10/2/25, 23:14 Acute viral encephalitis in children: Treatment and prevention - UpToDate

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Acute viral encephalitis in children: Treatment and

prevention
AUTHOR: Kevin Messacar, MD, PhD
SECTION EDITORS: Morven S Edwards, MD, Douglas R Nordli, Jr, MD
DEPUTY EDITOR: Carrie Armsby, MD, MPH

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2025.

This topic last updated: Nov 14, 2024.

INTRODUCTION

Encephalitis is inflammation of the brain parenchyma, manifest by neurologic dysfunction (eg,

altered mental status, behavior, or personality; motor or sensory deficits; speech or movement
disorders; seizure) and evidence of central nervous system inflammation (eg, cerebrospinal fluid
pleocytosis and/or findings consistent with encephalitis on neuroimaging or
electroencephalogram).

The treatment and prevention of viral encephalitis in children will be discussed here. The
pathogenesis, etiology, clinical manifestations, and diagnosis of viral encephalitis in children are
discussed separately. (See "Acute viral encephalitis in children: Pathogenesis, epidemiology, and
etiology" and "Acute viral encephalitis in children: Clinical manifestations and diagnosis".)

TERMINOLOGY

Central nervous system (CNS) infections are described according to the site of infection:

● Encephalitis – Encephalitis is defined as inflammation of the brain parenchyma and is

manifested by signs of neurologic dysfunction lasting at least 24 hours. Characteristic
clinical features include altered mental status (decreased level of consciousness, lethargy,
personality change, unusual behavior), seizures, and/or focal neurologic signs, often

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accompanied by fever, headache, nausea, and vomiting [1]. (See "Acute viral encephalitis in
children: Clinical manifestations and diagnosis", section on 'Clinical features'.)

● Meningitis – Meningitis is inflammation of the meninges and is typically manifested by

fever, headache, nausea, vomiting, photophobia, and stiff neck. (See "Viral meningitis in
children: Clinical features and diagnosis", section on 'Clinical features'.)

● Rhombencephalitis – Rhombencephalitis, or brainstem encephalitis, is characterized by

myoclonic jerks, tremor, ataxia, cranial nerve involvement, respiratory abnormalities,
shock, and coma.

● Myelitis – Myelitis is inflammation of the spinal cord and is characterized by weakness,

paralysis, bowel and/or bladder dysfunction, and changes in tone and reflexes. (See
"Disorders affecting the spinal cord", section on 'Acute viral myelitis'.)

● Radiculitis – Radiculitis is inflammation of the nerve roots and is characterized by

weakness, shooting pain, dysesthesia, and diminished reflexes.

Some viruses cause less discrete manifestations of CNS infection and are described with
broader terms:

● Meningoencephalitis – Meningoencephalitis refers to CNS infection manifesting signs

and symptoms consistent with inflammation of the meninges and brain parenchyma.

● Encephalomyelitis – Encephalomyelitis refers to CNS infection manifesting signs and

symptoms consistent with inflammation of the brain parenchyma and spinal cord.

Abnormal brain function distinguishes encephalitis from meningitis. The distinction between
these entities is frequently blurred as both may be present concurrently; however, it is
important to try to determine the presence of encephalitis because the likely causes may differ
somewhat ( table 1).

● Encephalopathy – Encephalopathy is a disruption of brain function in the absence of a

direct inflammatory process in brain parenchyma (eg, caused by metabolic disturbance,
hypoxia, ischemia, drugs, intoxications, organ dysfunction, systemic infection). This is
discussed separately. (See "Acute toxic-metabolic encephalopathy in children".)

SUPPORTIVE CARE

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Encephalitis is an acute, life-threatening emergency, requiring prompt intervention. Assessment

and management often are performed simultaneously ( table 2). Supportive care is a critical
aspect of the treatment of encephalitis. Initial supportive care measures may include
stabilization of cardiorespiratory status and treatment of seizures. (See "Initial assessment and
stabilization of children with respiratory or circulatory compromise" and "Management of
convulsive status epilepticus in children".)

Monitoring — Patients with severe encephalitis (ie, those with seizures, cardiorespiratory
compromise, coma, or severe neurologic compromise) should be cared for in an intensive care
unit with close monitoring, including:

● Cardiorespiratory status.

● Neurologic status – The Glasgow coma scale (GCS) score ( table 3), although not
specifically validated in patients with encephalitis, can be helpful in quantifying the level of
consciousness and monitoring neurologic progression. Acute deterioration in the
neurologic status (eg, new focal findings, loss of pupillary reactivity, acute decline in GCS)
should prompt repeat neuroimaging to evaluate for cerebral edema, hemorrhage, or
other acute changes. Repeat neuroimaging may also be warranted in patients who do not
improve as expected over the initial days to weeks. Computed tomography is typically
performed to evaluate acute changes, and magnetic resonance imaging is performed
when more detailed diagnostic and prognostic information is desired.

● Fluid balance and electrolytes – It is important to monitor fluid balance (eg, input, urine
output, daily weight) and electrolyte status in patients with severe encephalitis, as is the
case with all critically ill children. Hypovolemia (if present) should be addressed with
appropriate volume expansion (eg, 20 mL/kg normal saline bolus). Subsequent fluid
management generally consists of isotonic maintenance intravenous (IV) fluids to
maintain euvolemia. Fluid restriction is not typically necessary. Patients who have
depressed mental status and those in whom airway reflexes are not intact are kept nil per
os. Enteral feeding tubes are used to provide adequate nutrition in patients who are not
able to feed by mouth. Parenteral nutrition is generally reserved for patients who are
unable to resume enteral feeding after one week. (See "Maintenance intravenous fluid
therapy in children" and "Overview of enteral nutrition in infants and children" and
"Parenteral nutrition in infants and children".)

Management of complications — Potential complications that must be anticipated include [2]:

● Seizures and status epilepticus, which should be treated aggressively. There is insufficient
evidence to support or refute routine use of antiseizure medications for the primary or
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secondary prevention of seizures in patients with viral encephalitis [3]. We typically treat
with antiseizure medications only if the child has clinical or electroencephalographic
evidence of seizures. In most of these cases, ongoing treatment is necessary, at least
through the acute phase of illness. (See "Management of convulsive status epilepticus in
children", section on 'Emergency antiseizure treatment'.)

● Cerebral edema. (See "Elevated intracranial pressure (ICP) in children: Clinical

manifestations and diagnosis" and "Elevated intracranial pressure (ICP) in children:
Management".)

● Fluid and electrolyte disturbance (eg, the syndrome of inappropriate antidiuretic hormone
secretion [SIADH]). (See "Treatment of hyponatremia: Syndrome of inappropriate
antidiuretic hormone secretion (SIADH) and reset osmostat".)

● Abrupt cardiac and respiratory arrest of central origin. (See "Initial assessment and
stabilization of children with respiratory or circulatory compromise".)

