Download S. pyogenes

Streptococci
Morphology and Identification
Gram-positive cocci arranged in chains or pairs.
Most group A, B, and C strains produce capsules.
Most strains grow as discoid colonies, 1-2 mm in diameter.
Catalase-negative.
Grow better in media enriched with blood or tissue fluid.
Most are facultative
anaerobic and some
are capnophilic. For
most species growth
and hemolysis are
aided by incubation in
10% CO2.
Classification
Hemolysis
a-hemolysis: incomplete lysis of RBC with the formation
of green pigment.
b-hemolysis: complete hemolysis
No hemolysis
Lancefield classification: a serologic classification (A to V)
Biochemical reactions are used for species that can not
be classified into the Lancefield classification
(nongroupable), e.g. viridans streptococci.
Streptococcus pyogenes
Surface structure
Capsule: antiphagocytosis. The capsule of group A streptococci is
composed of hyaluronic acid.
Group-specific cell wall antigen (Lancefield group A)
Carbohydrate
A dimer of N-acetylglucosamine and rhamnose.
M protein
T protein: type-specific; function unknown.
M-like proteins: binds IgM, IgG and a2-macroglobulin; interfere with
phagocytosis.
Lipoteichoic acid: binds to epithelial cells.
Protein F: a major adhesin of S. pyogenes, binding with fibronectin.
Streptococcus pyogenes
Pathogenesis (via invasiveness and production of toxins)
Adherence to the epithelial cells;
>10 adhesion molecules
invasion into the epithelial cells;
mediated by M protein and protein F
important for persistent infections and invasion
into deep tissues
avoiding opsonization and phagocytosis;
M protein, M-like proteins, and C5a peptidase
producing enzymes and toxins
Streptococcus pyogenes
Enzymes and toxins
Streptokinase (fibrinolysin)
Can lyse blood clots and may be responsible for the rapid spread
of the organism.
Streptodornase (DNases A to D)
Decreases viscosity of DNA suspension.
Hyaluronidase (spreading factor):
Destroys connective tissue and aids in spreading infecting bacteria.
C5a peptidase
Prevents streptococci from C5a-mediated recruitment and
activation of phagocytes, and is important for survival of S.
pyogenes in tissue and blood.
Streptococcal pyrogenic exotoxins (Spe)
Produced by both the scarlet fever strains and new invasive
S. pyogenes strains.
More than four serologically distinct toxins (SpeA, B, C and F).
They are superantigens (except for SpeB, which is a cysteine
protease) and may exhibit the following biological activities:
Enhances release of proinflammatory cytokines
(pyrogenicity)
causes skin rash
Immunosuppression
Spe is associated with streptococcal toxic shock syndrome or
other invasive S. pyogenes diseases.
Hemolysins
Streptolysin O: O2-labile; causes hemolysis deep in blood
agar plates. ASO (antistreptolysin O) titer >160-200 units
suggests recent infection or exaggerated immune
response to an earlier respiratory infection. However, skin
infection does not induce ASO.
Streptolysin S: O2-stable. Causes b-hemolysis on the
surface of blood agar plates. Cell-bound, not antigenic.
Produced in the presence of serum. Kills phagocytes by
releasing the lysosomal contents after engulfment.
Streptococcus pyogenes
Epidemiology
S. pyogenes can transiently colonize the oropharynx and skin.
Diseases are caused by recently acquired strains that can
establish an infection of the pharynx or skin.
S. pyogenes causes pharyngitis mainly in children of 5 to 15
years old.
The pathogen is spread mainly by respiratory droplets.
Crowding increases the opportunity for the pathogen to spread,
particularly during the winter months.
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.
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.
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. 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%).
3. Poststreptococcal diseases (occurs 1-4 weeks after
acute S. pyogenes infection, hypersensitivity responses)
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.
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.
S. agalactiae (group B, b-hemolytic, contains type-specific capsular
polysaccharides which is the most important virulence factor and can
induce protective antibodies; may colonize at lower gastrointestinal tract
and genitourinary tract)
Neonatal sepsis or meningitis
Early-onset (during the first week of life): infection acquired in utero or at
birth. Pneumonia is common in addition to meningitis.
Late-onset (older infants): infection acquired from an exogenous source.
(Premature infants are at greater risk.)
Infection of pregnant women
Urinary tract infections, amnionitis, endometritis, and wound infections
Infection in men and nonpregnant women
Patients are generally older and have underlying conditions.
