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STREPTOCOCCIELIZABETH P. QUILES, M.D., FPASMAP
DEPARTMENT OF MICROBIOLOGYOUR LADY OF FATIMA UNIVERSITY
COLLEGE OF MEDICINE
CHARACTERISTICS
Gram positive cocci, in pairs or chains Catalase negative Facultative anaerobes Complex nutritional requirements (blood or
serum enriched medium) Ferment carbohydrates with formation of
lactic acid
CLASSIFICATION
1. Clinical – pyogenic, oral, enteric2. Serologic Lancefield Classification -
based on group specific cell wall carbohydrate
3. Hemolysisa. alpha – incomplete hemolysisb. beta – complete hemolysisc. gamma – no hemolysis
LANCEFIELD CLASSIFICATION
Group A – rhamnose-N-acetylglucosamine Group B – rhamnose-glucosamine
polysaccharide Group C –rhamnose-N-acetylglucosamine Group D – glycerol teichoic acid containing
alanine & glucose Group F – glucopyrasonyl-N-
acetylgalactosamine
CLASSIFICATION TABLE
SEROLOGIC BIOCHEMICAL HEMOLYTIC PATTERN
A S. pyogenes Beta
B S. agalactiae Beta, Alpha, Gamma
C S. equimilis Beta
D S. bovis
S. faecalis
Alpha, Gamma
Alpha, Beta, Gamma
F S. milleri Alpha, Beta, Gamma
G S. milleri -do-
- S. pneumoniae Alpha
VIRIDANS S. salivarius, S. sanguis, etc Alpha, Gamma
PRESUMPTIVE IDENTIFICATION OF STREPTOCOCCI
Organism Susceptibility
A P
Hydrolysis
hippurate esculin
Growth
Bile NaCl
Lysis
bile
S. pyogenes S R - - - - -
S. agalactiae R R + - - + -
Grp D
S. faecalis
S. bovis
R R
R R
- +
- -
+ +
+ -
-
-
Viridans R R
(var)
- - - - -
Pneumococcus R S - - - - +
Group A Streptococcus(S. pyogenes)
Structure:
1. Capsule – hyaluronic acid
2. Cell wall
a. protein antigens M,T,R
M protein major virulence factor
T & R protein no role in the virulence
b. group specific carbohydrates – rhamnose-N-acetylglucosamine
3. Pili consists partly of M protein & covered with lipoteichoic acid for attachment
VIRULENCE FACTORS
1. Capsule – non-immunogenic
2. M protein – hair-like projections on the cell wall
- major virulence factor
- promotes adherence
- antiphagocytic
- anticomplement
- type specific
3. Lipoteichoic acid – for adherence4. Erythrogenic toxin – pyrogenic exotoxins
A,B,C- responsible for the rash of Scarlet fever
5. Streptolysin O – lyses WBC, platelets, RBC
- immunogenic6. Streptolysin S – non-immunogenic
- responsible for the hemolytic zones around colonies
7. Streptokinase (fibrinolysin) – lyze blood clots plasminogen plasmin
digest fibrin & other proteins
- facilitates spread of infection
- used in the treatment of pulmonary emboli & coronary artery & venous thromboses
8. DNAse (streptodornase) – depolymerizes cell-free DNA in purulent materials
9. Hyaluronidase – spreading factor
- splits hyaluronic acid
streptodornase & streptokinase used in enzymatic debridement liquefy
exudates & facilitate removal of pus & necrotic tissue antibiotics gain better access
CLINICAL SYNDROMES
A. Suppurative Infections1. Skin Infections
a. impetigo – superficial blisters covered with pus or honey–colored
crustb. erysipelas – acute superficial cellulitis of the skin with lymphatic involvement
2. Pharyngitis – most common infection nasopharyngitis, tonsillitis, purulent
exudates, cervical lymphadenopathy & high fever
3. Sepsis –follows infection of traumatic or surgical wounds
4. Puerperal Fever – occurs ffg delivery
5. Acute Endocarditis – occurs in previously deformed heart valves
6. Scarlet fever – a complication of pharyngitis if the causative agent is capable of producing erythrogenic toxin initial symptoms of pharyngitis, diffuse
erythematous rash with sparing of the palms & soles
Circumoral pallor “strawberry tongue”
7. Pneumonia – rapidly progressive & severe
most commonly a sequela to viral infections like influenza or measles
B. Non-suppurative sequelae
