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BIOL 4405 > Staph Aureus > Flashcards

Staph Aureus Flashcards

1
Q

Staphlococcus aureus

how many virulence factors?

what can it cause?

due to things like what?

A

200-300 virulence factors

food poisoning, dermal infections of bone and joint, sinus, blood and skin

carriers, biofilms, facultative intracellular pathogen, fate depends on host response, isolate and genotype

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2
Q

toxins that induce host cell lysis: (3)

A

alpha-toxin

phenol-soluble modulins (PSM)

panton-valentine leukocidin (PVL)

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3
Q

secreted factors that inhibit neutrophil recruitment: (2)

A
  • chemotaxis inhibitory protein of staphylococci (CHIPS)
  • extracellular adherence protein (Eap)
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4
Q

factors that inhibit reactive oxygen species: (2)

A
  • golden caretenoid pigment
  • superoxide dismutase enzymes
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5
Q

FnBPA and FnBPB=

A

Fibrionectin binding proteins A and B

-epithelial, endothelial, fibroblasts, osteoclasts, keratinocytes and cellular surface proteins Hsp60 and Hsp70

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6
Q

Teichoic acids-

Zipper mechanism-

Kinases are?

A

teichoic acids in cell wall (WCT) and nasal colonization

Zipper mechanism- formation of actin cups

Kinases are host cell specific

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7
Q

MAPK=

P13K=

ERK=

A

mitogen-activated

phosphoinositide

extracellular regulated

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8
Q

1) extended phagocytic existence=
2) evasion of phagocytic lysis (lysosome)=

A

1) up regulation of anti-apoptotic factors
2) by disintegration of the lysosome membrane by alpha-toxin A, among other strategies.

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9
Q

Staph aureus is phagocytosed by? which leads to?

bacterium resists the action of reactive oxygen intermediates by?

A

S. aureus is phagocytosed by a neutrophil, the neutrophil is activated, and the bacterium is contained within a phagosome, where it encounters multiple antibacterial host defenses.

secreting superoxide dismutases (SODs), which dismutates O2- to O2, and inactivates radicals.

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10
Q

Reactive nitrogen intermediates are resisted by?

resistance to lysozyme is provided by?

resistance to cationic antimicrobial peptides is mediated by?

A

resisted by an inducible lactate dehydrogenase (iLDH) that is insensitive to the intermediates, allowing respiration to continue.

lysozyme resistance is provided by modifications to the muramic acid in peptidogylcan, this altering the cell wall.

is mediated by secretion of staphylokinase and aureolysin, which bind to the cationic peptides, by efflux pumps that remove the peptides from the cell, and by modifications in the cell wall that increase its positive charge, thereby decreasing the affinity of the positively charged antimicrobial peptides for the bacterium.

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11
Q

Bovine mastitis strains (sphingomyelinase)=

A

Beta-toxin in a minority of human strains, which selectively kills monocytes and destroys platelets.

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12
Q

Survival in the face of phagocytosis

dependent on?

log vs lag and stationary phases?

phagosomal acidification=

A

dependent on MOI (multiplicity of infection) and growth phase of the bacteria

Log phase vs lag and stationary phase; it is safer for the bacteria to be in lag or stationary phase because they do not produce any compounds which would “give” them away.

Phagosomal acidification (production of hypochorous acid HOCl) of rapidly-growing bacteria more efficient.

Acidification and digestion by the phagocyte is required for MyD88-dependent TLR responses to infection

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13
Q

not all bacteria are disinfected by phagolysosomes, stuff that keep it alive: (8)

A

1) persistence: attricuted to small colony variants (SVCs) metabolically quiescent
2) non-hemolytic
3) non-pigmented
4) reversible auxotrophy (heme and ocidative phosphorylation pathways)
5) deficiencies with quorum sensing-controlled virulence
6) thicker cell wall
7) improved stress responses
8) mutants in the accessory gene regulator locus (agr)

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14
Q

agr dependency-

alpha-toxin-

delta-toxin-

lyses-

activity similar to?

dependent on?

