Lecture Objectives

After completing this lecture student will be able to:

♦♦Classify streptococci.
♦♦Describe antigenic structure of Str. pyogenes.
♦♦List and describe toxins and enzymes of Streptococcus pyogenes.
♦♦Discuss pathogenicity of streptococci.
List and describe toxins and enzymes of Streptococcus pyogenes.
♦♦Describe nonsuppurative complications of Str. pyogenes infections.
♦♦Discuss labaratory diagnosis of streptococcal infections.
♦♦Discuss group B streptococci, group D streptococci and viridans group.
 Streptococci

 Characters of Streptococci
 Gram positive cocci
 1µm in diameter
 Chains or pairs
 Usually capsulated
 Non motile
 Non spore forming
 Facultative anaerobes
 Fastidious
 Catalase negative (Staphylococci are catalase positive)
Classification of Streptococci

 Streptococci can be classified according to:

Hemolysis on Blood Agar (BA)
Oxygen requirements
○ Anaerobic (Peptostreptococcus)
○ Aerobic or facultative anaerobic (Streptococcus)
Serology (Lanciefield Classification)
Classification of Streptococci Based
on Hemolysis on Blood Agar

 -hemolysis
Partial hemolysis
Green discoloration around the colonies
e.g. non-groupable streptococci (S. pneumoniae & S. viridans)
 -hemolysis
Complete hemolysis
Clear zone of hemolysis around the colonies
e.g. Group A & B (S. pyogenes & S. agalactiae)
 -hemolysis Streptococci

No lysis
e.g. Group D (Enterococcus spp)

-hemolysis -hemolysis -hemolysis

hemolysis
 Serology: Lanciefield Classification
Streptococci

Lanciefield classification

Group A Group B Group C Group D Other groups

S. pyogenes S. agalactiae S. equisimitis Enterococcus (E-U)

 Streptococci classified into many groups from A-K & H-V

 One or more species per group
 Classification based on C- carbohydrate antigen of cell wall
 Groupable streptococci
○ A, B and D (more frequent)
○ C, G and F (Less frequent)
 Non-groupable streptococci
○ S. pneumoniae (pneumonia)
○ viridans streptococci
 e.g. S. mutans
 Causing dental carries
Streptococcus : Habitat and
Clinical Infections
 Habitat
 Clinical infections
 Upper and lower
 Indigenous respiratory tract
respiratory tract infections
microbial flora of animals
 Urinary tract infections
and humans
 Certain species are also  Wound infections
found in the  Endocarditis
gastrointestinal and
urogenital tracts of humans
Group A streptococci
Beta-Hemolytic Streptococci

 Include only S. pyogenes

Epidemiology:
 S. pyogenes can transiently colonize the oropharynx and skin
 Group A streptococcal infections affect all ages peak incidence at 5-
15 years of age
 90% of cases of pharyngitis
 The pathogen is spread mainly by respiratory droplets.
 Soft tissue infections are preceded by skin colonization and the
organisms are introduced into the superficial or deep tissue through
a break in the skin.
Pathogenesis and Virulence Factors
 Structural components
 M protein , which interferes with opsonization and lysis of the
bacteria
 Lipoteichoic acid & F protein adhesion
 Hyaluronic acid capsule, which acts to camouflage the bacteria
 Enzymes
 Streptokinases(fibrinolysin)
 Deoxynucleases facilitate the spread of streptococci through
 C5a peptidase tissues
 Hyaluronidase
 Pyrogenic toxins that stimulate macrophages and helper T
cells to release cytokines ,they are superantigens .
 Streptolysins.
 Streptolysin O : O2-labile lyse red blood cells, white blood cells, and
platelets. ASO (antistreptolysin O) titer >160-200 units
 Streptolysin S: O2-stable not antigenic, kills phagocytes by releasing the
lysosomal contents after engulfment.
 Streptococcus pyogenes

Clinical Diseases

1. Local infection with S. pyogenes

Streptococcal sore throat (pharyngitis), and scarlet fever.

Streptococcal pyoderma (impetigo, local infection of

superficial layers of skin).

Strains that cause skin infections are different from those

that cause pharyngitis.
Streptococcal throat
infection
2. Invasion by S. pyogenes

Invasion from respiratory tract: otitis media, sinusitis,

pneumonia, meningitis, osteomyelitis, and arthritis.
Invasion from skin:erysipelas, cellulitis, and
necrotizing fasciitis WHICH IS Diffuse and rapidly
spreading infection that extends along lymphatic pathways
with only minimal local suppuration.
Sepsis (streptococcal toxic shock syndrome ,STSS):
the organism is introduced into the subcutaneous tissue
through a break in the skin cellulitis necrotizing
fasciitis systemic toxicity, multiple organ failure, and
death (mortality > 40%).
Impetigo caused by
S.pyogenes
3. Post-streptococcal
diseases =non
supurative complication
(occurs 1-4 weeks after acute S. pyogenes infection,
hypersensitivity responses)

1.Rheumatic fever: most commonly preceded by infection of

the respiratory tract. Inflammation of heart (pancarditis), joints,
blood vessels, and subcutaneous tissue.

