203 Aycaz, 295
anti-hepatitis drugs, 202 Azactam, 293
anti-herpesvirus drugs, 201–202 AzaSite, 315
anti-influenza drugs, 202 Azithromycin, 146
for children with obesity, 248 dosage form/usual dosage, 293, 315
hepatitis B or C, 183 neonates, 100
non-HIV, non–hepatitis B or C, 182 Azoles, 173–178
Appendectomy, non-perforated, surgical/ Aztreonam
procedure prophylaxis, 267 dosage form/usual dosage, 293
Appendicitis, 52, 67 for multidrug-resistant gram-negative
surgical/procedure prophylaxis, 268 bacilli, 241
Arakoda, 312 neonates, 100
Aralen, 296
Arbovirus, encephalitis, 60 B
Arcanobacterium haemolyticum, 115 Babesia spp, 212–213
Artemether/lumefantrine, 231–232 Babesiosis, 212–213
dosage form/usual dosage, 292 Bacillary angiomatosis, 116
Index

Artesunate, 292 Bacillus anthracis, 115

Arthritis Bacillus cereus or subtilis, 115
bacterial, 9–10 Bacitracin, 315
gonococcal, 10 Bacitracin + neomycin + polymyxin B, 319
 Index — 355

Bacitracin + neomycin + polymyxin B + Clostridium tetani, 120

hydrocortisone, 316 Corynebacterium diphtheriae, 120
Bacteremia, 38–39 Corynebacterium jeikeium, 120
abscess, brain, 58–59 Corynebacterium minutissimum, 120
Corynebacterium minutissimum, 120 Coxiella burnetii, 121
Leuconostoc, 126 Cutibacterium acnes, 121
Ralstonia, 133 Ehrlichia chaffeensis, muris, 121
Sphingomonas paucimobilis, 135 Ehrlichia ewingii, 121
Ureaplasma urealyticum, 139 Eikenella corrodens, 121
Bacterial and mycobacterial pathogens, Elizabethkingia meningoseptica, 121
107–139. See also Enterobacter spp, 110–111, 121
Antibiotics; Antimicrobials Enterococcus faecium, 108–109
Acinetobacter baumannii, 114 Enterococcus faecalis, 108–109
Acinetobacter spp, 110–111 Enterococcus spp, 122
Actinomyces israelii, 114 Erysipelothrix rhusiopathiae, 122
Aeromonas hydrophila, 114 Escherichia coli, 110–111, 122–123
Aggregatibacter actinomycetemcomitans, Francisella tularensis, 123
115 Fusobacterium spp, 123
Aggregatibacter aphrophilus, 115 Gardnerella vaginalis, 123
Anaplasma phagocytophilum, 115 group A streptococcus, 137
Arcanobacterium haemolyticum, 115 group B streptococcus, 137
arthritis, 9–10 Haemophilus ducreyi, 123
Bacillus anthracis, 115 Haemophilus influenzae, 110–111, 124
Bacillus cereus or subtilis, 115 Helicobacter pylori, 124
Bacteroides fragilis, 115 Kingella kingae, 124
Bacteroides spp, 116 Klebsiella, 110–111
Bartonella henselae, 116 Klebsiella granulomatis, 125
Bartonella quintana, 116 Klebsiella spp, 125
Bordetella burgdorferi, 116 Legionella spp, 125
Borrelia hermsii, turicatae, parkeri, 116 Leptospira spp, 125
Borrelia recurrentis, 117 Leuconostoc, 126
Brucella spp, 117 Listeria monocytogenes, 126
Burkholderia cepacia, 110–111, 117 meningitis, 60–61
Burkholderia pseudomallei, 117 Moraxella catarrhalis, 126
Campylobacter fetus, 117 Morganella morganii, 126
Campylobacter jejuni, 117 Mycobacterium abscessus, 127
Capnocytophaga canimorsus, 117 Mycobacterium avium complex, 128
Capnocytophaga ochracea, 117 Mycobacterium bovis, 128
Cellulosimicrobium cellulans, 118 Mycobacterium chelonae, 128
Chlamydia trachomatis, 118 Mycobacterium fortuitum complex, 128
Chlamydophila pneumoniae, 118 Mycobacterium hominis, 129
Chlamydophila psittaci, 118 Mycobacterium leprae, 129
Chromobacterium violaceum, 118 Mycobacterium marinum, balnei, 129
Citrobacter freundii, 118 Mycobacterium tuberculosis, 129
Citrobacter koseri, 118 Mycoplasma pneumoniae, 129
Index

Citrobacter spp, 110–111 Neisseria gonorrhoeae, 130

Clostridioides difficile, 119 Neisseria meningitidis, 110–111, 130
Clostridium botulinum, 119 Nocardia asteroides, 130
Clostridium perfringens, 120 Nocardia brasiliensis, 130
 356 — Index

Bacterial and mycobacterial pathogens susceptibility to antibiotics, 107–139

(continued) anaerobes, 112–113
Nocardia spp, 108–109 gram negative, 110–111
otitis externa, 18 gram positive, 108–109
otitis media, 262 tracheitis, 23
Pasteurella multocida, 130 Treponema pallidum, 138
Peptostreptococcus, 131 vaginitis, 57
perirectal abscess, 53 vaginosis, 123
pharmacodynamics of, 234–235 Vibrio cholerae, 139
Plesiomonas shigelloides, 131 Vibrio vulnificus, 139
pneumonia, 28–31 Yersinia enterocolitica, 139
postexposure antimicrobial prophylaxis, Yersinia pestis, 139
255 Yersinia pseudotuberculosis, 139
preferred therapy, 107, 114–139 Bacteroides fragilis, 115
Prevotella spp, melaninogenica, 131 Bacteroides spp, 116
Propionbacterium acnes, 131 appendicitis, 52
Proteus mirabilis, 131 necrotizing fasciitis, 8
Proteus vulgaris, 131 omphalitis and funisitis, 88
Providencia spp, 132 perirectal abscess, 53
Pseudomonas aeruginosa, 110–111, 132– sepsis and meningitis, 93
133 susceptibility to antibiotics, 112
Pseudomonas cepacia, mallei, Bactocill, 306
pseudomallei, 133 Bactrim, 313
purulent pericarditis, 45 Bactroban, 319
Ralstonia, 133 Balamuthia mandrillaris, 59, 210
Rhodococcus hoagii, 133 Balantidium coli, 212
Rickettsia rickettsii, 133 Baloxavir, 182, 202
Salmonella, 133 dosage form/usual dosage, 293
Salmonella typhi, 134 susceptibility of non-HIV, non–hepatitis
Serratia, 110–111 B or C viral pathogens to,
Serratia marcescens, 134 182
Shewanella spp, 134 Baraclude, 298
Shigella, 110–111 Bartonella henselae, 67, 116
Shigella spp, 135 Bartonella quintana, 116
Sphingomonas paucimobilis, 135 Baxdela, 297
Spirillum minus, 135 Baylisascaris procyonis, 212
Staphylococcus, coagulase-negative, 108– Bedaquiline, 293
109 Bell palsy, 70
Staphylococcus aureus, 135–136 BenzaClin, 316
Staphylococcus aureus, methicillin- Benzamycin, 317
resistant, 108–109 Benzimidazoles, 232
Stenotrophomonas maltophilia, 110–111, Benznidazole, 293
136 Benzyl alcohol, 315
Streptobacillus moniliformis, 136 Berdazimer, 315
Streptococcus, viridans group, 137 Besifloxacin, 315
Index

Streptococcus milleri/anginosus group, Besivance, 315

137 β-Lactam antibiotics, 142–146
Streptococcus pneumoniae, 108–109, 138 allergies to, 276–279
Streptococcus pyogenes, 108–109 for children with obesity, 247
 Index — 357

sequential parenteral-oral antibiotic Buccal cellulitis, 6

therapy, 251–252 Bullous impetigo, 5
β-Lactam/β-lactamase inhibitor (BLI) Bullous myringitis, 17
combinations, 141–142 Bunyavirus encephalitis, 60
Bethkis, 313 Burkholderia cepacia, 117
Bezlotoxumab, 294 cystic fibrosis (CF), 25
Biaxin, 296 susceptibility to antibiotics, 110–111
Biaxin XL, 296 Burkholderia pseudomallei, 70, 117
Bicillin L-A, 306 Butenafine, 315
Biltricide, 308 Butoconazole, 315
Bioterror-related illnesses, Clostridium
botulinum, 119 C
Bites Cabtreo, 316
dog and cat, 5 California encephalitis, 60
Capnocytophaga canimorsus, 117 Campylobacter, diarrhea/gastroenteritis, 47
human, 5 Campylobacter fetus, 117
Eikenella corrodens, 121 Campylobacter jejuni, 48, 117
Pasteurella multocida, 130 CA-MRSA. See Community-associated
postexposure antimicrobial prophylaxis, methicillin-resistant
255 Staphylococcus aureus
Blastocystis spp, 206, 213 (CA-MRSA) infections
Blastomyces dermatitidis, 150 Cancidas, 294
Blastomycosis, 156 Candida albicans, 150
Blephamide, 320 Candida auris, 150
Body surface area, nomogram, 323 Candida parapsilosis, 150
Bordetella burgdorferi, 116 Candida spp
Borrelia burgdorferi, 69 endocarditis, 44
postexposure antimicrobial prophylaxis, endophthalmitis, 16
256 neonates, 80–81
Borrelia hermsii, 116 otitis externa, 18
Borrelia parkeri, 116 urinary tract infection, 99
Borrelia recurrentis, 117 vaginitis, 57
Borrelia turicatae, 116 Candida tropicalis, 150
Botulism, infant, 68, 119 Candidiasis, 156–160
Bowel rupture, neonates, 83 Capillaria, 213
Brain abscesses, 58–59 Capnocytophaga canimorsus, 117
Aggregatibacter actinomycetemcomitans, bites, dog and cat, 5
115 postexposure antimicrobial prophylaxis,
Aggregatibacter aphrophilus, 115 255
Nocardia asteroides, brasiliensis, 130 Capnocytophaga ochracea, 117
Streptococcus milleri/anginosus group, 137 Carbapenem-resistant GNR, 93
Breastfeeding, antimicrobial therapy during, Carbapenems, 145–146
105–106 allergies to, 279
Brexafemme, 300 for children with obesity, 249
Bronchitis, 25 Cardiovascular infections, 38–46
Index

Moraxella catarrhalis, 126 bacteremia, 38–39

Brucella spp, 117 endocarditis, 40–44
Brucellosis, 67, 117 Lemierre syndrome, 45
Brugia malayi, timori, 213, 217 purulent pericarditis, 45–46
 358 — Index