EMPIRIC ANTIMICROBIAL THERAPY

Empiric antimicrobial treatment is warranted in children who present with suspected

encephalitis (eg, fever, seizures, decreased or altered mental status, cerebrospinal fluid [CSF]
pleocytosis, neuroimaging and/or electroencephalogram findings not attributable to another
identified cause). In most cases, initial empiric antimicrobial coverage includes intravenous (IV)
acyclovir for potential herpes simplex virus (HSV) infection and empiric antibiotics (eg,
vancomycin and a third-generation cephalosporin) for potential bacterial central nervous
system (CNS) infection ( table 2). Empiric coverage for other potential infectious causes (eg,
influenza, Mycoplasma pneumonia, cat scratch disease, Rocky Mountain spotted fever [RMSF],
ehrlichiosis, Q fever) is individualized based on the season, exposures, geographic region, and
presenting symptoms. Antimicrobial therapy should be started as soon as possible, and,
whenever possible, appropriate specimens should be collected prior to initiating antimicrobial
therapy.

Empiric acyclovir — The indications for empiric acyclovir in neonates are reviewed separately.
(See "Neonatal herpes simplex virus (HSV) infection: Management and prevention", section on
'Indications' and "The febrile infant (29 to 90 days of age): Management", section on 'Ill-
appearing' and "The febrile neonate (28 days of age or younger): Initial management", section
on 'Ill-appearing'.)

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For infants and children beyond the neonatal period who present with suspected encephalitis,
we recommend prompt initiation of IV acyclovir pending viral studies [4].

HSV encephalitis can be a devastating infection. The majority of survivors have neurologic
deficits even when appropriately treated [5,6]. Several small randomized controlled trials in
pediatric and adult patients found that antiviral therapy for HSV encephalitis reduces mortality
[7-11]. Initial placebo-controlled trials found vidarabine reduced mortality from approximately
70 to 30 percent [7,8]. Subsequent trials found lower mortality with acyclovir compared with
vidarabine [9-11]. (See "Herpes simplex virus type 1 encephalitis", section on 'Treatment'.)

Dose — The dose of acyclovir varies depending on age [12]:

● >28 days to <3 months – 20 mg/kg per dose IV every eight hours.

● ≥3 months to <12 years – 10 to 15 mg/kg per dose IV every eight hours; an increased dose
(20 mg/kg per dose every eight hours) is approved by the US Food and Drug
Administration for the treatment of HSV encephalitis in this age group, but the risk of
nephrotoxicity and encephalopathy may be increased; consultation with an infectious
disease or pharmacology specialist may be warranted if administered with other
nephrotoxic drugs or weight-based dosing exceeds 800 mg per dose [13].

● ≥12 years – 10 mg/kg per dose IV every eight hours.

Shortages of IV acyclovir have occurred. If IV acyclovir is not available, alternative agents must
be used. Specific recommendations are presented separately. (See "Acyclovir: An overview",
section on 'If there is an acyclovir shortage'.)

Duration — The duration of empiric acyclovir therapy depends upon laboratory results:

● HSV confirmed or probable – If HSV polymerase chain reaction (PCR) from CSF or another
site is positive, acyclovir should be continued for 21 days [14]. Lumbar puncture should be
performed near the end of acyclovir treatment to ensure that HSV PCR is negative;
acyclovir therapy should be continued if CSF HSV PCR remains positive. (See "Neonatal
herpes simplex virus (HSV) infection: Management and prevention", section on 'Duration
of therapy' and "Herpes simplex virus type 1 encephalitis", section on 'Discontinuation of
therapy based on PCR results'.)

● HSV PCR is negative – For patients in whom HSV PCR is negative, the decision to continue
acyclovir therapy must be individualized. If there are strong clinical indicators of HSV
encephalitis (eg, temporal spikes on electroencephalogram or temporal lobe involvement
on imaging), repeat lumbar puncture may be warranted to exclude the possibility of a
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false-negative result on initial testing [5,15,16]. Repeat lumbar puncture also may be
warranted in patients with severe neurologic dysfunction even in the absence of clinical
indicators of HSV, particularly if no specific alternative etiology has been identified.
Additional factors to consider in the decision to continue or discontinue acyclovir therapy
are discussed separately. (See "Herpes simplex virus type 1 encephalitis", section on
'Discontinuation of therapy based on PCR results'.)

Empiric antibiotics — The clinical manifestations and CSF indices of bacterial meningitis and
viral encephalitis overlap ( table 4). Given the serious consequences of delayed treatment for
bacterial meningitis, the usual practice is to initiate empiric antibiotic therapy pending cultures
in most patients who present with clinical findings suggestive of encephalitis (eg, fever,
decreased or altered mental status, seizures, and CSF pleocytosis). Empiric treatment for
bacterial meningitis usually consists of vancomycin plus a third-generation cephalosporin
(ceftriaxone or cefotaxime). Antibiotics can be discontinued after 48 hours if cultures remain
negative. Some experts advise discontinuing vancomycin sooner in cases with low suspicion for
bacterial meningitis if Gram stain and molecular testing for Streptococcus pneumoniae (eg, on
multiplex meningitis/encephalitis PCR panel) are negative [17,18]. (See "Bacterial meningitis in
children older than one month: Treatment and prognosis", section on 'Empiric therapy'.)

Other empiric therapy — Empiric therapy also may be indicated for other infectious causes of
encephalitis that are suspected based on epidemiologic or clinical information ( table 5 and
table 6 and table 7) [15]. Examples include:

● Mycoplasma pneumoniae – A prodrome of fevers and respiratory symptoms prior to onset

of neurologic symptoms may suggest M. pneumoniae; however, respiratory symptoms may
be less prominent in some patients. The diagnosis is confirmed with PCR and/or serology.
If M. pneumoniae encephalitis is suspected, we suggest empiric therapy with a
fluoroquinolone antibiotic (eg, levofloxacin) pending confirmation of the diagnosis. A
macrolide antibiotic (eg, azithromycin) is a reasonable alternative, though macrolide
resistance among M. pneumoniae isolates is increasing in some regions. (See "Mycoplasma
pneumoniae infection in children", section on 'Macrolide resistance'.)

Adjunctive therapies (eg, intravenous immune globulin [IVIG] or glucocorticoids) to

address immune-mediated symptoms in patients with suspected M. pneumoniae
encephalitis may be considered, though data are limited [19,20]. (See "Mycoplasma
pneumoniae infection in children", section on 'Other clinical syndromes'.)

● Influenza – Influenza infection may be suggested based upon the constellation of

symptoms in the appropriate season. Patients with encephalitis due to suspected

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influenza should have appropriate testing performed. In most cases, the diagnosis can
readily be confirmed with rapid testing. Treatment for seasonal influenza in children is
summarized in the table ( table 8) and discussed separately. (See "Seasonal influenza in
children: Management".)

