Streptococci Flashcards

1
Q

Classification system of streptococci based on visible hemolysis on sheep blood agar

A
  • α-hemolysis
  • ß-hemolysis
  • ɣ-hemolysis

*Note: some former Streptococci (mostly Enterococci) have variable hemolysis –> this is not a great way to recognize those strains on SBA

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2
Q

α-hemolysis

A
  • Incomplete destruction of erythrocytes –> green coloration of medium surrounding colonies
  • Examples:
    • Streptococcus pneumoniae
      • optochin susceptible
    • Streptococcus viridans
      • optochin resistant
      • implicated in subacute endocarditis in setting of dental procedure
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3
Q

β-hemolysis

A
  • Complete lysis of RBCs –> distinct clear zone around colonies
  • Examples:
    • S. pyogenes - Group A
    • S. agalactiae - Group B
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4
Q

ɣ-hemolysis

A
  • No hemolysis effect
  • Preferably noted “nonhemolytic”
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5
Q

Lancefield classification of streptococci

A
  • Based on antigenic characteristics of C carbohydrate found in cell wall
    • Called “Lancefield antigens”
    • Given letter names A-S
  • Used in conjunction with other methods of identification:
    • Hemolysis (SBA)
    • Genetics
    • Growth chracteristics
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6
Q

Lancefield group A: common streptococci, hemolysis pattern

A
  • Common streptococci:
    • Streptococcus pyogenes
  • Hemolysis:
    • Beta-hemolysis
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7
Q

Lancefield group B: common streptococci, hemolysis pattern

A
  • Common streptococci:
    • Streptococcus agalactiae
  • Hemolysis:
    • Beta-hemolysis
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8
Q

Lancefield group “formerly D”: common streptococci, hemolysis patterns

A
  • Enterococci
    • Streptococcus faecaelis, Streptococcus faecium
    • Hemolysis: alpha, beta, or gamma
  • Non-enterococci
    • Streptococcus bovis, Streptococcus equinus
    • Hemolysis: rarely alpha
  • Viridans group
    • Hemolysis: usually alpha, rarely gamma
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9
Q

Structure of streptococci

A
  • Capsule
    • Hyaluronic acid
  • Cell wall
    • Protein, M, T, R antigens
    • Group carbohydrate
      • N-acetyl glucosamine, rhamnose
    • Peptidoglycan
      • N-acetyl glucosamine, N-acetyl muramic acid, alanine, glutamid acid, lysine, glycine
  • Cytoplasmic membrane
    • Phospholipids, proteins
  • Glycerol teichoic acids
    • Location uncertain
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10
Q

Role in virulence: capsule

A
  • Hyaluronic capsule –> anti-phagocytic
    • Significant cause of illness in asplenic patients
  • Non-immunogenic
  • Glycocalyx = capsule slime
    • Allows some bacteria to adhere to surfaces
    • Ex. S. epidermidis to catheters
  • Quellung reaction = diagnostic test - specific antiserum causes capsule to swell
    • Ex. S. pneumoniae and H. influenzae type B
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11
Q

Role in virulence: cell wall components

A
  • T, R antigens unrelated to virulence
  • M protein (virulence factor for group A) –> antiphagocytic, prevents activation of complement
    • Weakest point in organism’s defense - plasma (B) cells generate Abs against M protein
    • Abs bind M protein (opsonization) –> aids in destruction of organism by macrophages and neutrophils
    • Immunity arises from Abs against M-protein
    • Protection is M-type specific
    • 80 serotypes exist
  • Teichoic acids
    • Lipoteichoic acids (LTA) bound to surface protein (ex. M protein) –> important virulence factor
    • Mediates initial adherence of streptococci cells to mucosal cells, epithelial cells –> facilitates colonization
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12
Q

Role in virulence: toxins

A
  • Pyrogenic exotoxins (A-C)
    • Pyrogenic
    • Immunosuppressive
    • Enhance host susceptibility to endotoxin shock
  • Streptococci erythrogenic toxins
    • Cardiac tissue damage
    • Rash of scarlet fever
  • Streptolysin O
    • Binds to cholesterol in RBC membranes –> polymerizes –> inserts as a pore precipitating lysis
  • Streptolysin S
    • Hemolytic to RBCs
    • Cytotoxic to leukocytes
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13
Q

Role in virulence: enzymes

A
  • Enzymes that are spreading factors promote spread of group A streptococci through tissue
  • Streptokinase
    • Degrades host-derived fibrin (normally acts to wall off lesions)
  • Hyaluronidase
    • Degrades ground substance of connective tissue
  • DNAase
    • Nucleases which digest DNA
  • Proteinase
    • Digests proteins and aids spread
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14
Q

Tissue invasive toxins from S. pyogenes

A
  • Hemolysis/Streptolysin O and S
    • Lyses RBCs
  • Streptokinase
    • Activates plasminogen to lyse fibrin clots (host-derived fibrin usually acts to wall off lesion), much like Staphylokinase
  • DNAases
    • Hydrolyzes DNA
  • Hyaluronidase
    • Breaks down proteoglycans
  • NADase
    • Hydrolyzes NAD and NADH
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15
Q

Complications of group A streptococci infections: acute rheumatic fever

A
  • Symptoms: carditis, chorea, migratory polyarthritis, erythema marginatum, subcutaneous nodules (Jones criteria!!)
  • Autoimmune:
    • Anti-streptolysin O (ASO) Abs crossreact with structural heart valve tissues (laminin)
  • Streptolysin O, other rheumatic toxins initiate cardiac damage, facilitating rheumatic process
  • L forms or streptococci strains (w/o cell wall) directly infect heart
  • Genetic determination of immune response
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16
Q

