Histotoxic - Enteropathogenic Clostridia Flashcards

(46 cards)

1
Q

C chauvoei diseases

A

black leg in cow and sheep

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2
Q

c chauvoei toxins

A

-a – oxygen stable hemolysis, lethal, necrotizing
-B – deoxyribosuclease
-y – hyaluronisase
-delta – oxygen labile hemolysin

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3
Q

c septicum diseases

A

-malignant edema in cow, pig, sheep
-abosastitis in sheep (braxy), occasionally calves

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4
Q

c septicum toxins

A

-a – lethal, hemolytic, necrotizing
-B – deoxyrobonuclease, leukocidin
-y – hyaluronidase
-delta – oxygen labile hemolysin

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5
Q

c novyi type A diseases

A

-big head in young rams
-wound infections

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6
Q

c novyi type A toxins

A

-alpha – cytotoxin, glucoylation of small GTPases, necrotizinf, lethat

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7
Q

c perfringens type A diseases

A

-gas gangrene
-necrotizing enteritis in pigs
-necrotic enteritis and gangrenous dermatitis in chickens

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8
Q

c perfringens type A toxins

A

-a – a phospholipase – hemolytic, necrotizing, lethal, lecithin digestion
-theta – perfringolysin O, a thiol activated cytolysin
-Net B – role unclear, essential virulence component in some strains causing necrotic enteritis in chickens

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9
Q

c soredellii diseases

A

-myositis in cow, sheep, horse
-abomastitis in lambs

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10
Q

c soredellii toxins

A

-a – lecithinase, hemolytic
-B – cytotoxin, glucosylation of small GTPase, lethal

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11
Q

c novyi type B diseases

A

-infectious necrotic hepatitis (black disease) in sheep, occasionally cow

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12
Q

c novyi type B toxins

A

-a – cytotoxin, glucosylation of small GTPases, necrotizing, lethal
-B – necrotizing, hemolytic, lethal, phospholipase C

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13
Q

egg yolk agar

A

-differentiation of species based on lecithinase activity
-digestion of leithin causes opaque zone of precipitation that spreads beyond edge of colony

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14
Q

c chauvoei disease characterisitics

A

-produces gas
-black leg

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15
Q

which clostridium cause exogenous infections

A

-perfringens type A, novyi, chauvoei, sordellii

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16
Q

malignnant edema charactersitics

A

-fibrin in pericardium
-edema in subcutaneous
-dark hemorrhagic muscle

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17
Q

c novyi disease characteristics

A

-black disease
-Fasicola hepatica (liver parasite)
-gas bubble in liver, spongy apperance of liver
-“aero chocolate” apperance

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18
Q

c haemolyticum disease characterisitcs

A

-bacillary hemoglobinuria
-yellow or pale color of gums and eye sclera (jaundice, icteric)
-dark purple-red urine (hemoglobinuria), dark colored feces

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19
Q

clostridium lab diagnostics

A

-immunofluorescence of infected tissue smears
-isolation on media rich in cysteine and water soluble vitamins
-PCR

20
Q

treatment and control of clostridium

A

-often disappointing
-IV penicillin
-vaccination of cattle at 3-6 months
-vaccination of pregnant ewes 3 weeks prior to parturition
-vaccination of lambs in first year

21
Q

enteropathogenic, enterotoxemia producing clostridia

A

-c perfringens type A, B, C, D, E
-present and replicate in GI tract

22
Q

predisposing factors of c perfringens insheep

A

-low proteolytic activity in neonatal intestine
-incomplete establishment of normal intestinal flora in neonates
-dietary influences in older animals – change in diet, energy rich diet

23
Q

c perfringens type A toxins and diseases

A

-membrane active toxins and connective tissue toxins
-yellow lamb disease
-gastritis and hemolytic disease in ruminants
-hemorrhagic enteritis in cow, horse, infant alpaca
-necrotic enteritis in poultry
-canine hemorrhagic gastroenteritis
-food poisoning in humans
-antibiotic associated diarrhea

