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What problems may thin ewes have in a flock?

Decreased ovulation rates, increased foetal resorption, increased deaths, increased perinatal mortality due to smaller lambs and decreased colostrum, metabolic diseases such as pregnancy toxaemia, decreased lamb growth rates, welfare concerns.


What types of disease may cause ill thrift in adult sheep?

Sheep scab, lameness, Johnes, fluke, PGE (haemonchus),teeth problems in old ewes, triplet ewes, gimmers/ewe lambs, Chronic pneumonia (MVV, spa, pasteurellosis), chronic lameness, CLA, chronic abscessation, neoplasia, scrapie etc.


What is Johne's disease?

Chronic bacterial enteritis of ruminants caused by mycobacterium avium subspecies paratuberculosis. Survives in the environment for months and is difficult to culture. There is a long preclinical stage with reduced production.


What are the clinical signs of Johne's?

Progressive loss of condition - protein loss, muscle wasting, brought on by stress. Faeces is normal or slightly soft. Usually have a high GI parasite burden. Up to 5% mortality in adult sheep.


What gross pathology will be seen in ovine Johne's disease?

The terminal ileum may be grossly thickened or congested, difficult to detect, may be pigmented yellow, may affect afferent lymphatics/nodes, and cause ascites etc.


What are the two forms of ovine johne's disease?

Multibacillary - weak CMI, strong antibody. Numerous Map in macrophages.
Paucibacillary - strong CMI, weak antibody, map sparce or absent.


How can Johne's be diagnosed?

Faecal smear, Faecal culture (8-14 weeks, sheep strains v poor growth), faecal PCR, Serology - ELISA, AGID, serum proteins.


What protein levels will be seen with chronic fasciolosis?

Hypoalbumin, hyperglobulin.


how is Johne's trasnmitted?

Oral faecal, in milk, possibly semen, possibly in utero


What are the costs associated to the farmer with Johne's?

Lost of cull ewe sale, cost of replacement, death /poor growth of lambs from affected ewes.


What are the control methods for Johne's?

Reducing environmental contamination and spread of infection, limiting introduction of infection, vaccination, eradication, remove clinical disease, don't keep lambs from affected ewes for breeding, diagnose and remove subclinical disease, farm hygiene, lambing is a high, avoid high stocking rates on bare pastures, purchase sheep from farms known to be free


Describe the gudair vaccination

Killed strain of MAP in oil. Give single cub cut dose 4 weeks to 6 months for replacements. £2-3 per dose.


Describe the problems seen with incisor loss in ewes?

Unable to bite short pasture so unable to raze - malnutrition, poor production and weight loss on marginal grazing and hill pastures.


What is the aetiology of incisor loss?

Repeated bouts of acute gingivitis, recession of gingival margin and damage to periodontal ligament, bacterial involvement, teeth appear elongated, loose then are lost, may take one to four years.


What are the clinical signs of respiratory disease in sheep?

Coughing, nasal discharge, dyspnoea, as well as crackles and wheeses.


How does Parainfluenza virus Type 3 infect sheep?

Most infections appear subclinical or mild but acute high morbidity outbreaks have been recorded. Infection with PI3 predisposes lambs to infection with manheimia haemolytica. Intranasal (cattle) vaccines have demonstrated a reduction in prevalence of pneumonia.


What type of disease does pasteurellosis cause?

Manhaemia haemolytica causes septicaemia in young lambs, pneumonia in growing lambs and mastitis in ewes. Pasteurella trehalosi causes septicaemia in 6-10 month old lambs. P multocida only rarely causes disease.


What are the clinical signs of infection with manhemia haemolytica?

Hyperacute - sudden death
Acute - sudden onset anorexia and dullness, pyrexia, hyperpnoea/dyspnoea, serous ocular and nasal discharges, frothy fluid at mouth in terminal stages. Chronic presentations may lead to ill thrift.


What findings are seen on pathology with manheimia haemolytica infections?

Ecchymoytic haemorrhages over the throat and over the ribs. The lungs are swollen and purple red in hyperacute cases, and the airways contain pink stained froth.


What are the clinical signs of septicaemic pasteurellosis?

This is an important cause of sudden death in lambs up to twelve weeks old. Affected lambs are depressed, easily caught, with injected mucous membranes and marked dyspnoea, most lambs are pyrexic.


What prediposing factors play a role in triggering clinical manheimia haemolytica?

Environmental conditions - extremes of temperature, wet weather, handling stress, PI3 virus, SPA, mycoplasma/bordetella.


What is the treatment for M haemolytica?

Clinical cases - oxytetracycline, NSAID. A decision must be made whether to gather and treat the lambs during an outbreak. handling may trigger further deaths/disease and most acute mortality occurs in the first day or two of the outbreak. Breeding ewes require a primary course four to six weeks apart followed by a booster four to six weeks before lambing often combined with clostridial vacicine.


What is the most common cause of sudden death in lambs between july and december?

Pasteurella trehalosi. confirmation via isolation of large numbers of P trehalosi from lung liver or spleen.


What are other causes of acute death in lambs?

Clostridial disease, ruminal acidosis, redgut (caecal torsion), acute fluke, brassica poisoning, nitrite poisoning, dog worry, phenol dip aspiration, rhododendron poisoning.


When is P trehalosi sudden death most common?

During october november and december. Outbreaks frequently follow movement of lambs onto rape, turnips or improved pastures. Outbreaks start with a few sudden deaths, but the number of deaths then reduces. GI erosions and ulcers caused by dietary change seem to be port of entry for the normal commensal bacteria, leading to septicaemic disease.


What is atypical pneumonia?

A non progressive chronic pneumonia of housed sheep under a year old caused by mycoplasma ovipneumoniae and possibly chlamydia psittaci. Predisposing factors may include PI3 and M haemolytica.


What are the clinical signs of atypical pneumonia?

A chronic soft cough with some mucopus nasal discharge that spreads slowly through a group of lambs. Some dullness and tachypnoea and growth rates are affected. Some lambs may develop a secondary pasteurellosis.


What is the most pathogenic lungworm in sheep?

Dictyocaulus filaria. Deaths are uncommon but may cause outbreaks of coughing and weight loss in the late autumn/early winter. Infection may trigger secondary pasteurellosis.


What other lungworm can infect sheep?

Protostrongylus rufescens - only a problem if very heavy infestation. Muellerius capillaris - more common but no clinical significance.


What is the life cycle of dictyocaulus filaria?

First stage larvae are passed in the faeces which develop to infective L3 on pasture. Spring pastures are inected by overwintered larvae or via faeces of ewes or hoggs. Clinical disease is seen in autumn, with adult worms in the bronchi.


What do Muellerius capillaris look like on gross pathology?

green/grey subpleural nodules in the caudal lung lobes


What do P rufescens look like on gross pathology?

Inhabits the bronchioles causing small yellow/grey granulomas, also in the caudal lobes.


How does chronic suppurative pnuemonia occur in sheep?

follows pneumonia and occurs when pockets of bacterial infection persist and are walled off as chronic abscesses in the lung tissue or pleural space. it may also be caused by bacteramic spread from a septic focus. Bacteria involved may include manhemia haemolytica, arcanobacterium pyogenes, pasteurella and E coli. Other causes of lung abscesses may include CLA and TB.