Results from cross reactivity of anti-M protein Ab and the

human heart tissue.

* Rheumatic fever can be reactivated by recurrent

streptococcal infections, whereas nephritis does not.
Post-streptococcal diseases
=non supurative complication
2. Acute glomerulonephritis: preceded by infection
of the skin (more commonly) or the respiratory
tract. Symptoms: edema, hypertension,
hematuria, and proteinuria. Initiated by Ag-Ab
complexes on the glomerular basement
membrane.
 * Rheumatic fever can be reactivated by
recurrent streptococcal infections, whereas
nephritis does not.
Laboratory Diagnosis:
Group A Streptococcus
 Identification
 Catalase-negative
 Bacitracin-susceptible

Group A streptococci is susceptible to

Bacitracin disk (left); The right shows
resistance
Group B -Hemolytic Streptococcus
(Streptococcus agalactiae)

 Has been known to cause mastitis in cattle

 Colonize the urogenital tract of pregnant women
 Cause invasive diseases in newborns
 Early-onset infection
 Late-onset disease
Stretococcus agalactiae:
Invasive Infections

 Early-onset infection

Occurs in neonates who are less than 7 days old

neonates
Vertical transmission of the organism from the
mother
Manifests in the form of pneumonia or meningitis
with bacteremia
Associated with a high mortality rate
 Streptococcus agalactiae:
Invasive Infections
 Late-onset infection
 Occurs between 1 week and 3 months after birth
 Usually occurs AS meningitis form
 Mortality rate is not as high as early-onset

 In adults
 Occurs in immunosuppressed patients or those with underlying diseases:
bacteremia, pneumonia, bone and joint infections, skin and soft tissue
infections. Mortality is higher.

 Often found in a previously healthy adult who just experienced childbirth:

Urinary tract infections, endometritis, and wound infections
 Laboratory Diagnosis:
Group B -Hemolytic
Streptococcus
 Colony morphology
 Grayish-white, mucoid, creamy,
narrow zone of -hemolysis
 Identification tests
 Catalase-negative
 Bacitracin-resistant
 Bile-esculin-hydrolysis–negative
 Does not grow in 6.5% NaCl
 CAMP-test–positive
 Treatment

All S. pyogenes are sensitive to penicillin G.

Effective doses of penicillin or erythromycin for 10 days

can prevent poststreptococcal diseases.

Drainage and aggressive surgical debridement must be

promptly initiated in patients with serious soft tissue
infections.

Group B streptococci are also susceptible to penicillin G.

Antibiotic sensitivity test is helpful for treatment of

bacterial endocarditis.
 Prevention and Control

Most streptococci are normal flora of the human body.

Source of S. pyogenes and S. agalactiae is a person harboring
these organisms (carrier).
Control:
1. Prompt eradication of streptococci from early infections.
2. Prophylactic antibiotic treatment for rheumatic fever
patients.
3. Eradication of S. pyogenes from carriers.
4. Dust control, ventilation, air filtration.
5. Intrapartum penicillin to mother at risk of giving birth to an
infant with invasive group B disease.
Streptococcus Group D
and Enterococcus Species
(E. faecalis, E. faecium)
 Members of the gut flora
 Associated infections:
 One of the leading causes of nosocomial infections. Urinary
tract (UTI), peritoneum (peritonitis) and heart tissue
(endocarditis- a severe complication) are involved most often.
 Particularly common in patients with intravascular or urinary
catheters, and in hospitalized patients with prolonged broad-
spectrum antibiotic treatment.
 Intra-abdominal abscess and wound infections: generally
polymicrobial.
 Many strains are completely resistant to all conventional
antibiotics. Vancomycin-resistant strains have been isolated
(first reported in England and France in 1987).
 Laboratory Diagnosis: Streptococcus
Group D and Enterococcus Species

 Microscopic morphology
 Cells tend to elongate
 Colony morphology
 Most are non-hemolytic, although
some may show or,
rarelyhemolysis
 Possess Group D antigen
 Identification tests
 Catalase: may produce a weak
catalase reaction
 Hydrolyze bile esculin
 Differentiate Group D ,with 6.5%
NaCl or PYR test
 Enterococci

Treatment, Prevention, and Control

Resistance in enterococci to aminoglycosides and vancomycin is

mediated by plasmids and can be transferred to other bacteria.
Combined antibiotic therapy: an aminoglycoside and a cell-wall-
active antibiotic.