● Cat scratch disease (Bartonella henselae) – Cat scratch disease may be suspected based
upon reported exposure to cats (particularly kittens) and other clinical findings (ie,
lymphadenopathy). The diagnosis is confirmed with serology. Empiric therapy consists of
doxycycline or azithromycin plus rifampin. (See "Treatment of cat scratch disease", section
on 'Neurologic and ocular manifestations'.)

● RMSF (Rickettsia rickettsia) – RMSF may be suspected based upon suggestive clinical
findings (maculopapular or petechial rash, particularly with centripetal spread
( picture 1)) in the setting of exposure to ticks in an endemic region (North, Central, and
South America as well as southeastern and south-central states in the United States)
( figure 1). The diagnosis is confirmed with serology and/or PCR. Empiric therapy
consists of doxycycline. (See "Epidemiology, clinical manifestations, and diagnosis of Rocky
Mountain spotted fever" and "Treatment of Rocky Mountain spotted fever".)

● Ehrlichiosis – Clinical and epidemiologic clues to ehrlichial infections (human

monocytotropic ehrlichiosis [Ehrlichia chaffeensis] and human granulocytotropic
ehrlichiosis [Anaplasma phagocytophilum]) include exposure to ticks in endemic regions
( figure 2A-B), headache, rash, leukopenia, thrombocytopenia, characteristic blood
smear ( picture 2A-B), and elevated transaminases. The diagnosis is confirmed with
serology. Empiric therapy consists of doxycycline (same dosing as for RMSF). (See "Human
ehrlichiosis and anaplasmosis".)

● Q fever – Exposure to farm animals (eg, sheep, goats, particularly placental tissue,
parturient fluids, newborn animals) may suggest Q fever. The diagnosis is confirmed with
serology and/or PCR. Empiric treatment consists of doxycycline. (See "Q fever:
Epidemiology, microbiology, and diagnostic tests", section on 'Diagnostic tests' and "Acute
Q fever in nonpregnant patients", section on 'Children'.)

THERAPY FOR SPECIFIC VIRUSES

Specific treatment options, when available, for the more common causes of viral encephalitis in
children and adolescents are discussed separately:

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● Enteroviruses and parechoviruses (see "Enterovirus and parechovirus infections: Clinical

features, laboratory diagnosis, treatment, and prevention", section on 'Treatment')

● Herpes simplex virus (HSV) (see "Herpes simplex virus type 1 encephalitis" and "Neonatal
herpes simplex virus (HSV) infection: Management and prevention", section on 'Initial
antiviral therapy')

● Influenza virus (see "Seasonal influenza in children: Management", section on 'Antiviral

therapy')

● Arboviruses (see "Arthropod-borne encephalitides" and "Treatment and prevention of

West Nile virus infection")

● Epstein-Barr virus (see "Clinical manifestations and treatment of Epstein-Barr virus

infection", section on 'Treatment')

● Cytomegalovirus (see "Overview of cytomegalovirus infections in children", section on

'Treatment')

● Human herpesvirus 6 (see "Human herpesvirus 6 infection in children: Clinical

manifestations, diagnosis, and treatment", section on 'Treatment')

● Varicella (see "Treatment of varicella (chickenpox) infection", section on 'Individuals with

complications')

ADJUNCTIVE THERAPIES

Based on the available evidence, we suggest not routinely treating children with viral
encephalitis with adjunctive therapies, including glucocorticoids, plasmapheresis, intravenous
immune globulin (IVIG), interferon alfa, and therapeutic hypothermia [2,15,21-24]. Although
observational reports have described beneficial effects of some of these adjunctive therapies in
limited settings, the reports vary and a clear benefit has not been established [2,15].

An exception is the child with viral encephalitis who has an underlying humoral
immunodeficiency (agammaglobulinemia, hypogammaglobulinemia), for whom replacement
IVIG therapy is appropriate, as discussed separately. (See "Common variable immunodeficiency
in children", section on 'Immune globulin'.)

In addition, immune-modifying therapies (eg, glucocorticoids, IVIG) are routinely used in the
management of the following conditions, which can present with clinical, laboratory, and

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imaging findings similar to those of acute infectious encephalitis. These conditions are
discussed separately:

● Acute disseminated encephalomyelitis (see "Acute disseminated encephalomyelitis (ADEM)

in children: Treatment and prognosis")

● Autoimmune encephalitis (see "Autoimmune (including paraneoplastic) encephalitis:

Clinical features and diagnosis")

● Coronavirus disease 2019 (COVID-19)-related multisystem inflammatory syndrome in

children (MIS-C) (see "COVID-19: Multisystem inflammatory syndrome in children (MIS-C)
management and outcome", section on 'Immunomodulatory therapy')

PROGNOSIS

The prognosis of viral encephalitis varies depending upon the age of the patient, neurologic
findings at the time of presentation, and pathogen. Poor outcome is associated with the
following factors [25-30]:

● Coma, convulsion, or focal neurologic findings in the acute phase

● Young age (<5 years)
● Need for intensive care
● Herpes simplex encephalitis
● Diffusion restriction on magnetic resonance imaging

Mortality — The overall risk of death in childhood encephalitis ranges from 0 to 7 percent
[25,26,31,32]. However, mortality is increased with specific pathogens (eg, in herpes simplex
encephalitis and eastern equine encephalitis). (See "Herpes simplex virus type 1 encephalitis",
section on 'Outcomes' and "Arthropod-borne encephalitides", section on 'Eastern equine
encephalitis virus'.)

Neurologic sequelae — In self-limited cases, lethargy and coma gradually improve over days to
weeks [31]. Focal deficits resolve more slowly. In a series of 71 patients from a single institution,
24 children (34 percent) made a complete recovery within 6 to 12 months [27]. Persistent
neurologic effects may include personality change, behavior disorder (including attention deficit
disorder), movement disorder (including tic disorders), intellectual disability, learning disorders,
blindness, paresis, ataxia, recurrent headaches, and sleeping problems [27-29].

In a study that evaluated neurologic outcomes in 99 children with encephalitis at a mean 35.6
months duration of follow-up, the following findings were noted [33]:
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● No neurologic sequelae (51 percent)

● Learning problems (23 percent)
● Developmental delay (19 percent, including 7 percent with global developmental delay)
● Behavioral problems (10 percent)
● Motor deficit (2 percent)
● Visual defects (1 percent)
● Hearing impairment (1 percent)
● Bladder spasticity (1 percent)

Outcomes of specific viral pathogens

● Herpes simplex virus (HSV) encephalitis – At least two-thirds of children and adolescents
surviving with HSV encephalitis have some form of neurologic debility (eg, seizure
disorder, global developmental delay, residual hemiplegia) [5,6,9,27].

