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8. GI Pathogens 2 (Steph) Flashcards

1
Q

4 major characteristics of clostridia

A
  • gram positive
  • anaerobic
  • spore forming
  • produce exotoxins
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2
Q

C. perfringens 5 toxinotypes

A

A,B,C,D,E

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3
Q

C. perfringens 4 major toxins

A

alpha, beta, epsilon, iota

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4
Q

common disease of C. perfringens toxinotype A

A

myonecrosis, fowl necrotic enteritis, bovine and ovine enterocolitis, porcine necrotic entercolitis

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5
Q

common disease of C. perfringens toxinotype B

A

ovine hemorrhagic enterotoxemia, hemorrhagic enteritis

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6
Q

common disease of C. perfringens toxinotype C

A

neonatal hemorrhagic or necrotizing enterotoxemia (ovine, porcine, bovine, equine)

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7
Q

common disease of C. perfringens toxinotype D

A

ovine enterotoxemia

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8
Q

common disease of C. perfringens toxinotype E

A

bovine hemorrhagic enteritis

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9
Q

what does C. perfringens alpha toxin act on

A

Phospholipase: acts on membranes; cytolytic, hemolytic, dermonecrotic

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10
Q

what does C. perfringens beta toxin act on

A

pore forming activity, HEMORRHAGIC, cytolytic, dermonecrotic

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11
Q

what does C perfringens epsilon toxin act on

A

alerations of cell membrane permeability –> edema in various organs (liver, kidney, CNS)

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12
Q

what does C. perfringens iota toxin act on

A

Hemolysin: pore forming, cytotoxic, lethal leakage of water and ions by enterocytes and diarrhea

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13
Q

Describe the zoonotic component of C.perfringens type A

A

some strains of C.perfringens type A produce an enterotoxin (CPE) at the moment of sporulation causing disease in humans

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14
Q

describe how CPE causes food poisoning in humasn

A
  1. pore formation: cytotoxic due to plasma membrane permeability alterations
  2. interactions with epithelial tight junctions –> alter paracellular permeability
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15
Q

Type A C.Perfringens in poultry

A

Necrotic enteritis, necrosis in jejunal and ileal mucosa, sometimes mild NE results in decreased rates of gain, short clinical course culminating in dealth

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16
Q

what predisposes poultry to Type A C.perfringens

A

high fiber diet and concurrent coccidiosis

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17
Q

Type A C.perfringens in sucking and feeder pigs

A

necrotizing enterocolitis with mild villous atrophy. jejunal and ileal lesions are heavily colonized with C. perfringens

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18
Q

Type A C.perfringens in equine:

A

neonatal hemorrhagic diarrhea. clinical pres: watery-mucoid diarrhea to peracute death with hemorrhagic mucosal necrosis

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19
Q

Type A C.perfringens in beef calves

A

abomasal ulceration and tympany

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20
Q

Type A C.perfringens in dairy calves

A

necrotic enteritis in newborn calves

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21
Q

Type A C.perfringens in adult cattle

A

haemorrhagic bowl syndrome

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22
Q

what is “red gut”? what is it caused by

A

post mortem finding in enterotoxemic and sudden death dairy and feedlot cattle. large segments of small intestine arereddish purple and filled with blood. large numbers of C.perfringens can be isolated from jejunum

