Bovine GIT 2

Question 1

1. Johne’s disease aetiology.
2. Johne’s disease progressions

Answer 1

1. Mycobacterium - similar to TB. Calves become infected very early in life (via mammary gland) - may be infected in-utero (trans-placental).
   If see any clinical disease, don’t see clinical disease until animal 4-5yrs old. - Difficult to pin-point cause of illness.
   - have had own offspring by this point. Specific progressive enteritis.
   Calves most susceptible.
   Small proportion become carriers
   A few of these then develop clinical signs mostly between 2-5yrs.

Question 2

Johne’s disease clinical signs.

Answer 2

Early sign drop in milk yield.
Profuse watery D+, no blood/mucus.
- but membranes of hind-gut quite friable so bleeding can be induced on rectal exam.
Gluteal muscle wastage.
Skin loses suppleness.
- condition loss due to PLE.
Cow still bright.
No anorexia.

Question 3

1. Dx of Johne’s disease.
2. Tx/prevention of Johne’s disease.

Answer 3

1. Hx, clinical signs.
   Definitive Dx by bacteria in faeces, and more lately an ELISA/PCR.
2. No effective tx.
   Consider vac.
   - but now difficult to get permission (effect on TB test - can cause positive test).
   Improvements in hygiene and husbandry essential.

Question 4

What can cause a major risk of Johne’s?

Answer 4

Pooling colostrum.
Group housing of calves.

Question 5

Johne’s disease (mycobacterium avium paratuberculosis) transmission.

Answer 5

Faecal-oral route.
Transplacental/transmammary.
Calves <6m most susceptible to infection.
Organisms shed in serum and milk.
Incubation long - usually >15m.

Question 6

Johne’s disease epidemiology.

Answer 6

Common.
Prevalence varies with region and breed.
Possible breed predisposition for Limousin and Jersey.
Temperate conditions allow survival of organism in environment >1yr.
Mostly acquired by purchase of clinically normal infected animal (carrier).
For every 15-25 others likely to be infected.
Also found in wild rabbits and their faeces - infective dose in a single rabbit faecal pellet.

Question 7

1. Why is the mycobacteria that causes Johne’s disease found in clumps in the faeces?
2. Where in the gut can the mucobacteria be found?
3. What does the Johne’s mucosa look like on pathology?

Answer 7

1. Because they are within macrophages.
2. Distal jejunum, ileum, caecum, ileocoecocolic junction, colon.
3. Very thickened gut wall, cannot be stretched out, enlarge LNs.

Question 8

Diagnosis of Johne’s disease on microscopy.

Answer 8

Faecal smears.
Stained with ZN.
Acid alcohol fast bacilli red.
Single organisms inconclusive.
Clumps pathognomonic.
Saprophytic organisms confusing.

Question 9

Diagnosis of Johne’s disease using culture.

Answer 9

Definitive diagnostic technique.
Technically difficult.
Time-consuming (months).
Gold standard.
Löwenstein-Jensen medium / Merkal medium.
Mycobacterium (johnin) supplement.
Decontaminate sample.
Colonies tiny and can take up to 12 weeks.

Question 10

Dx of Johne’s disease on PCR.

Answer 10

Very sensitive.
Primers from IS 900 area of genome.
Specific.
Can be used on faeces but some have questioned sensitivity on faeces.

Question 11

Inferior serology in diagnosis of Johne’s disease.

Answer 11

Complement fixation test.
Serum from animals with clinical disease best.
Antigen aqueous extract of bacteria.
Complement.
Sheep red cells + haemolysin.
Positive red cells ++ at 1/8 dilution.

Question 12

What is the best serooogical test at present for Johne’s disease?

Answer 12

ELISA.
Specificity increased by M. phlei absorption.
Equal to CF test for clinical cases and better for sub clinical cases.
Can detect antibody in blood and milk.
Gives ability to detect animals that are likely to be infected and incubating the infection before they develop clinical disease and producing larger numbers of organisms in their faeces.
- gives control approach.
— early detection and removal from herd to reduce overall infection burden and reduce risk of calves becoming infected, reducing herd prevalence.
Herd screening using milk now common place.
High specificity, lower specificity.
- may miss some infected animals and leave infection in the herd.
— needs to be done repeatedly.

Question 13

Delayed type hypersensitivity testing.

Answer 13

Avian PPD or Johnin.
Injected intradermally in prepared site.
Skin thickness measured before and at 72 hours.
Specificity depends on cut-off skin thickness.
Reactions to avian TB common.

Question 14

Vaccine for Johne’s disease.

Answer 14

Needs to be used under license as can disrupt TB test.
Live attenuated, incorporated with oil and pumice.
Heat killed adjuvanted.
Produce large nodules.
Induce sensitivity to other mycobacteria.
Require ‘ministry’ permission.
Now available from Lelystad, Netherlands.
Commercial vac available for sheep and goats but not cattle in uk.

Question 15

Zoonosis of Johne’s?

Answer 15

Hotly debated and controversial.
Present in milk.
Present on and in meat.
Not always killed by pasteurisation but processes modified now.
Recovered from some cases of Crohn’s disease.
Causality not establish.

