MLSCI 242 > LECTURE - Streptococcus > Flashcards

LECTURE - Streptococcus Flashcards

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1
Q

T or F. Streptococcus is catalase positive

A

F! Catalase negative

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2
Q

grandmother of Strep

A

Rebecca Lancefield

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3
Q

beta hemolytic

A 
Group A (S. pyogene)
Group B (S. agalactiae)
* both pyogenic
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4
Q

alpha hemolytic

A

S. pneumoniae

“viridans” streptococci

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5
Q

gamma hemolytic

A

group D

Enterococci

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6
Q

Three main disease presentations caused by GAS

A
  • superficial
  • invasive (toxin-mediated)
  • sequelae
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7
Q

superficial diseases caused by GAS

A
  • pharyngitis (sore throat)
  • soft tissue infections
  • impetigo
  • streptococcal cellulitis
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8
Q

invasive or toxin-mediated diseases caused by GAS

A
  • streptococcal toxic shock

- necrotizing fasciitis

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9
Q

Pharyngitis is characterized by presence of

A

strawberry tongue

- can’t tell if virl or bacterial just by looking

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10
Q

T or F. impetigo is very contagious

A

T! daycares (towels!!!)

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11
Q

Rheumatic fever

A
  • inflammatory lesions involving heart, joints, subcutaneous tissue & CNS
  • kids 6-15: polyarthritis, carditis
    > sequelae of pharyngitis and NOT impetigo
    > associated with large amount of M protein and a capsule
    > cross-reactive Ab against heart proteins
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12
Q

Sequelae of GAS

A
  • rheumatic fever

- acute glomerulonephritis

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13
Q

Acute glomerulonephritis

A
  • inflammatory disease of renal glomerulus (nephritogenic strains of GAS after strep throat or rarely, impetigo)
    > immune complex disease
    > edema, hypertension, headache malaise, dark urine, hematuria, proteinuria
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14
Q

T or F. GAS have MSCRAMMs

A

T! important to all gram + organisms

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15
Q

This is required for S. pyogenes virulence

A

M protein (identified by emm genes that encode them)

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16
Q

elicits a humoral immune response that is type-specific; also an MSCRAMM, has the LPXTG motif, and is antiphagocytic

A

M protein

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17
Q

Functional interactions of M protein

A
  • GAS aggregation through homotypic interactions
  • evasion of phagocytosis by fibrinogen recruitment or C4BP to the surface
  • M protein released by neutrophil proteases from surface interacts with fibrinogen and M-fibrinogen complexes activate neuts via B2 integrins along with IgGs that bind to M protein and interact with FcyRII; activated neuts release heparin BP (vasodilator)
  • M-fibrinogen complexes also activate platelets
  • synergizes a TLR2-dependent manner with HBP to activate monocytes = pro-inflammatory cytokines and up-reg pro-coagulatory protein tissue factor
  • neutralizing the antimicrobial effects of cathelicidins in NETSs
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18
Q

besides M protein, other anti-phagocytic virulence factors of GAS

A
  • hyaluronic acid capsule: discourages C3b binding; resembles self
  • C5a peptidase: extracellular enzyme that degrades C5a = reduced migration of neutrophils to infection site
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19
Q

pyo- vs pyro-

A 
pyo = pus-forming
pyro = fever-inducing
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20
Q

Why does GAS have a diverse disease spectrum?

A
  • differences in strains that produce…
  • different types of toxins
  • M type
  • invasive ability (linked to a 2-component regulatory system called CovRS)
  • differences in hosts
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21
Q

T or F. GBS is beta hemolytic

A

T! narrow zone

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22
Q

an emerging pathogen (Strep)

A

GBS

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23
Q

Disease caused by GBS in neonates

A
  • 1-2 %
  • early-onset disease (EOD); first 6 days
  • late-onset disease (LOD); over 7 days old
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24
Q

risk factors of GBS

A

mostly those who are elderly and have other underlying illnesses (chronic)

