9. Infection II Flashcards

(22 cards)

1
Q

What is the first step in the infection process?

A

Pathogen must encounter and attach to host

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2
Q

List the key steps in the infection process.

A
  • Facilitate entry and establish presence
  • Colonize host tissues
  • Develop mechanisms for multiplication and spread
  • Eventually shed to infect new hosts
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3
Q

True or False: Infections are always symptomatic.

A

False

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4
Q

What are some general pathogenic strategies?

A
  • Produce capsules to frustrate phagocytosis
  • Generate lipopolysaccharides (LPS) that can cause septic shock
  • Secrete toxins that aid invasion and cause host cell damage
  • Express adhesins (including lectins) to facilitate attachment
  • Produce enzymes (proteases, glycanases) to break down host matrix
  • Develop mechanisms to survive within phagosomes or cytosol
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5
Q

What are host defenses against pathogen attachment?

A
  • Rinsing microbes away from epithelial surfaces
  • Secretions (e.g., mucin in respiratory tract)
  • Ciliary activity to clear pathogens
  • Production of immunoglobulin A (IgA)
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6
Q

Name a pathogen countermeasure against host defenses.

A
  • Surface molecules that bind to specific host receptors
  • Production of toxins that inhibit ciliary activity
  • IgA proteases that break down host antibodies
  • Formation of microcolonies (as seen with enteropathogenic E. coli)
  • Fimbriae/pili that bind to mannose receptors (e.g., E. coli type 1 fimbriae)
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7
Q

What physical barrier does the host present against invasion?

A

Cell membrane

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8
Q

What are some pathogen mechanisms for invasion?

A
  • Fusion proteins (e.g., HIV envelope proteins)
  • Injection of proteins that trigger uptake
  • Blocking intracellular killing mechanisms
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9
Q

Give an example of a pathogen that uses fusion proteins for invasion.

A

HIV

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10
Q

How does Listeria monocytogenes facilitate cell-to-cell spread?

A

Uses ActA protein to polymerize actin, forming ‘rocket tails’

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11
Q

What is the role of siderophores in iron acquisition?

A

Pathogens secrete siderophores (iron-binding molecules) with higher affinity for iron than host transferrin/lactoferrin

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12
Q

How do pathogens resist oxidative burst from host phagocytes?

A
  • Diverting vesicles containing NADPH oxidase
  • Producing enzymes (catalase, superoxide dismutase) to detoxify reactive species
  • Breaking down hydrogen peroxide before hydroxyl radicals form
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13
Q

What strategies do pathogens use to evade complement and antimicrobial peptides?

A
  • Sialylation of bacterial surface (stealth mode)
  • Alterations to lipopolysaccharide structure
  • Production of proteases to degrade antimicrobial peptides
  • Expression of C3b receptors to interfere with complement cascade
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14
Q

How do pathogens evade antibodies?

A
  • Secretion of IgA proteases
  • Infecting lymphoid cells to hide within immune system
  • Binding antibodies in unusual orientation
  • Extended LPS chains to keep antibodies at a distance
  • Acquiring coating of host molecules (fibrin, actin)
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15
Q

What is one method pathogens use to shed and increase transmission?

A
  • Trigger sneezing/coughing via respiratory route
  • Cause diarrhea via fecal-oral route
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16
Q

Describe the composition of Vibrio cholerae cholera toxin.

A
  • Composed of A1, A2 catalytic units surrounded by five B units
  • B units bind to GM1 ganglioside receptors
17
Q

What is the LD50 of botulinum toxin type D?

A

0.8×10⁻⁸ mg

18
Q

What are the characteristics of Enterohemorrhagic E. coli (EHEC)?

A
  • Major foodborne pathogen
  • Causes diarrhea, hemorrhagic colitis, hemolytic uremic syndrome (HUS)
  • Typically O157 serotype
19
Q

What are the pathogenicity mechanisms of EHEC?

A
  • Shiga-like toxins (Stx1 and Stx2)
  • Locus of Enterocyte Effacement (LEE)
  • Multiple infection routes
20
Q

What is the function of Shiga-like toxins in EHEC?

A

Inhibit protein synthesis

21
Q

What does the Locus of Enterocyte Effacement (LEE) encode?

A

Type III secretion system (‘molecular syringe’)

22
Q

What is the outcome of the dynamic conflict between host defenses and pathogen virulence factors?

A

Depends on microbial virulence, infectious dose, and host immune status