1. Rheumatic fever – associated with M types causing URI & skin infections fever, malaise, migratory
nonsuppurative polyarthritis, evidence of inflammation of the heart
carditis leads to thickened & deformed valves & to small perivascular granulomas in the myocardium (Aschoff bodies)
2. Acute Glomerulonephritis – associated with M types producing URI & skin infections
particularly associated with types 12, 4, 2 & 49 which are nephritogenic
initiated by ag-ab complexes on the glomerular basement membrane
hematuria, proteinuria, edema & hypertension
DIAGNOSIS
1. Microscopy
2. Culture – Bacitracin Test (Taxo-A)
3. Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests
4. Antibody detection ASO titer – for respiratory disease antiDNAse & antihyaluronidase – for
skin infections
TREATMENT
1. Penicillin G – drug of choice
2. Erythromycin
Antistreptococcal chemoprophylaxis in persons who have suffered an acute attack of rheumatic fever Penicillin G 1.2 M units IM every 3-4 weeks or daily oral penicillin or oral sulfonamide
GROUP B STREPTOCOCCI(S. agalactiae)
Cell wall rhamnose-glucosamine polysaccharide
Colonize the URT, lower GIT & vagina Serotypes Ia, Ib, II & III – account for most
human infections
CLINICAL SYNDROMES
1. Early-Onset Neonatal Disease – can occur in utero, at birth or during the 1st 5 days of life
may occur as bacteremia, meningitis or pneumonia
2. Late-Onset Neonatal Disease – in older infants from exogenous sources
Bacteremia with meningitis
3. Post-partum Sepsis – as endometritis or wound infection with bacteremia
STREPTOCOCCUS PNEUMONIAE
Also known as Pneumococcus or Diplococcus pneumoniae
Gram (+) cocci, in pairs or short chains Lancet-shaped May or may not be encapsulated Normal inhabitant of the upper respiratory
tract
STRUCTURE
1. Capsule – complex polysaccharides Serologically typable (84 serotypes) Immunogenic principal determinant
of immunity
2. Teichoic acid
VIRULENCE FACTORS
1. Capsule - antiphagocytic
2. Pneumolysin - hemolysin
3. Purpura-producing principle – responsible for dermal hemorrhages
4. Neuraminidase – spreading factor
5. Amidase – autolysin & for cell division
EPIDEMIOLOGY
Common inhabitant of the nasopharynx of healthy individuals
Most common cause of bacterial pneumonia & meningitis above 5 years old & in adults
One of the two most common causes of acute sinusitis & otitis media
CLINICAL SYNDROMES
1. Pneumonia MOT: aspiration of endogenous oral
organisms thru droplets Cough, blood-tinged or rusty colored
sputum & sharp pleural pain Generally localized in the lower lobes
of the lungs lobar pneumonia May also occur as bronchopneumonia
2. Sinusitis & otitis media – preceded by viral infection of the URT
3. Meningitis – follows bacteremia, infections of the ear & sinuses or head trauma
4. Bacteremia – associated with pneumococcal pneumonia & meningitis
DIAGNOSIS
1. Microscopy
2. Capsule swelling test Quellung rxn
3. Culture Optochin test (Taxo-P) Biochemical test Autolysin activated by bile
4. Serologic tests – immunofluorescence & Latex (detects capsular polypeptides)
TREATMENT
1. Penicillin – drug of choice
2. Alternate drugs Erythromycin, chloramphenicol, cephalosporins
3. Severe infections with Penicillin resistance Vancomycin, Imipenem, 3rd generation cephalosporins
GROUP D STREPTOCOCCUS(ENTEROCOCCUS)
Grown in 6.5% NaCl Hydrolyze esculin in the presence of bile E. faecalis most common cause of
human infections Normal flora of GIT & URT
INFECTIONS
1. UTI – in hospitalized patients with in-dwelling catheters & receiving broad spectrum antibiotics
2. Intra-abdominal abscess
3. Wound infection
4. Endocarditis
5. Pulmonary infections in children
TREATMENT
Aminoglycosides combined with cell wall active antibiotics (Penicillin, ampicillin, vancomycin)