Download - Streptococci With Pics(2)
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STREPTOCOCCIELIZABETH P. QUILES, M.D., FPASMAP
DEPARTMENT OF MICROBIOLOGYOUR LADY OF FATIMA UNIVERSITY
COLLEGE OF MEDICINE
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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
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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
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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
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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
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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 - - - - +
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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
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b. group specific carbohydrates – rhamnose-N-acetylglucosamine
3. Pili consists partly of M protein & covered with lipoteichoic acid for attachment
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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
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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
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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
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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
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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
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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
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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”
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7. Pneumonia – rapidly progressive & severe
most commonly a sequela to viral infections like influenza or measles
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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)
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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
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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
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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
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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
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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
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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
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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
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STRUCTURE
1. Capsule – complex polysaccharides Serologically typable (84 serotypes) Immunogenic principal determinant
of immunity
2. Teichoic acid
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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
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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
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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
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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
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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)
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TREATMENT
1. Penicillin – drug of choice
2. Alternate drugs Erythromycin, chloramphenicol, cephalosporins
3. Severe infections with Penicillin resistance Vancomycin, Imipenem, 3rd generation cephalosporins
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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
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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
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TREATMENT
Aminoglycosides combined with cell wall active antibiotics (Penicillin, ampicillin, vancomycin)
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