Bacteremia, pneumonia, bone and joint infections, skin and soft tissue
infections. Mortality is higher.
Viridans streptococci (a-hemolytic or nonhemolytic, most are
nongroupable; they, except for S. suis, are divided into 5 subgroups
based on the specific diseases they cause)
These streptococci colonize the oropharynx, GI tract, and GU tract;
rarely on the skin surface.
Diseases:
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
Laboratory Diagnosis
Smears: useful for soft tissue infections or pyoderma, but not for
respiratory infections.
Antigen detection tests: commercial kits for rapid detection of
group A streptococcal antigen from throat swabs.
Detection of group A streptococci by molecular methods: PCR
assay for pharyngeal specimens.
Culture: Specimens are cultured on blood agar plates in air.
Antibiotics may be added to inhibit growth of contaminating
bacteria.
Identification: serological and biochemical tests.
Antibody detection
ASO titration for respiratory infections.
Anti-DNase B and antihyaluronidase titration for skin infections.
Antistreptokinase; anti-M type-specific antibodies.
Identification of Gram-positive cocci
None
CAMP test
Christie R, Atkins NE, and Munch-Peterson E. 1944. A note on a lytic phenomenon
shown by group B streptococci. Aust. J. Exp. Biol. Med. Sci. 22:197-200
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, UV irradiation and
aerosol mists are of doubtful efficacy.
5. Intrapartum penicillin to mother at risk of giving birth to an
infant with invasive group B disease.
S. pneumoniae
Morphology and Physiology
Gram-positive lancet-shaped diplococci for typical organisms.
a-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.
Smooth (capsular polysaccharideproducing) vs. rough colonies
*Quellung reaction (for rapid
identification or typing of the bacteria)
S. pneumoniae
Pathogenesis and Immunity
Pneumococci produce disease through their ability to multiply in the
tissues (invasiveness). Virulence factors: capsule, cell wall
polysaccharide, phosphocholine, pneumolysin, IgA protease, etc.
40-70% of humans are at sometimes carrier of virulent pneumococci.
Normal respiratory tract has natural resistance to the pneumococcus.
Major host defense mechanisms: ciliated cells of respiratory tract and
spleen. Loss of natural resistance may be due to:
1. Abnormalities of the respiratory tract (e.g. viral RT infections).
2. Alcohol or drug intoxication; abnormal circulatory dynamics.
3. Patients undergone renal transplant; chronic renal diseases.
4. Malnutrition, general debility, sickle cell anemia, hyposplenism
or splenectomy, nephrosis or complement deficiency.
5. Young children and the elderly.
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.
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.
S. pneumoniae
Laboratory diagnosis
Examination of sputum
Stained smears of sputum: a rapid diagnosis.
Quellung test with multivalent anticapsular antibodies.
Culture
Specimen: sputum, aspirates from sinus or middle ear, CSF.
cultured on blood agar plate in 5-10% CO2.
Identification: bile solubility, optochin sensitivity, etc. for
differentiation from other a-hemolytic streptococci. Additional
biochemical, serologic or molecular diagnostic tests for a definitive
identification.
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.
Enterococci
(E. faecalis, E. faecium)
Physiological properties are similar to the streptococci.
Form large colonies on blood plate;
most are nonhemolytic.
Microscopic morphology is similar to
S. pneumoniae.
Resistant to 6.5% NaCl, 0.1% methyl
blue and grow in bile-esculin agar.
More resistant to antibiotics than the
streptococci.
Colonize the large intestine of
humans and animals. An opportunist.
Clinical Diseases
Enterococci
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 broadspectrum 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
Enterococci can be differentiated by simple biochemical tests
(e.g., resistant to optochin and bile, hydrolyze PYR, etc.)
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-wallactive antibiotic.
New antibiotics have been developed for treatment of enterococci
resistant to both ampicillin and vancomycin.
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.)
M protein
Forms hair-like projections (fimbriae)
from the cell membrane.
Major virulence factor of S. pyogenes.
Enhances degradation of C3b via
binding with factor H, and
phagocytosis by PMNs is prevented.
Promotes adherence to epithelial cells.
Induces type-specific protective
immunity (>100 serotypes).
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Erysipelas
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STSS
High risk population for STSS: patients with HIV infection, cancer,
diabetes mellitus, heart or pulmonary disease, varicella-zoster virus
infection, and intravenous drug abusers and alcoholic.
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S. pneumoniae virulence factors
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