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60 Cards in this Set

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  • Back
How are clostridial organisms defined?
Anaerobic, spore-forming, opportunistic, toxin-producing organisms
Where are C perfringens organisms normally present?
The intestines of sheep
What causes an increase in C perfringen levels?
A change in diet, causing overflow of undigested foor into the SI allows the saccharolytic bacteria to multiply rapidly in the anaerobic presence of carbs.
What changes in diet/rumen can occur to increase C perfringens levels?
Sudden changes
Insufficient dietary fibre
Severe GI parasitism
What do C perfringens bacteria produce?
Non-toxic protixins thatthen are converted to toxins by action of digestive enzymes
What are the 3 manin conditions caused by C perfringens?
Pulpy Kidney
Lamb dysentery
What causes Lamb dysentery?
C. perfringens Type B and the beta and episilon toxins
What age group is affected by lamb dysentery?
Healthy lambs less than 2 weeks (usu 1-3 days)
Predisposing factors for lamb dysentery?
Bad hygeine
Cold/wet springs
C/S of lamb dysentery
Sudden death of w/in 4 hours
Acute abd pain
Lamb dysentery PM signs
Dark red, ulcered intestines
Blood-stained peritoneal fluid
Pale/friable kidneys
Diag of lamb dysentery?
beta and episilon ELISA
Intestinal scrape and G stain
What causes pulpy kidney?
C. perfringens Type D
C/S of pulpy kidney
Sudden death
Progresses to recumbency and death
What animals are affected by pulpy kidney?
Either well grown (greedy!) lambs aged 4-10 weeks or fattening lambs aged 6-12 months
Predisposing factors for pulpy kidney?
Greedy lambs that eat a CHO rich diet and sugars spill over ino the SI from the abomasum. Also assd with a change in diet.
Pulpy kidney PM?
Excess peritoneal fluid
Congested/friable liver
Pale/swollen/autolysed kidney
Swollen viscera
Diag pulpy kidney?
Glucose in urine (dipstick)
Episilon toxin ELISA test
Brain biopsy
What causes Struck?
C. perfringens Type C, beta toxin
C/S of struck
Sudden death
What causes clostridial abomasitis?
C. sordellii
C/S of abomasitis?
Sudden death
Cause of abomasitis?
Rapid change in dietary fermentable CHO (lambs get into the creep and have too much sugar)
Age group affected by abomasitis?
3-10 week lambs
Does abomasitis affect vacc or unvacc sheep?
What is the best way to prevent C. perfringen enterotoxaemias?
Vaccinate! Initial course is two vaccine inj 4-6 weeks apart when they enter breeding flock followed by an annula booster about 6 weeks before lambing.

Lambs protected for 16 weeks. Should get their first dose at 8-12 weeks followed by a booster 4 weeks later.
What 3 steps should occur in the face of an enterotoxaemia outbreak?
Start a vacc programme
Restrict feeding (decreases sugars)
Inject C. perfringens beta and episilon antitoxins in valuable animals
What causes blackleg in sheep and cattle?
C. chauvoei
What are the predisposing factors for blackleg?
Shearing under dirty conditions
Dirty needles
Root crops
Poor lambing hygeine
C/S of blackleg?
Depends on site of infection.

LIMBS - stiff, sc oedema, gas production

VULVA - swollen, purple vag, necrosis and erosion of extending muscles

HEAD - swollen whole face, bleeding from nose

All cases - dull, depressed, recumbency then DEATH
What do the toxins of C chauvoei cause?
Necrotising myositis
Gas production
PM of blackleg?

Oedematous, dark red m (esp spinal and legs)
Rancid smell
Oedema oozing from fascia
General toxaemia
How to diagnose blackleg
FRESH carcass PM
G+ rods in oedema fluid
Smear of bone marrow of rib as its the last place that the opportunistic C. septicum bacteria gets to!
Most common blackleg area in cattle?
Upper limbs
Spinal muscles
Treatment of blackleg?
Seldom effective.

Cleaning and surgical debridement
High dose penicillin
What causes black disease?
C. novyi Type B, beta and alpha toxins
What age is affected by black disease?
All ages of sheep
C/S of black disease?
Sudden death
What causes C. novyi to multiply?
They are part of the normal flora of soils and sheep intestine. When the sheep has liver flukes leaving tracks of necrotic debris and inflam exudate this provides an excellent condition for multiplications and toxin production.
PM signs of black disease?
Again, autolyses quickly!

Engorged SC blood vessels = black colour to carcass
Dark liver with areas of pale foci (fluke migration!)
Diag of black disease?
ID of G+ rods in smears of cut liver tissue
+ FAT from liver tissue

Care, as found in healthy animals too must go with hx and PM findings
What causes tetanus?
C. tetani
Who can get tetanus?
Where is C tetani found and how is it made infectious?
Found in soil and causes disease when spores enter deep wounds with devitalised tissue (esp docking wounds!)

Reaches brain after 1-3 weeks causing a state of sustained spasm and rigidity
C/S tetanus
Sustained spasm - animals cannot eructate or swallow, laterally recumbent with extended neck and limbs, open mouth (lock jaw), protruded 3rd eyelid and stiff tail head.
How do tetanus animals die?
Asphixiation due to paralysis of resp muscles
Diag of tetanus?
No PM findings - all based on hx and C/S
Treatment of tetanus?
Easly causes with IV tetanus antitoxin, AB and AF but with a guarded prog.
What causes braxy?
C. septicum
Who gets braxy?
Hoggs feeding on frosted feed or turnips
C/S of braxy?
Sudden death
Severe abomasitis
What causes malignant oedema?
C. novyi, septicum and chauvoei
What causes botulism?
C. botulinum Types B, C and D
Explain the types of C. botulinum
C and D - from poultry litter on fields
B - carcass contamination of big bale silage
Who gets botulism?
Why is C. botulinum different from the other forms of clostridia?
Its the only one that doesn't cause toxin production
C/S of botulism?
Flaccid paralysis and incoordination starting in the pelvic limbs
Tongue protrudes
Recumbent within 24 hours
What causes bacillary haemoglobinuria (red water)
C. novyi Type D
C/S of red water?
Similar to black disease as following the tracts of liver fluke

Rumen stasis
Anaemia and jaundice
Death after 2-3 days
Main vaccine for clostridial spp?
Heptavac, SC over neck