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
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
- Streptococcus pneumoniae
3
Q
β-hemolysis
A
- Complete lysis of RBCs –> distinct clear zone around colonies
- Examples:
- S. pyogenes - Group A
- S. agalactiae - Group B
4
Q
ɣ-hemolysis
A
- No hemolysis effect
- Preferably noted “nonhemolytic”
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
6
Q
Lancefield group A: common streptococci, hemolysis pattern
A
- Common streptococci:
- Streptococcus pyogenes
- Hemolysis:
- Beta-hemolysis
7
Q
Lancefield group B: common streptococci, hemolysis pattern
A
- Common streptococci:
- Streptococcus agalactiae
- Hemolysis:
- Beta-hemolysis
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
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
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
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
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
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
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
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
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
- Bacteria carried in maternal genital tract –> colonize neonate, especially following obstetric complications
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)
- Early-onset disease: within first 24 hours
- 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
CAMP test
* CAMP factor is diffusible, heat-stable protein produced by group B strep
* Group A = CAMP negative
* Group B = CAMP positive
26
Bacitracin sensitivity
* Differential test used to distinguish between organisms sensitive to bacitracin and those not
* Group A sensitive
* Group B resistant
27
Bile esculin hydrolysis
* 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
Growth in NaCl
* Group D streptococci cannot grow in 6.5% NaCl
* Enterococi CAN grow in 6.5% NaCl
