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Significant Streptococcal species
Pyogenes, agalactiae, and pneumoniae
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Doctor who instituted hand cleaning between patients, fought Pyogenes
Semmelweiss
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Historical Classification, Hemolysis Classifications
- -Separated based on hemolytic activity on blood auger plates
- -alpha, beta, or gamma hemolytics -Alpha:green coloration of surroundings
- -Beta:Complete lysis, clear surrounding -Gamma:No change
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Streptococcal Serology
- Discovered by Lancefield
- -Discovered that streptococci possessed unique cell wall carbohydrates
- -Allowed more specific serotyping
- -Pyogenes: Group A strep
- -Agalactiae:Group B
- -Pneumoniae: Originally classified as
- Diplococcus, after DNA sequencing went to Streptococcus
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Other Strains of Strep
- -Viridans group: represent oral commensal species
- -Cause endocarditis when it gets into blood
- -Will attack congenitally abnormal/damaged scarred heart valves
- -Stick to valve and multiply
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Group A Strep (S. pyogenes)
- -Capsule, M Protein, lipoteichoic acid, streptolysin O, C5a peptidase, tissue destroying
- enzymes
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Group A Strep (S. pyogenes) M protein
- -250 different M-protein types
- -Show differences in repeat regions and binding of host molecules
- -Binds and inhibits IgA/C4BP to stop classical pathway/IgAmediated phagocytosis
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Strep. pyogenes: C5a peptidase/SpeB
-Destroy C5a/CXC chemokines that serve as signaling molecules
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Strep. pyogenes: Cytolytic toxins:
- -Streptolysin S: is a 2.7 kD modified peptide
- -Streptolysin O: is a pore-forming toxin (cholesterol-dependent cytolysin)
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Strep. pyogenes enzymes: SpeA,
SpeC, SpeG-M, SmeZ, SSA
- -Superantigens
- -Cause release of IL-1, IL-2, IL-6, TNF-alpha, gamma-IFN
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Strep pyogenes Epidemiology
-Group A carried in throat of 15-20% of all children and adults w/o evidence of disease
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Strep. pyogenes causes:
- -Suppurative streptococcal diseases:
- -Pharyngitis:Strep_throat -Scarlet fever: results from erythrogenic toxin
- -Streptococcal Toxic Shock: fever
- rash, vomiting, diarrhea, desquamation, renal failure, confusion. Caused by
- superantigen
- -Impetigo: pustules around nose and mouth
- -Necrotizing fasciitis: Flesh-eating
- disease. Starts from trauma, excessive pain at site, progresses to blisters on
- skin/necrosis
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Rheumatic Fever
- -Inflammatory disease of connective tissue, usually manifested on heart valves
- -Anti-body response to Group A strep antigens leads to cross-reactive antibodies
- -attach to connective tissue, leads local complement activation
- -destroys tissuse
- -seen mostly in 5-15
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B. acute Glomerulonephritis (AGN)
- -Kidneys have filters (glomeruli)
- -Attach to small fluid collecting tubes
- -Filter blood
- -Waste to bladder
- -Inflammation of glomeruli
- -leads to loss of filtration
- -Accumulation of waste, kidney failure
- -Skin or throat Group A is followed by AGN
- -Caused by accumulation of Abs-Ags immune complexes in glomeruli
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Culture and Identification Group A streptococci
- -Readily grown on BAP
- -Beta (occasionally non hemolytic)
- -Identified (presumptive) with sensitivity to antibiotic bacitracin
- -Other betas are resistant
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Group B Strep: S. agalactiae Epidemiology
- Commensal human GI and 10-30% of healthy women
- Diseases
- -Neonatal: early onset: Pneumonia from
- inhaled amniotic fluids/vaginal secretions during birth
- -Late onset: Intestinal infection,
- sepsis and meningitis
- -Postpartum: Mastitis, endometritis,
- sepsis, meningitis
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Lab Identification and Growth
- -Readily grown overnight on BAP, beta zone
- -Resistant to bacitracin
- -Capable of hydrolysis of hippurate, other strep cannot do this
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Streptococcus pneumoniae Infections and Disease
- -Carriage:5-75% depending on time of year/age
- -Pneumonia:100,000 cases a year, 40,000 deaths
- -Otitis media:most common cause for visit to pediatrician -Meningitis, sepsis, severe disease
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Strept. pneumoniae Capsular polysaccharide
- -inhibits complement lysis, antibody binding, phagocytosis, > capsule serotypes
- -Capsular serotype change via cassette type mechanism of genetic recombination
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Strep. pneumoniae Pneumococcal surface
- -PspA: coiled-coil protein
- -Bound to choline on bacterial polysaccharides (teichoic/lipoteichoic)
- -Inhibits complement lysis
- -antibodies to PspA are protective
- -many, many serotypes
- - Other Choline binding proteins (CBPs)
- -8-14
- -cbpA mutant showed reduced adherence
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Strept. pneumoniae virulence mechanism
- -Pnemolysin
- -pore-forming toxin
- -Binds Fc of IgG, fixes complement
- -Limits inflammatory response
- -released by autolysin
- -IgA protease
- -cleaves IgA
- -Teichoic acid/Lipoteichoic acid:
- -Surface polysaccharide carrying phosphorylcholine
- -Potentially
- involved in adherence and invasion
- -Autolysin
- -Division of daughter cells
- -Lysis of bacteria in stationary phase
- -Release of pneumolysin and possibly other virulence factors
- -Autolysin mutants are reduced in virulence in the mouse model
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S. pnumoniae Variation: Transformation
- -Population structure is panmictic (non-clonal)
- -Pneumococci undergo transformation at high frequency (+95%)
- -Occurs at late log phase
- -Is induced by a secreted peptide (competence factor)
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S. pneumoniae: Phase Variation
- -18% of pneumococcal genes are predicted to phase-vary
- -Vary between opaque and translucent
- -Transparent less virulent
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Growth and Laboratory Identification of S. pneumoniae
- -Readily grown in laboratory
- -Forms large gooey colonies
- -Exhibit alpha hemolysis
- -Identified by sensitivity to compound Optochin
- -Serological identification not routine
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Most common source of vaccine preventable death in children
S. pneumoniae
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Polysaccharide vaccine for S. pneumoniae
- -23-valent vaccine available, contains
- mixture of most common types of capsular polysaccharides
- -Conjugate vaccine
- -2000: 7-valent
- -2009: 10-valent
- -2010: 13-valent
- -Implementation of 7-valent vaccine
- has changed most common serotype to non-7VPCV
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