| Question |
Answer |
| Large, Gram-positive rods |
Clostridium |
| Produce endospores |
Clostridium |
| Anaerobic |
Clostridium |
| Catalase-negative, oxidase-negative |
Clostridium |
| Enriched media required for growth |
Clostridium |
| Motile (except C. perfringens |
Clostridium |
| Present in soil & alimentary tracts of animals & in feces |
Clostridium |
| Neurotoxic Clostridia |
Clostridium tetaniClostridium botulinum (types A - G) |
| Causative agent of tetanus |
Clostridium tetani |
| Straight, slender, anaerobic, Gm +ve rod with special terminal endospores, giving characteristic “drumstick” appearance |
Clostridium tetani |
| Endospores resistant to chemicals & boiling but killed by autoclaving at 121 deg. C for 15 mins |
Clostridium tetani |
| Has swarming growth & hemolytic on blood agar |
Clostridium tetani |
| Ten serologic types based on flagellar antigens |
Clostridium tetani |
| Cross-neutralizing antibodies to neurotoxins between all serotypes |
Clostridium tetani |
| Infection occurs by entry of endospores into traumatized tissues (abrasions & wounds |
Clostridium tetani |
| Mode of action is by synaptic inhibition |
Clostridium tetani |
| Incubation period is 5 to 7 days, may extend to 3 weeks |
Clostridium tetani |
| Clinical effects of neurotoxins are similar in all domestic animals |
Clostridium tetani |
| Nature & severity of clinical signs are dependent on anatomical site of the replicating bacteria, amount of toxin produced & species susceptibility |
Clostridium tetani |
| Clinical signs include stiffness, localized spasms, altered facial expression, spasm of mastigatory muscles (“lock jaw”), generalized muscle stiffness (“saw-horse”) stance, especially in horses |
Clostridium tetani |
| Recovered animals are not necessarily immune (toxin concentration that induce clinical disease is usually below threshold required to stimulate production of neutralizing antibodies |
Clostridium tetani |
| Serious & fatal disease |
Botulism |
| cause most outbreaks in domestic animals |
C. botulinum types C and D |
| Inactivated by boiling for 20mins |
C. botulinum |
| Gm +ve rod with sub-terminal endospores |
C. botulinum |
| Occurs most commonly in waterfowl, cattle, horses, sheep, mink, poultry & farmed fish |
C. botulinum |
| Pigs & dogs are relatively resistant & rare in domestic cats |
C. botulinum |
| Poor quality baled silage & silage or hay containing rodent carcasses have been linked to outbreaks in horses & ruminants |
C. botulinum |
| the most potent biological toxin known |
Neurotoxins of C. botulinum |
| C. botulinum Mode of action is by |
inhibition of neuro-muscular transmission |
| Botulism Clinical signs Develops |
3 to 17 days after ingestion of toxin in all species of animals |
| Acute disease of cattle & sheep caused by C. chauvoei |
Blackleg |
| bomasitis in sheep caused by C. septicum |
Braxy |
| Manifests as cellulitis with minimal gas gangrene & gas formation |
Malignant edema |
| Acute disease affecting sheep & occasionally cattle, caused by C. novyi type B |
Infectious necrotic hepatitis |
| Occurs primarily in cattle & occasionally in sheep, caused by C. haemolyticum |
Bacillary hemogl |
| Neuro disorder in newborn foals under 2 months, due to stress in dam, high level of corticosteroids in milk, high mortality |
Shaker foal symptom |
| Cattle & Sheep: Gangrenous cellulitis & myositis caused by exotoxins, leading to rapid death |
Blackleg |
| Large muscle masses of limbs, back & neck are frequently affected |
Blackleg |
| Manifests as cellulitis with minimal gas gangrene & gas formation |
Malignant edema |
| Clinical features of toxemia are similar to malignant edema |
Gas gangrene |
| Hemoglobinuria: major clinical feature as a result of extensive red cell destruction |
Bacillary hemogl |
| Histotoxic clostridia |
Vaccination: Adjuvanted bacterin & toxoid is most effective |
| is the causative agent of Gas gangrene in human & domestic animals. |
C. perfringens type A |
| C. perfringens type B |
Lamb dysentery |
| Many animals die suddenly & high susceptibility of this group is attributed to the absence of microbial competition and the low proteolytic activity in the neonatal intestine |
C. perfringens type B |
| Occurs in sheep at pasture, usually manifests as sudden death |
perfringens type C:perfringens type C |
| Sudden death in goats & feedlot catle |
Clostridia |
| Necrotic enteritis in chickens |
Enteropathogenic & Enterotoxaemia-producing Clostridia |
| Haemorrhagic enteritis in neonatal pigs |
Enteropathogenic & Enterotoxaemia-producing Clostridia |
| Neuro disorder in newborn foals under 2 months, due to stress in dam, high level of corticosteroids in milk, high mortality |
Shaker foal symptom |
| Vax available |
immunize dam and passive transfer of neutralizing antitoxin to foal, or give antitoxin serum to foal |
Alva Jackson
on 2009-10-22
Spanish 3
