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block 4 > Digestive tract infections III > Flashcards

Digestive tract infections III Flashcards

1
Q

Clostridium spp. of intrest in gi tract

A
  • Clostridium perfringens
  • clostridium piliforme
  • CLOSTRIDIODES difficile is NOT a clostridium any longer it is reclassified BUT shares the characteristics of a clostridium spp.
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2
Q

clostridium spp. and clostridiodes difficile characteristics

A
  • gram pos
  • spore forming
  • anaerobic
  • bacilli
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3
Q

clostridium spp. and clostridiodes difficile found where

A
  • natural inhabitant digestive tract

- found in soil

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4
Q

clostridium spp. and clostridiodes difficile transmission (gi)

A

ingestion

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5
Q

clostridium spp. and clostridioudes difficile (GI) -> dx how

A
  • produce toxins that cause dx while they are inside host in GI the dx they cause really isn’t GI based but they are in GI making the toxin
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6
Q

clostridium difficile infection how

A
  • triggering event -> disturbance normal microbiome

- piglets can get infection when newborn before establish own microbiota to prevent infection or dx

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7
Q

clostridium piliforme infection how

A

usually stress to animal triggers infection

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8
Q

clostridium per fringes infection how

A
  • newly ingested spores germinate and -> dx
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9
Q

clostridiodes difficile effects who

A
  • horse
  • pig
  • dog
  • RARELY cats
  • maybe zoonotic?
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10
Q

clostridiodes difficile horse and pig (piglets0

A
  • hemorrhagic necrotizing enterocolitis ie bldy d+
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11
Q

clostridiodes difficile dogs and cats

A
  • chronic d+ may or may not contain blood

- RARELY EFFECTS CATS

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12
Q

clostridium perfringens types

A
  • a-e

- based on toxins they make

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13
Q

clostridium perfringens -> what in who

A
  • endotoxemia, usually acute and highly fatal
  • cattle, sheep, goat, pig, horse, dog
  • ZOONOTIC (some types not all)
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14
Q

clostridium perfringens dx spreads how

A
  • toxins made in intestine enter blood stream -> spread -> death (usually)
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15
Q

clostridium perfringenes diagnosis how

A

necropsy

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16
Q

clostridium perfringens necropsy what seen

A

congestive hemorrhagic ulceration on intestinal mucosa

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17
Q

clostridium perfringenes most comon in what types animals

A
  • v young

- overfed

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18
Q

clostridium perfringenes very young animals

A
  • young: digestive enzymes not made yet or are inhibited by colostrum bacteria making toxins and toxins not degraded -> toxins have effect
  • older animal: have trypsin and other enzymes so bacteria can mult and make toxins but toxins get degraded in intestinal tract
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19
Q

clostridium perfringenes overfed animals

A
  • food left undigested in li microbes can grow on also intestinal motility slowed so more time for toxins to get absorbed and cause dx
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20
Q

clostridium piliforme affects who

A
  • lab rodents
  • lagomorphs
  • occasionally foals, cats, dogs
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21
Q

clostridium piliforme general characteristics

A
  • gram variable (they are gram pos but sometimes appear gram neg on staining)
  • spore forming
  • obligate intracell (most clostridium = extra cell this is different)
  • anaerobic
  • bacillus
22
Q

clostridium piliforme -> what

A
  • tyzzer’s dx
23
Q

tyzzer’s dx = what / induced by what

A
  • hepatic necrosis -> rapid death

- induced by stress

24
Q

Clostridiodes difficile pathogenicity

A

spores endogenous in intestines germinate after triggering event ->

  • produce enterotoxins
  • cytotoxic to colonic epithelial cells and macrophages
  • cytotoxicity to colonic epithelial cells ->killing epithelial cells -> mucohemorragic d+
25
Q

clostridium perfringes pathogenesis

A
  • spores germinate in intestines and multiply to produce one toxin that damages intestine allowing other toxins they make to spread to bld stream then spread systemically and kill animal
  • diff strains produce diff toxin combinations
26
Q

