Final: New material Flashcards

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1
Q

exotoxins

A
  • produces and secreted by bacterium
  • specific role in pathogenesis
  • may act distant from bacterium
  • our bodies produce antitoxin
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2
Q

endotoxin

A
  • a part of the bacterial cell
  • LPS
  • acts systematically on host
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3
Q

hemolysins

A

red blood cells

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4
Q

leukocidins

A

white blood cells

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5
Q

what creates a channel in the membrane

A

hemolysins and leukocidins

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6
Q

what makes a lot of channels in the membrane

A

S. aureus and S. pyogenes

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7
Q

A-B subunit toxins

A
  • toxins with two subunits
  • toxin produced with subunits together
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8
Q

B subunit

A

binds cell surface

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9
Q

A subunit

A

active component

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10
Q

diphtheria toxin

A
  • classic A-B subunit toxin
  • transcribed, translated as a single gene unit
  • post translational cleavage, reduction to active form performed by host cell
  • B subunit binds to cell surface, endocytosed
  • in acidic compartment, conformational change creates membrane pore, A subunit enters cytoplasm
  • ADP ribosylation of EF-2
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11
Q

Super antigens

A
  • toxins that bind to TCR and MHC activate immune system
  • semi specific activation 3-30%
  • results in massive overstimulation
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12
Q

medically important exotoxins

A
  • botulinum
  • tetanus
  • cholera toxin
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13
Q

endotoxins

A
  • LPS-lipopolysaccharide
  • Lipid A portion is endotoxin
  • released during cell death
  • treatment w/ antibiotics may make this worse
  • septic shock
  • disseminated vascular clotting
  • detect with limulus amoebocyte lysate assay
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14
Q

endotoxin induces…

A

fever and shock
- LPS released when bacteria are lysed in macrophage
- stimulated IL-1, tumor necrosis factor, other cytokines

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15
Q

genetics of pathogenicity

A
  • mobile genetic elements contain toxin genes
  • bacteriophage-lysogenic conversion
  • plasmids
  • transposons
  • pathogenicity islands
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16
Q

plasmids and pathogens

A

toxin genes spread very rapidly
- virulence plasmids can be passed through the population
- tetanus toxin, staph. enterotoxins

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17
Q

lysogenic conversion

A
  • bacteriophage can lyse their host or integrate into chromosome
  • lysogens may carry virulence factor genes
  • cholera toxin
  • SEA
  • diphtheria toxin
  • botulinum toxin
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18
Q

pathogenicity islands

A

genomic elements containing virulence genes
- often id by different G+C content from rest of genome
- present in pathogenic strains, absent from avirulent
- potential horizontal transfer unclear

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19
Q

antimicrobial chemotherapy

A
  • based on exploiting differences between our physiology and invading organisms
  • antibiotic targets are enzymes or structures essential to pathogens success, but different from our essential parts
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20
Q

which microbe is hardest to treat?

A

viruses
- may essential parts to them are essential to us. makes it hard to make vaccine

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21
Q

which microbe is easiest to treat?

A

fungi? bacteria?

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22
Q

sources of antibiotics

A

natural compounds from bacteria (G+ rods), actinomycetes, fungi

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23
Q

example of a microbe that is very difficult to treat and needs specialized drugs

A

mycobacteria

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24
Q

bacteriostatic

A

inhibits growth

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25
Q

bacteriocidal

A

lyses cells

26
Q

antibiotic resistance

A
  • bacteria can develop resistance through several mechanisms
  • destruction of the antibiotic (B-lactamase)
  • mutations in the target site (alterations to ribosome)
  • efflux pumps (pump antibiotics out of cells
27
Q

beta-lactamases

A
  • broad or narrow spectrum
  • cleaves beta-lactamase ring
  • very widespread in medically relevant bacteria
28
Q

target alteration

A
  • mutations in the target site that dont affect function
  • affect binding of antibiotic
  • if antibiotic action closely associated with target activity, more difficult
29
Q

multi-drug efflux pump

A
  • MDR bacteria a rapidly growing concern
  • MDR-TB, MDR-pseudomonas
  • one major mechanism is efflux pump
  • can act on broad class of drugs
30
Q

antibiotic resistance

A
  • mutations may arise directly from selection pressure
  • antibiotics come from natural sources
  • organisms that make them are resistant to them
  • organisms may compete by developing resistance
  • genes for resistance spread by horizontal transfer
31
Q

misuse of antibiotics

A
  • Overprescription (colds, flus)
  • use of weakened, outdated drugs
  • failure to finish course
  • unsupervised use
  • long term use for sub-clinical infections
32
Q