What are the clinical signs of chronic suppurative pnuemonia in sheep?

Weight loss/ill thrift in individual animals, mild fluctuating pyrexia and normal temperature, dyspnoea, purulent nasal discharge, no respiratory signs, muffling on thoracic auscultation.


What is Jaagsiekte? (SPA)

An infectious tumour condition resulting from infection with a lentivirus, a herpes virus is also involved in the lesions. The incubation period is several months. Disease occurs in 2-4 year old sheep.


What are the clinical signs of SPA?

Loss of body condition, exercise intolerance, serous nasal discharge, episodes of mouth breathing, afebrile, then dyspnoea, tachypnoea, fluid gathers in resp tract and may flow freely when head is loweres, soft cough, fluid sounds may be heard on auscultation.


What do SPA tumours look like on growth pathology?

Tumours are confined to the lungs which are enlarged and heavy. Usually occupy the anteroventral lung fields, are solid and grey and are well demarcated from normal lung tissue. Lesions may contain abscesses or be hidden by extensive pleurisy. The bronchi and trachea contain copious frothy fluid. Tumour cells replace normal alveolar cells.


how is OPA diagnosed?

There are no commercial laboratory tests to support a diagnosis in the live animal. An afebrile wasting respiratory condition which free fluid running from the nostrils when the head is lowered gives a good indication.


What is the main route of transmission of OPA?

Infection is by respiratory aerosol. close confinement during housing or trough feeding increases the rate of spread of infection. Prompt culling of lean or dyspnoeic sheep may slow the spread of infection.


What is maedi visna virus?

A lentivirus infection causing respiratory disease (maedi) nervous disease (visna) mastitis and arthritis.


When do maedi signs occur?

In sheep over three years old. Earliest signs are exercise intolerance, noted during gathering. Affecte sheep stand with the neck extended, increased respiratory rate, flared nostrils and an abdominal component to the breathing. WAsting occurs and dyspnoea becoems obvious even at rest.


what neurological signs are seen with maedi visna?

Visna signs less common. nervous signs including gait abnormalities, e.g dragging a hind limb, knuckling, ataxia, incoordination, collapse and death.


What other clinical symptoms may occur in maedi visna other than respiratory and neurological?

A large number of affected sheep also have an indurative mastitis, identified as a flabby udder with diffuse hardening. milk production is significantly decreased.
Maedi visna arthritis is important in the USa bu has not been identified in the UK. straight legged gait, with swelling most commonly at the carpal joints.


How do maedi lungs appear on PM?

Lungs are firm, rubbery and heavy. They do not collapse.


how is maedivisna diagnosed?

Agar gel diffusion test to detect antibody to the virus. Elisa tests also now developed.


What are the most common causes of ill thrift in weaned lambs?

Poor nutrition, parasitic gastroenteritis, cobalt deficiency, selenium deficiency, liver fluke, other specific infectious and management problems such as respiratory disease, lameness, sheep scab, coccidiosis and border disease.


What should your basic history include when investigating ill thrift in lambs?

Farming system and feed management throughout the year, times of lambing and weaning, lambing percentage and spread, worming regime and anthelmintics used, previous trace element problems and supplements used, observations of scouring, coughing lameness or skin disease, weather conditions.


What are the clinical signs of cobalt deficiency in lambs?

Ill thrift, frequently empty, pot bellied and depressed in appearance, a watery ocular discharge is associated with low grade conjunctivitis, pale and anaemic.


Why is cobalt required by the animal?

for manufacture of vitamin b12 which is required in the liver for utilisation of rumen deprived propionic acid in energy production. Vitamin b12 is also required for the metabolism of certain S amino acids which are necessary for optimum growth and wool production.


When are pasture cobalt concentrations lowest?

Lowest during spring and highest during winter. Pasture cobalt uptake is lowest when pasture growth is rapid and in mature pasture, corresponding with the spring and summer periods. Pasture grown on waterlogged soil has a higher cobalt concentration than pasture grown on well drained soils.


When are clinical signs of cobalt deficiency seen?

In weaned lambs during the summer and in the newborn lambs of deficient dams during the spring.


What is a good method of diagnosing cobalt deficiency?

perform a dose response trial, comparing growth rates of supplemented animals with unsupplemented controls. The two groups need to be grazed and managed under the same conditions, however such an approach is not always practical or appropriate.


What methods of diagnosing cobalt deficiency are there?

Blood vitamin b12 concentrations reflect immediate dietary cobalt, whilst liver vitamin b12 provide a guide to limited continuous body storage. Serum vitamin B12 levels respond within a few days to an improvement in dietary cobalt therefore values must be interpreted with caution. Yarding for a period of more than 6 hours before sampling, liver damage and poor handling can result in elevated samples.


What is Methylmalonic acid?

MMA accumulates in the plasma of cobalt deficient sheep as a result of reduced vitamin b12 coenzyme activity, raised plasma concentrations of MMA can also be used to support a diagnosis of cobalt deficiency, although there are no defined reference values, so MMA concentrations cannot be used to predict the probability of a response to cobalt supplementation.


How can cobalt be supplemented?

Short term through oral drenching, foliage spraying with cobalt sulphate or vitamin b12 injections. Long term supplementation can be achieved using intraruminal cobalt bullets or by pasture top dressing with cobalt sulphate.


What type of virus is border Disease?

A congenital virus disease caused by a pestivirus. Serologically related to BVD in cattle and swine fever in pigs. characteristics of the disease include barren ewes, abortions, mummified foetuses and classical hairy shaker lambs which have excessively long fleeces and abnormal body tremors.


How does border disease cause disease in sheep?

Heathy newborn and adult sheep exposed to BD virus experience only mild often inapparent disease in the process of seroconverting to the virus. The most serious consequences occur when BD virus infects susceptible ewes during pregnancy with the outcome being dependent on the stage of pregnancy when infected.


What does infection before 60days gestation result in in BD?

foetal resorption, abortion or stillbirth. some foetuses may survive and become classical hairy shakers which are PI with virus but negative for antibody.


What happens when sheep are infected with BD between 6- and 85 days of gestation?

variable - some normal lambs but also some with major CNS irregularities and cerebellar hypoplasia. foetal infections after about 85 days are usually met with a competent immune system and lambs are born normal with detectable antibody levels. lambs persistently infected with virus do poorly.


What are the clinical signs of listeriosis in sheep?

Encephalitis is the predominant form in sheep, though abortion and septicaemia also occur. abortion can be caused by L ivanovii and L monocytogenes sensu stricto with the most common source of infection being poorly made silage.


When do abortions usually occur due to listeria?

Any stage but usually in third trimester. abortions due to L monocytogenes have been reported 7 days after consuming infected silage. diagnosis is dificult and relies on isolation of organism.


What is the minimum amount of treatment for scab?

Few flocks are able to remain totally closed so in most cases a minimum of one autumn acaricide treatment is required to mitigate the risk of scab introduction from stray sheep.


when is scab treatment ideally administered?

wait untill all replacement sheep have been introduced but ideally administered before tupping.


handling pens fields or buildings be considered to be a source of re-infestation with sheep scab?

At least 17 days and not used by previously treated animals during this period


How can sheep be treated with plunge dips?

