Virulence Factors Flashcards

(34 cards)

1
Q

is a causative agent of nosocomial infections due to living in biofilm

A

P. aeruginosa

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2
Q

bacteria grow in biofilms, in
which they are protected against disinfectants.
Workers in cooling towers, persons working in air
conditioned rooms and people taking a shower are
exposed to

A

Legionellosis

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3
Q

spreading factor. It is produced by streptococci, staphylococci and clostridia.
The enzyme attacks the interstitial cement (“ground substance”) of connective tissue

A

Hyaluronidase

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4
Q

produced by Cl. perfringens.
It breaks down collagen, the framework of muscles,
which facilitates gas gangrene due to these organisms.

A

Collagenase

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5
Q

produced by intestinal pathogens such as V. cholerae and Sh. dysenteriae. It degrades sialic acid, an intercellular cement of the epithelial cells of the intestinal mucosa.

A

Neuraminidase

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6
Q

Kinase enzymes convert inactive plasminogen to plasmin which digests fibrin and prevents clotting of the blood and allows more rapid diffusion of the infectious bacteria.

A

Streptokinase and staphylokinase

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7
Q

produced by Cl. perfringens, destroy (phosphatidyl choline) in cell membranes.

A

Lecithinases

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8
Q

produced by Cl. perfringens (i.e., alphatoxin), hydrolyze phospholipids in cell membranes by removal of polar head groups.

A

Phospholipases

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9
Q

produced by staphylococci (i.e., alphatoxin), streptococci (i.e., streptolysin) and various clostridia, that destroy red blood cells and other cells (i.e., phagocytes) by lysis.

A

Hemolysins

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10
Q

destroys both PML and macrophages.

A

Leukocidin

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11
Q

breaks down fat

A

Lipase

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12
Q

Coagulase, formed by S. aureus, is a cell-associated and diffusible enzyme that converts fibrinogen to fibrin which causes clotting.

A

Staphylococcal coagulase:

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13
Q

produced by N. gonorrhoeae, N. meningitidis, H. influenzae and S. Pneumoniae. It degrades the secretory IgA on mucous surfaces and thus eliminates protection of the host by antibody.

A

Immunoglobulin A (IgA) protease

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14
Q

survive by inhibiting

phagosome-lysosome fusion.

A

M. tuberculosis and Legionella

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15
Q

quickly escapes the phagosome into the cytoplasm

before phagosome-lysosome formation.

A

Listeria

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16
Q
  • The genes are carried on plasmids or bacteriophages rather than chromosomes.
  • Diffuse
  • +/-
  • toxoidable
  • release during life cell
17
Q

———- component binds,———enzymaically active

18
Q

bind non-specifically, activate large
numbers of T cells which in turn release large amounts of
cytokines.

A

Superantigens

19
Q

small proteins that regulate immune responses and in high
concentrations can cause many symptoms and signs: fever, nausea,
vomiting, diarrhea, shock and even death

20
Q

secrete hemolysins that cause the

complete lysis of RBC’s

A

Beta Hemolytic Streptococci (exo)

21
Q

preparations of exotoxins chemically treated to destroy their toxigenicity but retain their ability to elicit antibody formation in the body.
(Immunizes exotoxins)

22
Q

-produced only by Gram-negative
bacteria and released only when bacteria lyze.
-lipopolysaccharide
of the outer membrane of Gram-negative bacteria;Lipid A
-@ bacterial chromosomes
-release upon cell lysis

23
Q

produces IL-1 and TNF → fever-shock

24
Q

C3a and C5a→ release of mast cell

mediator as bradykinin→ vasodilatation and hypotension

25
early component of coagulation | →DIC→THROMBOSIS
Hageman factor
26
are mobile genetic DNA segments inserted into chromosome or plasmid
pathogenicity islands (PIs)
27
Bacteria change antigenicity of their surface as in (N. gonorrhea -Borrelia) to escape immune response
Antigenic Heterogenicity (variation)
28
Invasive factors
Anti phagocytic factors, EC enzymes, ability to survive IC
29
Neisseria, gonorrhoeae, E.coli
Pili- UTI
30
S.epidermidis , s.mutans
Glycocalyx | Heart, teeth
31
M protein cell wall
S. Pyogenes
32
Protein A cell wall
S. aureus
33
What are the types of bacteria that can change the surface of the ag
Antigen Hetrogenicity N.gonorrhea, borrleia
34
Bacteria that escapes phagocytosis
Listeria, legionella, m.tuberculosis