Cardiovascular surgical/procedure Cefotaxime

prophylaxis, 266–267 dosage form/usual dosage, 294
Carditis, Lyme disease, 70 neonates, 75, 101
Caspofungin, 179 Cefotetan, 142, 295
for children with obesity, 248 Cefoxitin, 142
dosage form/usual dosage, 294 dosage form/usual dosage, 295
susceptibility of fungal pathogens to, susceptibility of anaerobes to, 112
150–151 Cefpodoxime, 295
Catheter fungemia, 157–158 Cefprozil, 295
Catheter infections Ceftaroline, 143
Cellulosimicrobium cellulans, 118 for community-associated methicillin-
Mycobacterium chelonae, 128 resistant Staphylococcus
Mycobacterium fortuitum complex, 128 aureus (CA-MRSA)
Staphylococcus aureus, 136 infections, 242–243
Cat-scratch disease, 67 dosage form/usual dosage, 295
Bartonella henselae, 116 neonates, 101
CAZ/AVI, susceptibility of gram-negative susceptibility of gram-positive bacterial
bacterial pathogens to, pathogens to, 109
110 Ceftazidime, 142–143
Ceclor, 294 for children with obesity, 249
Cefaclor, 294 dosage form/usual dosage, 295
Cefadroxil, 294 neonates, 75, 101
Cefazolin, 142 susceptibility of gram-negative bacterial
for children with obesity, 249 pathogens to, 111
dosage form/usual dosage, 294 Ceftazidime/avibactam
neonates, 101 dosage form/usual dosage, 295
susceptibility of anaerobes to, 112 neonates, 101
susceptibility of gram-negative bacterial Ceftin, 295
pathogens to, 110 Ceftobiprole, 243
susceptibility of gram-positive bacterial Ceftolozane/tazobactam
pathogens to, 109 dosage form/usual dosage, 295
Cefdinir, 294 neonates, 101
Cefepime Ceftriaxone, 142–143
for children with obesity, 249 dosage form/usual dosage, 295
dosage form/usual dosage, 294 neonates, 76, 101
for multidrug-resistant gram-negative susceptibility of anaerobes to, 113
bacilli, 241, 242 susceptibility of gram-negative bacterial
neonates, 75–76, 101 pathogens to, 110
susceptibility of anaerobes to, 113 Cefuroxime, 142
susceptibility of gram-negative bacterial dosage form/usual dosage, 295, 296
pathogens to, 111 susceptibility of gram-negative bacterial
Cefiderocol, 143 pathogens to, 110
dosage form/usual dosage, 294 Cefzil, 295
for multidrug-resistant gram-negative Cellulitis
bacilli, 240–241 Aeromonas hydrophila, 114
Index

susceptibility of gram-negative bacterial Arcanobacterium haemolyticum, 115

pathogens to, 110 associated with entry site lesion on skin,
Cefixime, 294 13
Cefotan, 295 buccal, 6
 Index — 359

erysipelas, 6 Chlamydia trachomatis, 54, 118

Erysipelothrix rhusiopathiae, 122 lymphogranuloma venereum, 56
group A streptococcus, 137 neonates, 90
Haemophilus influenzae, 124 pelvic inflammatory disease, 56
Nocardia asteroides, brasiliensis, 130 pneumonia, 31
orbital, 13 Chlamydophila pneumoniae, 31, 118
periorbital, 13–14 Chlamydophila psittaci, 31, 118
peritonsillar, 22 Chloroquine, 221–222, 231
retropharyngeal; parapharyngeal; lateral Chloroquine phosphate, 296
pharyngeal, 23 Cholera, 139
true, 13 diarrhea/gastroenteritis, 48
of unknown etiology, 6 Chromobacterium violaceum, 118
Cellulosimicrobium cellulans, 118 Chromoblastomycosis, 161
Central nervous system infections, 58–63 Chronic mastoiditis, 18
abscess, brain, 58–59 Chronic osteomyelitis, 12
encephalitis, 59–60 Ciclopirox, 315
meningitis Cidofovir, 182, 201
bacterial, community-associated, dosage form/usual dosage, 296
60–61 susceptibility of non-HIV, non–hepatitis B
TB, 62 or C viral pathogens to, 182
shunt infections, 62–63 Ciloxan, 315
Staphylococcus aureus, 136 Cipro, 296
Cephalexin Ciprodex, 315
dosage form/usual dosage, 296 Ciprofloxacin, 148
susceptibility of gram-negative bacterial dosage form/usual dosage, 296, 315
pathogens to, 110 neonates, 101
susceptibility of gram-positive bacterial susceptibility of gram-negative bacterial
pathogens to, 109 pathogens to, 111
Cephalosporins Ciprofloxacin + dexamethasone, 315
allergies to, 277–278 Ciprofloxacin + fluocinolone, 315
for children with obesity, 247 Ciprofloxacin + hydrocortisone, 316
oral, 142 Cipro HC, 316
parenteral, 142–143 Cirrhosis, peritonitis, 53
Cervical adenitis Citrobacter freundii, 118
Mycobacterium avium, 128 Citrobacter koseri, 118
Mycobacterium tuberculosis, 129 Citrobacter spp, 110–111
Cervicitis Claforan, 294
Chlamydia trachomatis, 54, 118 Clarithromycin, 146
gonorrhea, 55 dosage form/usual dosage, 296
Cervicofacial actinomycosis, 114 Clarithromycin ER, 296
Cetraxal, 315 Clavispora, 150
CF. See Cystic fibrosis (CF) Cleocin, 297, 316
Chagas disease, 213, 228 Cleocin-T, 316
Chalazion. See Hordeolum (sty) or chalazion Clindamycin
Chancroid, 54, 123 for children with obesity, 247
Index

Chickenpox/shingles (VZV), 67, 199 for community-associated methicillin-

Children resistant Staphylococcus
arthritis, bacterial, 9, 10 aureus (CA-MRSA)
otitis media, acute, 19–20 infections, 244
 360 — Index

Clindamycin (continued) Coliform bacteria

dosage form/usual dosage, 297, 316 omphalitis and funisitis, 87
neonates, 101 osteomyelitis, suppurative arthritis, 88
sequential parenteral-oral antibiotic otitis media, 89
therapy, 252 purulent pericarditis, 46
susceptibility of anaerobes to, 113 urinary tract infection, neonates, 99
susceptibility of gram-positive bacterial Colistimethate, 297
pathogens to, 109 Colistin + neomycin + hydrocortisone, 316
Clindamycin + adapalene benzoyl peroxide, Coly-Mycin M, 297
316 Coly-Mycin S, 316
Clindamycin + benzoyl peroxide, 316 Combination therapy, 2
Clindamycin + tretinoin, 316 Community-acquired pneumonia, 25
Clindesse, 316 alternative antibiotic options for, 281
Clinical syndromes cystic fibrosis (CF), 25
antimicrobial therapy according to, 1–2 definitive therapy for pathogens of, 28–30
cardiovascular infections, 38–46 endocarditis, 44
central nervous system infections, 58–63 Community-associated methicillin-resistant
ear and sinus infections, 17–20 Staphylococcus aureus
eye infections, 13–17 (CA-MRSA) infections, 2,
gastrointestinal infections, 46–53 3
genital and sexually transmitted abscess, lung, 24
infections, 54–58 antimicrobials for, 242–245
lower respiratory tract infections, 24–37 arthritis, bacterial, 9
miscellaneous systemic infections, 66–73 bites
oropharyngeal infections, 21–23 dog and cat, 5
skeletal infections, 9–12 human, 5
skin and soft tissue infections, 3–8 bullous impetigo, 5
urinary tract infections, 64–66 cellulitis
Clonorchis/opisthorchis, 206 orbital, 13
Clonorchis sinensis, 213, 218 periorbital, 13
Clostridia spp of unknown origin, 6
necrotizing fasciitis, 8 empiric therapy for suspected, 245–246
omphalitis and funisitis, 88 impetigo, 7
susceptibility to antibiotics, 112 investigational gram-positive agents for,
Clostridioides difficile, 119 245
diarrhea/gastroenteritis, 48 Lemierre syndrome, 22, 45
susceptibility to antibiotics, 112 mastoiditis
Clostridium botulinum, 119 acute, 17
Clostridium perfringens, 120 chronic, 18
Clostridium tetani, 72, 120 myositis, suppurative, 7
postexposure antimicrobial prophylaxis, osteomyelitis, 11
257 of the foot, 12
Clotrimazole, 297 otitis, chronic suppurative, 18
dosage form/usual dosage, 316 otitis externa, 18
Clotrimazole + betamethasone, 316 peritonsillar cellulitis and abscess, 22
Index

CMV. See Cytomegalovirus (CMV) pneumonia, 27

Coartem, 292 postexposure antimicrobial prophylaxis,
Coccidioides immitis, 150 255
Coccidioidomycosis, 162 purulent pericarditis, 45
 Index — 361

pyoderma, cutaneous abscesses, 8 Cysticercosis, 214

retropharyngeal; parapharyngeal; lateral Cysticercus cellulosae, 214
pharyngeal cellulitis or Cystic fibrosis (CF), 25–26
abscess, 23 Burkholderia cepacia, 117
staphylococcal scalded skin syndrome mycobacteria, nontuberculous, 71
(SSSS), 8 Pseudomonas aeruginosa, 133
toxic shock syndrome (TSS), 73 Cystitis, acute, 64
tracheitis, bacterial, 23 Cystoisospora belli, 215
Congenital syphilis, 56, 96–98 Cystoisospora spp, 206
Conjunctivitis Cystoscopy surgical/procedure prophylaxis,
acute, 14 268
chlamydial, 77 Cytomegalovirus (CMV)
gonococcal, 77 encephalitis, 59
gonorrhea, 55 neonates, 78–79
herpetic, 14 pneumonia, 31
neonates, 77–78 preferred therapy, 185–186
Chlamydia trachomatis, 118 retinitis, 16
Pseudomonas aeruginosa, 78 susceptibility to antivirals, 182
Staphylococcus aureus, 77 Cytovene, 300
Coronavirus (SARS-CoV-2), 67
anti-coronavirus drugs, 203 D
neonates, 92 Dacryocystitis, 15
preferred therapy, 184 Dalbavancin
susceptibility to antivirals, 182 for community-associated methicillin-
Cortisporin, 316 resistant Staphylococcus
Cortisporin TC otic, 316 aureus (CA-MRSA)
Corynebacterium diphtheriae, 120 infections, 243
Corynebacterium jeikeium, 120 dosage form/usual dosage, 297
Corynebacterium minutissimum, 120 neonates, 101
Corynebacterium spp, surgical/procedure Dalvance, 297
prophylaxis, 266, 267 Dapsone, 297
COVID-19. See Coronavirus (SARS-CoV-2) dosage form/usual dosage, 317
Coxiella burnetii, 72, 121 Daptomycin
Creeping eruption, 214 for children with obesity, 247, 249
Cresemba, 301 for community-associated methicillin-
Cross-reactivity, allergic, 276–280 resistant Staphylococcus
Cryptococcosis, 163 aureus (CA-MRSA)
Cryptococcus spp, 150 infections, 244–245
Cryptosporidiosis, 206, 213 dosage form/usual dosage, 297
Cryptosporidium parvum, 213 neonates, 101
Cubicin, 297 susceptibility of gram-positive bacterial
Cutaneous anthrax, 4 pathogens to, 109
Bacillus anthracis, 115 DEC, 206–207
Cutaneous candidiasis, 156 Declomycin, 297
Cutaneous larva migrans, 206, 214 Deep head/neck space infections
Index