The outcome of neonatal HSV central nervous system (CNS) disease is discussed
separately. (See "Neonatal herpes simplex virus (HSV) infection: Management and
prevention", section on 'Outcome'.)

● Arboviruses – The outcome of arboviral encephalitis is discussed separately. (See

"Arthropod-borne encephalitides".)

● Enteroviruses – Enteroviral encephalitis generally causes milder clinical disease than other
viruses, except when it causes CNS infection in neonates with disseminated disease
[27,34]. Enterovirus A71 (EV-A71), which causes epdemics worldwide, can be associated
with higher morbidity and mortality [35-37]. Mortality risk is particularly high in patients
with associated cardiopulmonary failure; mortality rates as high 20 to 40 percent have
been reported in this setting [33,35]. Patients without cardiopulmonary involvement have
a better prognosis. In one retrospective study of 43 children with EV-A71 CNS infections
without cardiopulmonary failure, there were no deaths and 93 percent completely
recovered by one to two months; tremor and ataxia persisted in two children and paralysis
persisted in one child [38]. (See "Enterovirus and parechovirus infections: Epidemiology
and pathogenesis" and "Enterovirus and parechovirus infections: Clinical features,
laboratory diagnosis, treatment, and prevention".)

LONG-TERM FOLLOW-UP

Supportive care, rehabilitation, and monitoring should continue for at least one year after
discharge from the hospital [27]. Long-term sequelae of viral encephalitis may not manifest
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during the acute illness. These include motor incoordination, seizures, strabismus, amblyopia,
hearing loss, and behavioral disturbances [39].

Hearing evaluation should be performed at the time of or shortly after discharge from the
hospital. (See "Hearing loss in children: Screening and evaluation".)

Children who survive encephalitis are at risk for long-term neurodevelopmental disability.
Developmental surveillance should continue throughout childhood. Neuropsychologic testing
may be helpful in identifying neurologic deficits and formulating a treatment plan. (See
"Developmental-behavioral surveillance and screening in primary care".)

PREVENTION AND CONTROL

Because treatment options for encephalitis are limited, prevention is paramount.

Primary prevention — Primary prevention measures include:

● Handwashing (see "Infection prevention: Precautions for preventing transmission of

infection", section on 'Hand hygiene')

● Appropriate identification, monitoring, and treatment of genital herpes simplex virus (HSV)
infection during pregnancy to prevent neonatal HSV (see "Genital herpes simplex virus
infection and pregnancy")

● Routine immunization of infants, children, and adolescents (for measles, mumps, rubella,
varicella, influenza) and appropriate immunization of travelers depending upon their
destination(s) (eg, Japanese encephalitis vaccine, tick-borne encephalitis virus vaccine) (see
"Immunizations for travel")

● Insect control and avoidance of mosquito and tick exposure (eg, draining stagnant water,
appropriate dress, use of mosquito and tick repellants, mosquito netting, looking for ticks
after hiking, etc) (see "Prevention of arthropod and insect bites: Repellents and other
measures")

● Appropriate viral screening of blood products (eg, West Nile virus) (see "Blood donor
screening: Laboratory testing", section on 'Viruses')

Infection control — Patients who are hospitalized with encephalitis are usually placed on
droplet and contact precautions at the time of admission. Isolation precautions can be changed
if and when a specific pathogen is identified. Consultation with the hospital infection control

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practitioner or local health department may be helpful in making decisions regarding isolation
precautions and/or evaluation or treatment of contacts. (See "Infection prevention: Precautions
for preventing transmission of infection".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Infectious encephalitis".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or email these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient education" and the keyword[s] of interest.)

● Basics topics (see "Patient education: Encephalitis (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Overview table – A quick summary of the management of suspected encephalitis in

children is provided in the table ( table 2).

● Supportive care – Potential complications include status epilepticus, cerebral edema, fluid
and electrolyte disturbance, and cardiorespiratory failure. Patients with severe encephalitis
(ie, those with seizures, cardiorespiratory compromise, coma, or severe neurologic
compromise) should be cared for in an intensive care unit with close cardiorespiratory
monitoring and careful attention to neurologic status, fluid balance, and electrolyte status.
(See 'Supportive care' above.)

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● Empiric antimicrobial therapy – All children who present with clinical findings that are
consistent with encephalitis (ie, fever, seizures, decreased or altered mental status,
cerebrospinal fluid [CSF] pleocytosis, abnormal neuroimaging and/or
electroencephalogram findings not attributable to another identified cause) should
receive prompt empiric antimicrobial treatment. Whenever possible, appropriate
specimens should be collected prior to initiating antimicrobial therapy. (See 'Empiric
antimicrobial therapy' above.)

• Acyclovir – For all children who present with suspected encephalitis, we recommend
prompt initiation of acyclovir pending results of viral testing (Grade 1B). (See 'Empiric
acyclovir' above and "Herpes simplex virus type 1 encephalitis" and "Neonatal herpes
simplex virus (HSV) infection: Management and prevention", section on 'Initial antiviral
therapy'.)

• Antibiotics – Empiric antibiotic therapy for treatment of possible bacterial meningitis

(vancomycin plus a third-generation cephalosporin [ceftriaxone or cefotaxime])
pending results of bacterial cultures is also usually warranted since, in most cases,
bacterial meningitis cannot be excluded initially. Empiric treatment for bacterial
meningitis is discussed separately. (See "Bacterial meningitis in children older than one
month: Treatment and prognosis", section on 'Empiric therapy'.)

• Other empiric therapy – Empiric therapy also may be indicated for other infectious
causes of encephalitis that are suspected based on epidemiologic or clinical
information ( table 5 and table 6 and table 7). (See 'Other empiric therapy'
above.)

● Prognosis – The prognosis of viral encephalitis varies depending upon the age of the
patient, neurologic findings at the time of presentation, and pathogen. The overall risk of
death from childhood encephalitis ranges from 0 to 7 percent; however, the risk is
increased with specific pathogens (eg, in herpes simplex encephalitis and eastern equine
encephalitis). Long-term neurologic sequelae are common. (See 'Prognosis' above.)

● Long-term follow-up – Survivors of childhood encephalitis should be monitored for long-

term sequelae, including motor incoordination, seizures, strabismus, amblyopia, hearing
loss, and behavioral disturbances. Hearing evaluation should be performed at the time of
or shortly after discharge from the hospital. Developmental surveillance should continue
throughout childhood. (See 'Long-term follow-up' above.)

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ACKNOWLEDGMENTS

The UpToDate editorial staff acknowledges Paul Krogstad, MD, and Hordur Hardarson, MD, who
contributed to earlier versions of this topic review.

Use of UpToDate is subject to the Terms of Use.

