Clostridial Dz

Question 1

1. tends to affect which animals?
2. once in tissue kill quickly due to what?
3. where do clostridia spread from post mortem?

what is the most common cause of secondary?

Answer 1

1. the thriftiest
2. exotoxin
3. GI flora or spores in liver/spleen

C. novyii

Question 2

(Tetanus: clostridium tetani - anaerobe)

1. which animals especially susc?

tend to get when?

2. Cx?
3. why does jsut giving penicillin on day of tail docking not work?
4. tx?
5. prevention?

Answer 2

1. small ruminants

after tail docking with rubber band (necrotic tissue)

2. **stiffness (first) –> sawhorse, prolapse of third eyelid, **resp arrest
3. often takes 10-18 days after trauma for Cx (better is good vx, colostrum, mgmt)
4. put in dark/quiet location, ace/valium for sedation, treat wound, antitoxin if early
5. CD&T vx (ewe 30 days before kidding), dec anaerobic sites

Question 3

(Botulisism: Clostridium Botulinium) - not zoonotic

1. usual source of infection?
2. main cx?
3. Tx?

Answer 3

1. eating carcass or decayed stuff
2. lack of muscle tone (flaccid paralysis, tongue paralysis)
3. antitoxin - really $$$

Question 4

(Clostridial Myonecrosis: Blackleg - aka malignant edema, gas gangerene, gangrene myositis)

1. Caused by what bac?
2. affects what animals most?
3. source of infection?

most occur when?

4. Cx?
5. prog?
6. tx?
7. prevention?

Answer 4

1. C. Chauvoei, C. septicum, C. sordelli, or mixed
2. 3-24 mo (mostly healthy cattle)
3. soil, GIT, liver, spleen

late summer/fall

4. **CREPITUS, **death, fever, etc

(crepitus almost always this)

5. poor regardless of tx
6. debride, antitoxin, penicillin
7. vx

Question 5

(malignant edema)

1. caused by what?
2. causes what?
3. in what?

Answer 5

1. C. septicum
2. edema after IM injection
3. cattle and sheep

Question 6

(BRaxy)

1. caused by what?
2. causes what?

Answer 6

1. C. septicum
2. gangrenous abomasitis in lambs and calves

Question 7

(Fluke Related Liver Infections: Bacillary Hemoglobinuria)

1. caused by what bac?

aka what?

2. “red water in cattle”
3. lesions a result of activity from what 3 toxins?

cause what?

4. found where in environment?
5. how do liver flukes contribute?
6. Cx?
7. prevention?

Answer 7

1. C. haemolyticum

C. novyi type D

3. beta

localized hepatic necrosis & intravasc hemolysis

4. soil of pH of 8 (high mountain valley)
5. create anaerboic environment (allow bac to sporulate)
6. sudden death, red urine, bleeding from nose/rectum
7. vx, fluke control

Question 8

(BLACK DZ _ ON THE TEST)

1. causes what? in what?
2. what happens?
3. Cx?

Answer 8

1. infectious necrotic hepatitis in sheep and goats (mostly late fall)
2. fluke dmg liver -> allow C. novyi type B to replicate and kill the animal
3. black discolorization of skin, no red urine or bleeding from orificies

Question 9

(Enterotoxemia: “Pulpy Kidney Dz” “OVereating”)

1. common dz of what?
2. cause?
3. what abc likes this diet? what toxin dos it makes?
4. Cx?
5. lesions in lambs/calves?
6. lesions in goats?
7. how do you diff diff types of C. perfringens?
8. prevention?
9. control in goats?

Answer 9

1. feedlot lambs
2. high carb diet, poor titer
3. C. perfringens type D -> epsilon toxin
4. sudden death in 2 hrs, neuro
5. **pulpy kidney, thymus hemorrhage, **focal symmetric encephalomalacia, general congestion
6. fibrinohemmorhagic enterocolitis (more in GI)
7. PCR
8. **ALWAYS VX IN FACE OF OUTBREAK, **reduce carbs, ^ motility
9. vx TWICE yearly

Question 10

(Necrohemmorhagic enteritis)

1. caused by what?
2. Path for type C?

risk factors?

3. path for type A?
4. Cx (for both)?
5. tx (for foals)?
6. prevention?

Answer 10

1. C. perfringens type C or A
2. milk fed babies -> contaminated by inapparent shedder -> not enough proteases in GIT -> allow C. prefringens type C to proliferate

lots of milk, dams not vx or low colostrum

3. ovefeeding, bad colostrum, slowed gut motility
4. depression, rapid progression to death (10-30% morb, 100% mort)
5. supportive, metronidazole
6. vx (now have one dose)