Histotoxic - Enteropathogenic Clostridia Flashcards
C chauvoei diseases
black leg in cow and sheep
c chauvoei toxins
-a – oxygen stable hemolysis, lethal, necrotizing
-B – deoxyribosuclease
-y – hyaluronisase
-delta – oxygen labile hemolysin
c septicum diseases
-malignant edema in cow, pig, sheep
-abosastitis in sheep (braxy), occasionally calves
c septicum toxins
-a – lethal, hemolytic, necrotizing
-B – deoxyrobonuclease, leukocidin
-y – hyaluronidase
-delta – oxygen labile hemolysin
c novyi type A diseases
-big head in young rams
-wound infections
c novyi type A toxins
-alpha – cytotoxin, glucoylation of small GTPases, necrotizinf, lethat
c perfringens type A diseases
-gas gangrene
-necrotizing enteritis in pigs
-necrotic enteritis and gangrenous dermatitis in chickens
c perfringens type A toxins
-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
c soredellii diseases
-myositis in cow, sheep, horse
-abomastitis in lambs
c soredellii toxins
-a – lecithinase, hemolytic
-B – cytotoxin, glucosylation of small GTPase, lethal
c novyi type B diseases
-infectious necrotic hepatitis (black disease) in sheep, occasionally cow
c novyi type B toxins
-a – cytotoxin, glucosylation of small GTPases, necrotizing, lethal
-B – necrotizing, hemolytic, lethal, phospholipase C
egg yolk agar
-differentiation of species based on lecithinase activity
-digestion of leithin causes opaque zone of precipitation that spreads beyond edge of colony
c chauvoei disease characterisitics
-produces gas
-black leg
which clostridium cause exogenous infections
-perfringens type A, novyi, chauvoei, sordellii
malignnant edema charactersitics
-fibrin in pericardium
-edema in subcutaneous
-dark hemorrhagic muscle
c novyi disease characteristics
-black disease
-Fasicola hepatica (liver parasite)
-gas bubble in liver, spongy apperance of liver
-“aero chocolate” apperance
c haemolyticum disease characterisitcs
-bacillary hemoglobinuria
-yellow or pale color of gums and eye sclera (jaundice, icteric)
-dark purple-red urine (hemoglobinuria), dark colored feces
clostridium lab diagnostics
-immunofluorescence of infected tissue smears
-isolation on media rich in cysteine and water soluble vitamins
-PCR
treatment and control of clostridium
-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
enteropathogenic, enterotoxemia producing clostridia
-c perfringens type A, B, C, D, E
-present and replicate in GI tract
predisposing factors of c perfringens insheep
-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
c perfringens type A toxins and diseases
-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
c perfringens type B characterisitics
-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%
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
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
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
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
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
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
c difficile diseases in humans
-antibiotic associated diarrhea
-pseudomembranous colitis
-toxic megacolon
-septicemia
-myonecrosis
c difficile in lab animals
-typhlitis in hamsters
-antibiotic associated diarrhea in mice, rabbits, guinea pigs
c difficile in horses
-hemorrhagic necrotizing enterocolitis in neonatal foals
-nosocomial diarrhea and typhlitis in adult horses
-equine colitis
c difficile in dogs
- chronic diarrhea
c difficile in ratities
-enterotoxemia in ostrriches
c difficile in pigs
-neonatal necrotizing colitis
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)
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)
which antitoxin is protective for humans
-bovine antitoxin
lab diagnosis of c difficile
-PCR, immunological based tests from feces
-cycloserine, cefoxitin, fructose agar (CCFA)
treatment of c difficiles
-metronidazole (resistance, alternative is vancomycin)
-no vaccines available
control of c difficile
-hand washing
-disinfectants not effective against the spore
c piliforme
-acute fatal diarrhea, Tyzzer’s diseases
-high mortality events
c sordellii
-fatal myositis
-hepatic diseases
-most common out of c piliforme, c sordellii, c colinum, c sporiforme
c colinum
-quail disease
-ulcerative enteritis
-necrotizing hepatitis
-affects fowl
c sproiforme
-juvenile enteritis (mucoid enteritis) in rabbits
-antibiotic induced enteritis in rabbits
