Virulence Factors Definitions Flashcards

1
Q
  1. Cell wall – useful for bacterial viability, homeostasis, protect the bacteria
    from attack by host lysozyme
A
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2
Q
  1. protein A - bind Fc of IgG protects, blocks immune response, & opsonization
A
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3
Q
  1. binding or clamping factors – attachment to host proteins
A
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4
Q
  1. Capsule (slime layer) – useful for
     adhesion
     prevents chemotaxis and
     inhibit phagocytosis by polymorphonuclear leukocytes
A
  • Adhesion
  • Hide/cover the surface of the bacterial cell by depositing host sialic
    acid residues on their surfaces
  • Thus, capsule prevents bacterial recognition by phagocytes, prevents
    complement assisted opsonization (inhibit phagocytic killing)
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5
Q
  1. hyaluronidase - breaks down connective tissue between adjacent cells
    (digs deeper between cells)
A
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6
Q
  1. catalase – protects against host reactive oxygen species (ROS) e.g. H2O2
A
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7
Q
  1. coagulase - clots blood to hide in it
A
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8
Q
  1. staphylokinase - lyses clots (fibrin) to come out of it and disperse itself
A
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9
Q
  1. lipase - digest lipids, thus allows to colonize skin surface & sebaceous
    glands
A
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10
Q
  1. protease - destroys tissue proteins
A
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11
Q
  1. beta-lactamases - inactivate beta-lactam drugs’ thus, survive treatment
A
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12
Q
  1. hemolysin (alpha, beta, or gamma) - destroys red blood cells,
    neutrophils, macrophages, platelets
A
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13
Q
  1. cytolytic toxins (leukocidin)- destroy cell membranes of host cells
    (leukocytes)
A
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14
Q
  1. exfoliative toxin – separate skin layers, resulting in impetigo & skin
    layer peel off
A
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15
Q
  1. toxic shock syndrome (TSS) toxin – causes
    a. shock &
    b. superantigens (Mass T cell activation i.e. 20% of all body T cells)
A
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16
Q
  1. enterotoxins – 20 toxins in total. They cause
    a. food poisoning by stimulating the gut motility (vomiting) &
    b. superantigens
A
17
Q

Lipoteichoic
acid
* Adhesion
* Cytotoxic for most host cells

A
18
Q

Protein M

A
  • Adhesion and inhibition of phagocytic ingestion.
  • Protein M binds the Fc region of IgG & prevents opsonization
19
Q

Protein G
* Compete with complement to bind with the constant Fc region of IgG
of diverse animal species.
* It binds and accumulates IgG on the bacterial surface through non-
immune binding, leading to prevention for opsonization

A
20
Q

Nuclease
(Type A,B, C,
& D)
* Facilitate liquefaction of pus (converts pus to resources/substrates
to utilize it and grow)
* Have DNase activity (A & C) and RNase activity (B&D) to destroy
host cells and host defense

A
21
Q

Streptokinases
* Catalyze conversion of plasminogen to plasmin, leading to digestion
of fibrin (lyse blood clots to escape and spread from the clots)

A
22
Q

C5a
peptidases
* Destroy C’ chemotactic signals (C5a); thus blocks chemotaxis or
host defense cell recruitment to the infection site

A
23
Q

Hemolysin
(, , and )
* destroys RBCs, neutro/mac/plat

A
24
Q

Exotoxins
(streptolysin
O & S)
1. Hemolytic on blood agar
2. kills many cells including phagocytes
3. Inhibit phagocyte attraction (inhibit chemotaxis)

A
25
Q

enterococcus
Aggregation substance = binds to host cells or bacteria-to-bacteria (conjugation)
 Trafficker of AMR genes by transferring them horizontally to enterococci spp.
 Acquired broad-spectrum antimicrobial resistance (AMR).

A
26
Q

Cytolysin/hemolysin (also called bacteriocin or enterocin) =
1. kills by pore-forming on cell envelope of red and white blood cells
2. kills Gram-negative bacteria competitors = to defend its territory that contributes to niche control

A
27
Q

Sex pheromone = stimulate expression of aggregation substances which results in conjugation;
thus, it is a means of acquiring and accumulating plasmids

A
28
Q

Phospholipase
Pore-forming lysis on
endocytosis membrane of
the host to free itself from
lysosome (vacuoles) in the
cytoplasm of the host cell

A
29
Q

Beta-hemolysin and Listeriolysin O
Pore-forming lysis on endocytosis
membrane of the host to free
itself from lysosome (vacuoles)
in the cytoplasm of the host cel

A
30
Q

Actin-polymerizing protein (
actA)
 instructs host cell for deposition of its actin-
filaments on the end of Listeria
 Then Listeria uses the host actin filaments for
propelling to the nearby cells.
 Such host actin-based zipper mechanism for
propelling and transmission from cell to cell are
used by:
 Listeria, Rickettsia, and Yersinia pseudotuberculosis

A
31
Q

Surface protective proteins (spA, B and C antigens) – for biofilm formation,
adhesion, and to elicit immune response.
 These surface proteins can be used as a protective vaccine

A
32
Q

Neuraminidase (sialidase) – for bacterial attachment, invasion, destroy blood
vessels leading to hemorrhage and thrombosis
 This can lead to bacterial emboli and infarction in the heart valves (endocarditis), spleen, liver,
lung, kidney, and joints (polyarthritis)

A
33
Q

Neutrophils is the target of the oedema factor.
Macrophages, dendritic cells neutrophils and some epithelial and endothelial cells are
the target of the lethal factor

A
34
Q

Tetanus toxin (tetanospasmin)
* Zinc endopeptidase binds to the neurons, which release
gamma-aminobutyric acid (GABA) and glycine, the major
inhibitory neurotransmitters
* Hydrolyzes the docking proteins (VAMP aka synaptobrevin)
required by neurotransmitter-containing vesicles to fuse with the
pre-synaptic membrane
* Once the docking proteins are hydrolyzed, the synapse degenerates,
taking weeks-months to regenerate

A
35
Q
  • Botulinum neurotoxins (BoNT)
  • Act in the neuromuscular junction
  • Zinc endopeptidases with identical activity that binds to
    cholinergic nerve cells
  • Decreases the release of acetylcholine
  • Once hydrolyzed, the synapse degenerates, taking weeks to months
    to regenerate
  • BoNT are secreted with accessory proteins
  • Aid in the survival in the GI tract
A
36
Q

Epsilon toxin
* Increases intestinal permeability, causes vascular damages, fluid losses,
edema

A
37
Q

Clostridium difficile toxins
* Toxin A (Tox A or TcdA)
* ENTEROTOXIN
* Breakdown of cytoskeletal components of the affected
cell
* Disruption of the tight junctions between intestinal
epithelial cells
* RESULTS IN CELL DEATH
* Stimulates influx of polymorphonuclear cells
* Synthesis of prostaglandins
* RESULTS in secretion of chloride ions and water (Diarrhea)

A