Cutibacterium acnes, 121 Peptostreptococcus, 131

Cycloserine, 297 Prevotella spp, melaninogenica, 131
Cyclospora spp, 214 Streptococcus, viridans group, 137
Cyclosporiasis, 206 Delafloxacin, 297
 362 — Index

Demeclocycline, 297 drug concentrations at site of infection

Dental abscess, 21 and, 234
Prevotella spp, melaninogenica, 131 factors involved in recommendations for,
Deoxycholate, amphotericin B, neonates, 233
100 susceptibility data and, 233
Dermatophytoses, 168–169 target attainment, 2
Diagnostic stewardship, 283–285 Doxycycline, 231
Diarrhea/gastroenteritis, 46–51 dosage form/usual dosage, 298
Aeromonas hydrophila, 48, 114 Duration of therapy, 1–2
Bacillus cereus or subtilis, 115 Duricef, 294
Campylobacter jejuni, 48, 117 Durlobactam, 241
cholera, 48 Dynapen, 297
Clostridioides difficile, 48
Escherichia coli, 49 E
giardiasis, 50 Ear and sinus infections, 17–20
non-typhoid strains, 50 bullous myringitis, 17
Plesiomonas shigelloides, 131 mastoiditis
Salmonella, 133 acute, 17
salmonellosis, 50 chronic, 18
shigellosis, 51 otitis, chronic suppurative, 18
travelers, 47, 48 otitis externa, 18
typhoid fever, 51 otitis media, acute, 19–20
Yersinia enterocolitica, 47, 51, 139 sinusitis, acute, 20
Dibothriocephalus latus, 215 topical antimicrobials, 315–321
Dicloxacillin, 297 Eastern equine encephalitis, 60
Dientamoeba fragilis, 215 Ebola, 186
Dientamoebiasis, 206, 215 Echinocandins, 178–180
Dificid, 299 Echinococcosis, 215–216
Diflucan, 299 Echinococcus granulosus, 215
Diphtheria Echinococcus multilocularis, 216
Corynebacterium diphtheriae, 120 Econazole, 317
pharyngitis, 21 EES, 299
Diphyllobothrium latum, 226 Efinaconazole, 317
Dipylidium caninum, 215, 226 Egaten, 313
Disseminated candidiasis, 157–158 Ehrlichia chaffeensis, 68, 121
Disseminated disease, Mycobacterium avium Ehrlichia ewingii, 68, 121
complex, 128 Ehrlichia muris, 121
Disseminated gonococcal infection, 55 Ehrlichiosis, 68
Dog and cat bites, 5 Rickettsia rickettsii, 133
Capnocytophaga canimorsus, 117 Eikenella corrodens, 121
Pasteurella multocida, 130 bites, human, 5
postexposure antimicrobial prophylaxis, Elbasvir/grazoprevir, 183
255 dosage form/usual dosage, 298
Donovanosis, 55 Elimite, 320
Dosage/dosing, 1 Elizabethkingia meningoseptica, 121
Index

antimicrobial Empiric therapy, antibiotic stewardship,

for children with obesity, 247–249 285
neonates, 100–103 Emverm, 302
 Index — 363

Encephalitis, 59–60 Epidural abscess, Streptococcus milleri/

Epstein-Barr virus, 187 anginosus group, 137
herpes simplex virus, 191 Epiglottitis, 21
Endocarditis, 40–44 Haemophilus influenzae, 124
Aggregatibacter actinomycetemcomitans, Epstein-Barr virus
115 encephalitis, 59
Aggregatibacter aphrophilus, 115 preferred therapy, 187
antibiotic prophylaxis, 44 Eravacycline, 298
Bartonella quintana, 116 Eraxis, 291
Corynebacterium jeikeium, 120 Ertaczo, 320
Eikenella corrodens, 121 Ertapenem, 247
Enterococcus spp, 122 dosage form/usual dosage, 298
Erysipelothrix rhusiopathiae, 122 Eryderm, 317
postexposure antimicrobial prophylaxis, Erygel, 317
255–256 Ery Pads, 317
Streptococcus, viridans group, 137 EryPed, 299
Endophthalmitis, 15–16 Erysipelas cellulitis, 6
Endovascular infection, Campylobacter Erysipelothrix rhusiopathiae, 122
fetus, 117 Erythrocin, 299
Enmetazobactam, 242 Erythrasma, 120
Entamoeba histolytica, 208–209, 216 Erythromycin, 146
Entecavir, 183 dosage form/usual dosage, 317
dosage form/usual dosage, 298 neonates, 101
Enteritis, 135 Erythromycin base, 298
Yersinia enterocolitica, 139 Erythromycin + benzoyl peroxide, 317
Enterobacter spp, 121 Erythromycin ethylsuccinate, 299
osteomyelitis, suppurative arthritis, Erythromycin lactobionate, 299
88 Escherichia coli, 122–123
pneumonia, 32 bacteremia, 38
susceptibility to antibiotics, 110–111 cystitis, acute, 64
urinary tract infection, 99 diagnostic stewardship, 283
Enterobius vermicularis, 216 diarrhea/gastroenteritis, 46–47
Enterococcus faecium, 108–109 nephronia, lobar, 65
Enterococcus faecalis, 108–109 osteomyelitis, suppurative arthritis,
Enterococcus spp, 122 88
appendicitis, 52 otitis media, 89
endocarditis, 40–41, 43 pneumonia, 32
sepsis and meningitis, 93 pyelonephritis, acute, 65
surgical/procedure prophylaxis, 267, sepsis and meningitis, 94
268 susceptibility to antibiotics, 110–111
urinary tract infection, 99 urinary tract infection, 99
Enterovirus Esophageal candidiasis, 159
encephalitis, 59 Ethambutol, 248
preferred therapy, 186 dosage form/usual dosage, 299
sepsis and meningitis, 94 Ethionamide, 299
Index

Eosinophilic meningitis, 216 Evoclin, 316

Epclusa, 183 Exelderm, 320
Epididymitis, 54 Extina, 318
 364 — Index

Eye infections, 13–17 sequential parenteral-oral antibiotic

cellulitis therapy, 252
orbital, 13 Foodborne illnesses
periorbital, 13–14 Clostridium botulinum, 119
conjunctivitis Clostridium perfringens, 120
acute, 14 Foot, osteomyelitis of, 12
herpetic, 14 Fortaz, 295
dacryocystitis, 15 Foscarnet, 182, 201
endophthalmitis, 15–16 dosage form/usual dosage, 299
hordeolum or chalazion, 16 susceptibility of non-HIV, non–hepatitis
retinitis, 16 B or C viral pathogens to,
topical antimicrobials, 315–321 182
Foscavir, 299
F Fosfomycin, 241
Famciclovir, 182 dosage form/usual dosage, 299
dosage form/usual dosage, 299 Francisella tularensis, 73, 123
susceptibility of non-HIV, non–hepatitis B pneumonia, 32
or C viral pathogens to, 182 Fungal pathogens, 149–169. See also
Famvir, 299 Antifungal agents
Far East scarlet-like fever, 139 aspergillosis, 153–155
Fasciola hepatica, gigantica, 206, 216, 218 Aspergillus calidoustus, 150
Fasciolopsis buski, 216, 218 Aspergillus fumigatus, 150
Fetroja, 294 Aspergillus terreus, 150
Fexinidazole, 299 Blastomyces dermatitidis, 150
Fidaxomicin, 299 blastomycosis, 156
Filariasis, 216–217 Candida albicans, 150
Flagyl, 303 Candida auris, 150
Flavivirus, encephalitis, 60 Candida parapsilosis, 150
Floxin otic, 319 Candida spp
Fluconazole, 174 endocarditis, 44
for children with obesity, 248 endophthalmitis, 16
dosage form/usual dosage, 299 neonates, 80–81
neonates, 101 otitis externa, 18
susceptibility of fungal pathogens to, urinary tract infection, 99
150–151 vaginitis, 57
Flucytosine Candida tropicalis, 150
for children with obesity, 248 candidiasis, 156–160
dosage form/usual dosage, 299 chromoblastomycosis, 161
neonates, 101 Clavispora, 150
susceptibility of fungal pathogens to, Coccidioides immitis, 150
150–151 coccidioidomycosis, 162
Flukes, 218 cryptococcosis, 163
Fluoroquinolones, 147–148 Cryptococcus spp, 150
for children with obesity, 247 febrile, neutropenic patient, 68
for community-associated methicillin- Fusarium spp, 150
Index

resistant Staphylococcus Histoplasma capsulatum, 150

aureus (CA-MRSA) histoplasmosis, 165
infections, 245 hyalohyphomycosis, 164
 Index — 365

localized mucocutaneous infections, 168– Gastroenteritis. See Diarrhea/gastroenteritis

169 Gastrointestinal infections, 46–53
Lomentospora, 151 anthrax, 115
long-term antimicrobial prophylaxis, 264 diarrhea/gastroenteritis, 46–51
Meyerozyma (Candida) guilliermondii, intra-abdominal infection, 52–53
151 neonates, 83
mucormycosis, 166 perirectal abscess, 53
Mucor spp, 151 peritonitis, 53
Nakaseomyces (Candida) glabrata, 151 surgical/procedure prophylaxis, 267–268
neonates, 80–83 Gatifloxacin, 317
Paracoccidioides spp, 151 Genital and sexually transmitted infections,
paracoccidioidomycosis, 166 54–58
Penicillium spp, 151 chancroid, 54
phaeohyphomycosis, 155 Chlamydia trachomatis, 54
Pichia kudriavzevii (Candida krusei), 151 epididymitis, 54
Pneumocystis jirovecii, 167 gonorrhea, 54–55
pneumonia, 30, 32 granuloma inguinale, 55
preferred therapy, 149 herpes simplex virus, 55, 191
prophylaxis, 152 HIV testing, 54
Rhizopus spp, 151 lymphogranuloma venereum, 56
Scedosporium apiospermum, 151 pelvic inflammatory disease, 56
Sporothrix spp, 151 syphilis, 56–57
sporotrichosis, 167 trichomoniasis, 57
susceptibility to antifungal agents, 150–151 Ureaplasma urealyticum, 139
systemic infections, 152–167 urethritis, nongonococcal, 57
Trichosporon spp, 151 vaginitis, 57–58
vulvovaginal, 160 Genitourinary surgical/procedure
Fungizone, 291 prophylaxis, 268
Fungoid, 318 Gentamicin
Funisitis, 87–88 dosage form/usual dosage, 300, 317
Furadantin, 305 neonates, 104
Fusarium spp, 150 susceptibility of gram-negative bacterial
Fusobacterium necrophorum, Lemierre pathogens to, 111
syndrome, 22, 45 Gentamicin + prednisolone, 317
Fusobacterium spp, 123 Giardia duodenalis, 218–219
Giardia intestinalis, 218–219
G Giardiasis, 50, 218–219
Ganciclovir, 182, 201, 202 Giardia spp, 206, 218–219
for children with obesity, 248 Gingivostomatitis, herpetic, 22
dosage form/usual dosage, 300, 317 Glecaprevir/pibrentasvir, 183
neonates, 101 dosage form/usual dosage, 300
Garamycin, 317 GNB. See Gram-negative bacilli (GNB)
Gardnerella vaginalis, 123 Gonococcus
Gas gangrene, 6 arthritis, 10, 89
Clostridium perfringens, 120 endocarditis, 42
Index

