Bacterial Pathogenesis Flashcards

1
Q

asymptomatic, inapparent, subclinical infection

A

-host defenses clear pathogen before any symptoms of disease are notes

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2
Q

communicable infection

A

can be passed from host to host

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3
Q

contagious infection

A

highly communicable

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4
Q

noncommunicable infection

A
  • comes from environment, not a previous host

- botulism, legionnaires

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5
Q

latent infection

A

-disease subsides, but microorganisms remain in body and can restart disease later

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6
Q

chronic carrier state

A

-host survives disease but continues to shed the pathogen indefinitely

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7
Q

parasitism

A
  • pathogens are parasites in the sense that they harm the host by taking its resources to reproduce themselves
  • all viruses and a few bacteria are obligate intracellular parasites, must enter host cells to reproduce
  • more bacteria are facultative intracellular parasites, meaning that they can reproduce outside the host cells when they need to
  • be careful of confusion of parasites-protazoa and helminths
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8
Q

nonpathogens

A
  • very unlikely to cause disease
  • most environmental bacterial and normal flora
  • very low virulence
  • LD50 very high (lethal dose to kill 50% of pop)
  • ID50 high (infectious dose to 50% pop)
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9
Q

opportunistic pathogen

A
  • unlikely to cause disease in a healthy adult
  • will take advantage of injury of immunosuppression
  • legionella, pseudomonas, enterobacter
  • low virulence
  • LD50 high
  • ID50 med/low
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10
Q

pathogen

A
  • regularly causes disease in previously healthy hosts
  • n. gonorrheae, shigella, norwalk virus
  • Mid-high virulence
  • LD50 med/low
  • ID50 med/low
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11
Q

virulence

A
  • numerical measure of pathogenicity
  • lower ID50 means fewer infecting organisms are needed to cause symptoms of disease
  • lower LD50 means fewer infecting organisms needed to kill the host
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12
Q

virulence factors

A
  • genes found empirically to be determinants of pathogenicity
  • can be encoded in pathogenicity islands
  • can be plasmids or come from phages
  • E coli has an acquisition of virulence that makes it disease causing-uropathogenic gains the ability to attach to respiratory tract
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13
Q

survive extreme environments

A

-pH tolerance, siderophores, resistance to drying, resistance to detergents

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14
Q

siderophores

A
  • bind iron
  • need it to grow
  • need to steal it from us
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15
Q

Adhesion

A
  • pili/fimbrae/curli
  • slime layer
  • adhesins
  • biofilm formation
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16
Q

Immune evasion

A
  • capsule
  • IgA proteases
  • macrophage apoptosis inducers
  • antigenic variation (switching out)
  • serum resistance (stops complement)
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17
Q

host cell takeover

A
  • endosome escape routes
  • actin polymerization pathways (use cells actin to make pseudopods to get to neighboring cells)
  • type 3 and 4 secretion systems (3-peptides, 4-DNA)
18
Q

poison the host

A
  • tissue degrading enzymes (stop oxygen or immune from getting to bacteria-coagulase)
  • endotoxins
  • exotoxins
19
Q

endotoxins

A
  • cell wall/membrane components trigger septic shock
  • gram neg- LPS/LOS
  • gram pos-teichoic acids
  • exposure can lead to overproduction of TNF and IL1, DIC, SIRS, death
  • symptoms are immunogenic, antibody is not protective and vaccination is not useful
20
Q

exotoxins

A
  • polypeptides
  • secreted from cell or injected by T3SS
  • most toxic substances known
21
Q

exotoxin themes

A
  • often encoded in plasmids or bacteriophages rather than bacterial genome
  • common toxic strategies include superantigenicity, interference with signal transduction, depolymerization of actin
  • several exotoxins have a similar A-B subunit structure-B delivers A to A’s toxicity site- A can be ADP rybosylase
  • almost always heat liable, inactivated toxoids are often useful vaccines
22
Q

superantigens

A
  • undermine specificity of immune response (activates up to 25% of T cell repertoire instead of normal .001-.001 %)
  • can cause shock and multiple organ failure
  • most common are s aureus, strep pyrogens–>TSS
23
Q

Cholera, E coli, B cereus in gut

A
  • increase adenylate cyclase activity
  • leads to fluid and electrolyte loss (osmotic gradient)
  • watery diarrhea to spread bacteria
  • heat stable e coli enterotoxin (which is an exotoxin) causes same effect by stim guanylate cyclase
24
Q

diphtheria

A
  • tox gene encoded by lysogenic bacteriophage
  • A subunit ADP ribosylates TF EF-2- things allowed to cross nuclear membrane and affect gene expression
  • makes a pseudomembrane in resp tract
  • kills by suffocation
25
Q

C difficile A and B

A
  • glucosylate Rho GTPase

- leads to depolymerization of actin, apoptosis, and a major inflammatory response in the gut (pseudomembranous colitis)

26
Q

MRSA PV leukocidin

A
  • forms pore in cel membranes and leads to lysis- like our complement system
  • PVL genes are phage born
27
Q

Infection

A

-pathogen defeats innate immunity for successful colonization

28
Q

incubation period

A

-microbial numbers too low to produce symptoms, most rapid growth

29
Q

prodrome

A

-non-specific immunogenic symptoms as adaptive immunity is raised:fever/ fatigue

30
Q

specific illness period

A

-pathogen mediated symptoms emerge as large numbers of pathogens express virulence factors

31
Q

recovery/convalescence

A

-immune system gains upper hand and dramatically reduces pathogen numbers;patient begins to regain strength

32
Q

ways to be virulent

A
  • surviving extreme conditions
  • adhesion
  • immune evasion
  • host cell takeover (T3,4SS, actin)
  • poisoning host-toxins
  • other
33
Q

transmission of pathogens

A
  • respiratory droplets
  • fecal-oral
  • direct contact
  • sexual contact
  • blood blood
  • vertical-transplacental, vaginal delivery, breast milk
  • animal reservoir-zoonosis
  • fomite (washcloth, countertop)
  • vector (tick/mosquito)
34
Q

coagulase

A
  • breaks down fibrinogen to form a fibrin clot around S aureus
  • invasion of host tissue
35
Q

collagenase/hyaluronidase

A
  • break down tissue to s pyrogenes can penetrate

- invasion of host tissue

36
Q

pyrogenic IF response

A

-pus forming, predominantly neutrophils

37
Q

granulomatous IF response

A

-macrophages kill most of the bacteria, but some survive inside macrophages within a granuloma

38
Q

facultative intracellular

A
  • mycobacteria, legionella, brucella, listeria
  • legionella also inhibits fusion of lysosome with phagosome and inhibits acidification if fusion does occur along with chlamydia
39
Q

obligate intracellular

A

-chlamydia and rickettsia

40
Q

invasins

A

-virulence factors recognized by cell-surface integrins, docking leads to cell entry

41
Q

Q fever

A

-allows lysosome fusion and survives acidification