Question 16

How can we increase the predictive value of testing to diagnose Johne’s disease?

Answer 16

Combining test, including PE.

Question 17

What would be found on haematology/biochemistry in an animal with Johne’s disease?
- with what other rare condition could these parameters be affected in this way?

Answer 17

Hypoproteinaemia, anaemia, hypocalcaemia, hyponatraemia.
Hypokalaemia.
- amyloidosis of the kidneys.
— PLN.
— secondary diarrhoea.
— oedema due to protein loss.
— wasting.

Question 18

1. What should be done if animal found to have Johne’s disease.
2. Johne’s disease prevention and control.

Answer 18

1. Cull ASAP.
2. Segregation, culling.
   Breed dairy cows to a beef bull.
   Separate valves from dams and feed colostrum from know uninfected dams.
   Pasteurisation of colostrum.
   Avoid pooled colostrum.
   Cull offspring of infected cows.
   Ensure calf pastures not contaminated with adult faeces.
   Don’t use calves as followers on pastures.
   Vac - rarely used - need DEFRA approval.

Question 19

Johne’s disease - Cattle Health Schemes.

Answer 19

CHeCS = Cattle Health Certification Standards.
For BVDV, IBR, Johne’s, Leptospirosis, Neospora, (TB).
1st test = absorbed ELISA.
2nd test = faecal culture or PCR.
Reactor = faeces +ve, or in known infected herds, ELISA +ve (except vaccinated herds).
Cull all reactors.
Cull all calves of reactors.
Vaccinate if >5% of hers are reactors.
Tight biosecurity measures.
Categorises both individual animals AND herds in terms of risk level.

Question 20

Malignant Catarrhal Fever.

Answer 20

Caused by a herpesvirus that should not be in cattle.
An almost invariable fatal disease of cattle of worldwide distribution in which fever, oculonasal discharge, corneal opacity, mouth ulceration, and lymphadenopathy occur.
Very dramatic, severe pan systemic disease, usually of individual cattle.
UK - believed to be associated with contact with sheep (ovine herpesvirus type 2).
High case fatality rate (or euthanasia), but animals can recover.
- antibodies to heroes found in live and well individuals.
No cattle-to-cattle spread.

Question 21

Clinical signs of malignant catarrhal fever.

Answer 21

D+ not constant.
Almost all cases involve lesions on head/eyes and occasional urticaria.
Profuse mucopurulent nasal discharge and centripetal corneal oedema.
Superficial LNs enlarged (generalised lymphadenopathy).
Occasional nervous signs.
Dermatitis (esp. insides of HLs).
Very marked pyrexia.
Abort if pregnant.
Generalised severe vasculitis.
Sloughing of mucosal tissues (differential for FMD).
Lesions everywhere.

Question 22

Dx, Tx and control of malignant catarrhal fever?

Answer 22

Dx based on clinical signs.
No tx (may be treatable but advice against).
Advise euthanasia.
Control based on keeping cattle separate to sheep, esp. at lambing.
Occasional mild cases occur and spontaneously recover.

Question 23

Bovine papular stomatitis.

Answer 23

Similar to orf.
World-wide pox virus of little clinical importance (but can confuse new grads!)
Does not cause d+ but often occurs with coccidia or ostertagia.
Lesions (semi-circular or horse-shoe-shaped) confined to muzzle, nostril and buccaneers mucosa, NOT tongue.
Small circular shaped reddish papules (0.5-1cm).
Heals quickly, good immunity.

Question 24

What disease should be considered as a differential alongside malignant catarrhal fever?

Answer 24

Infectious Bovine Rhinotracheitis (IBR).

Question 25

Winter dysentery.

Answer 25

Caused by coronavirus.
Acute, severe disease over short period of time.
Highly contagious, high morbidity, housed cattle.
Faeco-oral transmission.
Incubation period 3-7d.
Explosive profuse dark D+, not much smell, occasional blood.
Precipitous drop in milk yield.
Recovery in 5-7 days.
Good immunity.
Usually in November (UK), 2-3 weeks after housing.
Relatively uncommon.
First lactation heifers more severely affected.
Disease tends to pass through within 2-3 weeks.
Outbreaks rarely occur on same farm within 2-3 years.

Question 26

Clinical signs of winter dysentery.

Answer 26

Acute onset of D+, sometimes containing blood.
Milk drop, lethargy and Inappetence.
Possible dehydration.
Not usually pyrexic.
Rumen motility might decrease.
Intestinal borborygmi might decrease.
Dilated loops of intestine on rectal exam.
Spontaneous recovery in 2-3 days.

Question 27

Winter dysentery tx.

Answer 27

Supportive tx - fluids, forage etc.
Only treat individual cases with antimicrobials if unable to distinguish from salmonellosis on CE and Hx.
Therefore, if treated, probably as for salmonellosis.

Question 28

Other causes of d+.

Answer 28

Plant toxins.

Copper deficiency - certain parts of UK.
— look for depigmentation, reduced milk yield and weight loss.
— persistent d+, not anorexic or febrile.
— check copper levels in blood and liver.

Tumours.

Amyloidosis.