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25
T or F. GBS is opportunistic
T
26
If mothers are colonized by GBS, approximately half of the infants will also be colonized...
- most will be asymptomatic but small % will develop invasive disease - intravenous penicillin G of carriers during labour to reduce likelihood of neonatal GBS infection
27
third leading cause of nosocomial infection
Enterococci | - opportunistic pathogen not taken seriously in the past
28
Virulence factors of Enterococci
- biofilm formation - Vancomycin resistance - ~21 MSCRAMMs - pathogenicity island (PI); genetic material acquired by an organism that has come from another organism
29
Virulence factor of Enterococci that contributes to biofilm formation
pili
30
Distinctive diagnostic features of S. pneumoniae
- Quellung test (capsular swelling) - latex agglutination (PCR for psaA) - bile solubility (S. pneumo is lysed by bile) - Optochin (ethyl hydrocupreine) sensitivity
31
Diseases caused by S. pneumoniae
- pneumonia (especially in infants and the elderly) - meningitis (<2 yr olds) - otitis media (inner ear infection in <10 yr olds)
32
What does the capsule of S. pneumoniae do ?
- anti-phagocytic - Fc portion of Abs is buried within capsule so can't opsonize - inhibits complement binding as well
33
PsaA
- S. pneumoniae - adherence - binding to disaccharide residues GlcNAc B1-3 on Gal on epithelial cells in naspopharynx, then to GalNAc B1-3(4) Gal on type II pneumocytes in lung and on endothelial cells in blood vessels - facilitated by inflammation & viral infection
34
keys to GAS (S. pyogenes) pathogenicity
- encounter - entry - spread
35
MSCRAMMs (adhesins) that contribute to entry of GAS (S. pyogenes)
- M protein: binds collagen and certain blood proteins (factor H, Fc of IgG, fibrinogen) - fibronectin-binding protein (F1, F2): binds fibronectin - Epa: collagen-binding protein
36
MSCRAMMs (adhesins) that contribute to entry of GAS (S. pyogenes)
- M protein: binds collagen and certain blood proteins (factor H, Fc of IgG, fibrinogen) - fibronectin-binding protein (F1, F2): binds fibronectin - Epa: collagen-binding protein
37
these GAS virulence factor causes intense inflammatory response
- streptolysin O - streptokinase - lipoteichoic acid (LTA)
38
streptolysin O (SLO) and SLS
- SLO = O2-sensitive hemolysin | - membrane-inserting toxin and streptolysin S (O2-stable hemolysin)
39
streptokinase
facilitates spread of organisms in body | - activates plasminogen, leading to dissolution of clots and degradation of extracellular matrix proteins in human cells
40
LTA
- component of the streptococcal cell wall - function can be analogous to LPS in gram negs (endotoxin-like); i.e. septic shock in host ; binds to TLR2 - synergism with SAGs?
41
SPEs
- streptococcal pyrogenic exotoxins - 7 variants - carried by temperate bacteriophages - SAGs = nonspecific stimulation of T cells, excess IL-2, TNF released leading to shock (cap leakage, hypotension, rash, fever) - historically known as 'erythrogenic toxins' associated w scarlet fever (fever + red rash)
42
Early Onset Disease (EOD) of GBS neonatal infection
first week of life; pneumonia, sepsis, meningitis
43
Late onset disease (LOD)
second week of life up to 3 months; meningitis is the most frequent manifestation
44
Virulence factors of GBS
- polysaccharide capsule - pili - beta hemolysin - laminin-binding protein (Lmb) - fibronectin-binding proteins (Fnb, A, B, C) - C5a peptidase (ScpB) - CAMP factor
45
polysaccharide capsule of GBS
- helps organism evade opsonophagocytosis by binding complement factor H which degrades C3b before it can bind
46
Polysaccharide capsular types of GBS
Ia, Ib, II, III, IV, V, VI, VII, VIII
47
Spe A
- GAS | - seems to be the most important exotoxin; associated with recently emerging, problematic strains
48
Spe B
- GAS | - cysteine protease
49
Where organisms invade between cells
paracellular invasion of GBS
50
