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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
clostridium perfringes pathogenesis
- 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
diagnosis clostridium spp. gi and clostridiodes difficile
- id toxins (elisa or toxin gene pcr) - C. perfringens- gross finding on necropsy - C. piliforme- pcr
27
clostridioides difficile tx
- abs (once spores germinate can treat with abs)
28
clostridium spp. tx
- rapid onset so can't really treat | - antitoxin if progress slowly
29
clostridiodes difficile and clostridium piliforme prevention
avoid stress
30
clostridium perfringens prevention
- redue w/ high fiber low protein diet | - a and b toxoid vac for preg animals
31
escherichia coli general charcteristics
- gram neg - bacillus - facultative anaerobe
32
eschreichai coli found where
- natural inhabitant of intestines | - widely distributed in environment
33
escherichia coli transmission
fecal-oral
34
types E. coli gi
- enterotoxigenic -> secretory gi | - shiga toxin-producing E. coli (STEC) which includes subset (enterohemorrhagic E.coli EHEC)
35
STEC causes what in who
- edema dx in pigs - mostly outbreaks in recently weaned pigs - some of these are important foodborn pathogens
36
edema dx signs
- case fatality risk 90% | - found dead or clinical signs = neuro, sq edema, rarely d+
37
EHEC causes what in who
- carried by cows where -> nothing BUT is ZOONOTIC - in humans -> - watery d+ - more severe bldy d+ - most severe hemolytic uremic syndrome
38
pathogenesis shiga-toxin producing e. coli STEC
- 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
GB4 receptor
- receptor for porcine STEC toxin
40
pathogenesis shiga-toxin producing e.coli EHEC
- 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
pilli STEC binds
- in si - same pilli enterotoxigenic E. coli bind - found in post weaning pigs = time these receptors available
42
EHEC binding
their attachment via attaching/ effacing factors -> attaching/ effacing lesions in colon when adhere to colon adherence results in effacement of microvilli
43
diagnosis shigatoxin producing E. coli
- elisa for toxin (intestinal samples) - pcr toxin gene (intestinal samples) - clinical signs
44
shigatoxin producing E. coli tx
- antibiotics but once see neurosigns = too late for piglets treat other animals in herd to prevent issue
45
prevention shigatoxin producing e. coli
- stx2e vac not in us yet
46
yersinia spp. general characteristics
- fam= enterobacteriacea - rod shapped - fan an - gram neg
47
yersinia spp. found where
- intesitnes and environment
48
yersinia spp. of interst
- yersinia enterocoliti | - yersenia pseudotuberculosis ZOONOTIC
49
yersinia spp. -> what in who
- rarely dx in animals usually food born pathogen of ppl - -> - enteritis - mesenteric lymphadenitis
50
diagnosis yersinia spp.
- grow at low temp so cold enrichment
51
how do ppl get yersinia spp. ingested
- contaminated pork

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