chap 15 Flashcards

1
Q

basic steps of causing disease

A
  • enter host
  • penetrate/invade host defenses - using capsule, enzyme, and fimbriae/pili
  • damage host - use toxins, intracellular pathogens
  • exit host
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2
Q

portals of entry

A

mucous membranes - respiratory tract; GI tract;
genitourinary tract

skin - hair follicles, sweat glands, conjunctiva

parenteral route - deposition of microbes directly
under skin or mucous membrane

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3
Q

what is the preferred method of entry for pathogens?

A

respiratory tract and GI tract

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4
Q

ID50

A

infectious dose needed to cause symptoms in 50% of experimental hosts

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5
Q

LD50(lethal dose 50%)

A

dose of pathogen needed to kill 50% experimental animal hosts(measure potency)

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6
Q

how specifically do pathogens enter the host

A
  • bind via adhesion/ligands on pathogen to cell membrane
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7
Q

biofilm formation

A
  • microbial community contain in exopolysaccharide matrix
  • adhere to surfaces
  • very resistant
  • dental plaque, catheters, ivs, heart valves
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8
Q

factors that allow for penetration of host defenses

A
  • capsule - impairs phagocytosis by host cells
  • cell wall comp: mycolic acids in some
    M protien- for attachment,
    antiphagocytic, inactive complement
  • extracellular enzymes
  • antigenic variation - alter pathogen surface proteins;
    possess alternate genes
  • opa protein - tight attachment for transcytosis
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9
Q

extracellular enzymes to penetrate host

A
  • coagulases: clot blood, isolate bacteria from host
  • kinases: destroy blood clots
  • collagenase: digests collagen in connective tissue,
    muscles, organs, tissues
  • protein A - make antibodies inactive
  • proteases - destroy host proteins; IgA protease
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10
Q

process of opa protien(transcytosis)

A
  • pilli anchor pathogen to epitheial cells
  • opa protein attach for tight adherence
  • pathogen travels through the cells to other cells and it keeps going
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11
Q

penetration into cytoskeleton

A
  • penetrate using actin filaments in cytoskeleton
  • invasions(salmonella) - pathogen surface proteins
    that rearrange actin filaments
    - make membrane ruffling(pathogen engulfed
    into cell
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11
Q

pathogen damage to host cells

A
  • use host’s nutrients: pathogen get host
    siderophores(Fe chelators)
  • cause direct dmg in vicinity of infection: intracellular
    pathogen(viral infection)
  • production of toxins: transported by blood, lymph
    - inhibit protein synthesis
    - disruption of membrane
  • induction of hypersensitivity reaction: overproduction
    of cytokines
  • release of toxins
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12
Q

exotoxins

A
  • types: a-b toxins, membrane disrupting, superantigens
  • secreted into environment
  • water soluble proteins(lot enzymes); most plasmid
    based or in phages
  • antitoxins: toxoid forms to provide immunity
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13
Q

toxigenicity

A

ability for pathogen to produce substances that damage the host

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14
Q

toxemia

A

disease caused by spread of bacteria and its toxins in blood steam

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15
Q

a-b toxins

A

diphtheria toxin: inhibits proteins synthesis; phage
carries tox gene

botulism toxin: neurotoxin; prevents nerve impulses to
muscles; causes flaccid paralysis

tetanus toxin: neurotoxin tetanospasmin; blocks
inhibitory nerve impulses to muscles; cause
spasmodic contractions

vibrio enterotoxin: cholera toxin; causes cellular
secretion of fluids and electrolytes –> severe
diarrhea and dehydration

16
Q

membrane - disrupting toxin

A
  • cause lysis host cells by disrupting the plasma
    membrane
    - leukocidins: kill phagocytic white
    - hemolysins: kill red blood cells
16
Q

superantigens

A
  • stimulate intense immune response of T cells
  • t cells stimulated to produce cytokines; regulate
    immune response

erythrogenic toxins: damage blood capillaries under
skin cause rash and scarlet fever

staphylococcal enterotoxin(s. aureus)

17
Q

endotoxin

A
  • lipid protein(A) of LPS of gram neg -> released when
    cells die and lyse
  • stimulates macrophages release too much cytokines
  • can activate blood clotting proteins and induce fever
  • endotoxic shock: drastic drop in blood pressure
18
Q

cytopathic effects

A
  • visible effects of viral infection
    cytocidal effect: results in cell death
    - cytocidal viruses stop host biosynthesis and make
    cell lysosomes release contents
  • syncytium formation
  • granules formation
  • virus infected cells form interferons(protects non-
    infected cells)
  • antigenic changes on cell surface caused by virus
19
Q

what is syncytium and how is it formed?

A

multinucleate infected cell

  • virus entry(membrane fusion)
  • viral replication(viral envelope on outside)
  • noninfected cell fuses w infected
  • syncytium forms are more cells get fused
20
Q

what do oncogenic viruses do

A

transform cells into cancerous cells

21
Q

portal of exit

A

secretion, excretion, discharges, tissue that is shed

  • related to part of the body that was infected
  • usually same portal entry and exit