It is difficult to prevent and control enterococcal infections.

Control: careful restriction of antibiotic treatment and appropriate
infection-control practices (isolation of infected patients; use of
gowns and gloves by anyone in contact of patients.)
 Other Streptococcal Species
 Viridans group
 Members of the normal oral and nasopharyngeal flora
 Includes those that lack the Lancefield group antigen
 Most are  hemolytic but also includes nonhemolytic species


The most common cause of subacute bacterial endocarditis(SBE )after
tooth extraction(S. mutans )
 Subacute endocarditis (group: Mitis)
 Intra-abdominal infections (group: Anginosus)
 Dental caries (group: Mutans)
 Cariogenicity of S. mutans is related to its ability to synthesize
glucan from fermentable carbohydrates (e.g. sucrose) as well as
to modify glucan in promoting increased adhesiveness.
 S. pneumoniae

Morphology and Physiology

Gram-positive lancet-shaped diplococci for typical organisms.

-hemolytic (pneumolysin is similar to streptolysin O).
Form small round colonies on the plate, at first dome-shaped
and later developing a central plateau with an elevated rim.
Autolysis is enhanced in bile salt.
Growth is enhanced by 5-10% CO2.
Capsular polysaccharide:
type-specific, 90 types.
*Quellung reaction (for rapid
identification or typing of the bacteria)
S. pneumoniae
 General characteristics
 Inhabits the nasopharyngeal areas of healthy individuals 40-70%
 Typical opportunist
 Possess C substance( Capsular polysaccharide)
 Pathogenesis:
Pneumococci produce disease through their ability to
multiply in the tissues (invasiveness).
Virulence factors: Capsular polysaccharide (type-
specific, 90 types), cell wall ,phosphocholine,
pneumolysin, IgA protease.
 S. pneumoniae
Clinical diseases
Pneumococcal pneumonia develops when the bacteria multiply
rapidly in the alveolar space after aspiration. The affected area
is generally localized in the lower lobes of the lungs (lobar
pneumonia). Children and the elderly can have a more
generalized bronchopneumonia. Resolution occurs when
specific anticapsular antibodies develop.
THE COMMNE CAUSE OF COMMNITY AQUIRED
PNEUMONIA
Sudden onset with fever, chills and sharp chest pain. Bloody,
rusty sputum. Empyema (mostly caused by type 3) is a rare but
significant complication.
Complications caused by spreading of pneumococci to other
organs: sinusitis, middle ear infection, meningitis, endocarditis,
septic arthritis.
Laboratory Diagnosis:
Streptococcus pneumoniae
 Microscopic morphology
Stained smears of sputum a rapid
diagnosis
 Gram-positive cocci in pairs;
lancet-shaped
 Colony morphology
 Smooth, glistening, wet-looking,
mucoid
 -Hemolytic
 5-10% CO2 enhances growth
 Laboratory Diagnosis:
Streptococcus pneumoniae

 Identification
 Catalase negative
 Optochin-susceptibility-test–
susceptible
 Bile-solubility-test–positive
 Quellung test with multivalent
anticapsular antibodies
 Antigen detection: detect
pneumococcal C polysaccharide
(teichoic acid; type-specific) in
urine (bacteremic) or CSF
(meningitis).
 S. pneumoniae
Treatment, Prevention, and Control

Penicillins are the drugs of choice. However, strains

resistant to penicillin and other antibiotics are common
nowadays.

Healthy carriers are the source of dissemination. In the

development of illness, predisposing factors are more
important than exposure to the bacteria.
Vaccination of high-risk population (too old, too young,
and people losing natural resistance) with vaccines
containing multiple capsular polysaccharide types.
7-valent conjugate vaccine for infants <2 years.
23-valent vaccine for older children and adults.
Differentiation between -hemolytic streptococci

Hemolysis Bacitracin CAMP test

sensitivity
S. pyogenes  Susceptible Negative

S. agalactiae  Resistant Positive

Differentiation between -hemolytic streptococci

Hemolysis Optochin Bile Inulin

sensitivity solubility Fermentation
S. pneumoniae  Sensitive (≥ Soluble Not ferment
14 mm)

Viridans strep  Resistant Insoluble Ferment

(≤13 mm)
Outline of differentiation between
Gram-Positive cocci

e.g. S. epidermidis