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Bacteriology and Mycology Exam 1 > Histotoxic - Enteropathogenic Clostridia > Flashcards

Histotoxic - Enteropathogenic Clostridia Flashcards

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
Q

c perfringens type C characteristics

A

-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
Q

c perfringens type D characteristics

A

-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
Q

lab diagnosis of c perfringens type D

A

-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
Q

diagnosis of c perfringens

A

-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
Q

treatment and control of c perfringens

A

-too acute for successful treatmetn
-antitoxin (for correct type) – pretection for 2-3 weeks
-bacterin-toxoid combination injections prior to parturition
-prevent overeating

30
Q

clostridium difficile characteristics

A

-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
Q

c difficile diseases in humans

A

-antibiotic associated diarrhea
-pseudomembranous colitis
-toxic megacolon
-septicemia
-myonecrosis

32
Q

c difficile in lab animals

A

-typhlitis in hamsters
-antibiotic associated diarrhea in mice, rabbits, guinea pigs

33
Q

c difficile in horses

A

-hemorrhagic necrotizing enterocolitis in neonatal foals
-nosocomial diarrhea and typhlitis in adult horses
-equine colitis

34
Q

c difficile in dogs

A
  • chronic diarrhea
35
Q

c difficile in ratities

A

-enterotoxemia in ostrriches

36
Q

c difficile in pigs

A

-neonatal necrotizing colitis

37
Q

c difficile toxin A

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
Q

pathogenesis of c difficile

A

-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
Q

which antitoxin is protective for humans

A

-bovine antitoxin

40
Q

lab diagnosis of c difficile

A

-PCR, immunological based tests from feces
-cycloserine, cefoxitin, fructose agar (CCFA)

41
Q

treatment of c difficiles

A

-metronidazole (resistance, alternative is vancomycin)
-no vaccines available

42
Q

control of c difficile

A

-hand washing
-disinfectants not effective against the spore

43
Q

c piliforme

A

-acute fatal diarrhea, Tyzzer’s diseases
-high mortality events

44
Q

c sordellii

A

-fatal myositis
-hepatic diseases
-most common out of c piliforme, c sordellii, c colinum, c sporiforme

45
Q

c colinum

A

-quail disease
-ulcerative enteritis
-necrotizing hepatitis
-affects fowl

46
Q

c sproiforme

A

-juvenile enteritis (mucoid enteritis) in rabbits
-antibiotic induced enteritis in rabbits

Bacteriology and Mycology Exam 1 (26 decks)

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