Plunge dipping for one minute in an approved organophosphate or pyrethroid based solution is a proven method for treatment of sheep scab. Sheep should be immersed for one minute with their heads dipped twice and care should be taken to limit faecal or soil contamination of the dipsolution. When correctly applied plunge dips kill any scab mites present with 24 hours/ Pyrethroid scab dips have a nil or short meat withdrawal period but residues in wool.


What mite causes sheep scab?

Psoroptes ovis.


What are the clinical signs of sheep scab?

Mainly a winter disease. Restless sheep, rubbing against posts, soiled areas of wool, tags of fleece, loosing condition, open wounds can occur.


Which systemic endectocides can be used for the treatment of scab?

Two subcutaneous injections of ivermectin seven days apart. or a single IM injection of doramectin. It may be atleast 7 days before all mites are killed and ivermectin provides no significant residual protection against reinfestation. A single subcutaneous injection of moxidectin provides residual protection against sheep scab for atleast 28 days but two injections 10 days apart are recommended for treatment of scab outbreaks.


How can blowflies be controlled?

Freshly dead animals, faecal material and rotting vegetation provide protein for blowflies so the prompt burial of carcasses and attention to general farm hygiene can aid in their control. blow flies prefer a warm moist and sheltered environment so the risk of strike can be reduced by moving sheep to more exposed pasture. The smell of wool grease, presence of foot rot, urine soaked wool, skin disease, scour or infection attracts blowflies to sheep. Shear sheep often.


How can plunge dipping be used to protect against blowfly strike?

plunge dipping in organophosphorus or high cis cypermethrin can provide protection from blowfly strike for 3-8 weeks depending on the product used. Sheep should have at least 3 weeks fleece growth at the time of dipping. Flumethrin plunge dips which are licensed for sheep scab are ineffective for the control of blow fly strike.


How can louse be controlled in sheep?

Shearing significantly reduces the louse burden by removing a large proportion of the lice and exposing those remaining to the lethal effects of dessication. Pyrethroid plunge dips can provide effective louse control. Pyrethroid pour ons disperse around the body in wool grease. They require 6 weeks to disperse around the body and kill lice therefore fail to prevent infection of newborn lambs.


What type of virus is orf?

Parapox virus in the poxvirus family.


What is caseous lymphadenitis?

A contagious skin disease of sheep caused by corynebacterium pseudotuberculosis.


How does transmission of CLA occur?

Directly between sheep during close confinement or indirectly via contaminated shearing equipment, fighting causing skin lesions


What is the clinical presentation of CLA?

Abscessation of superficial LN - parotid, submandibular, popliteal, precrural and prescap. (cutaneous form). spread of infection to LN within the chest and internal organs including lungs, spleen, kidneys and liver, constitutes the visceral or internal form.


How can CLA be treated?

Despite the sensitivity of C pseudotuberculosis to a number of antibiotics therapy is often unsuccessful due to the intracellular site of the bacteria and the fibrous capsule surrounding the lesions. Lancing lesions only results in contamination of the environment thus increasing the potential for disease spread. Abscesses frequently recur after drainage and lavage with antiseptics.


What can fusobacterium necrophorum cause in sheep feet?

Footrot, scald, foot abscess, toe abscess.


Describe the pathogenesis of footrot in sheep.

Wet conditions and trauma of the interdigital skin predispose. Interdigital dermatitis occurs. F necrophorum penetrates the stratum corneum, D nodosus proteases cause hoof separation and allow the deeper penetration of F necrophorum. With virulent strains, under running spreads form axial heel, laterally and anteriorly under sole to abaxial wall and toe.


What are the clinical signs of footrot?

Mixture of interdigital dermatitis, under run heels and severe under run hooves. mild strains only result in separation at the heels and back of the sole, while virulent strains can result in complete separation of the horn of the hoof wall and sole, there is a characteristic smell. In chronic cases there will be a misshapen hoof, trapping dirt and inflammatory exudates. in advanced footrot the sheep will be extremely lame and recumbent for long periods.


What treatment can be used for footrot?

Gentle paring and application of oxytet spray, footbathing with 3% formalin, 10% zinc sulphate, clean feet and dry standing afterwards is important. cure rates of up to 80% feet, but not great against advanced lesions. There is also a vaccination possible which has a therapeutic effect. some respond to first injection. Parenteral antibiotics are effective against advanced lesions, paring is not needed but dry conditions are required 24 hours post treatment. Use oxytet or pen & strep.


How is footrot controlled and prevented?

Aim of control is to achieve low incidence of footrot, low % of early lesions developing into severe lesions, two doses needed for protection with vaccination. 4-6 months protection. Footbaths useful for stopping development of early interdigital lesions into severe lesions. Footparing HAS NO RULE IN PREVENTING FOOTROT.


How can footrot be completely eradicated?

De stocking for 7 days and re stocking with clean sheep. this involves intensive effort during a non transmission phase when all virulent footrot infections should be clinically apparent, and all pastures safe for clean sheep. Cases must be treated or culled, isolated, and non responders culled. Avoid re introduction via purchasing clean replacements, quarantine before adding to flock.


What is interdigital dermatitis in sheep? (scald)

Scald is a major cause of lameness, and the first stage in the pathogenesis of footrot and septic pedal arthritis. It is caused by F necrophorum infection alone and does not require D nodosus. Moist conditions, trauma caused by long wet grass is often the predisposing factor. Straw bedding may play a similar role in housed ewes.


What are the clinical signs of interdigital dermatitis (scald)

Sheep are lame on one or more foot. interdigital skin is inflamed and swolen, layer of white necrotic material, may progress to erosions of ID skin tissue, no under running of horn, no smell. Lameness can persist for several months if untreated.


What is the treatment of scald in sheep?

Oxytetracycline sprays, move to dry pastures, management of areas around troughs and gates, zinc sulphate or formalin footbaths followed by dry standing for 1 hour.


What is ovine digital dermatitis? (new varient footrot)

A virulent rapidly spreading foot disease similar to digital dermatitis in cattle. An association has been made with motile spirochaetes.


What are the clinical signs of new varient footrot?

High morbidity rate, severe lameness, initially full thickness skin ulceration at coronary band, hoof wall under run from coronary band and often shed to expose the sensitive laminae which may bleed profusely. 1cm areas of hair loss and ulceration sometimes seen on skin below fetlock joints.


How can ODD be treated?

Lesions heal quickly after topical treatment with oxytetracycline sprays. response to foot trimming and footbathing in formalin or zinc sulphate is poor. footbathing for 20 minutes in tylosin or lincomycin antibiotic solutions followed by dry standing appears to be effective for prevention and treatment of ovine digital dermatitis.


How can dietary energy supply relative to metaboilc demands be accurately determined during late gestation?

By measuring ewes serum or plasma 3-OH butyrate concentration. increased values reflect ineffcient fatty acid utilisation caused by high glucose demand from developing foetuses not matched by dietary propionate glucogenic amino acid supply.


When should ewes be blood sampled and body condition scored?

four to five weeks before start of lambing time thereby allowing sufficient time to implement dietary changes. Ewe lambs and gimmers should be avoided as they have more singletons and may give a skewed population. a random sample of 15-20 ewes should be blood sampled.


What is the target value for 3-OH butyrate in sheep?

