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Flashcards in Bovine Deck (459)
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181

Which samples should be submitted for testing?

The whole foetus, placenta with cotyledons, lesions and normal tissue and possibly a maternal blood sample. if the whole foetus cannot be submitted, fresh samples should be taken including foetal stomach contents, pleural or peritoneal fluid, liver, lung, thymus and blood.

182

What is freemartinism?

Hormones, blood cells and other cells cross the placental anastomoses, leading to chimerism. Testosterone or male clels lead to masculinisation of female twin. clinical signs may include an enlarged clitoris with tuft of hair, vagina less than normal lenngth and blind, gonads hypoplastic, uterus difficult to palpate, epididymides and vasa deferentia seen on ultrasound.

183

What is the difference between primary and secondary infectious infertility?

Primary - acting directly on the reproductive tract, placenta, foetus. Secondary - systemic diseases, secondary effect on conception/pregnancy.

184

List all the infectious agents that cause abortion commonly?

Leptospirosis
Campylobacter
Brucella
Salmonella dublin
Listeria monocytogenes
Bovine viral diarrhoea BVD
Bovine herpes virus BHV1 (IBR)
Transmissible viral papillomatosis
PI3
Bovine herpes virus 4
Neospora
Mycoplasmosis
Aspergillus
Q fever
Epizootic bovine abortion (chlamydophila abortus)
Trochomonas foetus (trichomoniasis) not in UK

185

How is campylobacter fetus var venerealis transmitted?

Natural habitat is the prepuce, glans penis and distal urethra. Service leads to mechanical transmission. Herd infection usually occurs after introduction of new infected bull.

186

What are the clinical signs of campylobacter fetus var venerealis?

Usually no systemic illness, females experience a mild endometritis and cervicitis with mucopurulent vaginal dischage. Cases present as repeat breeder which eventually holds, with abortion and RFM at 4-7 months or pregnancy survives to term. in herd - large number of returns, then abortions.

187

Do animals develop immunity to campylobacter?

Untreated bulls are usually permanently infected, cows and heifers develop immunity over 3-6 months.

188

How can campylobacter be diaganosed?

Isolation form post service discharges, vaginal mucus agglutination test, C foetus venerealis in products of abortion. For males - qualitative and bacteriological examination of semen, FAB on preputial washings, virgin heifer test.

189

How can campylobacter be controlled?

AI all stock or AI infected stock and use clean male on clean females. Two normal pregnancies by AI before resuming natural breeding advised.

190

What is the treatment for campylobacter?

Females not usually treated. Streptomycin will shorten course of disease. Bulls are usually culled or treated systemically plus topically (preputial irrigation and antibiotic cream). Four negative FAB or virgin heifer test advised before bull re used.

191

How is brucella abortus transmitted?

Infection is primarily by ingestion, with haematogenous spread at around 6 months gestation to uterus/placenta. This causes a necrotic placentitis and endometritis. In bulls, the infection localizes in the seminal vesicles and testes. It is introduced by silent carriers and excreted in fluids/faeces before and after abortion. Cattle normally only abort once but remain infected and excrete as carriers.

192

What are the clinical signs associated with brucella abortus?

No systemic disease. Abortion and placental retention. Some foetuses are born alive, newly infected herd, abortion seen in cows in late pregnancy, then those earlier in pregnancy. When endemic, abortions are seen in clean replacements and home bred heifers.

193

What does IBR cause?

Respiratory disease, milk drop and reproductive disease Non veneral infection at service or AI can lead to repeat breeding, or later in gestation to abortion. Infection in late pregnancy may lead to stillborn or non viable calves. Venereal infection at natural service can lead to infectious pustular vulvo vaginitis.

194

How does infectious pustular vulvo vaginitis present?

Sudden on set vulval hyperaemia, leading to vesicles and ulcers 48 hours post mating. This leads to pain, anorexia and pyrexia, preventing further service. Males develop similar preputial lesions and mating is interrupted for 2-4 weeks.

195

What are the definitive hosts of neospora caninum?

Dogs - they shed oocysts in their faeces. These oocysts are picked up by intermediate hosts.

196

What are the intermediate hosts of neospora caninum ?

Dogs, cattle, mice , horses& sheep

197

How does neospora cause disease in cows?

When a CONGENITALLY infected animal becomes pregnant, bradyzoite cysts multiply and spread to the placenta and foetus. the consequences may be abortion in the 3rd to 9th month of gestation, premature birth/stillbirth and a full term calf with neurological signs, a clinically normal infected calf or rarely a clinically normal uninfected calf.

198

What may infection with neospora during pregnancy lead to?

Infection in early pregnancy can lead to later abortion, while infection in late pregnancy can lead to a full term clinically normal congenitally infected calf.

199

How is diagnosis of neospora made?

Diagnosis is based on pathology and serology. There is non inflammatory necrotic foci in CNS, bradyzoites in myocardium and liver, inflammatory and necrotic placental lesions. positive maternal serology indicates exposure but may go negative, positive foetal serology indicates exposure after 17 weeks gestation.

200

How can neospora infection be controlled?

No vaccine in the uk or treatment. control BVD. prevent animal contamination of feed, prevent bovine/canine contact with placenta or abortion tissues, embryo transfer from valuable seropositive cows.

201

What is the cause of ringworm in cattle?

Trichophyton verrucosum. Spores survive for months/years. Transmitted by clinical cases and fomites.

202

What are the common sites for ringworm infection?

Calves - periorbital, ears, back
Adults - thorax, limbs, udder
Non pruritic, alopecic lesions, greywhite with powdery surface, often roughly circular.

203

What is the pathogenesis of ringworm?

Infection of keratin of hair and skin, enzymes attack keratin of actively growing hair, breaks off, mild inflammatory reaction

204

What is the treatment for ringworm?

Often self limiting.
Griseofulvin in feed not available in the UK.
Sodium iodide - repeat in 7 days (toxicity)
Ringvac vaccine.
Topical enilconazol (imaverol)

205

Which lice species infect cattle?

Novicola bovis (biting lice)

Haematopinus eurysternus, linognathus vituli, solenopotes capillatus (sucking lice)

206

Describe the life cycle of lice in cattle

3-6 weeks, entirely on host, lay eggs which attach to hairs, nymphs undergo several moults to become adult, survival off host is short.

207

Where are lice seen in cattle?

Biting lice - neck, withers, tailhead
Sucking lice - more generalised, head neck withers brisket tail axillae groin.

208

What can lice be treated with?

Deltamethrin pour on, permethrin pour on, endectocides. Only eprinex can be used in dairy cows. Injectable endectocides not very effective vs biting lice.

209

Which mites cause mange in cattle?

Chorioptes bovis surface mite, psoroptes ovis, sarcoptes scabiei, demodex.

210

Describe the life cycle of chorioptes bovis?

Surface mite, life cycle is 2-3 weeks. lives off epidermal debris. Transmission via direct contact.