diagnosis clostridium spp. gi and clostridiodes difficile

A
  • id toxins (elisa or toxin gene pcr)
  • C. perfringens- gross finding on necropsy
  • C. piliforme- pcr
27
Q

clostridioides difficile tx

A
  • abs (once spores germinate can treat with abs)
28
Q

clostridium spp. tx

A
  • rapid onset so can’t really treat

- antitoxin if progress slowly

29
Q

clostridiodes difficile and clostridium piliforme prevention

A

avoid stress

30
Q

clostridium perfringens prevention

A
  • redue w/ high fiber low protein diet

- a and b toxoid vac for preg animals

31
Q

escherichia coli general charcteristics

A
  • gram neg
  • bacillus
  • facultative anaerobe
32
Q

eschreichai coli found where

A
  • natural inhabitant of intestines

- widely distributed in environment

33
Q

escherichia coli transmission

A

fecal-oral

34
Q

types E. coli gi

A
  • enterotoxigenic -> secretory gi

- shiga toxin-producing E. coli (STEC) which includes subset (enterohemorrhagic E.coli EHEC)

35
Q

STEC causes what in who

A
  • edema dx in pigs
  • mostly outbreaks in recently weaned pigs
  • some of these are important foodborn pathogens
36
Q

edema dx signs

A
  • case fatality risk 90%

- found dead or clinical signs = neuro, sq edema, rarely d+

37
Q

EHEC causes what in who

A
  • carried by cows where -> nothing BUT is ZOONOTIC
  • in humans ->
  • watery d+
  • more severe bldy d+
  • most severe hemolytic uremic syndrome
38
Q

pathogenesis shiga-toxin producing e. coli STEC

A
  • ingested bacteria adhere to intestinal mucosa via pilli in SI -> adherent bacteria produce shiga toxin -> inhibit protein synth -> toxin kills epithelial cells and endothelial cells -> spreads to blood stream -> bind GB4 receptor on endothelial cells of small artier and articles -> damage endothelium -> edema -> death
39
Q

GB4 receptor

A
  • receptor for porcine STEC toxin
40
Q

pathogenesis shiga-toxin producing e.coli EHEC

A
  • ingested bacteria adhere to intestinal mucosa via attaching/ effacing factors in colon ->adherent bacteria produce shiga toxin -> inhibit protein synth -> toxin kills epithelial cells and endothelial cells -> hemorrhagic d+ in humans
41
Q

pilli STEC binds

A
  • in si
  • same pilli enterotoxigenic E. coli bind
  • found in post weaning pigs = time these receptors available
42
Q

EHEC binding

A

their attachment via attaching/ effacing factors -> attaching/ effacing lesions in colon when adhere to colon adherence results in effacement of microvilli

43
Q

diagnosis shigatoxin producing E. coli

A
  • elisa for toxin (intestinal samples)
  • pcr toxin gene (intestinal samples)
  • clinical signs
44
Q

shigatoxin producing E. coli tx

A
  • antibiotics but once see neurosigns = too late for piglets treat other animals in herd to prevent issue
45
Q

prevention shigatoxin producing e. coli

A
  • stx2e vac not in us yet
46
Q

yersinia spp. general characteristics

A
  • fam= enterobacteriacea
  • rod shapped
  • fan an
  • gram neg
47
Q

yersinia spp. found where

A
  • intesitnes and environment
48
Q

yersinia spp. of interst

A
  • yersinia enterocoliti

- yersenia pseudotuberculosis ZOONOTIC

49
Q

yersinia spp. -> what in who

A
  • rarely dx in animals usually food born pathogen of ppl
  • ->
  • enteritis
  • mesenteric lymphadenitis
50
Q

diagnosis yersinia spp.

A
  • grow at low temp so cold enrichment
51
Q

how do ppl get yersinia spp. ingested

A
  • contaminated pork

block 4 (23 decks)

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