Target below 1mmol/l. 3-OH butyrate concentrations above 1.6mmol/l in individual ewes represent severe energy underfeeding with the likelihood of pregnancy toxaemia, 3-OH butyrate concentrations greater than 3.0mmol/l are consistent with a diagnosis of ovine pregnancy toxaemia.


How can protein status in pre partum ewes be evaluated?

Blood samples can also be analysed for BUN which indicates short term protein intake and albumin which reflects longer term protein status. Care must be exercised with the interpretation of these parameters as recent feeding can increase BUN concentration. Lw BUN usually indicates a shortage of rumen degradable protein.


What happens to serum albumin in ewes during late gestation?

Serum albumin concentrations usually fall during the last month of gestation as immunoglobulins are manufactured and accumulate in the udder thus serum albumin concs in the region of 26-30g/l are normal during last month of the gestation.


When must ewes be vaccinated for clostridial disease?

Four weeks before lambing. Vaccinate as two separate groups with later lambing ewes one week to 10 days later than those lambing during first week.


What does maternal undernutrition result in?

Inadequate placental development which causes poor oxygen, nutrient and electrolyte transfer and ultimately results in poor lamb birth weights. Long term foetal hypoxaemia inhibits the new born lambs capacity for thermoregulation thereby increasing its susceptibility to hypothermia. Severe maternal under nutrition during the final six weeks of pregnancy results in the birth of hypoglycaemic lambs with poor accumulations of liver glycogen and brown fat and in poor udder development and colostrum production.


What happens during dystocia?

Compression of the umbilical cord, protracted labour or trauma to the foetal central nervous system results in short term, usually reversible hypoxaemia, parturient deaths result from acute anoxia of vital centres of the CNS or from the compounding effect of parturition hypoxaemia on pre existing foetal hypoxia due to placental insufficiency. Maintenance of body temperature, teat searching and suckling behaviour are inhibited in surviving lambs. Soft tissue trauma occuring during parturition and subsequent infection may compromise maternal behaviour.


What are the causes of dystocia?

Poor maternal pelvic conformation, foetal oversize, malpresented lambs, partial uterine inertia in polytocous ewes, vaginal prolapse, ringwomb and unskilled shepherding.


How much colostrum does an average 5kg lamb require?

around 1Litre of colostrum during first 24 hours. Failure of the neonatal lamb to suckle or failure of the newly lambed ewe to provide adequate colostrum results in starvation and poor passive immunity to the disease.


What are the maternal reasons which could cause lamb starvation?

Genotype, inexperience, undernutrition, dystocia, concurrent diseases, mastitis, multiple births.


What are the lamb related reasons which could cause lamb starvation?

genotype, multiple litters, birth stress, prenatal malnutrition, hypothermia (dont suckle), infectious disease.


What extrinsic reasons on farm could lead to lamb starvation?

High stocking density of lambing ewes, disturbance of lambing or newly lambed ewes, human interference, poor pasture availability near to the lambing site, exposure.


At what temperature do lambs become hypothermic?

Normal temp - 39-40C - healthy lamb exhibiting normal suckling behaviour. rectal temp 37-39 - weak, still capable of following the dam and suckling. rectal temp


What is the treatment for moderate hypothermia? (37-39C)

dry thoroughly, ensure a colostrum or milk feed, return to ewe, supervise closely.


What is the treatment for severely hypothermic lambs under 5 hours old?

Dry thoroughly, warm to >37C, give a colostrum feed at a rate of 50ml/kg, warm to 39C, return to the ewe, monitor closely and check dam for milk supply or poor maternal behaviour.


What is the treatment for severely hypothermic lambs over 5hours old?

Inject intraperitoneal 20% glucose at a rate of 10ml/kg, dry thoroughly, warm to 37C, give a colostrum feed at a rate of 50ml/kg, warm to 39C, return to the ewe, monitor closely, check dam for milk supply.


Why should lambs over 5 hours old be given intraperitoneal glucose before warming?

Severely hypothermic lambs over 5hours old are hypoglycaemic, warming results in increased cerebral metabolism which rapidly leads to convulsions, coma and death if the hypoglycaemia is not corrected by intraperitoneal administration of glucose. oral administration of fluids to hypothermic lambs causes regurgitation and inhalation asphyxia or pneumonia.


What is watery mouth?

A disease of 1-3 day old lambs characterised by lethargy, profuse salivation and abdominal distension. Usually highest in intensive indoor lambing flocks of prolific ewes.


What are the clinical signs of watery mouth?

Lamb is depressed, anorexic, mouth is cold and commissures of lips and lower jaw are wet due to drooling of saliva, dehydrated with abdominal distension, cold extremities, scleral blood vessels dilated and ocular mucous membranes are congested.


How can watery mouth be treated?

Intravenous flunixin meglumine, oral dextrose electrolyte solutions, enemas of metoclopramide and broad spectrum systemic antibiotics.


How can watery mouth be prevented?

Correc nutrition of pregnant ewe, management of abortion and dystocia, adequate supervision to ensure all lambs suckle and receive colostrum, maintenance of a clean lambing environment, prophylactic use of oral aminoglycoside antibiotics administered to all lambs within 15 minutes of birth.


How does cryptosporidiosis affect lambs?

Cryptosporidium parvum is not species specific and is potentially zoonotic. Infection causes villous atrophy of the distal small intestine, leading to malabsorption. Rarely causes severe in disease in lambs but if environmental oocyst contamination is high or lambs are other wise compromised or stressed then the organism may cause acute onset, pale green coloured watery and occasionally blood stained diarrhoea in lambs between 2 and 20 days old.


How do outbreaks of salmonellosis occur in lambs?

rare - usually follow the purchase of infected carrier sheep or calves. most cases are caused by salmonella typhimurum or salmonella dublin.


What is the pathogenesis of salmonella spp?

They cause severe intestinal inflammation destroying the absorptive capacity and stimulating secretion. They are also invasive leading to bacteraemia and infection of other organ systems. Endotoxins are released into the systemic circulation on bacterial death resulting in depression, circulatory failure and cardiovascular collapse. the clinical signs are depression and profuse green/brown coloured blood stained diarrhoea with variable pyrexia, dehydration and dyspnoea, rapidly progressing to recumbency and death.


How can diagnosis of salmonella be confirmed?

Diagnosis of salmonella confirmed by faecal culture or culture from liver, gall bladder, small intestine and mesenteric lymph nodes at PM examination.


How does E coli cause disease in lambs?

Enterogenic E coli posess K99 adherence pili which enable attachment to the intestinal mucosa. A stable toxin is produced which causes severe watery, brown coloured diarrhoea. The disease is uncommon and only affects lambs less than 48 hours old. Most lambs die unless prompt fluid therapy is administered.


How do non specific bacteraemias occur in lambs?

In colostrum deprived lambs, tonsilar or enteroinvasion by E coli, P haemolytica and P multocida, arcanobacterium pyogenes, staph and strep from a contaminated environment may be followed by multiplication in other organ systems and subsequent polyarthritis, omphalophlebitis, endocarditis or meningitis.


How does meningitis affect lambs?

Usually occurs 2-4 weeks old. isolation from dam and failure to suckle with episceral congestion, lack of suck reflex, weakness, altered gait and depression extending to stupor but hyperaesthesia to auditory and tactile stimuli. Opisthotonus is observed during the agonal stages of the disease.


What is joint ill and how does this appear in lambs?