a pore-forming cytolysin, active against a variety of cell types
beta hemolysin
51
T or F. Like GAS, GBS is still treatable with penicillin G
T!
52
Features of enterococci
- formerly classified as Group D - can grow with or without O2 (facultative anaerobes = don't need O2) -can grow in 6.5% NaCl at pH 9.6 can grow at temps from 10 to 45 degrees C - can hydrolyze esculin and L-pyrrolidonul-beta-naphthylamide (PYR)
53
Group II enterococci
E. faecalis, E. faecium, E. casseliflavus, E. gallinarum, E. mundtii - cinstitutes almost ALL human enterococcal isolates - all mannitol + and sorbitol -
54
enterococcal disease
- opportunistic organisms that were not taken seriously in the past - enterococci have become the 3rd leading cause of nosocomial infections = UTI, wound infections, endocarditis, catheter-associated infections
55
occurs as a consequence of the immune response to certain strains of GAS
GAS can cause disease as an aftermath of actual infection. With rheumatic fever, for example, you may not see any evidence of active GAS infection
56
help neutrophils trap bacteria to make it easier to phagocytose them
NETs | - M protein can neutralize anti-bacterial proteins inside NET
57
an inhibitor of cell wall synthesis
vancomycin | - inhibits both final steps of peptidoglycan synthesis, transglycosylation, and transpeptidation
58
T or F. Proteins make better vaccines than capsular polysaccharides
T! they are T-dependent antigens
59
What does the cell wall polysaccharide in Pneumococcal species do?
stimulate inflammation by strongly activating complement and stimulating release of cytokines
60
Pneumolysin
cytotoxic; activates complement and cytokines ; also pore-forming
61
this pneumococcal component inhibits phagocytosis by blocking activation and deposition of complement on the bacterial surface
PspA
62
this pneumococcal factor inhibits phagocytosis by binding complement factor H
PspC
63
PsaA
pneumococcal constituent | mediates adherence
64
Autolysin (LytA)
- pneumococcal - causes bacterial disintegration - releases components like pneumolysin
65
Autolysin (LytA)
- pneumococcal - causes bacterial disintegration - releases components like pneumolysin
66
neuraminidase
possibly mediates adherence; pneumococcal
67
Some activities attributed to pneumolysin
- inhibits the activity of ciliated cells - cytotoxic for alveolar and endothelial cells - activates classical complement pathway by binding to Fc portion of an antibody - causes inflammation in the lung - decreases the effectiveness of PMNs - stimulates monocytes to produce cytokines
68
LTA in S. pneumo binds to _____ and triggers cytokine release (like effect of gram neg bacterial LPS on ___)
TLR2; TLR4
69
Two known quorum sensing eptides for S. pneumoniae
ComC and BlpC
70
How does S. pneumoniae mutate in response to antibiotic therapy
- chromosomal mutation in PBPs (b-lactam resistance) - conjugative transposons confer resistance to other antibiotics like erythromycin - some bacteria shut own metabolism until antibiotics disappear; for ex: > depletion of autolysins through bacterial starvation > cell wall structure changes to make it resistant to autolysin
71
T or F. No antibiotics work against S. pneumoniae
F! Although they have some antimicrobial resistance strategies, we are still okay for now!
72
T or F. DNA uptake is easier in gram pos than in gram neg bacteria
T, case for S. pneumoniae
73
The transformability or DNA uptake of S. pneumoniae may provide the basis for:
- heterogeneity of capsular polysaccharide | - changes in PBPs
74
Leading cause of death in children worldwide
pneumonia
75
The majority of mortality associated with the influenza pandemic of 1918 was attributable to...
bacterial infections, esp. pneumococcus - PCV (pneumococcal conjugate vaccines) are important in preparedness (children); pneumococcal polysaccharide vaccine for adults)
MLSCI 242
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