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26. Fowler A, Stödberg T, Eriksson M, Wickström R. Childhood encephalitis in Sweden: etiology,

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acute encephalitis. Pediatrics 2014; 133:e546.
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31. Willoughby RE, Long SS. Encephalitis, meningoencephalitis, acute disseminated encephalo
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ork 2008. p.310.
32. Kolski H, Ford-Jones EL, Richardson S, et al. Etiology of acute childhood encephalitis at The
Hospital for Sick Children, Toronto, 1994-1995. Clin Infect Dis 1998; 26:398.
33. Rismanchi N, Gold JJ, Sattar S, et al. Neurological Outcomes After Presumed Childhood
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California encephalitis project, 1998-2005. J Infect Dis 2008; 198:1685.
35. Chang LY, Hsia SH, Wu CT, et al. Outcome of enterovirus 71 infections with or without
stage-based management: 1998 to 2002. Pediatr Infect Dis J 2004; 23:327.
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Topic 5977 Version 39.0

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GRAPHICS

Clinical clues to viral infections of the central nervous system in children

Relative frequency of
Etiology meningitis versus Potential clinical clues
encephalitis

Enteroviruses

Coxsackie A and B viruses Meningitis > Encephalitis Rash, herpangina, hand-foot-

mouth disease, conjunctivitis,
Echoviruses
pharyngitis, pleurodynia,
Numbered enteroviruses (eg, myopericarditis
A71)

Polioviruses Meningitis > Encephalitis Flaccid paralysis

Parechoviruses

Parechovirus type 3 Meningitis > Encephalitis Palmar and plantar rash; sepsis-
like illness in young infants

Arthropod-borne viruses (arboviruses)

West Nile virus Encephalitis > Meningitis Rash; mosquito exposure

St. Louis encephalitis virus Encephalitis = Meningitis Mosquito exposure

La Crosse (California) Encephalitis > Meningitis Mosquito exposure

encephalitis virus

Eastern equine encephalitis Encephalitis > Meningitis Mosquito exposure

virus

Western equine encephalitis Encephalitis = Meningitis Mosquito exposure

virus

Powassan virus Encephalitis > Meningitis Tick exposure

Herpesviruses

Herpes simplex type 1 Encephalitis > Meningitis Oral lesions

Herpes simplex type 2 Meningitis > Encephalitis Genital lesions, sacral

radiculopathy (urinary retention,
constipation, paresthesia,
weakness)

Cytomegalovirus Encephalitis > Meningitis Preterm neonate;

immunocompromised host

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Varicella zoster virus Meningitis > Encephalitis Vesicular rash; shingles (rash may
not be present in some cases of
viral reactivation)

Epstein-Barr virus Encephalitis > Meningitis Preceding signs of infectious

mononucleosis – Malaise,
headache, fever, pharyngitis,
cervical lymph node enlargemen

Other viruses

HIV (ie, acute retroviral Encephalitis = Meningitis Intravenous drug use, high-risk
syndrome) sexual behavior

Influenza virus Encephalitis > Meningitis Classic influenza symptoms –

Fever, cough, vomiting,
headache, diarrhea

Lymphocytic choriomeningitis Meningitis > Encephalitis Rodent pets or contact with

virus rodent droppings or urine

Measles virus Encephalitis > Meningitis Cough, coryza, conjunctivitis;

occurs in unvaccinated or
incompletely vaccinated
individuals

Mumps virus Meningitis > Encephalitis Painful parotitis; occurs in

unvaccinated or incompletely
vaccinated individuals

Rabies virus Encephalitis > Meningitis Animal exposure; prodrome of

nonspecific symptoms (fever,
headache, malaise, myalgia,
cough, sore throat, nausea,
vomiting)

SARS-CoV-2 Encephalitis = Meningitis Preceding signs of COVID-19 –

Fever, cough, respiratory
symptoms

Zika virus Encephalitis > Meningitis Mosquito exposure; residence in

or travel to an endemic region

COVID-19: coronavirus disease 2019 (COVID-19); HIV: human immunodeficiency virus; SARS-CoV-2: severe
acute respiratory syndrome coronavirus 2.

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Initial evaluation and management of suspected encephalitis in children older

than one month of age

History

Symptoms – Fever, decreased level of consciousness, irritability or personality/behavior change,

seizures, focal neurologic abnormalities

Travel

Exposure (animals, insects, freshwater swimming, toxins)

Immunizations and immune status

Physical findings
Vital signs and general examination

Neurologic examination, particularly for GCS and focal findings

Laboratory studies
Blood tests:
CBC
Glucose, electrolytes, BUN, creatinine
LFTs, ammonia
Coagulation studies
Blood cultures
Serologies for EBV, HIV, and Mycoplasma pneumoniae (IgM and IgG)
EBV PCR
Acute serum sample (to hold for subsequent serologic testing if necessary)

Urine tests:
Urine drug screen
Urinalysis

CSF studies (perform lumbar puncture after neuroimaging if a mass lesion has not been ruled out):
Opening pressure (if feasible)
CSF cell count/differential
CSF glucose and protein
CSF Gram stain and bacterial culture
CSF PCR testing *
If possible, save a sample of CSF (to hold for subsequent testing)

Other laboratory tests to consider:

Testing for influenza and other respiratory viruses (ie, respiratory panel/PCR, viral culture)
Throat swab for HSV, enterovirus, M. pneumoniae PCRs
Stool or rectal swab for enterovirus PCR and viral culture

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Tests for toxic metabolic encephalopathy and inborn errors of metabolism ¶

Testing for autoimmune encephalitis (NMDAR and VGKC antibodies), if clinically indicated ¶
CSF acid fast stain and Mycobacterium tuberculosis culture, if clinically indicated

Ancillary studies
Neuroimaging – MRI preferred, but perform CT if MRI not promptly available, impractical, or cannot be
performed

EEG – As soon as is feasible

Presumptive diagnosis
Based upon ALL of the following:
Altered mental status, focal neurologic deficits, and/or seizures, plus
CSF pleocytosis, plus
Abnormal neuroimaging or EEG, plus
No other etiology identified

Treatment

Stabilization

Support airway, breathing, and circulation

Endotracheal intubation for GCS ≤8 or compromised airway

Fluid resuscitation with normal saline (20 mL/kg, initial bolus) for signs of hypovolemia or shock

Treat seizures with lorazepam (0.1 mg/kg IV)

Empiric antimicrobial therapy

Empiric acyclovir Δ (for all patients with suspected acute infectious encephalitis):
Age >28 days to <3 months – 20 mg/kg IV every 8 hours ◊
Age ≥3 months to <12 years – 10 to 15 mg/kg IV every 8 hours ◊
Age ≥12 years – 10 mg/kg IV every 8 hours ◊

Empiric antibiotics (give until bacterial meningitis has been excluded):

Vancomycin 15 mg/kg IV every 6 hours (maximum 4 g/day) ◊ , plus
Either ceftriaxone 50 mg/kg IV every 12 hours (maximum 4 g/day) or cefotaxime (if available)
100 mg/kg IV every 8 hours (maximum 2 g/dose)