Polyarthritis may occur in lambs as young as 5 days old and is characterised by sudden onset lameness with pain, heat and flutuating swelling of several limb joints, leading to poor suckling behaviour and ill thrift. At PM examination, incised joints contain pus, synovial membranes are thickened and congested and articular surfaces eroded.


Which pathogen is usually identified in joint ill in lowland flocks?

Streptococcus dysgalactiae


How does navel ill occur in lambs?

May follow bacteraemia or infection of the umbilical vessels and urachus form a contaminated environment. affected lambs may adopt a hunched back stance with a poor body condition and hollow flanks due to poor suckling behaviour. the navel is moist, swollen and painful and may exude a purulent material.


What is Erysipelothrix rhusopathiae and how does it cause disease in lambs?

It is a bacteria that has a wide host range and can survive for long periods in the soil, especially at low temperatures. Recently born lambs acquire the infection in the same way they acquire other forms of joint ill. A bacteraemia results in organisms settling in the joints, where they cause a fibrinopurulent polyarthritis in addition to osteomyelitis and in some cases endocarditis. Morbidity can reach 40% although mortality is low. affected lambs are stiff and may be pyrexic.


What is the treatment for E rhusopathiae?

high doses of parenteral penicillin is effective in the early stages. in flocks with a recognised problem, vaccination of the dam with two doses of bacterin 4-6 weeks apart in the first year and one booster dose 3-4 weeks before lambing is effective.


What does navel infection with F. necrophorum result in in lambs?

Characteristic white spot, 2-10 mm diameter abscesses in the liver and secondary spread to joints and lungs.


What are the signs of iodine deficiency in lambs?

Goitre, pot bellied, wool is scant and lacks crimp. lambs from the same litter can be afefcted to different extremes. Typically high lamb losses occur during adverse weather conditions due to starvation or stillbirths where the foetal membranes still cover the lambs nose. this is due to the role of iodine in thyroid hormones in foetal maturation and thermoregulation.


What radio of thyroid:body weight suggests flock needs iodine supplementation?

A production response to iodine supplementation is likely when ratio of thyroid:body weight of newborn lambs exceeds 0.4g/kg.


What are the main pathogens in acute mastitis in ewes?

Staphylococcus aureus or pastuereulla haemolytica


which species of coccidia cause outbreaks in lambs?

eimeria crandallis and E ovinoidalis.


What clinical signs to lambs show when infected with coccidiosis?

Acute onset diarrhoea, dullness, anorexia, dehydration, weight loss affecting a high proportion of the lamb flock.


How does coccidia infection progress?

Following the ingestion of coccidia oocysts from a contaminated environment, the parasite invades and multiplies several times in the cells of the lining of the intestine, causing epithelial erosion. After a period of 2-3 weeks oocysts are shed in the faeces, further contaminating the environment. Under cool and moist conditions many oocysts survive over winter in buildings and on pasture.


How can outbreaks of coccidiosis in lambs be managed?

Usually managed by whole flock treatment with sulphonamide drugs and avoidance of intensive grazing. The coccidiostat drug decoquinate can be included in lamb creep feed for disease prevention or fed to ewes to reduce their contribution to environmental oocyst contamination. Diclazuril can be administered orally to lambs as a single preventative treatment in anticipation of a problem.


Where are the usual sites of urolithiasis obstruction in sheep?

vermiform appendage and sigmoid flexure. Most outbreaks due to intensive concentrate feeding and due to calcium magnesium phosphate and magnesium ammonium phosphate. Ewe rations should never be fed to wether lambs.


What are the clinical signs of urolithiasis in sheep?

Anorexia, discomfort, frequent straining and dribbling of small amounts of urine. The ventral abdomen and prepuce become swollen due to leakage of urine into subcutaneous tissues, which eventually slough.


How can severely affected lambs with urolithiasis be treated?

amputation of the urethral process or by pelvic urethrotomy. The long term prognosis is poor because of hydronephrosis. Acidification of the urine by feed withdrawal for 24 hours and daily dosing with ammonium chloride in solution reduces the likelihood of calculus formation.


What is tick borne fever?

A disease cause by erlichia phagocytophilia. The primary disease is usually benign but it has a profound effect on the immune system. Begins with a high fever, then intracellular infection of white blood cells. Most animals become carriers and suffer periodic spontaneous relapses.


What are the clinical syndromes seen with tick borne fever?

Prolonged fever may influence spermatogenesis in rams. pregnant animals may abort, although native sheep are unlikely to be infected for the first time during pregnancy. the main importance is potentiation f other infections, in particular louping ill and tick pyaemia.


How can tick borne fever be diagnosed?

Depends on knowledge of tick activity and identification of rickettsias in gimsa stained blood smears. Positive serology indicates exposure but does not confirm the cause of the disease.


How can tick borne fever be prevented?

Prevention is by dipping or applying pour on treatments of flumethrin or cypermethrin when new born lambs are introduced to the hill. E phagocytophilia is sensitive to oxytetracycline and some hill farmers combine pour on with a single long acting injection.


What is louping ill?

Diffuse non suppurative meningoencephalomyelitis in sheel caused by a flavivirus.


What are the clinical signs of louping ill?

transient ataxia to sudden death, usually starts with incoordination and progresses to recumbency, convulsions, coma and death within 24-48 hours. In non fatal cases residual torticollis or posterior paralysis may remain for several months.


How is louping ill transmitted?

Via ixodes ricinus and linked to annual periodicity of tick feeding activity. Older sheep are usually immune. Colostrum derived antibodies proide good protection in lambs born to immune ewes. Lambs protected by colostral antibodies are fully susceptible during their second spring so most losses are in ewe lambs retained for breeding.


How is diagnosis of louping ill made?

Clinical signs, knowledge of tick activity, histological exmaination of brain and virus isolation from brain tissue can be used to confirm. Serum can be submitted for ELISA to record exposure.


What is tick pyaemia?

A bacteraemia and joint ill which results from physical injection of staphylococcus aueus, commensal on the skin surface, by the feeding activity of I ricinus. The disease is potentiated by the effect of E phagocytophilia. Spinal abscesses, leading to posterior paralysis are common.


What are the main differentials for sudden death in several lambs?

Lamb dysentry, nematodirosis, coccidiosis, tetanus, pulpy kidney, clostridium sordelli, acute haemonchosis, redgut, nitrate poisoning, black disease, acute liver fluke, systemic pasteurellosis, grain overload.


Describe How enterotoxaemias due to clostridum occur?

Clostridium perfringens are normally present int he intestinal contents of sheep, which under certain conditions can cause enterotoxaemia. in healthy animals a balance exists between multiplication and passage into faeces, maintaining a low level of infection. C perfringens is saccharlolytic and can multiply rapidly when the anaerobic conditions in the abomasum and small intestine are combined with presence of large quantities of fermentable carbohydrate. These conditions occur when sudden changes in diet enable the overflow of undigested feed to the small intestine.


What is lamb dysentery?

A peracute and fatal disease of young lambs. Caused by beta and epsilon toxins of C perfringens type B. Affected lambs are usually less than two weeks old. Sporadic sudden death of stronger single lambs occur. Lambs are seen with acute abdominal pain but die within four hours. Faeces may be semi fluid and blood stained but in most cases they are normal.


How does pulpy kidney occur?

