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
What are SPEs
Strep Pyrogenic exotoxins
- Intense inflamm response in tissues
- Superantigens activate macrophages and T cells to release cytokines
- Three types: SPEA, B, and C
- Responsible for rash of scarlet fever
- Similar to TSST-1
- Produce Strep TSS
GBS characteristics
- More common but less notorious than GAS
- Inhabit lower GI and female genital tract
- Cause neonatal sepsis and meningitis (S. agalactiae)
- Cause cellulitis, arthritis, and meningitis
- Polysaccharide capsule that is antigenic (unlike GAS capsule)
B-hemolytic strep groups other than GAS and GBS
C, G, and F
GCS, GGS, and GFS characteristics
- M protein, bind fibrinogen and secrete similar extracellular enzymes
- Group C also has hyaluronic acid capsule (like GAS)
- Implicated in AGN but not ARF
GDS
- alpha or gamma hemolytic
- enterococci on nonenterococci strains
- S. faecalis=enterococcus faecalis
- normal flora of GI and GU tracts
- Low virulence
Enterococci is referred to as _____? why?
Worlds toughest pathogenic bacteria
- Grows in high salt and in detergents
- Inhibited but not killed by penicillin
- Resistant to most antibiotics (synergism required)
Vancomycin resistant enterococci (VRE)
- Low virulence but untreatable
- Transfer vancomycin resistance to staph.
- dalfopristin-quinipristin combination
Nonenterococcal GDS
S. bovis.=most common for human disease
- Subacute bacterial endocarditis-affects abnormal heart valves
- Bactermia-colonic lesions-colon cancer
- Does not grow in high salt
- Penicillin is effective
Viridans strep.
- alpha hemolytic-aka “greening”
- 30-60% of oropharyngeal flora
- Low virulence
- Most common cause of subacute bacterial endocarditis-affects heart valves
- Produce dextrans for adherence
What is responsible for caries
Viridans streptococci-mutans group
-includes S. mutans, s. sanguis, s. salivarius, s. mitis, s minitor, and s. milleri
How to viridans streptococci mutans group cause caries
- Surface proteins bind salivary glycoprotein on teeth (pellicle)
- Thrive on sucrose
- Ferment sugar to lactic acid that demineralizes enamel