Streptococcal Species Flashcards
what is the most common cause of pharyngitis
viral; most commonly diagnosed bacterial cause is Group A strep
How are strep species classified
based on hemolysis, Lancefield groups (based on C carbohydrate in cell wall), Type specific antigens
Group A strep
S. pyogenes
Group B strep
S. agalactiae
- primarily infection of babies (pneumonia, meningitis, sepsis)
- 20-25% prego women colonized in rectum/vagina, so babies can acquire through birth– very high mortality
- Gropu B vaccine given during pregnancy
- beta hemolytic, lipoteichoic acid, polysaccharide capsule
- NO M, T, R proteins
- Ab to polysaccharide capsule
what is purpose to treat streptococcal pharyngitis
to prevent rheumatic fever, not necessarily to get rid of pharyngitis
Group D strep
-kinda 2 categories but not really called Group D anymore– Enterococci and non-enterococci group D (S. bovis)
Enterococci
- formerly group D– colonize nl GI tract
- usually opportunistic
- Adults: nosocomial infections– UTI, bacteremia, biliary tract infections, line sepsis, endocarditis
- Children: nosocomial bacteremia
- inducible transferable high level vancomycin resistance (VRE)
- can grow in 6.5% NaCl
- variable hemolysis
- E. faecalis more common but E. faecium more dangerus
Major virulence factor of group A strep
M protein– contributes ability to adhere by binding lipoteichoic acid (LTA) in correct orientation
- in the form of fine fimbriae
- 80 serotypes
- certain M types associated with predilection for pharyngeal infection or skin infection, as well as possible non-suppurative complications (ARF, AGN)
Group A spreading factors
Streptokinase, hyaluronidase, DNAse, proteinase
Which type of group B strep in newborn can be prevented b y giving antibiotics prior to delivery
early onset disease
alpha hemolytic strains
- S. pneumoniae
- Viridans group (S. mutans, S. sanguinis)
- have green ring around colony–biliverdin/heme degradation products
Streptococci Metabolism
- Gram positive
- Catalase negative
- aerotolerant
- ferment carbohydrates to lactic acid
- fastidious nutritionally (hard to grow)
- ## blood/serum enhances growth
beta hemolytic bugs
Group A, Group B,
M protein
major virulence factor present on group A strep (S. pyogenes)
- phagocytes ingest and kill strains without this protein but can’t kill bugs with it
- Ab against M-protein allows killing but is serotype specific
- N terminus where variation occurs
Group A Antigens
- capsule (hyaluronic acid)
- cell wall (surface protein–M, T, R)
- Group Carbohydrate (A)
- Mucopeptide
- glycerol teicholic acid
- cytoplasmic membrane
GAS extracellular virulence products
- Streptolysin O (hemolysin- antigenic)
- Streptolysin S (hemolysin–non antigenic)
- Pyogenic exotoxins (A-C; immunosuppressive and enhance susceptibility to endotoxin shock)
- Spreading factors (hyaluronidase, DNAse, proteinase, streptokinase)
- streptokinase lyses clots
Streptolysin O
- Oxygen labile hemolysin
- binds RBC, polymerizes, forms pore in membrane–causes hemolysis)
- Antistreptolysin O (ASO) antibody increases after infection
Diseases caused by group A strep
- Pyogenic (pharyngitis, osteomyelitis, cellulitis, impetigo, erysipelas)
- Toxigenic (Toxic chock-like syndrome, scarlet fever, necrotizing fasciitis)
- Immunogenic (rheumatic fever, acute glomerulonephritis)
Acute Rheumatic Fever
Nonsuppurative complication of S pyogenes 3-6 weeks after pharyngitis infection (NOT skin) but bug not recovered from site inflammation
- inflammation of heart valve, skin, joints, CNS
- Best model = autimmune disease– M3 and M18 strains associated with ARF; genetic predisposition (HLA and B cell alloantigen)–think genetically programmed abnormal immune response to common infection
- JONES criteria
(Joint polyarthritis, Carditis, Nodules (subcutaneous) erythema marginatum–annular arythema, Syndenham chorea)
-
Scarlet Fever
scarlet rash with sandpaper like texture, strawberry tongue, circumoral pallor, subsequent desquamation
- due to infection with strains producing pyrogenic exotoxins
Post streptococcal glomerulonephritis (PSGN)
- Nonsuppurative complication from S. pyogenes 2-4 weeks after infection but don’t recover organism from site of inflammation
- some M types associated with increased
- Best model = immune complex disease (Type III sensitivity reaction)– complexes trapped below glomerular basement membrane– complement deposition and neutrophil recruitment results in kidney damage
- Dark urine, facial swelling from edema
- can be after pharyngitis and skin infections
CAMP factor
produced by gropu B– enlarges area of hemolysis formed by S. aureaus
- distinguishes S. galactiae
GBS virulence factors/toxins
Neuraminidase, C protein, Beta hemolysin, Protease, Hyaluronidase
Non-enterococcus Group D strep
- i.e. Strep bovis
- colonizes gut, upper respiratory tract, GU, skin
- opportunistic! (intra-abdominal infections, TUI, abscesses post appendicitis/diverticulitis/other GI dz, endocarditis/heart valve infection; in-dwelling IV catheter infection common
- can cause bacteremia with subacute endocarditis
- associated with colon cancer
- can grow in bile but NOT 6.5% NaCl (diff from Enterococci)
Pus in strep vs Staph
strep is more watery, thin vs thicker pus from staph
Which nonsuppurative complications does antibiotic therapy prevent
- ARF, probably not APSGN
nephitogenic GAS strains
M12, M4, M49
Viridans strep
- alpha hemolytic
- S. salivarius, S pyogenis sanguis, S. mitis, S mutans
- mutans assd with dental caries
- bacterial endocarditis from ability of strains to adhere to previously damaged valves (about 50% cases due to viridans strep)
Group G strep
similar to goup A
- many produce streptolysin O, streptokinase
- several M proteins
- uncommon cause of pharyngitis; can cause othe rinfections
- ARF doesn’t occur but APSGN can
Group C strep
animal pathogens with occasional human disease
- some pharyngitis oubreaks
- streptolysin O produced
- No ARF but occasional APSGN
GBS cell wall components
- C carbohydrate
- Lipoteichoic acids - -mediate adhesion
- polysaccharide capsule in virulent forms with capular types Ia, Ib, II, III; resist phagocytosis (we develop Ab against capsule )
- NO M, T, R Ag
Extracellular products of GBS
- neuraminidase, protease, betahemolysin, hyaluronidase
- CAMP factor – soluble protein enhancing hemolysis of S. aureus–used to ID group B strep
forms of neonatal group B strep dz
- Early onset within first 24 hrs– high mortality; all capsular types can cause this
- Late onset after 24 hrs, usually 1 wk or later; almost all due to type III organisms
- Vaccines have been produced but not all women produce Ab