Gastritis, Helicobacter pylori, 124 endophthalmitis, 15

Gastroduodenal surgical/procedure pelvic inflammatory disease, 56
prophylaxis, 267 Gonorrhea, 54–55, 130
 366 — Index

Gram-negative bacilli (GNB) Group B streptococcus, 137

appendicitis, 52 bacteremia, 38
cystic fibrosis (CF), 25 neonates, 92
endocarditis, 43 omphalitis and funisitis, 88
febrile, neutropenic patient, 68 osteomyelitis, suppurative arthritis, 89
head and neck surgery prophylaxis, 269 otitis media, 89
multidrug-resistant, 2, 237–240 sepsis and meningitis, 94, 96
necrotizing fasciitis, 8 Gynazole-1, 315
peritonitis, 53 Gyne-Lotrimin-3, 316
pneumonia, 30, 31 Gyne-Lotrimin-7, 316
shunt infections, 63
surgical/procedure prophylaxis, 267, H
268 HACEK (Haemophilus, Aggregatibacter,
susceptibility to antibiotics, 110–111 Cardiobacterium, Eikenella,
Gram-positive bacilli Kingella spp), 42
agents for CA-MRSA, 245 Haemophilus ducreyi, 54, 123
susceptibility to antibiotics, 108–109 Haemophilus influenzae, 124
surgical/procedure prophylaxis, 267 osteomyelitis, suppurative arthritis, 89
Granuloma inguinale, 55, 125 susceptibility to antibiotics, 110–111
Grifulvin V, 300 Haemophilus influenzae non–type b
Griseofulvin microsize, 300 otitis media, acute, 19–20
Griseofulvin ultramicrosize, 300 pneumonia, 27
Gris-PEG, 300 sinusitis, acute, 20
Group A streptococcus, 137 Haemophilus influenzae type b
abscess, lung, 24 arthritis, bacterial, 9–10
adenitis, acute bacterial, 3 bacteremia, 38, 39
alternative antibiotic options for, 281 cellulitis
arthritis, bacterial, 9–10 buccal, 6
cellulitis of unknown origin, 6 periorbital, 13
endocarditis, 42 conjunctivitis, acute, 14
impetigo, 7 epiglottitis, 21
lymphangitis, 7 mastoiditis, acute, 17
mastoiditis, acute, 17 meningitis, 61
necrotizing fasciitis, 8 pneumonia, 27
omphalitis and funisitis, 88 purulent pericarditis, 45
osteomyelitis, 11 tracheitis, bacterial, 23
otitis media, 89 Hansen disease, 69
peritonitis, 53 Harvoni, 183, 311
peritonsillar cellulitis and abscess, 22 HCV. See Hepatitis C virus (HCV)
pharyngitis, 23 Head and neck surgery prophylaxis, 269
pneumonia, 27, 30 Helicobacter pylori, 124
purulent pericarditis, 45 diarrhea/gastroenteritis, 49
pyoderma, cutaneous abscesses, 8 Helminths, 232
sepsis and meningitis, 94 Hematologic malignancies, fungal infection
sinusitis, acute, 20 prophylaxis, 152
Index

toxic shock syndrome (TSS), 73 Hepatitis B virus (HBV)

tracheitis, bacterial, 23 preferred therapy, 188
vaginitis, 58 susceptibility to antivirals, 183
 Index — 367

Hepatitis C virus (HCV) I

anti-hepatitis drugs, 202 Ibrexafungerp, 180
preferred therapy, 189–190 dosage form/usual dosage, 300
susceptibility to antivirals, 183 IFN-γ receptor deficiency, 71
Hepatosplenic candidiasis, 158 Imidazoles, 173–178
Herpes simplex virus (HSV) Imipenem
anti-herpesvirus drugs, 201–202 for multidrug-resistant gram-negative
encephalitis, 60 bacilli, 241
genital infection, 55 susceptibility of anaerobes to, 113
keratitis, 259 susceptibility of gram-negative bacterial
neonates, 84 pathogens to, 111
postexposure antimicrobial prophylaxis, Imipenem/cilastatin, 300
258–259 Imipenem/cilastatin/relebactam, 301
preferred therapy, 191 Imiquimod, 317
prophylaxis in children who have Immunocompromised children. See also
asymptomatic infection/ Unimmunized infants and
latent infection, 253, 265 children
susceptibility to antivirals, 182 arthritis, bacterial, 9, 10
Herpetic conjunctivitis, 14 Burkholderia cepacia, 117
Herpetic gingivostomatitis, 22 Corynebacterium minutissimum, 120
Histoplasma capsulatum, 150 human herpesvirus 6, 194
Histoplasmosis, 165 mycobacteria, nontuberculous, 71
HIV. See Human immunodeficiency Mycobacterium avium complex, 128
virus (HIV) Pneumocystis jirovecii pneumonia, 35
Hookworm, 206, 214, 219 pneumonia, 30, 31
Hordeolum (sty) or chalazion, 16 retinitis, 16
HSV. See Herpes simplex virus (HSV) tuberculosis, 37
Human African trypanosomiasis, 228 Impaired splenic function, 262–263
Human bites, 5 Impavido, 303
Eikenella corrodens, 121 Impetigo, 7
Pneumocystis jirovecii pneumonia, 35 group A streptococcus, 137
postexposure antimicrobial prophylaxis, Inhalational anthrax, 115
255 Infants
Human granulocyte anaplasmosis, 66 arthritis, bacterial, 9, 10
Anaplasma phagocytophilum, 115 botulism, 68, 119
Human herpesvirus 6, 194 otitis media, acute, 19–20
Human immunodeficiency virus (HIV), 68 pneumonia, Chlamydia trachomatis, 118
mycobacteria, nontuberculous, 71 Infection prevention, antibiotic stewardship,
preferred therapy, 192–194 283
prophylaxis, neonates, 85–87 Infection site drug concentration, 234
retinitis, 16 Influenza A and B
testing, 54 anti-influenza drugs, 202
Human monocytic ehrlichiosis, 68, 121 neonates, 87
Hyalohyphomycosis, 164 pneumonia, 33
Hydroxychloroquine, 231 postexposure antimicrobial prophylaxis,
Index

Hydroxychloroquine sulfate, 300 260

Hymenolepis nana, 219, 226 preferred therapy, 195–196
susceptibility to antivirals, 182
 368 — Index

Interferon alfa-2b, 183 Ketoconazole, 301

Interferon-PEG alfa-2a, 301 dosage form/usual dosage, 318
Internal fixation of fractures, 269 Kingella kingae, 124
Interstitial pneumonia syndrome of early arthritis, bacterial, 9–10
infancy, 28 osteomyelitis, 11
Intestinal fluke, 218 Klebsiella granulomatis, 125
Intra-abdominal infection, 52–53 Klebsiella spp, 125
Enterococcus spp, 122 granuloma inguinale, 55
sequential parenteral-oral antibiotic osteomyelitis, suppurative arthritis, 88
therapy, 251 pneumonia, 33
Invanz, 298 susceptibility to antibiotics, 110–111
Invasive infection urinary tract infection, 99
Bacillus anthracis, 115 Krintafel, 312
Cutibacterium acnes, 121
Propionbacterium acnes, 131 L
Iquix, 318 La Crosse encephalitis, 60
Isavuconazole, 177–178 L-AmB. See Liposomal amphotericin B
susceptibility of fungal pathogens to, (L-AmB)
150–151 Lamisil, 313
Isavuconazonium sulfate, 301 Lamisil-AT, 320
Isoniazid, 248 Lamivudine, 183
dosage form/usual dosage, 301 Lampit, 304
Isospora belli, 219 Lariam, 302
Itraconazole, 174–175 Latent infection, 253, 265
dosage form/usual dosage, 301 Latent tuberculosis, 37, 265
susceptibility of fungal pathogens to, Lateral pharyngeal cellulitis or abscess, 23
150–151 Lefamulin, 302
Ivermectin, 206–207 Legionella spp, 125
dosage form/usual dosage, 301, 318 Legionnaires disease, 34, 125
Leishmaniasis, 219–220
J Leishmania spp, 219–220
Japanese encephalitis, 60 Lemierre syndrome, 22, 45
Jublia, 317 Arcanobacterium haemolyticum, 115
Fusobacterium spp, 123
K Leprosy, 69, 129
Kala-azar, 219–220 Leptospira spp, 125
Kawasaki syndrome, 69 Leptospirosis, 69, 125
Keflex, 296 Letermovir, 182, 201
Keratitis dosage form/usual dosage, 302
postexposure antimicrobial prophylaxis, susceptibility of non-HIV, non–hepatitis
259 B or C viral pathogens to,
prophylaxis in children who have 182
asymptomatic infection/ Leuconostoc, 126
latent infection, 265 Levaquin, 302
Keratoconjunctivitis, 191 Levofloxacin, 302
Index