Consider empiric treatment for other causes (eg, Mycoplasma pneumoniae, influenza, Rocky
Mountain spotted fever, cat scratch disease, Q fever, ehrlichiosis) as indicated based upon clinical
findings, season, exposure history, and other risk factors §

BUN: blood urea nitrogen; CBC: complete blood count; CMV: cytomegalovirus; CNS: central nervous
system; CSF: cerebrospinal fluid; CT: computed tomography; EBV: Epstein-Barr virus; EEG:
electroencephalography; GCS: Glasgow coma scale; HHV-6: human herpesvirus 6; HIV: human
immunodeficiency virus; HSV: herpes simplex virus; IV: intravenous; LFT: liver function test; NMDAR: anti-

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N-methyl-D-aspartate receptor; MRI: magnetic resonance imaging; PCR: polymerase chain reaction; VZV:
varicella zoster virus; VGKC: voltage-gated potassium channel; WNV: West Nile virus.

* PCR testing may consist of multiplex testing for multiple viral and bacterial pathogens simultaneously
in a single CSF sample (eg, FilmArray meningitis/encephalitis panel [BioFire]) or individual PCR tests for
specific pathogens. Testing for HSV, enterovirus, and parechovirus should be performed in all patients;
testing for additional pathogens may be warranted based upon history and epidemiology (eg,
Mycoplasma pneumoniae, influenza, CMV, EBV, HHV-6, VZV, WNV).

¶ Refer to separate UpToDate topics for details regarding the approach to diagnostic testing in children
with suspected toxic metabolic encephalopathy, inborn errors of metabolism, or autoimmune
encephalitis.

Δ Empiric acyclovir therapy is provided to all patients with suspected encephalitis until HSV infection has
been excluded (ie, by negative CSF PCR). Refer to UpToDate topics on HSV for additional details.

◊ The doses of acyclovir and vancomycin listed in this table are for patients with normal kidney function.
Dosing adjustment is required in patients with kidney function impairment. Refer to drug monographs
for details.

§ Empiric therapy for M. pneumoniae typically consists of a macrolide antibiotic (eg, azithromycin). Several
agents are available for treatment of influenza in children (oseltamivir, peramivir, baloxavir, and
zanamivir); refer to UpToDate's topics on seasonal influenza in children for details. Empiric therapy for cat
scratch disease, Rocky Mountain spotted fever, Q fever, or ehrlichiosis typically consists of doxycycline
(rifampin is added in the case of cat scratch disease). Risk factors for these infections include exposure to
or bites/scratches from cats or kittens (cat scratch disease), exposure to ticks in endemic regions (Rocky
Mountain spotted fever and ehrlichiosis) and exposure to farm animals (Q fever). Refer to separate
UpToDate content on these infections for additional details.

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Glasgow Coma Scale and Pediatric Glasgow Coma Scale

Glasgow Coma
Sign Pediatric Glasgow Coma Scale [2] Score
Scale [1]

Eye opening Spontaneous Spontaneous 4

To command To sound 3

To pain To pain 2

None None 1

Verbal response Oriented Age-appropriate vocalization, smile, or orientation 5

to sound; interacts (coos, babbles); follows objects

Confused, Cries, irritable 4

disoriented

Inappropriate Cries to pain 3

words

Incomprehensible Moans to pain 2

sounds

None None 1

Motor response Obeys commands Spontaneous movements (obeys verbal command) 6

Localizes pain Withdraws to touch (localizes pain) 5

Withdraws Withdraws to pain 4

Abnormal flexion Abnormal flexion to pain (decorticate posture) 3

to pain

Abnormal Abnormal extension to pain (decerebrate posture) 2

extension to pain

None None 1

Best total score 15

The Glasgow Coma Scale (GCS) is scored between 3 and 15, with 3 being the worst and 15 the best. It is
composed of 3 parameters: best eye response (E), best verbal response (V), and best motor response (M).
The components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS of 9.
Traditionally, the GCS defines the severity of traumatic brain injury (TBI) as follows: ≤8: severe brain
injury, 9 to 12: moderate injury, and a score ≥13 or higher: mild injury. However, a significant minority of
patients with TBI and a GCS score of 13 have potentially life-threatening intracranial lesions. While a
revised classification has not been widely adopted, a GCS score of 9 through 13 likely best represents the
TBI population at moderate risk for death or long-term disability (ie, "potentially severe").

The Pediatric Glasgow Coma Scale (PGCS) was validated in children 2 years of age or younger.

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Data from:
1. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; 2:81.
2. Holmes JF, Palchak MJ, MacFarlane T, Kuppermann N. Performance of the pediatric Glasgow coma scale in children with
blunt head trauma. Acad Emerg Med 2005; 12:814.

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Typical cerebrospinal fluid findings in central nervous system infections*

Total white blood cell

Glucose (mg/dL) Protein (mg/dL)
(cells/microL)

100 to 100 to
<10 ¶ 10 to 40 Δ ◊ 50 to 300 § >1000
500 1000

More Bacterial Bacterial Bacterial Viral meningitis Bacterial Bacterial or Ea

common meningitis meningitis meningitis meningitis viral ba
Nervous system
meningitis me
Lyme disease
(neuroborreliosis) TB Vir
meningitis me
Encephalitis
Ne
Neurosyphilis
TB
TB meningitis ¥
me

Less TB Neurosyphilis Early bacterial Some Encephalitis En

common meningitis meningitis cases of
Some viral
mumps
Fungal infections
and LCMV
meningitis (such as
mumps and
LCMV)

TB: tuberculosis; LCMV: lymphocytic choriomeningitis virus.

* It is important to note that the spectrum of cerebrospinal fluid values in bacterial meningitis is so wide
that the absence of one or more of these findings is of little value. Refer to the UpToDate topic reviews on
bacterial meningitis for additional details.

¶ <0.6 mmol/L.

Δ 0.6 to 2.2 mmol/L.

◊ 1 to 5 g/L.

§ 0.5 to 3 g/L.

¥ Cerebrospinal fluid protein concentrations may be higher in some patients with tuberculous meningitis;
concentrations >500 mg/dL are an indication of blood-brain barrier disruption or increased intracerebral
production of immunoglobulins, and extremely high concentrations, in the range of 2 to 6 g/dL, may be
found in association with subarachnoid block.