A common peracute and usually fatal disease of sheep of all ages. Epsilon toxin of C perfringens type D. commonest in well grown lambs between 4 and 10 weeks old, or fattening lambs betwen 6 months and 1 year old. Associated with a change in diet. Animals are occasionally seen alive with hyperaesthesia and ataxi, which progresses rapidly to recumbency, opisthotonus, convulsions and death, signs associated with focal symmetrical encephalomalacia and diarrhoea are seen in lambs which live longer.


What is struck?

A rare peracute disease of adult sheep, beta toxin of clostridium perfringens type C, enteritis, peritonitis and sudden death. The initial diagnosis of enterotoxaemia is made on the basis of history of sudden deaths in well grown, unvaccinated lambs fed on a carbohydrate rich diet, supported by PM findings.


How can clostridial entertoxaemia be prevented?

effective prevention of enterotoxaemia is achieved through vaccination. Previously unvaccinated ewes should be given an initial course of two vaccine injections 4-6 weeks apart when they enter the breeding flock, followed by an annual booster about 6 weeks before lambing.


What is blackleg caused by?

Toxins produced by clostridium chauvoei which survive in soil for many years. Outbreak of the disease in sheep usually requires some predisposing factor such as docking, castration, shearing under dirty conditions, or wintering hoggs on root crops.


What are the clinical signs of blackleg?

The signs depend on the site of infection. When the limbs are involved, sheep become stiff and unable to move. There is a subcutaneous oedema and gas production. Cases associated with parturition injury are characterised by erosion of the vulval mucosa and vulval and perineal oedema with dark red and gassy necrosis extending to adjacent muscles. When the head is affected, as sometimes occurs in rams after fighting, the whole face may swell. Such cases may bleed form the nose and are referred to as malignant oedema.


What are the signs of blackleg in cattle?

If seen alive, cattle may be pyrexic, depressed, tachypnoeic and anorexic. they are stiff or lame in one or more limbs and there is usually swelling and pain at the site of infection. any skeletal muscle mass can be affected, though the most common sites are upper limbs Wounds may discharge rancid smelling serosanguinous fluid. Over a period of 12 to 24 hours the disease progresses, with the development of tremors, ataxia recumbency coma and death.


How can control of blackleg be achieved?

By vaccination with formalin killed bacteria and toxoid. these are administered to catle as a single vaccine, but in sheep are usually included in a multi component vaccine. Also hygienic precautions should be taken when lambs are castrated and docked and when assisting ewes with dystocia.


What is black disease?

A fatal peracute infection of sheep of all ages caused by alpha and beta toxins of clostridium novyi type B. C novyi are part of the normal flora of soils and sheep intestinal contents. Under aerobic conditions the bacteria become motile and it is believed that some pass through the intestinal wall and become lodged as spores in the liver of healthy animals. liver fluke migrating through the liver parenchyma leave tracts of necrotic debris and inflammatory exudate which provide suitable conditions for germination and multiplication of C novyi and toxin production.


What are the clinical signs of blacks disease?

sudden deaths following a short incubation period. Losses can occur throughout the high risk period of liver fluke larval migration, which often amount to 5% and occasionally reach 30%.


What is tetanus?

A fatal paralysing disease of all species caused by a neurotoxin which is produced following multiplication and bacterial death of clostridium tetani. C tetani is ubiquitous in soil and causes disease when spores form the environment enter deep wounds with devitalised tissue. In sheep the disease is commonly associated with docking wounds, especially following the use of rubber rings.


Describe the pathogenesis of tetanus?

Following an incubation period of 1-3 weeks the neurotoxin reaches the brain via peripheral nerves and spinal cord and causes a state of sustained spasm and rigidity of voluntary muscles. AFfected animals are unable to swallow or eructate. As the disease progresses animals become laterally recumbent with characteristic saw horse appearance due to extension of the neck, thoracic and pelvic limbs. V painful - humane destruction recommended.


What is braxy and what is the cause?

Infection of the abomasum in sheep caused by clostridium septicum. Usually seen in hoggs after ingesting frozen food in late autumn.


What does clostridium sordelli abomasitis cause?

Sudden death of vaccinated and unvaccinated sheep, reared creep pfed lambs 3-10 weeks old, with abdominal distension, the abomasum is distended and displaced, with a thickened wall. avoid changes in dietary fermentable carbohydrate.


what type of reproductive cycle do ewes have?

They are seasonally polyoestrus short day breeders. Melatonin increases as day length shortens and sexual activity increases.


When is peak fertility for most breeds?

october/november but scottish blackface have v short breeding season and dorset horn type breeds capable of lambing all year.


What are the benefits of AI synchronisation in sheep?

Compact lambing with better utilisation of labour, more accurate feeding and ration control, even batches of lambs.


how long is the ewes oestrus cycle?

16/17 days. the luteal phase is 13-14 days and the follicular phase is 3-4 days.


How long is the doe oestrous cycle?

19/20 days.


Define the different stages of the reproductive year of the sheep flock.

Anoestrus - mid dec to mid june - no ewes or ovulating or exhibiting behavioural oestrus.
transition - mid june to mid sept - a proportion of the flock are ovulating with or without behavioural oestrus.
Breeding season - mid sept to mid dec - greater proportion of ewes are ovulating and exhibiting behavioural oestrus.


Describe how using a ram/teaser effect can synchronise ewes?

Most useful in transition period. Can be used to encourage ewes to cycle a few weeks earlier than the breed would do naturally. Ideal teaser is a vasectomised ram. The introduction will cause ewes to ovulate within 2/3 days of introduction. this heat is usually non fertile and silent, then the ewes will either have a normal oestrus in 18-20 days later or have a second silent oestrus followed by a normal cycle from 24 to day 28 after introduction. Fertile rams should replace teasers no later than 2 weeks after teasers were introduced due to the two peaks of oestrus a peak of lambing should be produced over two and a half weeks.


How can progestagen sponges be used to syncrhonise ewes?

Intravaginal progestagen sponges with or without PMSG injection are most common products used. sponges are inserted for 12 - 14 days to provide a period of progesterone priming, when sponges are removed, the sudden fall in progestogen precipitates a surge of gonadotrophin hormones that leads to oestrus activity. If used during breeding season PMSG is not generally required, whereas ewes in the transitional period or anoestrum will require a dose of PMSG to stimulate follicular activity.


When should the fertile ram be introduced after progestagen sponges?

The majority of ewes require 36-47 hours to come into season post sponge removal so rams should be introduced at 36-40 hours for maximal conception rates. If they are joined any earlier, rams may deplete their semen reserves on the first ewes to begin cycling.


How can melatonin be used to manipulate the ewes oestrus cycle?

Slow releasing melatonin implants can be used to mate sheep early in the season before the usual peak of reproductive activity. one implant per ewe is administered subcut near the base of the ear. Ewes must be kept separate from all male sheep and goats.35 days after implantation introduce rams Vasectomised rams may be used approx 14 days before fertile rams to improve conception rates to first service.


How can PGf2a be used to synchronise ewes?

Causes regression of the CL - has no use for out of season breeding programmes. the CL is responsive to pg from days 4-14. Oestrus occurs approx 40 hours after PG with ovulation 03 hours later.


