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35 Cards in this Set
- Front
- Back
Clostridium species |
Clostridium tetani Clostridium botulinum Clostridium perfringens (type A) |
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Clostridium Bacterial characteristics (tetani) |
Gram positive obligate anaerobe endospore forming |
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Clostridium Bacterial characteristics (botulinum & perfringens) |
gram positive obligate anaerobe endospore forming fastidious anaerobe |
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Clostridium tetani host species |
many |
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Clostridium tetani where did it come from |
soil, feces, sewage, environment |
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Clostridium tetani how are animals exposed |
spores entering following trauma |
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Clostridium tetani how does it cause disease |
incubation only days to 2 weeks |
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Clostridium tetani how does it cause disease (virulence factors) |
tentanolysin (hemolysin) --> promotes anaerobic microenvironment for growth Tetanospasmin (neurotoxin) - not present on all strains inactive protoxin released by lysis of bacterial wall - proteolyis activates toxin heavy chain - receptor binding and entry into axon. light chain - prevents neurotransmitter release by cleaving synaptobrevin necessary for export of intracellular vesicles |
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Clostridium tetani clinical signs |
early -> muscle fasciculations and exaggerated responses to stimuli --> impaired muscle function in head and neck advanced--> total body rigidity --> respiratory failure |
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Clostridium tetani how to diagnose |
culture clinical signs |
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Clostridium tetani will the infection spread to other animals |
no, separate infections! |
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Clostridium tetani how to treat |
clean and debride wound antibiotics (penicillin) antitoxin to neutralize unbound toxin (will not reverse CNS effects) supportive care |
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Clostridium tetani how to prevent |
vaccination |
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Clostridium tetani in horses... |
highly sensitive to toxin compared to other species. - post partum mares with traumatic deliveries and foal via umbilicus - guarded prognosis 50% mortality |
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Clostridium botulinum host species |
many |
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Clostridium botulinum where did it come from |
soil, invertebrates, nematodes (environment) |
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Clostridium botulinum how are animals exposed |
toxin C = carcasses Toxin C & D = affect animals toxin A, B, C = horses |
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Clostridium botulinum how does it cause the disease |
same as tetanus but target neuromuscular junction intoxication - ingestion of toxin in contaminated feeds toxicoinfectious - foals ingest spores (infection and toxin release). spores gain entry via wound (infection and toxin release) |
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Clostridium botulinum clinical signs |
- restlessness, incoordination, rear limb weakness - inability to stand - head and neck signs (paraylsis of tongue, drooling, poor pupillary light response) - death |
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Clostridium botulinum how to diagnose |
culture clinical signs |
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Clostridium botulinum will it spread to other animals |
no, separate infections |
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Clostridium botulinum how to treat |
heptavalent antitoxin to neutralize unbound toxin supportive care antibiotics for secondary infection wound botulism -> surgical debridement/antibiotics |
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Clostridium botulinum prognosis |
death if not treated early |
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Clostridium botulinum how to prevent |
prepare food properly |
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Clostridium botulinum zoonotic |
no |
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Clostridium perfringens (type A) common name |
Histotoxic Clostridia |
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Clostridium perfringens (type A) host species |
many |
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Clostridium perfringens (type A) where did it come from |
environment/normal flora |
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Clostridium perfringens (type A) how are animals exposed |
predisposing factos - wound = inoculates clostridia into tissue - tissue damage = anaerobic conditions - clostridium secretes necrotizing toxins = progressive necrosis and gas formation - rapid expansion of pathology muscle sheath = death |
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Clostridium perfringens (type A) how does it cause diesease |
clostridial spores & tissue trauma - germinate and release toxins - tissue necrosis + edema + hemolysis = death |
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Clostridium perfringens (type A) why does it cause disease (virulence factors) |
- alpha toxin = phopholipase that damages host cell membranes - beta toxin = mucosal necrosis, CNS and cardiac signs, lethal - epsion = secretes as prototoxin by proteolysis -> pore forming toxin -> K & fluid leakage from host cells -> toxin in blood stream --> CNS signs |
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Clostridium perfringens (type A) Clinical signs |
Type C strain (poor quality feed) - necrotic enteritis - neonates - NO diarrhea Type D strain (upset GI flora) - alpha and epsilon toxin --> edema, tissue necrosis, CNS signs, respiratory distress - brain edema, glucose in urine - older animals - sudden death |
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Clostridium perfringens (type A) how to diagnose |
sample submission of intestinal contents, blood clots, liver, blood , serum, feces. must find organism and toxin compatible with history |
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Clostridium perfringens (type A) how to treat |
no effective treatment |
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Clostridium perfringens (type A) how to prevent |
vaccination (dry cow) good colostrum feeding proper food |