Kerion, 168 dosage form/usual dosage, 318

Kerydin, 320 Lice, 220
 Index — 369

Likmez, 303 community-acquired pneumonia, 25

Linezolid cystic fibrosis (CF), 25–26
for children with obesity, 247, 249 interstitial pneumonia syndrome of early
for community-associated methicillin- infancy, 28
resistant Staphylococcus pertussis, 26
aureus (CA-MRSA) pleural fluid/empyema, 28
infections, 244 pneumonia
dosage form/usual dosage, 302 aspiration, 24
neonates, 101 atypical, 25
susceptibility of gram-positive bacterial definitive therapy for pathogens of
pathogens to, 109 CAP, 28–30
Lipid complex, amphotericin B (ABLC), empiric therapy, 26–27
neonates, 100 tuberculosis, 36–37
dosage form/usual dosage, 291 Ludwig angina, 7
Liposomal amphotericin B (L-AmB), 172– Lung abscess, 24
173 Lung fluke, 206, 218
neonates, 100 Lyme disease, 69–70, 116
Listeria monocytogenes, 126 postexposure antimicrobial prophylaxis,
Listeria spp 256
bacteremia, 38 Lymphadenitis, 7
sepsis and meningitis, 94 Lymphogranuloma venereum, Chlamydia
Liver abscesses, 209 trachomatis, 118
Liver flukes, 206, 218
Livtencity, 302 M
Loa loa, 216 Macrobid, 305
Lobectomy, surgical/procedure prophylaxis, Macrodantin, 305
267 Macrolides, 146
Localized mucocutaneous infections, 168– alternative antibiotic options for allergies
169 to, 281
Loiasis, 206 Mafenide, 318
Lomentospora, 151 Malaria, 221
Long-term antimicrobial prophylaxis, 253 prevention, 231
bacterial otitis media, 262 treatment, 231–232
fungal, 264 Malarone, 292
impaired splenic function, 262–263 Malathion, 318
rheumatic fever, 263 Mansonella ozzardi, 206, 216, 224
urinary tract infection, recurrent, 263 Mansonella perstans, 206, 216, 224
Loprox, 315 Mansonella streptocerca, 217, 224
Lotrimin, dosage form/usual dosage, 316 Maribavar, 182
Lotrimin-Ultra, 315 Maribavir
Lotrisone, 316 dosage form/usual dosage, 302
Louse-born relapsing fever, 117 susceptibility of non-HIV, non–hepatitis
Lower respiratory tract infections, 24–37 B or C viral pathogens to,
abscess, lung, 24 182
allergic bronchopulmonary aspergillosis, Mastoiditis, acute, 17
Index

24 Mavyret, 183, 300

bronchitis, 25 Maxipime, 294
 370 — Index

Maxitrol, 318 Meropenem/vaborbactam, 303

Measles, 196 Merrem, 302
Mebendazole, 206–207, 232 Mesenteric adenitis, 129, 139
dosage form/usual dosage, 302 Mesenteric enteritis, 139
Mefloquine, 232 Methenamine hippurate, 303
dosage form/usual dosage, 302 Methenamine mandelate, 303
Mefoxin, 295 Methicillin, susceptibility of gram-positive
Melioidosis, 70, 117 bacterial pathogens to, 108
Meningitis Metronidazole, 206–207, 232
Acinetobacter baumannii, 114 for children with obesity, 247
bacterial, community-associated, 60–61 dosage form/usual dosage, 303, 318
Campylobacter fetus, 117 neonates, 102
Citrobacter koseri, freundii, 118 susceptibility of anaerobes to, 113
Eikenella corrodens, 121 Meyerozyma (Candida) guilliermondii, 151
Elizabethkingia meningoseptica, 121 Micafungin, 179
Escherichia coli, 123 for children with obesity, 248
Haemophilus influenzae, 124 dosage form/usual dosage, 303
Klebsiella spp, 125 neonates, 102
Mycobacterium tuberculosis, 129 susceptibility of fungal pathogens to,
Neisseria meningitidis, 130 150–151
neonates, 93–95 Micatin, 319
group B streptococcus, 137 Miconazole, 318
Mycobacterium hominis, 129 Miltefosine, 303
Proteus mirabilis, 131 Minocin, 303
Proteus vulgaris, 131 Minocycline, 303
Ralstonia, 133 dosage form/usual dosage, 319
Streptococcus milleri/anginosus group, 137 Minocycline ER, 304
Streptococcus pneumoniae, 138 Monistat-1, 319
TB, 62 Monistat-3, 319
Meningococcus Monistat-7, 319
bacteremia, 38, 39 Monobactams, allergies to, 279
endophthalmitis, 15 Mononucleosis, 187
meningitis, 61 Monurol, 299
postexposure antimicrobial prophylaxis, Moraxella
256 otitis media, acute, 19–20
purulent pericarditis, 45 sinusitis, acute, 20
Meningoencephalitis, 67 Moraxella catarrhalis, 126
Bacillus anthracis, 115 Morganella morganii, 126
Mentax, 315 Moxidectin, 304
Mepron, 292 Moxifloxacin, 304
Meropenem dosage form/usual dosage, 319
for children with obesity, 247 Mpox (monkeypox), 197
dosage form/usual dosage, 302 MRSA. See Community-associated
for multidrug-resistant gram-negative methicillin-resistant
bacilli, 241 Staphylococcus aureus
Index

neonates, 102 (CA-MRSA) infections

susceptibility of anaerobes to, 113 Mucocutaneous herpes simplex virus, 191
susceptibility of gram-negative bacterial Mucormycosis, 166
pathogens to, 111 pneumonia, 32
 Index — 371

Mucor spp, 151 Nebupent, 307

Multidrug-resistant gram-negative bacilli Necator americanus, 219, 224
(GNB), 2, 237–240 Necrotizing enterocolitis, 83
Mupirocin, 319 Necrotizing fasciitis, 8
Myambutol, 299 Aeromonas hydrophila, 114
Mycamine, 303 Clostridium perfringens, 120
Mycelex, 297 group A streptococcus, 137
Mycobacteria, nontuberculous Vibrio vulnificus, 139
adenitis, 71 Necrotizing pneumonia, Rhodococcus
pneumonia, 34, 71 hoagii, 133
Mycobacterium abscessus, 127 Neisseria gonorrhoeae, 94, 130
Mycobacterium avium complex, 128 Neisseria meningitidis, 61, 130
Mycobacterium bovis, 128 postexposure antimicrobial prophylaxis,
adenitis, tuberculous, 4 256
meningitis, 62 sepsis and meningitis, 94
tuberculosis, abdominal, 52 susceptibility to antibiotics, 110–111
Mycobacterium chelonae, 128 Neomycin, 304
Mycobacterium fortuitum complex, 128 Neomycin + polymyxin B + dexamethasone,
Mycobacterium leprae, 129 318
Mycobacterium marinum, balnei, 129 Neomycin + polymyxin B + hydrocortisone,
Mycobacterium tuberculosis, 129 316
adenitis, tuberculous, 4 Neonates
meningitis, 62 aminoglycosides, 104
pneumonia, 34 antimicrobial therapy, 75–76
tuberculosis, abdominal, 52 dosages, 100–103
Mycobutin, 309 during pregnancy or breastfeeding,
Mycolog II, 319 105–106
Mycoplasma hominis, 129 arthritis, bacterial, 9
Mycoplasma pneumoniae, 129 candidiasis, 158–159
abscess, lung, 24 conjunctivitis, 77–78
pneumonia, 27, 34 Chlamydia trachomatis, 118
Mycostatin, 305, 319 cytomegalovirus, 78–79
Myositis Elizabethkingia meningoseptica, 121
Staphylococcus aureus, 136 fungal infections, 80–83
suppurative, 7 gastrointestinal infections, 83
gonorrhea, 54
N herpes simplex infection, 84
Naegleria fowleri, 59, 209, 224 postexposure antimicrobial
Nafcillin prophylaxis, 259
dosage form/usual dosage, 304 herpes simplex virus, 191
neonates, 102 influenza A and B, 87
Naftifine, 319 meningitis, 61
Naftin, 319 Campylobacter fetus, 117
Nakaseomyces (Candida) glabrata, 151 Mycobacterium hominis, 129
Nallpen, 304 omphalitis and funisitis, 87–88
Index

Natacyn, 319 osteomyelitis, 10

Native valve endocarditis, 40–43 suppurative arthritis, 88–89
Natroba, 320 otitis media, 89
Nebcin, 313 acute, 19
 372 — Index

Neonates (continued) Nosocomial (health care–associated/

parotitis, suppurative, 90 ventilator-associated)
pneumonia, 139 pneumonia, 31
pulmonary infections, 90–92 Acinetobacter baumannii, 114
sepsis and meningitis, 93–95 Corynebacterium jeikeium, 120
Capnocytophaga ochracea, 117 Pseudomonas aeruginosa, 132
group B streptococcus, 137 Serratia marcescens, 134
Morganella morganii, 126 Shewanella spp, 134
Plesiomonas shigelloides, 131 Staphylococcus aureus, 136
Shewanella spp, 134 Noxafil, 308
syphilis, congenital, 56, 96–98 Nucleoside analogues for children with
tetanus neonatorum, 98 obesity, 248
toxoplasmosis, congenital, 98 Nuvessa, 318
urinary tract infection, 99 Nuzyra, 305
vancomycin, 105–106 Nydrazid, 301
Neosporin, 319 Nystatin, 171
Nephronia, lobar, 65 dosage form/usual dosage, 305, 319
Neuroborreliosis, 70 Nystatin + triamcinolone, 319
Neurosurgery prophylaxis, 269
Neurosyphilis, 56 O
Nifurtimox, 304 Obesity, antibiotic therapy for, 247–249
Nirmatrelvir/ritonavir, 182, 203 Obiltoxaximab, 305
dosage form/usual dosage, 304 Occult bacteremia, 38
susceptibility of non-HIV, non–hepatitis Ocuflox, 319
B or C viral pathogens to, Ocular infection, Sphingomonas
182 paucimobilis, 135
Nirsevimab, 305 Off-label use, 1
Nitazoxanide, 206–207 Ofloxacin, 319
dosage form/usual dosage, 305 Omadacycline, 305
Nitrofurantoin, 305 Omnicef, 294
Nitrofurantoin macrocrystals, 305 Omphalitis, 87–88
Nitrofurantoin monohydrate and Onchocerca volvulus, 217, 224
macrocrystalline, 305 Onchocerciasis, 207
Nitroimidazoles, 232 Onychomycosis, 168
Nix, 320 Open or laparoscopic surgery, 268
Nizoral, 301, 318 Opisthorchis spp, 218, 224
Nizoral A-D, 318 Optimization of administration, antibiotic
Nocardia asteroides, 71, 130 stewardship, 286
Nocardia brasiliensis, 71, 130 Oral cephalosporins, 142
Nocardia spp, 108–109 Oral step-down therapy, 251–252
Nocardiosis, 71 Orbactiv, 306
Nomogram, body surface area, 323 Orbital cellulitis, 13
Non–β-lactam antibiotics, allergies to, 279– Oritavancin, 245
280 dosage form/usual dosage, 306
Nongonococcal urethritis, 57, 129 Ornidazole, 232
Index

