Exam 3 Lecture 25 Flashcards

1
Q

Falkow’s Molecular Koch’s Postulates

A
  1. phenotype must be associated with pathogenic strain
  2. specific inactivation should lead to loss in virulence
  3. replacement of the mutated gene should restore pathogenicity

(this is kind of like find it lose it rescue)

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2
Q

Mechanisms of bacterial pathogenesis:

A
  1. production of toxins
  2. attaching and colonizing a host surface
  3. invasion of host tissues
  4. avoiding host defenses
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3
Q

exotoxin

A

protein toxins

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4
Q

What does a pore-forming toxin do?

A

Oligomerizes in the host cell membrane and forms a pore that allows cytoplasmic contents to leak out

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5
Q

pore forming toxin mechanism?

A

First present as inactive monomers in solution. When they bind to protein or lipid receptor, they recruit other monomers and this forms a pore. Or a preformed oligomer can just insert into the membrane.

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6
Q

What is Pore Forming Toxin structure in the membrane?

A

Forms beta barrel, 7 monomers

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7
Q

What is AB exotoxin?

A

A is the toxin, B is the binding portion that will bind to receptor

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8
Q

What kind of activity does A have of AB toxin?

A

ADP ribosyltransferase activity. Depending on the target protein, this transfer can either inactivate or constitutively express

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9
Q

Cholera toxin mechanism

A

AB toxin binds to receptor, A enters cell and locks G protein in on position, turning on adenylate cyclase, increases cAMP concrentation, causes ion channels to open and release ions out of cell, water follows due to osmosis

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10
Q

How can bacteria adhere to cell surfaces?

A

Express adhesins, such as pili, cell surface proteins, capsules

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11
Q

True or false: bacteria can adhere to any type of cell to cause infection

A

False. The adherence is cell type specific and hijack certain hsot receptors. This causes localized infections

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12
Q

impediments to colonization

A

compete with host microbiome; obtain nutrients; mucosal immunity

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13
Q

____ is the most limiting nutrient during infection

A

Iron

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14
Q

What proteins do the host make to prevent iron toxicity?

A

lactoferrin, transferrin, hemoglobin

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15
Q

Siderophores

A

Small molecules that bind to iron very tightly that can then be used by bacteria

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16
Q

Main antibody present at mucosal surface

A

Secretory IgA (secreted by plasma cells)

17
Q

How can bacteria protect against secretory IgA?

A

capsule, secrete protease to cleave IgA, antigenic variation (changes type of surface protein expressed)

18
Q

examples of invading host tissue

A

through damaged skin, maybe even hair follicle, through mucous membrane (entry through damaged epithelium, or forced invasion)

19
Q

Salmonella invasion mechanism

A

TYPE 3 Secretion System!!!

Uses injectosome to “inject” effector molecules

20
Q

What do effector molecules?

A

cause dramatic rearrangement of host cytoskeleton. this can cause engulfing of the bacteria to force its way in

21
Q

M cell

A

samples environment in intestinal lumen, passes on these to macrophages on basolateral side of M cell

22
Q

How does shigella avoid M cell/macrophage?

A

It can survive inside a macrophage, then goes back into intestinal cells to protect itself (hides)

23
Q

Examples of phagocytes

A

Neutrophils, macrophages, dendritic cells

24
Q

How can bacteria avoid being killed by phagocytes?

A

prevent phagocytosis; survive inside phagocytes

25
Q

Opsonization

A

Bacteria is covered with antibodies to attract a phagocyte

26
Q

How can S. aureus prevent phagocytosis?

A

Has an Fc receptor that binds antibodies that face the wrong way. Fab regions will not be recognizable to macrophage (as it is not foreign), thus will not be engulfed

27
Q

Host cell mimicry

A

Bacteria can have hyaluronic acid capsule to appear non-foreign to host

28
Q

How does Listeria monocytogenes survive insside phagocyte?

A

engulfed into phagosome but secretes pore forming toxin (14 monomers) called LLO, allows bacterium to escape phagosome within 5 min before lysozyme fuses