Bailey 3 Flashcards
Streptococcus sp characteristics
Gram + Cocci -Chains or diplococci Non-spore forming Facultative anaerobes Catalase neg Infect humans and animals
Streptococcus sp classification/identification
-Hemolysis pattern
alpha-partial clearing (green)
beta-clearing
gamma-no clearing
-Lancefield group-cell wall carb antigens
*Agglutinated antigen-latex=positive result
-Metabolic reactions
GAS diseases
- Acute pharyngitis
- Pyoderma
- Impetigo (skin)
- Erysipelas (skin and subQ)
- Cellulitis
- GAS pneumonia
- Necrotizing fascitis and myositis
- Childbed (peurperal) fever
- Foodborne outbreaks
GAS-S. pyogenes causes what?
Strep throat and scarlet fever (strep w/ red skin rash)
What is ARF
Acute rheumatic fever
- Nonsuppurative sequelae following GAS infection
- Inflammation of heart and joints
- polyarthritis, carditis
- Severe valvular scarring
- All but carditis resolve over time
- Infection must invoke immune response
- Hypersensitivity rxn caused by cross-reacting antibodies
- Few people susceptible
- Can occur after asymptomatic infection
How is ARF treated
Can be prevented by treating strep w/ full course of penicillin
-ARF does not respond to drugs but can be prevented
High susceptibility to recurrence-prophylactic antibiotics for life
What is APSGN
Acute Post-streptococcal glomerulonephritis
- Active inflammation in the glomeruli of kidney
- Selectively removes uremic waste products
- Urine smoky due to proteins, WBC, RBCs and renal failure->dialysis
- Only caused by a few types of GAS
How do ARF and APSGN differ?
ARF: -Only follows pharyngitis -Few people susceptible -Susceptibility of recurrence is high -Prevented by penicillin APSGN: -Follows pharyngitis or pyodermal inf. -Many people susceptible -Susceptibility of recurrence is low -Not prevented by penicillin
GAS encounter, reservoir, transmission
- Live on skin and mucous membranes (nasopharynx)
- Person to person transmission
- Resp or hand to mouth
- Food
- Skin/wound
GAS entry and adherence
- Cannot penetrate intact skin
- Bacteria bind to epithelial cells using adhesins
- LTA makes GAS sticky and binds to fibronectin of host
- Protein F-fibronectin binding protein
- M protein-keratinocytes (outer skin) adhesin
GAS spread in body
Depends on how infection was acquired
- Skin or mucous membrane->localized inf
- Deeper tissue infections->rapid spread due to digestive enzymes
GAS virulence factors
DNAses Hyaluronidase Chemotaxins Hemolysins Streptokinase-clot lysis by breaking down fibrin
GAS antiphagocytic factors
M protein Hyaluronic acid capsule -most capsules-made of polysaccharides! C5a peptidases -inactivates phagocyte chemotaxin
M protein
- most important antiphagocytic factor
- central to pathogenesis and required for virulence
- binds to host serum proteins->forms dense coating->complement cant bind so no opsonization and no complement cascade
- contain antigenic protein tips that antibody can opsonize
Hyaluronic acid capsule
- most capsules-made of polysaccharides!
- makes GAS slippery so phagocytes cannot attach
- ARF isolates heavily encapsulated