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Gram + rods (large)Endospores Clostridium
CAT –Oxidase –Enriched media required Clostridium
Strict AnaerobeMotile (except perfringes)Exotoxinstoxemia Clostridium
Present in soil, alimentary tract and fecesExogenous infmalignant edema & gas gangreneEndogenous inf: dormant spores in muscle and liver Clostridium
Tetanus Terminal endospores (“drumstick”) C. tetani(neurotoxic
All animalsSame clinical effects of neurotoxins C. tetani(neurotoxic
Lock Jaw (spasm-masticatory mm); Saw Horse stance (esp horses)/generalized muscle stiffness, altered facial expression, arched back.Tx: antitoxin(passive immunity) + toxiod + penicillin C. tetani(neurotoxic
Endospores enter abrasions/ woundsinfectionToxinSynaptic inhibition =mode of actionSeverity: site of bact., amt of toxin, spp susceptibility C. tetani(neurotoxic
Only killed by autoclavingBA: swarming/hemolyticFlagellar Ag’s: 10 serotypesD/D: strychnine poisoningRecovered animals not immune. C. tetani(neurotoxic
Most potent biological toxin known C. botulinum(neurotoxic
BotulismSubterminal endospores C. botulinum(neurotoxic
Dilatd pupils, dry mmemb, decreased salivation, tongue flaccidity, dysphagia, paralysis of resp musclesabdominal breathing, paralysis neck muscles (“limberneck”), straddled stance.Fatal C. botulinum(neurotoxic
Cattle, Waterfowl, HorsesSheep, mink, poultry farmed fishPigs/dogs/cats:rare/resistantPoor quality silage w/rodent carcassesoutbreaks(Ingestion of preformed toxin) C. botulinum(neurotoxic
Toxininhibition of neuromuscular transmission=mode of actionTx: antiserum(neutralizes unbound toxin) C. botulinum(neurotoxic
Inactivated by boiling 20min.Type C&D-most outbreaksTypes may be geographically restricted C. botulinum(neurotoxic
Foals <2months(neurological dz) “Shaker-foal Syndrome”
Stress on damcorticosteroids in milk “Shaker-foal Syndrome”
Botulinum type B “Shaker-foal Syndrome”
Vacc dam: passive transfer of neutralizing antitoxins “Shaker-foal Syndrome”
“Shaker-foal Syndrome” C. botulinum(neurotoxic
Blackleg C. chauvoei(histotoxic
Cattle: 3months-2 years=endogenous infectionSheep: any age=exogenous infection C. chauvoei(histotoxic
Gangrenous cellulites and myositis due to exotoxinsrapid death C. chauvoei(histotoxic
“Braxy” (abomasitis) C. septicum(histotoxic
Sheep C. septicum(histotoxic
Anorexia, depression, feverrapid death C. septicum(histotoxic
Winter: ingestion of frozen herbage C. septicum(histotoxic
Malignant Edema C. septicum(histotoxic
=cellulitis w/minimal gas gangrene Malignant Edema
Tissue swelling (edema),Coldness, discoloration of overlying skin, depression, prostration (due to toxemia) Malignant Edema
Rapid death w/extensive lesions Malignant Edema
Gas Gangrene C. perfringensType A(histotoxic
Humans/Domestic animals C. perfringensType A(histotoxic
Gas productionSubcutaneous crepitation, clinical signs of toxemia (above). C. perfringensType A(histotoxic
Necrotizing lethal alpha toxin (has lecithinase activityopalescence on yolk agar= Nagler Rxn) C. perfringensType A(histotoxic
Anaerobic culture on BA: circular, flat, grey colonies/ double hemolysis+CAMP w/S. agalactiae C. perfringensType A(histotoxic
Food poisoning C. perfringensType A(histotoxic
Necrotizing enterocolitis C. perfringensType A(histotoxic
Necrotic enteritis C. perfringensType A(histotoxic
Canine hemorrhagic gastroenteritis C. perfringensType A(histotoxic
Necrotizing enterocolitis Pigs
Necrotic enteritis Chickens
Canine hemorrhagic gastroenteritis Dogs
Lamb dysenteryHemorrhagic enteritis C. perfringens Type B
1 week old-high mortalityCalves/Foals C. perfringens Type B
(All Clostridium produce immunologically distinct exotoxins) C. perfringens Type B
Sudden death: absence of microbial competition/low proteolytic activity in neonatal intestine. C. perfringens Type B
“Struck”(acute enterotoxemia- specific geog. regions) C. perfringens Type C
Adult Sheep+Goats, feedlot cattle, chickens, neonatal pigs C. perfringens Type C
Sudden death on pasture;Gut is hemorrhagicbloody diarrhea C. perfringens Type C
Pulpy Kidney Dz C. perfringens Type D
Sheep C. perfringens Type D
“Over-eating disease”-high grain diet/succulent pasture- worldwide. C. perfringens Type D
HyperglycemiaGlycosuriaSymmetrical hemorrhagic lesions in basal ganglia and midbrain. C. perfringens Type D
PM: Kidney autolysispulpy/cortical softening C. perfringens Type D
Enteritis C. perfringens Type E
RabbitsHemorrhagic in calves C. perfringens Type E
Young rams C. novyi Type A: “Big Head”
Infection of head wounds due to fighting possible rapid death C. novyi Type A: “Big Head”
Necrotizing lethal alpha toxin C. novyi Type A: “Big Head”
SheepCattle (+/-) C. novyi Type Type B: “Black Disease”(Infectious necrotic hepatitis)
Dark skin discoloration due to SQ venus congestion C. novyi Type Type B: “Black Disease”(Infectious necrotic hepatitis)
Liver damage by migrating parasitesexotoxins of C. novyihepatic necrosis C. novyi Type Type B: “Black Disease”(Infectious necrotic hepatitis)
Bacillary hemoglobinuria C.haemolyticum
CattleSheep (+/-) C.haemolyticum
Extensive RBC destruction & liver lesions C.haemolyticum
Tyzzer’s disease C. piliformeGram –Spore forming/filamentousIntracellular pathogen
Foals< 6 weeksMice C. piliformeGram –Spore forming/filamentousIntracellular pathogen
Severe hepatic necrosis and enteritis C. piliformeGram –Spore forming/filamentousIntracellular pathogen
Chronic diarrheaHemorrhagic enterocolitis C. difficile
DogsNewborn foals C. difficile
Quail dzRabbits C. colinumC. spiroforme
Created by: alljacks