Complications of Group A streptoccoci infections: acute post-streptococcal glomerulonephritis (APSGN)

A
  • Symptoms: hematuria, periorbital edema, hypertension
  • I. Immune complex deposition (most accepted)
    • Immune complexes form in systemic circulation –> filtered by glomerulus –> localized beneath glomerular basement membrane
    • Result: self-limited inflammation due to ability of immune complexes to fix complement, elicit vigorous immune response
  • II. Production of cross-reacting Abs
  • III. Production of nephrotoxins
  • Certain antigens from nephritogenic (able to cause glomerulonephritis) streptococci induce Ab response –> Ag/Ab complexes –> deposition in glomerular basement membrane –> activate complement cascade –> local glomerular destruction
17
Q

Acute rheumatic fever: characteristics/epidemiology

A
  • Age
    • Rare in infants and elderly
  • Gender incidence
    • Equal
  • Genetics
    • Familial
  • Season
    • Winter/spring
  • Site of infection
    • Pharynx
  • Attack rate
    • 1-3%
  • Pathogenesis
    • Autoimmune
  • Recurrence with reinfection
    • Common
  • Strain
    • M18, M3 large capsules
  • Relation to ASO titer rise
    • Increased ASO titer –> increased risk of ARF
  • Prevention by therapy of acute infection
    • Yes
18
Q

Acute post-streptococcal glomerulonephritis: characteristics/epidemiology

A
  • Age
    • Any age
  • Gender incidence
    • M > F
  • Genetics
    • None known
  • Season
    • Summer
  • Site of infection
    • Pharynx/skin
  • Attack rate
    • 1-25%, variable
  • Pathogenesis
    • Immune complex
  • Recurrence with reinfection
    • Rare
  • Strain
    • M12, M4, M9 small capsules
  • Relation to ASO titer rise
    • No relation
  • Prevention by therapy of acute infection
    • Probably not
19
Q

Pathogenesis of group B streptococci infections

A
  • Capsule is anti-phagocytic
  • Lipoteichoic acid helps with adherence, thus colonization
    • Also stimulates immune response
  • Pathogenesis:
    • Bacteria carried in maternal genital tract –> colonize neonate, especially following obstetric complications
      • Causes meningitis and pneumonia
20
Q

“Random but useful” information about group B streptococci

A
  • 20% of pregnant women colonized with GBS in rectum or vagina
  • Newborns acquire organism before birth by ascending infection or at time of birth
  • About 1/100 colonized infants will develop serious infxns
  • Group **B **streptococci correlated to Baby
    • Most common cause of meningitis in newborn (followed by E. Coli and Listeria)
  • Neonatal infection occurs in 2 forms:
    • Early-onset disease: within first 24 hours
      • Many babies ill at birth
      • Mortality very high
      • All capsular types cause early onset disease
    • Late-onset disease: after 24 hours of life (usually 1 week or later)
      • Almost all late-onset disease due to Type III organisms (70% of neonatal infections)
  • Low/absent levels of Ab against capsular polysaccharide correlates with risk of serious infection
  • High levels of maternal IgG Ab against capsular polysaccharide cross placenta –> hypothesized to protect newborn
  • Mothers who lack antibody –> little or no transfer of protective Ab to baby
21
Q

Differentiation between enterococci and group D streptococci

A
  • Unlike group D enterococci - group D streptococci cannot grow in 6.5% NaCl and are sensitive to pencillins
  • Enterococci: can live in both bile and salt
    • E. faecalis
    • E. faecium
  • Group D streptococci: can live in bile, not salt
    • S. bovis
    • S. equinus
  • Enterococci used to be classified as group D but have been shown to be significantly different and now are own category
22
Q

Common infxns due to viridans streptococci

A
  • S. mutans:
    • Dental caries via production of dextrans from sucrose, permits adherence to tooth surfaces
  • S. sanguis
    • 50% of subacute bacterial endocarditis - adhering to previously damaged heart valves

*Note: S. viridans (subacute bacterial endocarditis); S. Aureus (Acute Bacterial Endocarditis)

S. pyogenes is initial offender –> rheumatic fever –> damages heart valve

Then easier for S. viridans or GDS to more easily adhere to heart valves and cause SBE

23
Q

Metabolism of streptococi & common tests used for classification

A
  • Aerotolerant bacteria, ferment carbohydrates to form lactic acid
    • Catalase-, oxidase-negative
  • Catalase: enzyme possessed by staphylococci but not streptococci
  • Biochemical reactions
    • Optochin test
    • CAMP test
    • Bile esculin hydrolysis
    • Growth in NaCl
24
Q

Optochin test

A
  • S. pneumoniae is optochin sensitive
  • S. viridans is optochin resistant
25
Q

CAMP test

A
  • CAMP factor is diffusible, heat-stable protein produced by group B strep
    • Group A = CAMP negative
    • Group B = CAMP positive
26
Q

Bacitracin sensitivity

A
  • Differential test used to distinguish between organisms sensitive to bacitracin and those not
    • Group A sensitive
    • Group B resistant
27
Q

Bile esculin hydrolysis

A
  • Medium that is both selective and differential
  • Tests ability of organisms to hydrolyze esculin in presence of bile
  • Commonly used to identify members of genus Enterococcus
    • E. faecalis and E. faecium
28
Q

Growth in NaCl

A
  • Group D streptococci cannot grow in 6.5% NaCl
  • Enterococi CAN grow in 6.5% NaCl