Ch 15 Mechanisms of Pathogenicity Flashcards

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1
Q

what is a microbes ID50?

A

number of microbes needed when presented to a population to infect 50% w the disease. (ID= infectious dose)

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2
Q

is a higher or lower ID50 better?

A

higher- more microbes needed to cause disease

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3
Q

what is a microbes LD50?

A

concentration of toxin needed to cause 50% of test population to die (LD= lethal dose)

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4
Q

3 portals of microbial entry and examples

A
  1. MM- resp. tract, GI tract, conjun., genitourinary tract
  2. skin- openings like sweat glands and hair follicles (acne)
  3. parenteral- damage due to cuts, insect bites, drying out of skin (cracking)
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5
Q

what is adherence of a microbe

A

latching on to particular receptors on cell surface of host via ligands/adhesins

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6
Q

examples of enzymes used by pathogens to escape host defenses

A

coagulase- clots blood creating a barrier from IS

kinase- blocks formation of clots, once a certain number of pathogens is reached, kinase used to launch attack

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7
Q

theraputic application of kinase

A

streptokinase used to break up blood clots that cause heart attacks

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8
Q

how antigenic variation is used to escape host defenses

A

ability of microbes to change its surface antigens, ecading antibodies

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9
Q

what are siderophores, how damage host cells?

A

protein secreted by some pathogens, have high affinity for iron, take iron (ex: from hemoglobin RBCs), pathogen will take-up iron for growth and reproduction

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10
Q

exo v endo toxins- gram neg or pos?

A

exo- pos

endo- neg

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11
Q

difference between endo and exo toxins (where they are)

A

endo- w/in outer membrane

exo- secreted by growing cell

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12
Q

what component of gram neg cell acts as endo toxin

A

lipid A

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13
Q

which usually has a lower LD, exo or endo toxins

A

exo (less needed to be deadly)

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14
Q

which causes fever, endo or exo toxins

A

endo toxins- lipid A released in macrophage-> produces cytokines->bloodstream-> hypothalamus-> make porstaglandin-> changes thermostat

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15
Q

why, if someone has a gram ned infection, we are not TOO aggressive w treatment

A

killing all at once releases endotoxins all at once-> bad fever

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16
Q

how A-B toxins work

A
  1. B component attaches to host cell receptor
  2. host cell invaginates A-B (receptor-mediated endocytosis)
  3. A part separates, disrutes cellular metabolism and prevents protein synthesis
17
Q

why the A part of A-B toxin acts as an enzyme (what does that mean?)

A

repeated and continuous disruptive effect

18
Q

how a virus can cause cancer?

A

insert into host genome leading to mutations and cancer.

can also decrease contact inhibition- stop knowing that, when they bump into each other, stop growing-> tumors

19
Q

Bacterial enzyme associated w blackening of infected wounds, how does this aid in pathogenicity?

A

Hyalauronidase, helps microorganisms spread from initial site of infection (hydrolyzes hylaronic Acid)

20
Q

How exotoxins are produced

A

Part of cells growth and metabolism

21
Q

How exotoxins harm host

A

Inhibiting certain metabolic functions or destroying parts of host cell

22
Q

A-B is a kinda of endo or exotoxins?

A

Exo