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Mega Step 1 Deck > Bacterial Virulence Mechanisms > Flashcards

Bacterial Virulence Mechanisms Flashcards

1
Q

host-pathogen relationship

A

*dynamic relationship, each modifying the activities and functions of the other
*outcome is dependent on:
-virulence of the pathogen
-relative degree of susceptibility or resistance of the host

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2
Q

pathogenesis

A

ability of an agent of infection to produce disease

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3
Q

virulence

A

an agent of infection’s degree of pathogenicity
*how effectively it causes the disease
*the severity of the disease

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4
Q

virulence mechanisms

A

genetic or biochemical features which allow an organism to produce disease

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5
Q

pathogens must be able to accomplish the 5 requirements for infection:

A
  1. entry
  2. colonization
  3. immune evasion
  4. propagation
  5. transmission
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6
Q

portals of entry for pathogens

A

*mucus membranes
*skin
*parenteral (needles, bites, maternal-neonatal)

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7
Q

LD50

A

lethal dose required to kill 50% of experimentally inoculated test animals

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8
Q

ID50

A

infectious dose required to cause disease in 50% of inoculated test animals

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9
Q

which pathogen has a very HIGH ID50

A

vibrio cholera
(requires a lot of vibrio to become infected)

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10
Q

what pathogen has a really LOW ID50

A

shigella
(does not require very much shigella to become infected)

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11
Q

quorum sensing

A

*organisms sense and respond to their environment (produce, release, and sense extracellular signals to regulate gene expression)
*cell-to-cell communication

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12
Q

quorum sensing in gram NEGATIVE bacteria

A

*use acyl-homoserine lactones (AHL’s)
*diffuse freely through bacterial membrane

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13
Q

quorum sensing in gram POSITIVE bacteria

A

*use processed oligo-peptides
*two-component system: membrane-bound sensor kinase receptors and cytoplasmic transcription factors that direct gene expression

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14
Q

pathogenicity islands

A

*virulence genes in CLUSTERS (present in pathogens, absent in benign relatives)
*pick up genes from environmental gene pool by horizontal transfer
*large, distinct chromosomal regions

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15
Q

colonization by an organism

A

*the initial establishment of an organism within a particular habitat or of a colony at a particular site
*usually colonize sites that connect to the external environment
*often requires:
-IgA protease
-motility
-adherence
-biofilm production

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16
Q

IgA protease

A

-secretory IgA is the principal immunologic defense of respiratory and other mucosal surfaces in the body
***IgA protease causes LYSIS of IgA, allowing adherence of the organism to the mucus membrane

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17
Q

flagella

A

*motility
*can function as adhesins
*flagellin or FliC, filament forming component of bacterial flagella

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18
Q

type IV pili

A

*filaments at the poles of bacilli
*allow for gliding motility along a solid surface
*pili are extended and attach to a surface and then retract (causing a twitching motility) or can slingshot

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19
Q

examples of adhesins (virulence factors)

A

fimbria & MSCRAMMS

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20
Q

fimbria

A

*adhesive hair-like structures extending from surface
*usually binds to a specific sugar on the cell surface (the adhesin in LECTIN)

21
Q

P fimbria in E. coli

A

*virulence factor found in a pathogenicity island of uropathogenic E. coli
*binds to Gal-Gal on uroepithelial cells
*this is the most common cause of UTIs in the world

22
Q

MSCRAMMs (microbial surface components recognizing adhesive matrix molecules)

A

*proteins that bind components of the ECM of epithelial cells, such as fibronectin, collagen, or laminin
*secreted by staph, strep, and others

23
Q

biofilms

A

*irreversibly attach to a surface and produce extracellular polymers (matrix formation)
*provides antimicrobial resistance
*ALL bacteria CAN form biofilms, but some are really good at it

24
Q

type III secretion systems (T3SSs)

