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)