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23
Q

C. perfringens lesions

A

necro-haemorrhagic enteritis: severe dilated and congested small intestine

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24
Q

C. perfringens histological lesions

A

sloughing in large intestine, lots of immune cells and cell death

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25
what does type D C. perfringens cause and in which species
causes enterotoxemia, pulpy kidney, which affects calves, goats, horses and adult cattle, but mostly prevalent in young lambs
26
which toxin does Type D C perfringens produce
mainly produces epsilon toxin --> is converted to its active form in the intestinal tract and can cause systemic affects in various organs
27
what is overeating disease and what is it caused by and what is it associated with
upsets in gut microbiota from sudden changes to a rich diet or from continuous feeding of highly concentrated ration -->short clinical course and fatal associated with Type D C.perfringens
28
what percentage of antibiotic-associated diarrhea is C.difficile assoiated disease responsible for
25% (this is high!)
29
C. difficile associated disease presentation and mechanism for presentation
diarrhea, colitis, speudomembranous collitis, fulminant colitis spores germinate in colon and vegetative cells multiply rapidly, filling empty niches and producing toxins
30
what is the main cause of colitis in pigs
CDAD (C. difficile associated disease)
31
presentations of pigs with CDAD
1-7 days of age present with early onset scours. gross pathology = severe mesocolonic edema, large intestines filled with paty to watery yellowish feces
32
histologic lesions fo C. difficile
colon with focal infiltration of neutrophils and macrophages in lamina. propria and lumen like erupted volcano. "volcano lesion"
33
what is neutrophilic diarrhea caused by
clostridium difficile production of toxin a (enterotoxin) and B (cytotoxin)
34
function of clostridium difficile toxin A and B in neutrophilic diarrhea
inactivate proteins involved in regulation of actin cytoskeleton --> disaggregation of polymerized actin leads to opening of tight junctions and cell death - also release of proinflammatory mediators and cytokines and activation of enteric nervous system leading to PMN chemotaxis and fluid secretion
35
how would you diagnose C.perfringens
- clinical signs and gross microscopic lesions - multiplex PCR for toxins - ELISA for toxins - bacterial culture (but hard to grow in lab)
36
how would you diagnose C.difficile
- culture - gold standard is toxin detection via neutrilization test or ELISA
37
how to prevent clostridium infection
common clostridial vaccination is 7 way type
38
what causes tyzzers disease in foals
clostridium piliforme
39
what are the key characteristics of clostridium piliforme
- spore forming - extremely oxygen sensitive (strict anaerobic) - gram labile: gram -ve but gram positive when stained under strictly anaerobic conditions - obligate INTRACELLULAR bacterium - spores can survive up to 1 year in soiled bedding
40
transmissiion of tyzzers disease in foals
ingestion of spores from environement
41
prognosis for foals with tyzzer's disease
poor
42
prevention of tyzzers disease in foals
- no vaccines available - farm hygeine - well grassed paddocks proposed as preventative measure to decrease exposure to contaminated soil
43
how is tyzzers dogs and cats pathogenesis
- ingestion of rodent feces containing spores - local proliferatiion of organisms in the intestinal epithelial cells - after stress or imunosupression of host --> spread by portal circulation - colonization in hepatic parenchyma --> multifocal periportal hepatic necrosis, presumably as the result of an unidentified toxin
44
tyzzers disease post mortem findings in dogs and cats
1. multifocal periportal hepatic necrosis and icterus 2. necroti ileitis or colitis - numberous filamentous organisms in hepatocytes - thickening of intestinal mucosa at terminal ileum and proximal colon, foamy dark brown feces
45
what is a risk factor for clostridia infection
disruption of normal gut flora
46
what does clostridium perfringens primarily affect and what are the clinical signs
primarily afffects neonatal farms - enterotoxemia - bloody diarrhea
47
what does clostridium dificile primaily affect and what are and what is it associated with
primarily affects horses, piglets, humans and some lab animals
48
brachyspira hyodysenteriae general characteristics
-anaerobe but oxygen tolerate - obligate symbiotic microorganism, relatively resistant in environemnet
49
what does brachyspira pilosicoli cause in pigs
porcine colonic spirochetosis (PCS) affecting colon and resultts in diarrhea and decreased growth
50
what does brachyspira pilosicoli cause in horses,dogs and humasn
diarrhea
51
is swine dysentry common or uncommon in canada
uncommon in US/canada
52
clinical signs of swine dysentry
emaciation, lare amounts of mucus in feces, dehydration, edema of walls of large intestine, low mortality (but large economic losses)
53
what is swine dysentry caused by
Brachyspira hyodysenteriae
54
treatment of swine dysentry
antibiotics
55
how to diagnosis swine dysentry
Post mortem, fluorescent stain on smears, anaerobic culture, PCR
56
Brachyspira pilosicoli virulence factors
1. highly motile in mucin 2. chemotaxis via mucin to enterocytes 3. serine protease secretion affects tight junction integrity (parcytosis, chronic exxtracellular infection)
57
pathogenesis of brachyspira pilosicoli
1. attaches to apical membrane of enterocytes: loss or effacement of microvili 2. persistance extracellularily in lamina propria and intracellularly goblet cells 3. Beta-Haemolysin 4. induction of outpouring mucus into lumen 5. diarrhea results from colonic malabsorption due to failure of epithelial transport mechanisms
58
Camylobacter spp. general characteristics
- gram negative - microaerophilic - commensals of intestines and repro tract
59
what is intestinal campylobacterosis
cause of diarrhea in many species, including small animals. --> typically mucoid, sometimes blood-flecked, sometimes with fever - may worsen affects of other GI pathogens -
60
who is most at risk for intestinal camylobacteriosis
young and immunocompromised
61
is inteswstinal campylobacteriosis zoonotic
yes it is! and is becoming resistanrw
62
what are helicobacter species associated with
chronic gastritis.. but is a causative relationship not proven
63
general characteristics of yersinia
gram negative, facultative anaerobes
64
3 main pathogenic species in genus yersinia
Y. psudotuberculosis Y. enterocolitica, Y pestis
65
significance of yersinia psydotuberculosis and enterocolitica
enterocolitis and sporatic abortions in farm and wildlife. Gastriennterocolitis in humans
66
what does Y. pestis cause
plague in humans, cats, rodents
67
what age does enteric yersiniosis affect
young farm animals (often multiple animals in herd)
68
enteric yersiniosis clinical signs
diarrhea, sometimes death in farm animals (sheep and deer (most important disease of farmed deer. progressive diarrhea, emaciation and death in lab animals
69
which yersinia species is mroe severe when it comes to enteric yersinosis
Y.psudotuberculosis > enterocolitica

Bacteriology (19 decks)

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