Nontuberculous mycobacteria Oropharyngeal infections, 21–23

adenitis, 4 candidiasis, 159
cystic fibrosis (CF), 25 dental abscess, 21
Noritate, 318 diphtheria pharyngitis, 21
 Index — 373

epiglottitis, 21 P
gingivostomatitis, herpetic, 22 Papules, Mycobacterium marinum, balnei,
Lemierre syndrome, 22 129
peritonsillar cellulitis and abscess, 22 Paracoccidioides spp, 151
pharyngitis, 23 Paracoccidioidomycosis, 166
retropharyngeal; parapharyngeal; lateral Paragonimus westermani, 35, 218, 224
pharyngeal cellulitis or Parapharyngeal cellulitis or abscess, 23
abscess, 23 Parasitic pathogens
Streptococcus, viridans group, 137 Acanthamoeba, 208, 210
tracheitis, bacterial, 23 amebiasis, 208–209
Orthopedic surgery prophylaxis, 269 amebic meningoencephalitis, 209–210
Oseltamivir, 182, 202 Ancylostoma braziliense, 210
dosage form/usual dosage, 306 Ancylostoma caninum, 210
susceptibility of non-HIV, non–hepatitis Ancylostoma duodenale, 210, 219
B or C viral pathogens to, angiostrongyliasis, 211
182 Angiostrongylus cantonensis, 211
Osteochondritis, 12 Angiostrongylus costaricensis, 211
Osteomyelitis, 10–12 ascariasis, 206, 211
acute, 11 babesiosis, 212–213
chronic, 12 Balamuthia mandrillaris, 210
of the foot, 12 Balantidium coli, 211
Kingella kingae, 124 Baylisascaris procyonis, 211
Mycobacterium tuberculosis, 129 Blastocystis spp, 206, 213
Ralstonia, 133 Brugia malayi, timori, 213, 217
Sphingomonas paucimobilis, 135 Capillaria, 213
Staphylococcus aureus, 136 Chagas disease, 213, 228
Streptococcus pneumoniae, 138 Clonorchis sinensis, 213
suppurative arthritis, neonates, 88–89 cryptosporidiosis, 206, 213
Otiprio, 315 cutaneous larva migrans, 206, 214
Otitis Cyclospora spp, 214
chronic suppurative, 18 cyclosporiasis, 206
Moraxella catarrhalis, 126 cysticercosis, 214
Streptococcus pneumoniae, 138 Cystoisospora belli, 215
Otitis externa, 18 Cystoisospora spp, 206
Otitis media Dibothriocephalus latus, 215
acute, 19–20 dientamoebiasis, 206, 215
Haemophilus influenzae, 124 Dipylidium caninum, 215
long-term antimicrobial prophylaxis, 262 Echinococcosis, 215–216
neonates, 19–20, 89 Echinococcus granulosus, 215
Otovel, 315 Echinococcus multilocularis, 216
Ovide, 318 Entamoeba histolytica, 208–209, 216
Oxacillin Enterobius vermicularis, 216
dosage form/usual dosage, 306 eosinophilic meningitis, 216
neonates, 102 Fasciola hepatica, gigantica, 206, 216
susceptibility of gram-positive bacterial Fasciolopsis buski, 216
Index

pathogens to, 108 filariasis, 216–217

Oxiconazole, 319 flukes, 218
Oxistat, 319 Giardia spp, 206, 218–219
Ozenoxacin, 319 hookworm, 206, 219
 374 — Index

Parasitic pathogens (continued) Pasteurella multocida, 130

Hymenolepis nana, 219 bites, dog and cat, 5
intestinal fluke, 218 postexposure antimicrobial prophylaxis,
Isospora belli, 219 255
leishmaniasis, 219–220 Paxlovid, 203, 304
lice, 220 Pediculosis capitis, 220
liver fluke, 206, 218 Pediculosis humanus, 220
Loa loa, 216 Pegasys, 301
loiasis, 206 Pegylated interferon alfa-2a, 183
lung fluke, 206, 218 Peliosis hepatis, 116
malaria, 221 Pelvic inflammatory disease, 56
Mansonella ozzardi, 206, 216, 224 Penicillin
Mansonella perstans, 206, 216, 224 allergies to, 276–277
Mansonella streptocerca, 217, 224 alternative antibiotic options for allergies
Naegleria fowleri, 209, 224 to, 281
Necator americanus, 219, 224 endocarditis, 41, 43
onchocerciasis, 207, 224 penicillinase-resistant, 143–144
Opisthorchis spp, 224 susceptibility of anaerobes to, 112
Paragonimus westermani, 224 susceptibility of gram-positive bacterial
pinworm, 207, 224 pathogens to, 108
Plasmodium falciparum, vivax, ovale, Penicillinase-resistant penicillins, 143–144
malariae, 221–224 Penicillin G benzathine
Plasmodium spp, 224 dosage form/usual dosage, 306
pneumocystis, 225 neonates, 102
preferred therapy, 205, 208–229 Penicillin G crystalline, neonates, 102
prophylaxis, 221–222 Penicillin G IM, 306
river blindness, 217 Penicillin G IV, 307
scabies, 225 Penicillin G potassium, 307
schistosomiasis, 207, 225 Penicillin G procaine
sheep liver fluke, 218 dosage form/usual dosage, 307
Strongyloides spp, 207 neonates, 102
strongyloidiasis, 225 Penicillin G sodium, 307
tapeworm, 207, 226 Penicillin V PO, 307
toxocariasis, 207, 226 Penicillin V potassium, 307
toxoplasmosis, 226–227 Penicillium spp, 151
travelers diarrhea, 227 Penlac, 315
treatment of disease, 222–224 Pentam, 307
trichinellosis, 207, 227 Pentamidine, 307
trichomoniasis, 207, 227 Pneumonia
Trichuris trichiura, 227, 229 aspiration, 24
tropical pulmonary eosinophilia, 217 immunosuppressed, neutropenic host, 30
trypanosomiasis, 228 necrotizing, Rhodococcus hoagii, 133
Uncinaria stenocephala, 228 Peptic ulcer disease, 49
whipworm, 229 Helicobacter pylori, 124
Wuchereria bancrofti, 207, 217, 229 Peptostreptococcus, 131
Index

yaws, 229 Peramivir, 182

Parenteral cephalosporins, 142–143 dosage form/usual dosage, 307
Paromomycin, 206–207 susceptibility of non-HIV, non–hepatitis B
Parotitis, 90 or C viral pathogens to, 182
 Index — 375

Periodontitis, Aggregatibacter conjunctivitis, acute, 14

actinomycetemcomitans, 115 endocarditis, 42
Periorbital cellulitis, 13–14 endophthalmitis, 15
Perirectal abscess, 53 meningitis, 61
Peritoneal dialysis indwelling catheter otitis media, acute, 19–20
infection, 53 pneumonia, 27, 28–29
Peritoneal dialysis peritonitis, Shewanella purulent pericarditis, 45
spp, 134 sinusitis, acute, 20
Peritonitis, 53 tracheitis, bacterial, 23
Bacteroides fragilis, 115 Pneumocystis, 225
neonates, 83 Pneumocystis jirovecii, 167
Peritonsillar cellulitis or abscess, 22 long-term antimicrobial prophylaxis, 264
Permethrin, 320 pneumonia, 35
Pertussis, 26 Pneumonia
neonates, 90 aspiration, 24
postexposure antimicrobial prophylaxis, atypical, 25
256–257 Bacteroides spp, 116
Pfizerpen, 307 Burkholderia cepacia, 117
Phaeohyphomycosis, 155 Chlamydia trachomatis, 118
Pharmacodynamics, 234–235 Chlamydophila pneumoniae, 118
Pharmacokinetics, 235–236 Chlamydophila psittaci, 118
Pharyngitis, 23 Chromobacterium violaceum, 118
Arcanobacterium haemolyticum, 115 community-acquired, 25
group A streptococcus, 137 definitive therapy for pathogens of CAP,
Lemierre syndrome, 22, 45 28–30
Phthirus pubis, 220 empiric therapy, 26–27
Pichia kudriavzevii (Candida krusei), 151 Enterobacter spp, 121
Pinworm, 207, 224 Escherichia coli, 123
Piperacillin/tazobactam group A streptococcus, 27, 30
for children with obesity, 247, 249 group B streptococcus, 137
dosage form/usual dosage, 307 Haemophilus influenzae, 124
neonates, 102 interstitial pneumonia syndrome of early
susceptibility of anaerobes to, 113 infancy, 28
susceptibility of gram-negative bacterial Klebsiella spp, 125
pathogens to, 111 mycobacteria, nontuberculous, 34, 71
Piperonyl butoxide + pyrethrins, 320 Mycobacterium abscessus, 127
Pityriasis versicolor, 169 Mycobacterium avium complex, 128
Plague, 72, 139 Mycobacterium tuberculosis, 129
Plaquenil, 300 Mycoplasma pneumoniae, 129
Plasmodium falciparum, vivax, ovale, Nocardia asteroides, brasiliensis, 130
malariae, 221–224 nosocomial. See Nosocomial (health
Plasmodium spp, 224 care–associated/ventilator-
Plazomicin, 241 associated) pneumonia
dosage form/usual dosage, 307 of other established etiologies, 31–35
Plesiomonas shigelloides, 131 pneumococcus, 28–29
Index

Pleural fluid/empyema, 28 Pseudomonas aeruginosa, 132–133

Pneumococcus Ralstonia, 133
abscess, lung, 24 respiratory syncytial virus (RSV)
bacteremia, 38, 39 infection, 35
 376 — Index

Pneumonia (continued) Priftin, 310

Serratia marcescens, 134 Primaquine, 231
Shewanella spp, 134 Primaquine phosphate, 308
Staphylococcus aureus, 27, 29, 136 Primaxin, 300
Streptococcus milleri/anginosus group, 137 Proctitis, gonorrhea, 55
Streptococcus pneumoniae, 138 Prophylaxis/prevention of symptomatic
Ureaplasma urealyticum, 139 infection, 253–270
Polyenes, 171–173 antimicrobial, 253–270
Polymyxin B, 307 in children who have asymptomatic
Polymyxin B + bacitracin, 320 infection/latent infection,
Polymyxin B + trimethoprim, 320 253, 265
Polysporin, 320 endocarditis, 44
Polytrim, 320 fungal infections, 152
Posaconazole, 176–177 HIV, neonates, 85–87
dosage form/usual dosage, 308 long-term antimicrobial, 253
susceptibility of fungal pathogens to, bacterial otitis media, 262
150–151 fungal, 264
Postexposure antimicrobial prophylaxis, 253 impaired splenic function, 262–263
bacterial, 255 rheumatic fever, 263
bites, animal and human, 255 urinary tract infection, recurrent,
endocarditis, 255–256 263
herpes simplex virus, 258–259 Lyme disease, 116
influenza viruses A and B, 260 parasitic pathogens, 221–222
Lyme disease, 256 postexposure antimicrobial prophylaxis,
meningococcus, 256 253
pertussis, 256–257 bacterial, 255
rabies, 260–261 bites, animal and human, 255
tetanus, 257 endocarditis, 255–256
tuberculosis, 258 herpes simplex virus, 258–259
varicella-zoster virus, 261 influenza viruses A and B, 260
viral, 258 Lyme disease, 256
Postoperative wounds meningococcus, 256
Cutibacterium acnes, 121 pertussis, 256–257
Propionbacterium acnes, 131 rabies, 260–261
Posttransplant patients tetanus, 257
lymphoproliferative disorder, 187 tuberculosis, 258
pneumonia, 30 varicella-zoster virus, 261
Praziquantel, 206–207 viral, 258
dosage form/usual dosage, 308 recurrent UTI, 66
Pred-G, 317 respiratory syncytial virus, 198
Pregnancy surgical/procedure, 253, 266–270
antimicrobial use during, 105–106 travel-related exposure, 254
herpes simplex virus, 191 Propionbacterium acnes, 131
postexposure antimicrobial Prosthetic joints, 269
prophylaxis, 258 Prosthetic valve endocarditis, 43–44
Index