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Epidemiologic and historic clues to the etiology of encephalitis in children

Epidemiologic clues Potential etiologies

Age (0 to 28 days) Infectious – CMV, HSV (type 1 or 2), enteroviruses,

parechoviruses, rubella virus

Noninfectious – Inborn error of metabolism (eg, organic

acidemia, urea cycle disorder)

Season:

Summer Enterovirus, free-living amebae

Late summer/fall Arbovirus

Winter Postinfectious encephalitis in countries with low rates of

MMR immunization

Infection in horses, birds Arbovirus, Hendra virus

Blood transfusion or transplant recipient CMV, EBV, HIV, rabies, tick-borne encephalitis, WNV

Immunodeficiency CMV, HHV-6, HSV, VZV, WNV, enterovirus (especially in X-

linked agammaglobulinemia and common variable
immunodeficiency)

Historic clues

Rash

Vesicular HSV, VZV, enterovirus (hand, foot, and mouth disease),

herpes B virus

Hand, foot, mouth Enterovirus

Erythematous macules and papules Measles

with cephalocaudad spread

Maculopapular WNV

Maculopapular/petechial begins on Rocky Mountain spotted fever

ankles and wrists

Exposures

Mosquitoes Arbovirus

Ticks Borrelia burgdorferi, Powassan virus, Rickettsia rickettsii, tick

borne encephalitis

Animal bite/exposure (dog, bat, cat, Rabies, arboviruses, cat scratch disease, Q fever
birds, livestock, others)

Blood transfusion or transplant CMV, EBV, HIV, rabies, tick-borne encephalitis, WNV
recipient

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Recent infectious illness ADEM

Recreational activity

Swimming Enteroviruses, free-living amebae

Spelunking Rabies

Sexual activity HIV, Treponema pallidum

Travel

Immunization

Lack of immunization for specific Japanese encephalitis, MMR, VZV, polio, tick-borne
agent encephalitis

Recent immunization ADEM

CMV: cytomegalovirus; HSV: herpes simplex virus; MMR: measles, mumps, rubella; EBV: Epstein-Barr
virus; WNV: West Nile virus; HHV-6: human herpesvirus 6; VZV: varicella-zoster virus; ADEM: acute
disseminated encephalomyelitis.

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Travel history and possible etiologic agent(s) of viral encephalitis

Travel Possible infectious agent(s)

Africa Rabies virus, West Nile virus, Plasmodium falciparum, Dengue virus, Trypanosoma bruce
gambiense, Trypanosoma brucei rhodesiense

Australia Murray Valley encephalitis virus, Japanese encephalitis virus, Hendra virus

Central America Rabies virus, Eastern equine encephalitis virus, Western equine encephalitis virus,
Venezuelan equine encephalitis virus, St. Louis encephalitis virus, Dengue virus,
Rickettsia rickettsii, P. falciparum, Taenia solium

Europe West Nile virus, tick-borne encephalitis virus, Borrelia burgdorferi, Anaplasma
phagocytophilum

India, Nepal Rabies virus, Japanese encephalitis virus, P. falciparum, Dengue virus

Middle East West Nile virus, P. falciparum

Russia Tick-borne encephalitis virus

South America Rabies virus, Eastern equine encephalitis virus, Western equine encephalitis virus,
Venezuelan equine encephalitis virus, St. Louis encephalitis virus, Dengue virus, R.
rickettsii, Bartonella bacilliformis (Andes mountain), P. falciparum, T. solium

Southeast Asia, Japanese encephalitis virus, tick-borne encephalitis virus, Nipah virus, P. falciparum,
China, Pacific Gnathostoma species, T. solium, Dengue virus
Rim

Modified with permission from: Tunkel AR, Glaser CA, Bloch KC, et al. The management of encephalitis: clinical practice guidelines
by the Infectious Diseases Society of America. Clin Infect Dis 2008; 47:303. Copyright © 2008 University of Chicago Press.

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Clinical findings that may suggest specific etiologic agent(s) in children with
encephalitis

Clinical presentation Possible infectious agent(s)

General findings

Hepatitis HSV (especially in infants), enterovirus (especially in infants),

Coxiella burnetii; any severe encephalitis causing
impaired systemic perfusion can cause hepatitis due to shock liver

Lymphadenopathy HIV, EBV, cytomegalovirus, measles virus, rubella virus, WNV,

Treponema pallidum, Bartonella henselae and other Bartonella
species, Mycobacterium tuberculosis, Toxoplasma gondii,
Trypansoma brucei gambiense

Parotitis Mumps virus

Rash HSV, VZV, herpes B virus, human herpesvirus 6, WNV, rubella virus
some enteroviruses, HIV, Rickettsia rickettsii, Mycoplasma
pneumoniae, Borrelia burgdorferi, Treponema pallidum, Ehrlichia
chaffeensis, Anaplasma phagocytophilum

Respiratory tract findings Influenza virus, adenovirus, M. pneumoniae, Venezuelan equine

encephalitis virus, Nipha virus, Hendra virus, C. burnetii, M.
tuberculosis, Histoplasma capsulatum

Retinitis Cytomegalovirus, T. gondii, WNV, B. henselae, T. pallidum

Urinary symptoms (dysuria, St. Louis encephalitis virus (during prodrome)

urgency, incontinence)

Neurologic findings

Cerebellar ataxia Enteroviruses (especially A71), VZV, EBV, mumps virus, St. Louis
encephalitis virus, Tropheryma whipplei, T. brucei gambiense

Cranial nerve abnormalities HSV, enteroviruses, EBV, Listeria monocytogenes, M. tuberculosis, T.

pallidum, B. burgdorferi, T. whipplei, Cryptococcus neoformans,
Coccidioides species, H. capsulatum

Dementia HIV, human transmissible spongiform encephalopathies (sCJD and

vCJD), measles, T. pallidum, T. whipplei

Myorhythmia T. whipplei (oculomasticatory)

Parkinsonism (bradykinesia, Japanese encephalitis virus, St. Louis encephalitis virus, WNV,
masked facies, cogwheel rigidity, Nipah virus, T. gondii, T. brucei gambiense
postural instability)

Poliomyelitis-like flaccid paralysis Japanese encephalitis virus, WNV, tick-borne encephalitis virus,
enteroviruses (enterovirus 71, coxsackieviruses, poliovirus)

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Rhomboencephalitis Enterovirus 71, HSV, WNV, L. monocytogenes

HSV: herpes simplex virus; EBV: Epstein-Barr virus; WNV: West Nile virus; VZV: varicella-zoster virus; sCJD:
sporadic Creutzfeldt-Jakob disease; vCJD: variant Creutzfeldt-Jakob disease.

Modified with permission from: Tunkel AR, Glaser CA, Bloch KC, et al. The management of encephalitis: clinical practice guidelines
by the Infectious Diseases Society of America. Clin Infect Dis 2008; 47:303. Copyright © 2008 University of Chicago Press.