A

*complex bacterial structures in gram NEGATIVE pathogens for injecting effector proteins directly into the host cell
*effector proteins commonly interfere with host cell cytoskeleton to promote attachment and invasion, create cytotoxicity and barrier dysfunction, and block immune system

25
Q

T3SS apparatus

A

*consists of rings that provide a tube across the inner and outer bacterial membranes, including the peptidoglycan layer
*needle-like structure extends from outer membrane ring and projects from the bacterial surface (effector proteins transported through the hollow “center” of the needle)

26
Q

type IV secretion systems (T4SSs) - subfamilies

A

2 subfamilies:
1) conjugation systems (mediate interbacterial DNA transfer)
2) effector translocators (used by gram - for delivery of virulence proteins)

27
Q

what pathogen has a T4SS

A

H. pylori

28
Q

invasins

A

enzymes that promote invasion, including:
-hyaluronidase
-streptokinase
-collagenase

29
Q

what is invasion by an organism affected by

A

*colonization
*production of invasins
*ability to evade host defenses
*blocking of phagocytosis

30
Q

examples of enzymes that help an organism evade host defenses

A

-leukocidins
-hemolysins
-coagulase

31
Q

leukocidins

A

*kill WBCs; releases and ruptures lysosomes
*can create more tissue damage

32
Q

hemolysins

A

*cause lysis of RBCs
*alpha or beta hemolysis

33
Q

coagulase

A

stimulates clotting to protect bacteria from phagocytosis

34
Q

collagenase

A

*breaks down collagen (connective tissue)
*RAPID SPREAD through tissue

35
Q

hyaluronidase

A

*breaks down hyaluronic acid (connective tissue)
*“spreading factor”

36
Q

how can organisms survive host defenses

A

*antiphagocytic factors (kill phagocytes or facilitate avoidance of phagocytes)
*kill the leukocyte (using leukocidins)
*intracellular survival (readily engulfed but capable of surviving internally)

37
Q

capsule - anti-phagocytic virulence factor

A

*polysaccharide layer outside the cell envelope
*found in both Gram + and -
*resists phagocytosis

38
Q

protein A

A

*protein on cell wall of Staph aureus
*impairs phagocytosis by binding the Fc portion of antibodies**
*staph with protein A is more likely to be a colonizer of the nose

39
Q

M protein

A

*produced by some species of strep
*messes up complement by binding to factor H, destroying C3-convertase and preventing opsonization, therefore STRONGLY ANTI-PHAGOCYTIC
*our cells can generate antibodies against M protein

40
Q

siderophores

A

iron chelators that are excreted into the environment, bind iron, and then re-enter the cell
*iron is very important for bacteria

41
Q

bacteriocins

A

toxins produced by bacteria to inhibit growth of related strains

42
Q

toxins

A

bacterial products that directly harm tissue or trigger destructive biological activities

43
Q

exotoxins

A

*generated by gram pos or neg
**ACTIVELY SECRETED
*each toxin has a specific action
*generally does NOT produce fever
*heat labile (inactivated at high temps)

44
Q

types of exotoxins

A

-cytotoxins: kill cells
-neurotoxins: interfere with normal nerve impulses
-enterotoxins: cause changes in function of GI cells (usually resulting in diarrhea)

45
Q

endotoxins

A

*part of the outer cell wall of gram NEG bacteria ONLY (lipid A in LPS)
*no specific action: host response to endotoxin can result in severe inflammation
*heat STABLE
*PYROGENIC and can cause shock

46
Q

antitoxins

A

antibodies against exotoxins

47
Q

toxoids

A

inactivated exotoxins (from heat, etc)
-don’t cause disease
-DO stimulate antitoxin production
*we can inject toxoids as vaccines to stimulate antitoxin production and provide immunity

48
Q

superantigens

A

exotoxins that cause non-specific activation of T cells, resulting in polyclonal T cell activation and massive cytokine release
*excessive uncoordinated cytokine release causes rash, fever, and can lead to multi-organ failure

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