Prepubertal vaginitis, 58, 135 Proteus mirabilis, 131

Pretomanid, 308 Proteus vulgaris, 131
Prevotella spp, melaninogenica, 131 Protozoa, 232
Prevymis, 302 Providencia spp, 132
 Index — 377

Pseudomonas aeruginosa, 132–133 Reactive arthritis

appendicitis, 52 Yersinia enterocolitica, 139
cystic fibrosis (CF), 25 Yersinia pseudotuberculosis, 139
endocarditis, 43 Rebetol, 309
endophthalmitis, 15 Recarbrio, 301
febrile, neutropenic patient, 68 Recurrent UTI, prophylaxis, 66
mastoiditis Reevaluation of therapy, antibiotic
acute, 17 stewardship, 285
chronic, 18 Relapsing fever, 116, 117
necrotizing fasciitis, 8 Relebactam, 241
neonates, 90 Relenza, 314
osteomyelitis of the foot, 12 Remdesivir, 182, 203
otitis, chronic suppurative, 18 dosage form/usual dosage, 309
otitis externa, 18 susceptibility of non-HIV, non–hepatitis B
pneumonia, 30, 31 or C viral pathogens to, 182
sepsis and meningitis, 94 Respiratory syncytial virus (RSV) infection,
susceptibility to antibiotics, 35, 91
110–111 preferred therapy, 197–198
tracheitis, bacterial, 23 Retapamulin, 320
urinary tract infection, 99 Retinitis, 16
Pseudomonas cepacia, mallei, pseudomallei, Retropharyngeal cellulitis or abscess, 23
133 Rezafungin, 180
Psittacosis, 118 dosage form/usual dosage, 309
Pulmonary infections, neonates, 90–92 susceptibility of fungal pathogens to,
Purulent pericarditis, 45–46 150–151
Pustules, Mycobacterium marinum, balnei, Rezzayo, 309
129 Rheumatic fever, 263
Pyelonephritis, acute, 65 Rhizopus spp, 151
Pyoderma, cutaneous abscesses, 8 Rhodococcus hoagii, 133
Pyrantel pamoate, 206–207 Ribavirin, 309
dosage form/usual dosage, 308 dosage form/usual dosage, 309
Pyrazinamide, 248 Rickettsialpox, 133
dosage form/usual dosage, 309 Rickettsia rickettsii, 72, 133
Rid, 320
Q Rifabutin, 309
Q fever, 72, 121, 133 Rifadin, 310
Quinine, 232 Rifampin
Quixin, 318 for children with obesity, 248
dosage form/usual dosage, 310
R neonates, 102
Rabies, postexposure antimicrobial Rifampin/isoniazid/pyrazinamide, 310
prophylaxis, 260–261 Rifamycin, 310
Raccoon roundworm, 212 Rifapentine, 310
Ralstonia, 133 Rifaximin, 310
Rapivab, 307 River blindness, 217
Index

Rat-bite fever, 8 Rocephin, 295

Spirillum minus, 135 Rocky Mountain spotted fever, 72, 133
Streptobacillus moniliformis, 136 RSV. See Respiratory syncytial virus (RSV)
Raxibacumab, 309 infection
 378 — Index

S Pasteurella multocida, 130

Salmonella, 133 Peptostreptococcus, 131
diarrhea/gastroenteritis, 47, 50 Propionbacterium acnes, 131
neonates, 83 Proteus mirabilis, 131
susceptibility to antibiotics, 110–111 Proteus vulgaris, 131
Salmonella typhi, 134 Providencia spp, 132
Sarcoptes scabiei, 225 Pseudomonas aeruginosa, 132
Sarecycline, 311 Serratia marcescens, 134
SARS-CoV-2. See Coronavirus Staphylococcus aureus, 136
(SARS-CoV-2) Stenotrophomonas maltophilia, 136
Scabies, 225 Streptococcus milleri/anginosus group,
Scedosporium apiospermum, 151 137
Schistosoma haematobium, intercalatum, Streptococcus pneumoniae, 138
japonicum, masoni, Vibrio vulnificus, 139
mekongi, 225 Yersinia enterocolitica, 139
Schistosomiasis, 207, 225 Septra, 313
Secnidazole, 232 Sequential parenteral-oral antibiotic therapy,
dosage form/usual dosage, 311 251–252
Selenium sulfide, 320 Seromycin, 297
Selsun, 320 Serratia marcescens, 134
Selsun Blue, 320 Serratia spp, 99
Sepsis susceptibility to antibiotics, 110–111
Acinetobacter baumannii, 114 Sertaconazole, 320
Aeromonas hydrophila, 114 Sexually transmitted infections. See Genital
Aggregatibacter aphrophilus, 115 and sexually transmitted
Bacillus cereus or subtilis, 115 infections
Bacteroides fragilis, 115 Seysara, 311
Bacteroides spp, 116 Sheep liver fluke, 218
Burkholderia cepacia, 117 Shewanella spp, 134
Campylobacter fetus, 117 Shigella spp, 135
Capnocytophaga canimorsus, 117 diarrhea/gastroenteritis, 47, 51
Chromobacterium violaceum, 118 susceptibility to antibiotics, 110–111
Citrobacter koseri, freundii, 118 Shingles, 67
Clostridium perfringens, 120 Shunt infections, 62–63
Corynebacterium jeikeium, 120 Cutibacterium acnes, 121
Cutibacterium acnes, 121 Propionbacterium acnes, 131
Elizabethkingia meningoseptica, 121 Shewanella spp, 134
Enterobacter spp, 121 Staphylococcus aureus, 136
Erysipelothrix rhusiopathiae, 122 Silvadene, 320
Escherichia coli, 123 Silver sulfadiazine, 320
Fusobacterium spp, 123 Sinusitis
Klebsiella spp, 125 Haemophilus influenzae, 124
Neisseria meningitidis, 130 Moraxella catarrhalis, 126
neonates, 93–95 Streptococcus milleri/anginosus group,
Capnocytophaga ochracea, 117 137
Index

group B streptococcus, 137 Streptococcus pneumoniae, 138

Morganella morganii, 126 Sirturo, 293
Plesiomonas shigelloides, 131 Sitavig, 315
Shewanella spp, 134 Sivextro, 312
 Index — 379

Skeletal infections, 9–12 Soolantra, 318

arthritis, bacterial, 9–10 Spectazole, 317
osteomyelitis, 10–12 Sphingomonas paucimobilis, 135
of the foot, 12 Spinal and rod replacement, 269
Skin and soft tissue infections, 3–8 Spinosad, 320
adenitis Spirillum minus, 135
acute bacterial, 3 rat-bite fever, 8
nontuberculous mycobacterial, 4 Splenectomy, 262–263
tuberculous, 4 Sporanox, 301
alternative antibiotic options for, 281 Sporothrix spp, 151
anthrax, cutaneous, 4 Sporotrichosis, 167
bites SSSS. See Staphylococcal scalded skin
dog and cat, 5 syndrome (SSSS)
human, 5 Staphylococcal scalded skin syndrome
bullous impetigo, 5 (SSSS), 8
cellulitis Staphylococcus, coagulase-negative, 108–109
buccal, 6 Staphylococcus aureus, 135–136. See also
erysipelas, 6 Community-associated
of unknown etiology, 6 methicillin-resistant
Fusobacterium spp, 123 Staphylococcus aureus
gas gangrene, 6 (CA-MRSA)
impetigo, 7 abscess, lung, 24
Ludwig angina, 7 adenitis, acute bacterial, 3
lymphadenitis, 7 alternative antibiotic options for, 281
Mycobacterium abscessus, 127 arthritis, bacterial, 9–10
Mycobacterium fortuitum complex, bacteremia, 39
128 bites
myositis, suppurative, 7 dog and cat, 5
necrotizing fasciitis, 8 human, 5
pyoderma, cutaneous abscesses, 8 bullous impetigo, 5
rat-bite fever, 8 cellulitis
staphylococcal scalded skin syndrome orbital, 13
(SSSS), 8 periorbital, 13
Staphylococcus aureus, 135 of unknown origin, 6
Streptococcus milleri/anginosus group, cystic fibrosis (CF), 25
137 dacryocystitis, 15
topical antimicrobials, 315–321 endocarditis, 44
Sklice, 318 endophthalmitis, 15
Sofosbuvir/ledipasvir, 183 febrile, neutropenic patient, 68
dosage form/usual dosage, 311 head and neck surgery prophylaxis,
Sofosbuvir (Sovaldi) plus ribavirin, 183 269
Sofosbuvir/velpatasvir, 183 hordeolum (sty) or chalazion, 16
dosage form/usual dosage, 311 impetigo, 7
Sofosbuvir/velpatasvir/voxilaprevir, 183 lymphangitis, 7
dosage form/usual dosage, 311 mastoiditis
Index

Solid-organ transplants, fungal infections acute, 17

prophylaxis, 152 chronic, 18
Solodyn, 304 myositis, suppurative, 7
Solosec, 311 neonates, 92
 380 — Index

Staphylococcus aureus (continued) Strongyloides spp, 207, 225

omphalitis and funisitis, 87, 88 Strongyloidiasis, 225
osteomyelitis, 11 Subdural empyema, Streptococcus milleri/
of the foot, 12 anginosus group, 137
suppurative arthritis, 89 Sulbactam, 241
otitis, chronic suppurative, 18 Sulbactam/durlobactam, 311
otitis externa, 18 Sulconazole, 320
otitis media, 89 Sulfacetamide sodium, 320
peritonitis, 53 Sulfacetamide sodium + prednisolone,
pneumonia, 27, 29, 30 320
postexposure antimicrobial prophylaxis, Sulfadiazine, 311
255 Sulfamylon, 318
purulent pericarditis, 45 Suprax, 294
pyoderma, cutaneous abscesses, 8 Surgical/procedure prophylaxis, 253, 266–
shunt infections, 63 270
staphylococcal scalded skin syndrome cardiovascular, 266–267
(SSSS), 8 gastrointestinal, 267–268
surgery prophylaxis, 269 genitourinary, 268
surgical/procedure prophylaxis, 266, 267 head and neck, 269
susceptibility to antibiotics, 108–109 neurosurgery, 269
toxic shock syndrome (TSS), 73 orthopedic, 269
tracheitis, bacterial, 23 thoracic (noncardiac), 267
Staphylococcus epidermidis trauma, 270
sepsis and meningitis, 95 Susceptibility data and dosing, 233
shunt infection, 63 Swimmer’s ear, 18
surgery prophylaxis, 269 Swimming pool granuloma, 129
surgical/procedure prophylaxis, 266, 267 Syphilis, 56–57, 138
Stenotrophomonas maltophilia, 136 neonates, 96–98
cystic fibrosis (CF), 25 Systemic infections, 66–73
susceptibility to antibiotics, 110–111 actinomycosis, 66
St Louis encephalitis, 60 anaplasmosis, 66
Streptobacillus moniliformis, 136 anthrax, sepsis/pneumonia, community
Streptococcus, viridans group, 137 vs bioterror exposure, 67
Streptococcus epidermidis, endocarditis, 44 appendicitis, 67
Streptococcus milleri/anginosus group, 137 aspergillosis, 153–155
Streptococcus moniliformis, rat-bite fever, 8 blastomycosis, 156
Streptococcus pneumoniae, 138 brucellosis, 67
susceptibility to antibiotics, 108–109 candidiasis, 156–160
Streptococcus pyogenes cat-scratch disease, 67
cellulitis, erysipelas, 6 chickenpox/shingles (VZV), 67
susceptibility to antibiotics, 108–109 chromoblastomycosis, 161
Streptococcus spp coccidioidomycosis, 162
bites COVID-19, 67
dog and cat, 5 cryptococcosis, 163
human, 5 ehrlichiosis, 68
Index