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Dosing recommendations for antiviral agents for the treatment of influenza in

children and adolescents [1-3]

Drug/formulation Dosing recommendations

Oseltamivir (Tamiflu) *

30 mg capsule 1 through 12 years

45 mg capsule Children ≥12 months should receive approximately 4 mg/kg per day orally
75 mg capsule divided into 2 doses for a 5-day treatment course
6 mg/mL
≤15 kg >15 to 23 kg >23 to 40 kg >40 kg
suspension ¶
60 mg/day 90 mg/day orally 120 mg/day orally 150 mg/day orally
orally divided divided into 2 divided into 2 divided into 2
into 2 doses for doses for 5 days doses for 5 days doses for 5 days
5 days

≥13 years

150 mg/day orally divided into 2 doses for 5 days

Baloxavir (Xofluza) Δ

40 mg tablet ≥5 years
80 mg tablet
Weight <20 kg (oral suspension) – 2 mg/kg orally as a single dose
2 mg/mL oral
Weight 20 to <80 kg (oral suspension or tablet) – 40 mg orally as a single
suspension
dose
Weight ≥80 kg (oral suspension or tablet) – 80 mg orally as a single dose

Peramivir (Rapivab) *

200 mg in 20 6 months through 12 years

mL (10 mg/mL)
12 mg/kg per dose IV as a single dose (maximum dose 600 mg)
in a single-use
vial ≥13 years

600 mg IV as a single dose

Zanamivir (Relenza) ◊

5 mg per ≥7 years
inhalation
(Diskhaler) 2 inhalations (10 mg total per dose) twice daily for 5 days §

This table is meant for use with UpToDate content related to treatment of seasonal influenza in children.
The choice of agent for treatment may vary with the age of the child and susceptibility patterns of
circulating strains. Refer to UpToDate content for additional details, including indications for treatment
and dosing recommendations for oseltamivir in infants younger than 1 year.

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IV: intravenously.

* Dose adjustment is necessary for patients with kidney function impairment.

¶ When dispensing the oral suspension of oseltamivir, providers and pharmacists must take care to
provide a dosing device that matches the units of measure on the prescription.

Δ Baloxavir is available in Japan for the treatment of influenza in children <12 years of age who weigh at
least 10 kg. Refer to Japanese prescribing information for dosing information for children <12 years of
age.

◊ Zanamivir is not recommended for the treatment of hospitalized patients, because of limited data in
patients with severe influenza. Zanamivir inhalation powder should not be reconstituted in any liquid
formulation and is not recommended for use in nebulizers or mechanical ventilators.

§ Two doses should be administered on day 1, provided that the doses can be spaced at least 2 hours
apart.

References:
1. Kimberlin DW, Barnett ED, Lynfield R, Sawyer MH (Eds). Non-HIV antiviral Drugs. In: Red Book: 2021-2024 Report of the
Committee on Infectious Diseases, 32nd ed, American Academy of Pediatrics 2021.
2. Rapivab (peramivir injection) for intravenous use. US Food and Drug Administration (FDA) approved product information.
Revised January 2021. US Food and Drug Administration. http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm
(Accessed on February 3, 2021).
3. Xofluza (baloxavir marboxil) prescribing information. US Food and Drug Administration (FDA) approved product
information. Revised August 2022. US Food and Drug Administration.
https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm (Accessed on August 16, 2022).

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Rocky Mountain spotted fever rash

Child with Rocky Mountain spotted fever has the rash that is characteristic but typically does not appear
until several days after fever onset.

From: Fatal Cases of Rocky Mountain Spotted Fever in Family Clusters --- Three States, 2003. MMWR Morb Mortal Wkly Rep 2004;
53(19):407. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5319a1.htm.

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Annual incidence (per million persons) for Rocky Mountain Spotted Fever in the
United States, 2018

Although RMSF cases have been reported throughout most of the contiguous United States, five states
(North Carolina, Oklahoma, Arkansas, Tennessee, and Missouri) account for over 60% of RMSF cases. The
primary tick that transmits Rickettsia rickettsii in these states is the American dog tick (Dermacentor
variabilis, Dermacentor andersoni).

RMSF: Rocky Mountain Spotted Fever; NN: not notifiable.

Reproduced from: Rocky Mountain Spotted Fever (RMSF): Data and Statistics. Centers for Disease Control and Prevention. Available
at: https://www.cdc.gov/rocky-mountain-spotted-fever/data-research/facts-stats/index.html (Accessed on May 27, 2024).

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Annual reported incidence (per million population) for anaplasmosis – United

States, 2019

The figure shows the incidence of anaplasmosis cases by state in 2019 per million persons.

NN: not notifiable.

Reproduced from: Centers for Disease Control and Prevention. Anaplasmosis: Epidemiology and Statistics. Available at:
https://www.cdc.gov/anaplasmosis/hcp/statistics/?CDC_AAref_Val=https://www.cdc.gov/anaplasmosis/stats/index.html (Accessed
on May 27, 2024).

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Annual reported incidence (per million population) for Ehrlichia chaffeensis in

the United States for 2019

This figure shows the incidence of ehrlichiosis cases caused by Ehrlichia chaffeensis by state in 2019 per
million persons.

NN: not notifiable.

Reproduced from: United States Centers for Disease Control and Prevention. Ehrlichiosis: Epidemiology and Statistics, 2019.
Available at: https://www.cdc.gov/ehrlichiosis/stats/index.html (Accessed on January 4, 2022).

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Wright-Giemsa stain morula

Wright-Giemsa stain of a buffy coat specimen revealed the presence of a morula, or cluster of
intracellular coccobacilli, inside of a polymorphonuclear leukocyte (arrow).

Reproduced with permission from: Donato, AA, Chaudhary, A. Photo Quiz: A 78-Year-Old Man with the "Summer Flu" and
Cytopenias. Clin Infect Dis 2009; 48:1433. Copyright ©2009 University of Chicago Press.

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Morulae of anaplasmosis in circulating neutrophils

A 51-year-old man with no significant past medical history presented with a 5-day history of fever,
malaise, and diffuse myalgias with no recollection of a tick bite. He was found to have thrombocytopenia,
elevated transaminase levels, and renal insufficiency. Examination of the peripheral smear suggested the
diagnosis of anaplasmosis. He was started on a course of doxycycline, with eventual complete resolution
of symptoms. The peripheral smear (1000x, "feather edge") shows morulae of anaplasmosis in the
patient's granulocytes. Photomicrographs B and C were taken from the extreme feather edge and show
exploded neutrophils containing well-delineated morulae.

Peripheral smear and patient information kindly provided by Dr. Eddy J Chen and Dr. German Pihan, Departments of Medicine
and Pathology, Beth Israel Deaconess Medical Center, Boston, MA.

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Contributor Disclosures
Kevin Messacar, MD, PhD No relevant financial relationship(s) with ineligible companies to
disclose. Morven S Edwards, MD No relevant financial relationship(s) with ineligible companies to
disclose. Douglas R Nordli, Jr, MD No relevant financial relationship(s) with ineligible companies to
disclose. Carrie Armsby, MD, MPH No relevant financial relationship(s) with ineligible companies to
disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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