24
Q

c perfringens type B characterisitics

A

-old world diseases
-lamb dysentry in newborns (absence of microbial competition in intestines, low proteolytic activity)
-beta toxin – hemorrhagic enteritis
-depression, anorexia, abdominal pain, diarrhea
-mortality approaching 100%

25
c perfringens type C characteristics
-neonates -- absence of normal intestinal flora, hemorrhagic enteritis -beta toxin principle virulence factor -depression, anorexia, abdominal pain, diarrhea -mortality ~100% "Struck" in older sheep -- fatal toxemia-bacteriemia
26
c perfringens type D characteristics
-enterotoxins in older lambs -- overeating disease, pulp kidney disease -upset in gut flora -- change to rich diet, energy rich diet, intestinal hypomotility -epsilon toxin -- increased intestinal permability, vascular damage, fluid loss, edema -pulp kidney -- acute death, few symptoms, few lab findings (glycosuria) -encephalomalacia
27
lab diagnosis of c perfringens type D
-non motile, polysaccharide capsule, spores rarely in exudate -blood agar -- non proteolytic, not associated with odor, grey-yellow, translucent -blood agar with transmitted light -- double zone of hemolysis -- inner clear zone, hazy outer zone
28
diagnosis of c perfringens
-alpha toxin associated hemolytic activity -positive CAMP test with S agalactiae -geimsa, gram stains reveal gram positive rods -PCR -ELISA -stormy formation -- clotting of milk followed by gaseous disruption
29
treatment and control of c perfringens
-too acute for successful treatmetn -antitoxin (for correct type) -- pretection for 2-3 weeks -bacterin-toxoid combination injections prior to parturition -prevent overeating
30
clostridium difficile characteristics
-gram positive -motile -encapsulated -spore forming -anaerobic -rod -significant cause of diarrheal disease in humans -associated with antibiotic resistance or animals treated with antibiotics
31
c difficile diseases in humans
-antibiotic associated diarrhea -pseudomembranous colitis -toxic megacolon -septicemia -myonecrosis
32
c difficile in lab animals
-typhlitis in hamsters -antibiotic associated diarrhea in mice, rabbits, guinea pigs
33
c difficile in horses
-hemorrhagic necrotizing enterocolitis in neonatal foals -nosocomial diarrhea and typhlitis in adult horses -equine colitis
34
c difficile in dogs
- chronic diarrhea
35
c difficile in ratities
-enterotoxemia in ostrriches
36
c difficile in pigs
-neonatal necrotizing colitis
37
c difficile toxin A
-enterotoxin -breakdown cytoskeleton components -disruption of tight junctions between intestinal epithelial cells -- cell death -stimulate influx of polymorphonuclear cells -- prostaglandin synthesis, secretion of chloride ions and water (diarrhea)
38
pathogenesis of c difficile
-trigger event -- antibiotics, chemotherapy, etc -adherence to large intestine and toxin production -intense inflammatory response -- fluid and electrolyte secretion, diarrhea (with or without blood)
39
which antitoxin is protective for humans
-bovine antitoxin
40
lab diagnosis of c difficile
-PCR, immunological based tests from feces -cycloserine, cefoxitin, fructose agar (CCFA)
41
treatment of c difficiles
-metronidazole (resistance, alternative is vancomycin) -no vaccines available
42
control of c difficile
-hand washing -disinfectants not effective against the spore
43
c piliforme
-acute fatal diarrhea, Tyzzer's diseases -high mortality events
44
c sordellii
-fatal myositis -hepatic diseases -most common out of c piliforme, c sordellii, c colinum, c sporiforme
45
c colinum
-quail disease -ulcerative enteritis -necrotizing hepatitis -affects fowl
46
c sproiforme
-juvenile enteritis (mucoid enteritis) in rabbits -antibiotic induced enteritis in rabbits