febrile, neutropenic patient, 68 febrile, neutropenic patient, 68

Streptomycin, 311 fungal pathogens, 152–167
Stromectol, 301 histoplasmosis, 165
 Index — 381

human immunodeficiency virus Terconazole, 321

(HIV), 68 Tetanus, 72, 120
hyalohyphomycosis, 164 postexposure antimicrobial prophylaxis,
infant botulism, 68 257
Kawasaki syndrome, 69 Tetanus neonatorum, 98
leprosy, 69 Tetracycline, 313
leptospirosis, 69 Thoracic actinomycosis, 114
Lyme disease, 69–70 Thoracic (noncardiac) surgical/procedure
melioidosis, 70 prophylaxis, 267
mucormycosis, 166 Thoracotomy, 267
mycobacteria, nontuberculous, 71 Tick-borne encephalitis, 60
nocardiosis, 71 Tick-borne relapsing fever, 116
paracoccidioidomycosis, 166 Tigecycline, 245
phaeohyphomycosis, 155 Tinactin, 321
plague, 72 Tindamax, 313
Pneumocystis jirovecii, 167 Tinea capitis, 168
Q fever, 72 Tinea corporis, 168
Rocky Mountain spotted fever, 72 Tinea cruris, 168
sporotrichosis, 167 Tinea pedis, 168
tetanus, 72 Tinea unguium, 168
toxic shock syndrome (TSS), 73 Tinea versicolor, 169
tularemia, 73 Tinidazole, 206–207, 232
dosage form/usual dosage, 313
T Tioconazole, 321
Taenia saginata, 226 Tobi, 313
Taenia solium, 214, 226 Tobi Podhaler, 313
Tafenoquine, 231 Tobradex, 321
dosage form/usual dosage, 312 Tobramycin
Tamiflu, 306 for children with obesity, 248
Taniborbactam, 241 dosage form/usual dosage, 313, 321
Tapeworm, 207, 226 neonates, 104
Target attainment, 2 Tobramycin + dexamethasone, 321
Tavaborole, 320 Tobramycin inhalation, 313
Tazicef, 295 Tobramycin + loteprednol, 321
Tecovirimat, 312 Tobrex, 321
Tedizolid, 245 Togavirus, 60
dosage form/usual dosage, 312 Tolnaftate, 321
Teflaro, 295 Tolsura, 301
Telavancin, 245 Topical antimicrobials, dosing and
dosage form/usual dosage, 312 dose forms for,
Telithromycin, 146 315–321
Tenofovir, 183 Toxic shock syndrome (TSS), 73
Tenofovir alafenamide, 312 Toxin-mediated gastroenteritis, 115
Tenofovir disoproxil fumarate, 312 Toxocara canis, 226
Tenosynovitis, 89 Toxocara cati, 226
Index

Terazol, 321 Toxocariasis, 207, 226

Terbinafine, 313 Toxoplasma encephalitis, 60
dosage form/usual dosage, 320 Toxoplasma gondii, 226–227
 382 — Index

Toxoplasmosis, 226–227 Tularemia, 73, 123

congenital, 98–99 Typhoid fever, 51, 134
Tpoxx, 312 Typhus, 133
Tracheitis, bacterial, 23
Trachoma, 118 U
Trauma surgical prophylaxis, 270 Ulesfia, 315
Travelers diarrhea, 47, 48, 227 Unasyn, 291
Travel-related exposure prophylaxis, 254 Uncinaria stenocephala, 214, 228
Treatment of infections only, antibiotic Unimmunized infants and children. See also
stewardship, 285–286 Immunocompromised
Trecator, 299 children
Treponema palladium, 138 arthritis, bacterial, 9, 10
Triazoles, 173–178 bacteremia, 38
Trichinella spiralis, 227 cellulitis, periorbital, 13
Trichinellosis, 207, 227 epiglottitis, 21
Trichomonas vaginalis, 227 Haemophilus influenzae, 124
Trichomoniasis, 57, 207, 227 meningitis, 61
Trichosporon spp, 151 pneumonia, 27
Trichuriasis, 229 purulent pericarditis, 45
Trichuris trichiura, 227, 229 Upper respiratory tract infections,
Triclabendazole, 206–207, 232 Haemophilus influenzae,
dosage form/usual dosage, 313 124
Trifluridine, 321 Ureaplasma spp, neonates, 92
Trimethoprim/sulfamethoxazole (TMP/ Ureaplasma urealyticum, 139
SMX), 206–207 Urethritis
for children with obesity, 247 Chlamydia trachomatis, 54, 118
for community-associated methicillin- gonorrhea, 55
resistant Staphylococcus nongonococcal, 57, 129
aureus (CA-MRSA) recurrent UTI, prophylaxis, 66
infections, 244 Urinary tract infection (UTI), 64–66
dosage form/usual dosage, 313 candidiasis, 160
susceptibility of gram-negative bacterial cystitis, acute, 64
pathogens to, 111 Enterobacter spp, 121
Triterpenoid, 180 Enterococcus spp, 122
Tropical pulmonary eosinophilia, 217 Escherichia coli, 122, 123
Trypanosoma cruzi, 213 Klebsiella spp, 125
Trypanosomiasis, 228 long-term antimicrobial prophylaxis,
TSS. See Toxic shock syndrome (TSS) 263
Tuberculosis, 36–37 Morganella morganii, 126
abdominal, 52 neonates, 99
Mycobacterium bovis, 128 nephronia, lobar, 65
Mycobacterium tuberculosis, 129 Proteus mirabilis, 131
postexposure antimicrobial prophylaxis, Proteus vulgaris, 131
258 Pseudomonas aeruginosa, 132
prophylaxis in children who have pyelonephritis, acute, 65
Index

asymptomatic infection/ Shigella spp, 135

latent infection, 265 Staphylococcus aureus, 136
Tuberculous adenitis, 4 surgical/procedure prophylaxis, 268
Tuberculous purulent pericarditis, 46 UTI. See Urinary tract infection (UTI)
 Index — 383

V coronavirus, 184
Vabomere, 303 cytomegalovirus, 185–186
Vaborbactam, 241 Ebola, 186
Vaginitis, 57–58, 135 enterovirus, 186
Vaginosis, 123 Epstein-Barr virus, 187
Valacyclovir hepatitis B or C, 183, 188–190
dosage form/usual dosage, 314 herpes simplex virus, 191
susceptibility of non-HIV, non–hepatitis B human herpesvirus 6, 194
or C viral pathogens to, 182 human immunodeficiency virus, 192–194
Valcyte, 314 influenza A and B, 33, 195–196
Valganciclovir, 182, 201, 202 measles, 196
dosage form/usual dosage, 314 Mpox (monkeypox), 197
neonates, 102 non-HIV, non–hepatitis B or C, 182
Valtrex, 314 pneumonia, 30, 33
Vancocin, 314 postexposure antimicrobial prophylaxis,
Vancomycin 258
for children with obesity, 247, 248–249 preferred therapy, 181, 184–199
for community-associated methicillin- respiratory syncytial virus, 197–198
resistant Staphylococcus varicella-zoster virus, 199
aureus (CA-MRSA) Virazole, 309
infections, 243 Viread, 312
dosage form/usual dosage, 314 Viridans streptococci
neonates, 105–106 endocarditis, 40, 43
susceptibility of anaerobes to, 113 sepsis and meningitis, 94
susceptibility of gram-positive bacterial Viroptic, 321
pathogens to, 109 Vistide, 296
Vantin, 295 Voriconazole, 175–176
Varicella-zoster virus (VZV), 67 for children with obesity, 248
postexposure antimicrobial prophylaxis, dosage form/usual dosage, 314
261 neonates, 102
preferred therapy, 199 susceptibility of fungal pathogens to,
susceptibility to antivirals, 182 150–151
Veklury, 309 Vosevi, 183, 311
Veltin, 316 Vulvovaginal candidiasis, 160
Vemlidy, 312 Vulvovaginitis, gonorrhea, 55
Ventricular shunt infection, Shewanella spp, Vusion, 319
134 VZV. See Varicella-zoster virus (VZV)
Ventriculitis, 129
Vfend, 314 W
Vibativ, 312 Western equine encephalitis, 60
Vibramycin, 298 West Nile virus, 60
Vibrio cholerae, 139 Whipworm, 229
Vibrio spp, necrotizing fasciitis, 8 Wound infections
Vibrio vulnificus, 139 Acinetobacter baumannii, 114
Video-assisted thoracoscopic surgery, 267 Cellulosimicrobium cellulans, 118
Index

Vigamox, 319 Clostridium botulinum, 119

Viral pathogens. See also Antiviral agents Cutibacterium acnes, 121
adenovirus, 184 Enterobacter spp, 121
conjunctivitis, acute, 14 Morganella morganii, 126
 384 — Index

Wound infections (continued) Yersinia pestis, 72, 139

Shewanella spp, 134 Yersinia pseudotuberculosis, 139
Sphingomonas paucimobilis, 135
Wuchereria bancrofti, 207, 217, 229 Z
Zanamivir, 182, 202
X dosage form/usual dosage, 314
Xacduro, 311 Zelsuvmi, 315
Xaciato, 316 Zemdri, 307
Xenleta, 302 Zepatier, 183, 298
Xepi, 319 Zerbaxa, 295
Xerava, 298 Ziana, 316
Xifaxan, 310 Zidovudine, neonates, 103
Ximino, 304 Zika, 60
Xofluza, 293 Zinacef, 296
Xolegel, 318 Zinplava, 294
Zirgan, 317
Y Zithromax, 293
Yaws, 229 Zosyn, 307
Yeast Zovirax, 290
febrile, neutropenic patient, 68 Zylet, 321
peritonitis, 53 Zymar, 317
Yersinia enterocolitica, 139 Zymaxid, 317
diarrhea/gastroenteritis, 47, 51 Zyvox, 302
Index