What are the clinical signs associated with chlamydial abortion in ewes (enzootic abortion of ewes)

Chlamydophila abortus. Rarely any signs of impending abortion and ewes are usually unaffected unless placenta is retained and metritis develops. Abortion seen usually in the last 2-3 weeks of gestation and majority of lambs are well developed and quite fresh indicating recent death in utero. Although necrosis of foetal membranes with thickened intracotyledonary areas is a classical findings.


How is diagnosis of C abortus made?

Abortion of well preserved lambs in the last 2-3 weeks of pregnancy and associated necrotic placentitis. confirmation by the demonstration of large numbers of chlamydial elementary bodies in smears from affected cotyledons.


How is chlamydial abortion treated?

With long acting oxytetracycline - limits the severity of losses in an outbreak. two im injections at a two week interval are recommended. Vaccination against EAE is widely undertaken. must be completed 4 weeks prior to breeding. vaccinate ewe lambs at 5 months of age.


What is the lifecycle of toxoplasma gondii and how does this infect sheep?

The life cycle of toxoplasma gondii can be separated into two parts, an asexual cycle with ltitle host specificity and a sexual cycle confined to cats which results in the production of oocysts in cat faeces. in a farm situation rodents often host the asexual cycle where infective tachyzoites penetrate a host cell and form encysted bradyzoites. cats acquire infection through ingesting these infected mice and breaking down the tissue cysts to form oocysts which are shed in their millions onto bedding and feedstores creating a potential source of infection for pregnant sheep.


What are the clinical signs of infection of sheep with toxoplasma gondii?

Usually stillbirths in the very late stages of pregnancy or abortions. some stilborn lambs accompanied by a mummified foetus. ewes are normally unaffected. Infection in early pregnancy can produce foetal resorption with a large number of ewes ending up barren. Infection in late pregnany produces infected but clinicaly normal lambs.


What gross pathology is seen in toxoplasma abortions?

the main changes are the foetal membranes which are engorged, with necrotic cotyledons with speckled white necrotic foci on the surface. inter cotyledonary areas appear normal.


how can toxoplasmosis be diagnosed?

Serology. indirect fluorescent antibody tests to detect toxoplasma natibodies in foetal fluids can also be used if abortion products are available. Latex agglutination test can be performed on blood from the ewe.


How can toxoplasmosis be controlled and prevented?

Once an outbreak has occured little can be done to prevent further spread as infection is via contaminated feed and bedding and is not thought to be sheep to sheep. control of rodent and cat population on farm is important. Young cats are most likely to shed oocysts. Fedding the coccidiostat drug decoquinate to ewes during pregnancy has been shown to reduce toxoplasma related perinatal lamb mortality but the practicalities of feeding throughout pregnancy is limited. Vaccination with a live vaccine toxovax is the best available method of control. Once a ewe has been vaccinated or has aborted immunity is solid and revaccination should not be necessary.


what salmonella strains cause abortion in sheep?

S typhimurium, S dublin, S montevideo and S abortus ovis.


What are the clinical signs seen with salmonella abortion in sheep?

May or may not include general systemic and enteric signs. Main sign with s montevideo and s abortus is abortion in last 6 weeks of gestation and ewes are rarely seen ill. With S typhimurium and S dublin, enteric and systemic signs predominate, affected ewes are sick and pyrexic and may scour profusely.


How does the foetus/placenta appear when infected with salmonella?

The foetus and placenta is moderately to severely autolsed in most cases, with necrotic membranes and rotten lamb smell. the lambs may be emphysematous which often makes removal difficult.


How can diagnosis be made of salmonella infection?

Isolation of causal organisms along with gross signs of salmonellosis. typical gram negative organisms are seen on direct smears of placenta and stomach contents of foetuses. culture on desoxycholate cirate agar or maconkey agar should confirm diagnosis.


How is salmonella controlled during an outbreak?

Strict isolation of aborting ewes and good hygiene is paramount where salmonella is suspected or confirmed as being present as the zonotic danger is great. May mass medicate remaining ewes to lamb, changing the lambing field or shed after a week or so will help prevent build up, usually due to infected feed or water (apart from s abortus ovis), keep secure feedstores, avoid poaching in fields, turn over feed boxes when sheep have been fed.


How does campylobacter cause abortion in sheep?

Campylobacter fetus intestinalis/ jejuni causes abortion in the last 6 weeks of pregnancy with a placentitis developing 7-25 days after infection. Infection is transmitted orally though it occurs in many closed flocks.


How is diagnosis of campylobacteriorsis made?

Ziehl neelson smears made from cotyledons and stomach contents to observe the characteristic small, comma shaped bacteria.


How is campylobacteriosis spread?

no venereal spread as in cattle. usually self limiting from one year to the next with good immunity developing in the flock. Not always clear where the source of infection has come from. wildlife vectors such as crows and other birds have been implicated.


What are the major causes of abortion in goats?

Late stage - listeriosis, campylobacter, salmonellosis, border disease, multiple foetuses, corticosteroids.
At any stage - toxoplasmosis, chlamydophila, tick borne fever, stress, prostaglandins. goats more prone to abortion by stress due to maintenance of pregnancy by CL.


What are the differences in chlamydophila abortus abortion in goats compared to sheep?

Abortion can be at any stage of pregnancy unlike sheep where abortion is restricted to last trimester, incubation period may be as short as 2 weeks. Source of infection can be from aborted material, faeces and milk. carrier animals - kids born alive to infected does.


How can chlamydophila abortus be controlled in goats?

Disposal of infected material an ddisinfection, segregation of aborting animals for 2 weeks, cull any live kids from aborting does, treatment of pregnant does with oxytetracycline and move to clean pastures, vaccination.


Which lungworm species can also infect goats?

Dictyocaulus filaria - not often a major pathogen, seen in SE england in late summer. Muelleris capillaris - goats more likely than sheep. Clinical disease generally adult goats over 3 years old. treatment with fenbendazole or ivermectin.


What is beta mannosidosis?

An autosomal recessive lysosomal storage disease of anglo nubians. Usually bright, alert and able to suck but often unable to stand, have a head and neck tremor, nystagmus and deafness, dome shaped skull, carpal contracture, fetlock hyperextension, thickened skin.


Which organisms commonly cause mastitis in goats?

Staph aureus, strep uberis, streptococci, s dysgalactiae, s agalactiae, e coli, proteus, klebsiella, C pyogenes. Most common peracute cause is coagulase positive staphylococci.


What is the most common cause of diarrhoea in 3-7 week old goat kids?

Coccidiosis - major cause, esp housed dairy goat kids at weaning time, then kids acquire immunity with a good resistance by 5 months old, Watery, darkish scour, can be rapid dehydration, stress factors decrease immunity and predispose but management factors and kidding period all involved.


What is caseous lymphadenitis?

A chronic contagious disease mainly in sheep and goats. the causal agent is corynebacterium pseudotuberculosis. Entry is via cuts/abrasions with incubation of 2-6 months before abscesses noted in superficial LNs. Abscesses may rupture spontaneously and shed infection to others. The organism is extremely resistant, surviving on wool 1 week, in hay for 2 months and in soil for up to 8 months.


What are the clinical signs of caseous lymphadenitis in goats?

abscesses in parotid, prescapular and mandibular LN.. Internal abscesses may develop especially in the lungs, leading to the signs of respiratory disease and weight loss. Most common cause of carcase condemnation in sheep and goats in the USA.


