Streptococcus Flashcards
GAS infection treatment
- penicillin
- clindamycin or linezolid for toxic shock syndrome
Rheumatic fever treatment
penicillin for 10 days,
anti-inflmmatory drugs for symptoms relieve e.g. corticosteroid, aspirin
surgery: uncontrolled heart failure secondary to acute MR
Post infectious/streptococcal GN
1-2 weeks after pharyngitis (high ASO)
4-6 weeks after pyoderma (low ASO)
GAS prop
- S. pyogenes
- bacitracin susceptible
- PYR +ve, VP -ve
GAS - pathogenesis
- directly caused by present of GAS: pharyngitis, skin and soft tissue infection, streptococcal toxin shock syndrome, scarlet fever
- immunological reaction (non-suppurative complications): rhuematic fever, acute poststreptococcal glomerunephritis
GAS- virulent factors
- adherence to epithelial cells/ anti-phagocytic: M proteins and capsule
- spread and tissue invasion: streptokinase, hyaluronidase, protease
- systemic toxicity: streptolysin O
GAS- clinical presentations
- pharyngitis +/- scarlet fever
- skin and soft tissue infection
- streptococcal toxic shock syndrome
- bacteremia
scarlet fever
- day 2 rash (diffuse redish blue rash on upper chest that spread centrifugally, bleach on pressure)
- strawberry tongue
- Pastia’s line
- facial flushing with perioral pallor
- eosinophilia
GAS- skin and soft tissue infection
impetigo
cellulitis (rash with no distinct boundary), erysipelas (distinct boundary)
necrotising faciitis, myositis, myonecrosis
Streptococcal toxic shock syndrome
Lab diagnosis: isolation of GAS
Clinical presentation:
shock/ hypotension AND
multiorgan involvement (more than or equal to 2): renal involvement, liver involvement, coagulopathy, ARDS, skin and soft tissue infection, generalised erythematous macular rash with desquamation
caused by presence of superantigen which binds to non-specfic region of TCR
Lab diagnosis of GAS
- culture of site of infection (skin or throat swab) or blood culture
- antigen detection (rapid antigen detection test)
- serology (antistreptolysin O titre) not for acute
Rheumatic fever
valvular damage caused by abnormal immune response to GAS infection
usually 3 weeks after GAS pharyngitis or skin infection
pathogenesis: molecular mimicry. Immune response directed against M proteins also attack cardiac proteins
Consequence: rheumatic heart disease
Rheumatic fever- Jone’s criteria
2 major or 1 major + 2 minor
Major: pan-carditis, arthritis, subcutaneous nodules, erythema marginatum, sydenham’s chorea
Minor: fever, arthralgia, prolonged PR interval, elevated CRP or ESP
Rheumatic fever- prophylaxis
Primary prophylaxis: same as treatment
Secondary prophylaxis: IM penicillin once every 21-28 days
5 years/till 18 if no carditis, resolved carditis 10 years or till 25, lifelong if moderate to severe rheumatic heart disease
post streptococcal GN
- 1-2 weeks after pharyngitis with high ASO titre, 4-6 weeks after pyoderma with low ASO
- may be caused by molecular mimicry, circulating immune complexes deposit or deposition of streptococcal Ag in glomerulus