ramifications

A
  • MRSA, VRE drug resistant nosocomial infections
  • prophylaxis before surgery now requires harsher, higher doses of antibiotics
  • gram-negative pathogens are almost always totally resistant B-lactams
  • newer antibiotics are necessarily more costly, often have more side effects
33
Q

filamentous fungi

A

growing as multinucleate, branching hyphae, forming a mycelium

34
Q

yeasts fungi

A

growing as ovoid or spherical single cells multiply by budding and division

35
Q

superficial mycoses fungi

A
  • epidermophyton
  • microsporum
  • trichophyton
35
Q

deep mycoses fungi

A
  • aspergillus
  • candida
  • blastomyces
36
Q

local fugal infections

A
  • thrush
  • tinea
37
Q

systemic fungal infections

A
  • cryptococcal meningitis
  • aspergillosis
38
Q

treatment options

A
  • far fewer drugs
  • ergosterol
    (amphotericin B - binds ergosterol)
  • azoles (interfere with synth)
39
Q

protozoa

A
  • single celled
  • intracellular and extracellular
  • systemic infections
  • immune evasion
40
Q

insect borne protozoa

A
  • leishmania - sand fly
  • trypanosoma - chagas disease - reduviid bug
  • African sleeping sickness - tsetse fly
  • plasmodium - anopheles mosquito
41
Q

ingestion of cysts

A
  • systemic disease (toxoplasma)
  • GI disease (amoebas, giardia, cryptosporidia)
41
Q

treatment of cysts

A
  • not many drugs options
  • metronidazole
  • immune evasion
  • quinines and related for malaria
  • resistance
42
Q

helminths

A
  • flatworms (tapeworms)
  • flukes (schistosomes)
  • roundworms (filarial worms)
43
Q

routes of infection

A
  • intermediate host (accidental ingestion)
  • active skin penetration
  • insect
  • fecal-oral route
44
Q

schistosomiasis

A
  • affects 300-600 million people worldwide - blood fluke
  • snail intermediate host
  • other fluke infections (liver and lung)
  • few available drugs
45
Q

tapeworms

A
  • adult form (intestinal tract)
  • larval forms (intermediate host, disseminated tissue, cysts in brain, organs, varies by species)
46
Q

roundworms-nematodes

A
  • very diverse
  • protective cuticle
  • plant parasitic
  • free living bacteriovorus
  • pathogenic (person to person, arthropod vectors, zoonotic)
47
Q

arthropods vectors of disease

A
  • widespread
  • many associations
  • transmit many diseases
  • plants, animals, humans
  • control insects-control disease
48
Q

herpesviridae

A
  • often neurotropic
  • causes various diseases (fever/genital herpes, chicken pox/shingles, infectious mono)
49
Q

chicken pox/shingles

A

varicella zoster
- childhood CP
- adulthood shingles
- vaccines for both

50
Q

papilloma virus

A
  • HPV causes common warts, genital warts, cervical cancer
  • very common
  • HPV 6 and 11 cause genital warts
51
Q

HIV

A
  • human immunodeficiency virus
  • a retrovirus
  • RNA genome
  • incorporates into host cell as cDNA
  • infects CD4+ T-cells
52
Q

Infection of Host Cells by
HIV

A

HIV surface glycoproteins bind CD4, CXCR4 molecules on T-cell

53
Q

HIV latency andactivation

A

Provirus integrates into host cell genome, may be activated to produce virus particles

54
Q

influenza

A

 Influenza kills ~50k per year in
the US
 Orthomyxovirus
 Segmented genome
 Surface antigens(spikes) hemagglutinin and neuraminidase
 Large shifts in antigenic structure give rise to pandemics

55
Q

antigenic drift and shift

A
  • Drift-point mutations in
    H,N antigens
     Flu virus reassortment
    leads to shift —Pandemic
    strain
56
Q

poxviridae

A

 smallpox, cow pox viruses
 Smallpox ~30% fatality rate
 NOT chicken pox
(a herpes virus)
 Double stranded DNA
 Enveloped

57
Q

smallpox (edward jenner)

A

 Smallpox was a universal
disease
 80% of Europeans
contracted it
 30% mortality
 Vaccine invented by
Jenner 1769
 Based on cowpox (Vacca-
cow)
 Last natural case in 1977

58
Q

The black death

A

bubonic - fleas on rates
septicemic - in the bloodstream, results in septic shock

59
Q

yersinia pestis

A

forms biofilm to block fleas digestive tract
- starving flea will now bite people
- c. elegans

60
Q

SIR model of disease

A

Vaccine allows you to go
from Susceptible to
Recovered without passing
through Infected!
When S gets below 1/Ro,
that is when the epidemic