A

accessory gene locus

alpha-toxin facilitates translocation into the cytoplasm

delta-toxin is encoded by the agr-effector RNA III and is translated approx 1 hour after transcription

lyses a variety of organelles

activity and mode of action simlar to nonionic detergents

dependent on presence of sphingomyelinase beta-toxin

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15
Q

alternative factors: (4)

A

1) lipases
2) phenol-soluble modulins (PSM)
3) delta-toxin is a PSM, other incl. PSM-alpha and PSM-beta
4) part of the agr system and quorum-sensing system

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16
Q

molecular patterns of pathogens are detected by?

PG casues?

alpha-toxin interferes with?

A

molecular patterns of pathogens are detected by NOD proteins (that detect CW components, NOD1 and NOD2) of host cells.

PG causes a conformational change in NOD proteins, leads to NFKB and inflammation

alpha-toxin interferes with NOD2 and phagosomal membrane integrity

17
Q

PCD-

location?

proteins?

A

panton-valentine leokocidin

mitochondrial localization

Bax and Bcl proteins/ pro and anti apoptotic proteins

18
Q

For Bax-independent PCD, alpha-toxin and PVL cause?

Bcl overexpressing cells were protected from?

A

alpha-toxin and PVL cause caspase activation via pore formation, leakage of cytochrome C

Bcl overexpressing cells were protected from alpha-toxin mediated cell death

19
Q

CHIPS are?

complement labels bacteria with?

bacterial human pathogens have evolved differents strategies to impair?

A

Chemotaxis inhibitory protein of staphylococcus aureus (CHIPS)
the plasma proteins of the complement system are essential in the innate immune response against bacteria.

complement labels bacteria with opsonins to support phagocytosis and generates chemoattractants to attract phagocytes to the site of infection.

impair the complement response

20
Q

FPRs=

PRRs are used as?

these molecules known as?

A

FPRs= formylated peptide receptors

PRRs are used as microbial sensors to detect a set of enoltionarily conserved molevules found in a variety of pathogens.

these molecules known as PAMPs (pathogen associated molecular patterns) which do not cause disease but are the major external stimulator of inflammatory response

21
Q

CHIPS are a?

a potent inhibitor of?

their target cells by

A

CHIPS are exoprotein produced by several strains of S. aureus

potent inhibitor of neutrophil and monocyte chemotaxis towards C5a and formylated peptides

these chemoattractants act on their target cells by binding and activating the C5aR and formylated peptide receptor (FPR)

22
Q

CHIPS could be promising for?

A

leading to development of a new anti-inflammatory compound for diseases in which damage by neutrophils plays a key role.

23
Q

Eap=

facilitate?

also been shown to?

A

Eap= extracellular adherence protein, responsible for imparied wound healing

wide range of protein, protein interactions that facilitate the initiation and dissemination of staphylococcal disease

also shown to interfere directly with complex, signaling-dependent events such as leukocyte recruitment

24
Q

Eap interacts with

A

interactions of Eap with epithelial and endothelial cells, fibroblasts and the extracellular matrix (ECM)

25
Q

golden carotenoid pigment

impairs?

A

impairs neutrophil killing and promotes virulence through its antioxidant activity

overview of oxidative and nitrosative stressors and their potential targets

26
Q

metal ion homestasis: (3)

Stress response: (4)

A

1) iron
2) manganese
3) copper
1) metabolic regulation
2) general stress response
3) stringent response
4) SOS response

27
Q

Virulence: (3)

Metaolic response: (3)

A

1) exoproteins
2) cell surface proteins
3) antibiotic resistance
1) metabolite pool
2) redox status
3) energy status

28
Q

mutants lacking the pigment are?

A

less virulent

29
Q

protective vaccines should be able to elicit three major immune responses:

A

1) ABs to directly inhibit bacterial viability and/or toxicity
2) ABs to mediate epsonophagocytosis
3) cell-mediated immunity to stimulate recruitment of phagocytes at the site of the infection

BIOL 4405 (12 decks)

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