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MLSCI 242 > LECTURE - Streptococcus > Flashcards

LECTURE - Streptococcus Flashcards

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
Q

T or F. GBS is opportunistic

A

T

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26
Q

If mothers are colonized by GBS, approximately half of the infants will also be colonized…

A
  • most will be asymptomatic but small % will develop invasive disease
  • intravenous penicillin G of carriers during labour to reduce likelihood of neonatal GBS infection
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27
Q

third leading cause of nosocomial infection

A

Enterococci

- opportunistic pathogen not taken seriously in the past

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28
Q

Virulence factors of Enterococci

A
  • biofilm formation
  • Vancomycin resistance
  • ~21 MSCRAMMs
  • pathogenicity island (PI); genetic material acquired by an organism that has come from another organism
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29
Q

Virulence factor of Enterococci that contributes to biofilm formation

A

pili

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30
Q

Distinctive diagnostic features of S. pneumoniae

A
  • Quellung test (capsular swelling)
  • latex agglutination (PCR for psaA)
  • bile solubility (S. pneumo is lysed by bile)
  • Optochin (ethyl hydrocupreine) sensitivity
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31
Q

Diseases caused by S. pneumoniae

A
  • pneumonia (especially in infants and the elderly)
  • meningitis (<2 yr olds)
  • otitis media (inner ear infection in <10 yr olds)
32
Q

What does the capsule of S. pneumoniae do ?

A
  • anti-phagocytic
  • Fc portion of Abs is buried within capsule so can’t opsonize
  • inhibits complement binding as well
33
Q

PsaA

A
  • 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
Q

keys to GAS (S. pyogenes) pathogenicity

A
  • encounter
  • entry
  • spread
35
Q

MSCRAMMs (adhesins) that contribute to entry of GAS (S. pyogenes)

A
  • 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
Q

MSCRAMMs (adhesins) that contribute to entry of GAS (S. pyogenes)

A
  • 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
Q

these GAS virulence factor causes intense inflammatory response

A
  • streptolysin O
  • streptokinase
  • lipoteichoic acid (LTA)
38
Q

streptolysin O (SLO) and SLS

A
  • SLO = O2-sensitive hemolysin

- membrane-inserting toxin and streptolysin S (O2-stable hemolysin)

39
Q

streptokinase

A

facilitates spread of organisms in body

- activates plasminogen, leading to dissolution of clots and degradation of extracellular matrix proteins in human cells

40
Q

LTA

A
  • 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
Q

SPEs

A
  • 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
Q

Early Onset Disease (EOD) of GBS neonatal infection

A

first week of life; pneumonia, sepsis, meningitis

43
Q

Late onset disease (LOD)

A

second week of life up to 3 months; meningitis is the most frequent manifestation

44
Q

Virulence factors of GBS

A
  • polysaccharide capsule
  • pili
  • beta hemolysin
  • laminin-binding protein (Lmb)
  • fibronectin-binding proteins (Fnb, A, B, C)
  • C5a peptidase (ScpB)
  • CAMP factor
45
Q

polysaccharide capsule of GBS

A
  • helps organism evade opsonophagocytosis by binding complement factor H which degrades C3b before it can bind
46
Q

Polysaccharide capsular types of GBS

A

Ia, Ib, II, III, IV, V, VI, VII, VIII

47
Q

Spe A

A
  • GAS

- seems to be the most important exotoxin; associated with recently emerging, problematic strains

48
Q

Spe B

A
  • GAS

- cysteine protease

49
Q

Where organisms invade between cells

A

paracellular invasion of GBS

50
Q

a pore-forming cytolysin, active against a variety of cell types

A

beta hemolysin

51
Q

T or F. Like GAS, GBS is still treatable with penicillin G

A

T!

52
Q

Features of enterococci

A
  • 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
Q

Group II enterococci

A

E. faecalis, E. faecium, E. casseliflavus, E. gallinarum, E. mundtii

  • cinstitutes almost ALL human enterococcal isolates
  • all mannitol + and sorbitol -
54
Q

enterococcal disease

A
  • 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
Q

occurs as a consequence of the immune response to certain strains of GAS

A

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
Q

help neutrophils trap bacteria to make it easier to phagocytose them

A

NETs

- M protein can neutralize anti-bacterial proteins inside NET

57
Q

an inhibitor of cell wall synthesis

A

vancomycin

- inhibits both final steps of peptidoglycan synthesis, transglycosylation, and transpeptidation

58
Q

T or F. Proteins make better vaccines than capsular polysaccharides

A

T! they are T-dependent antigens

59
Q

What does the cell wall polysaccharide in Pneumococcal species do?

A

stimulate inflammation by strongly activating complement and stimulating release of cytokines

60
Q

Pneumolysin

A

cytotoxic; activates complement and cytokines ; also pore-forming

61
Q

this pneumococcal component inhibits phagocytosis by blocking activation and deposition of complement on the bacterial surface

A

PspA

62
Q

this pneumococcal factor inhibits phagocytosis by binding complement factor H

A

PspC

63
Q

PsaA

A

pneumococcal constituent

mediates adherence

64
Q

Autolysin (LytA)

A
  • pneumococcal
  • causes bacterial disintegration
  • releases components like pneumolysin
65
Q

Autolysin (LytA)

A
  • pneumococcal
  • causes bacterial disintegration
  • releases components like pneumolysin
66
Q

neuraminidase

A

possibly mediates adherence; pneumococcal

67
Q

Some activities attributed to pneumolysin

A
  • 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
Q

LTA in S. pneumo binds to _____ and triggers cytokine release (like effect of gram neg bacterial LPS on ___)

A

TLR2; TLR4

69
Q

Two known quorum sensing eptides for S. pneumoniae

A

ComC and BlpC

70
Q

How does S. pneumoniae mutate in response to antibiotic therapy

A
  • 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
Q

T or F. No antibiotics work against S. pneumoniae

A

F! Although they have some antimicrobial resistance strategies, we are still okay for now!

72
Q

T or F. DNA uptake is easier in gram pos than in gram neg bacteria

A

T, case for S. pneumoniae

73
Q

The transformability or DNA uptake of S. pneumoniae may provide the basis for:

A
  • heterogeneity of capsular polysaccharide

- changes in PBPs

74
Q

Leading cause of death in children worldwide

A

pneumonia

75
Q

The majority of mortality associated with the influenza pandemic of 1918 was attributable to…

A

bacterial infections, esp. pneumococcus
- PCV (pneumococcal conjugate vaccines) are important in preparedness (children); pneumococcal polysaccharide vaccine for adults)

MLSCI 242 (39 decks)

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