What is caprine arthritis encephalitis?

A lentivirus closely related to maedi visna virus in sheep.


How is CAE transmitted?

milk is the major mode of transmission, also direct contact, carriers infected for life but may be symtomless.


What are the clinical signs of CAE?

Arthritis - chronic progressive synovitis in joints, tendons and bursae with progressive stiffness. Carpal joints primarily affected and may be grossly swollen. Encephalitis not seen in the UK yet - seen in kids which are bright alert but ataxic progressing to hemi or tetraplegia, hyperaesthesia, blindness, adults showing neurological signs often preceeded by other signs of CAE.


Which type of poisoning are goats susceptible to?

Susceptible to rhododendron poisoning - clinical signs include abdominal pain, depression, projectile vomiting and regurgitation. Pieris belongs to a similar family of plants as rhododendron is deadly to goats.


How should faecal worm egg counts be interpreted?

In conjunction with knowledge of general farm management, parasite control practices, climate and time of year. mean faecal egg counts of 800 indicate low moderate and high levels of GI parasitisim. Variation in egg production between genera, sheep breed, age and reproductive status, length of time that sheep have been off pasture and dry matter content of faeces. They only indicate the presence of ADULT WORMS.


What is safe grazing?

Pasture which has not been grazed by sheep or goats during the previous 12 months.


What is periparturient rise?

A major source of summer pasture larval contamination derives from the periparturient rise faecal egg output of the ewes. The periparturient rise in faecal egg output by ewes normally persists for about 6 weeks after lambing. During this period significant pasture larval contamination occurs.


How often should periparturient ewes be wormed?

In the majority of cases, clean pasture is not available for newly lambed ewes and their lambs, under these conditions conventional anthelmintic dosing of periparturient ewes needs to be repeated at 3 weekly intervals or a persistent acting anthelmintic used.


Which is the most common parasite species present during the summer months?

Usually T circumcinta. Parasitic gastroenteritis can therefore be controlled using a dosing interval of 7 or 11 weeks for oral injectable moxidectin respectively.


What are the meat withdrawal periods for oral and injectable moxidectin?

14 days for oral and 70 days for injectable.


Which parasite is most resistant to anthelmintics?

Resistance is predominantly in T circumcinta. BZ resistance is present in about 80% of lowground flocks. Resistance to both BZ and LEV is seen.


How can a diagnosis of anthelmintic resistance be made?

Drench check, faecal egg count reduction test, in vitro assays, critical efficacy studies.


Which strategies can reduce the rate of development of anthelmintic resistance?

Quarantine treatments, Reduction in anthelmintic usage (only dosing ewes, clean grazing), dose correctly for weight of heaviest in group (weigh sheep, calibrate equipment), annual drench rotation, periodic use of narrow spectrum anthelmintics, prolongation of anthelmintic activity - yarding for 24 hours.


Which is the most common type of gastrointestinal parasite in cattle?

Ostertagia ostertagi.


When is clinical disease seen with ostertagia ostertagi?

Type 1 disease is seen in young cattle during late summer and autumn of their first grazing season, type II disease is occasionally seen in yearling cattle in the late winter or spring following their first grazing season.


How does ostertagia ostertagi cause clinical disease in dairy cattle?

The majority of eggs deposited during april, may and june all reach the infective L3 stage from late summer. Ingestion of large numbers of L3 results in clinical type I disease after about 18 days. During autumn, low environmental temperatures condition a proportion of ingested L3 to become inhibited at the early L4 stage in the abomasal glands. the presence of arrested l4 in the abomasum is usually asymptomatic until late winter to spring when they simultaneously complete their development and emerge as adults (type II ostertagiosis).


How does ostertagia cause disease in beef cattle?

In spring calving herds most of the overwintered l3 are ingested and killed in the gi tracts of immune cows. Overwintered l3 which remain on the pasture mostly die before calves are old enough to ingest significant amounts of herbage is low. consequently the level of pasture contamination in late summer and autumn is low, but these calves are susceptibleto PGE during their second season grazing.


Which anthelmintics are effective against early arrested L4 ostertagia?

Albendazole, fenbdendazole, oxfendazole and macrocylic lactones.


What are the clinical signs of lungworm infection in cattle and sheep?

Larvae in the alevoli cause an eosinophilic exudate, blocking small airways, resulting in gradual onset coughing and tacypnoea. In the patent phase, there is parasitic pnuemonia with consolidation in the ventral areas of the caudal lobes, treacheitis and bronchitis causing marked coughing, tachypnoea, dyspnoea, fever and anorexia.


How is diagnosis of lungworm made?

Based on grazing history, worming history and identification of adventitious lung sounds over the caudal lobes. Identification of larvae in the faeces can be useful.


which anthelmintics should be used to treat lungworm?

ganglion blocking agents which first paralyse the worms are arguably safer than benzimidazoles and macrocyclic lactones which kill the worms immediately. Anthelmintic treatment can exacerbate clinical signs due to allergic reaction to dead parasites in the lung and may even precipitate daeth.


Can dairy calves be vaccinated for lungworm?

Dairy calves can be vaccinated with oral vaccination of gamma irradiated L3. Calves over 2 months old are given two doses separated by 4 weeks.


What is acute fascioliasis?

Caused by massive liver parenchymal damage due to the presence of up to 1000 migrating immature flukes. Acute disease is characterised by lethargy, pallor, dyspnoea and deaths of sheep of all ages from september to december.


What is chronic fascioliasis?

Caused by the presence of adult flukes in the bile ducts of the liver. the chronic disease is usually seen in february and march, and is characterised by poor body condition, anorexia, anaemia and death. Ascites and submandibular oedema are present in advanced cases.


What is the seasonal appearance of fascioliasis determined by?

The effects of moisture and temperature on the snail populations and free living stages of F hepatica. At temperatures below 10C fluke eggs don't develop and hatch and snail development is halted.


How can a diagnosis of liver fluke be made?

PM findings, identification of fluke egg in faeces, serum GLDH and GGT concentrations, ELISA serology. GLDH increase in acute disease, GGT in chronic disease.


What is the treatment of acute fascioliasis?

Triclabendazole which has good efficacy against immature flukes. When safe pasture is available, a single treattment is given before moving sheep. Safe pasture is seldom available so repeated treatments at 3 weeks intervals are required throughout the high risk period in autumn and early winter.


How can chronic fascioliasis be treated?

Any available flukicide - triclabendazole, albendazole, closantel


What is dicrocelium dendriticum?

A small lancelate liver fluke which causes disease in sheep in a few islands off the west coast of scotland. The parasite has a different life cycle - The host is infected by ingestion of ants. Adult lives in bile duct. Eggs shed in faeces. Eggs ingested by an intermediate snail host. Cercariae are released by snail in a slime ball. Then become metacercariae after being eaten by an ant.


What is monenzia expansa and how does it cause disease in sheep?

2cm long segmented tapeworms. The mature proglottids are passed in the faeces. oncosphered on pasture are ingested by forage mites. Sheep are infected by ingestion of forage mites with herbage. Adults are short lived and patent infections only persist for about 3 months. Overwinters in the forage mites. A large proportion of the lamb flock between 2 and 6 months old are often affected. Generally regarded as non pathogenic.


What is taenia ovis and how does it cause disease in sheep?

Cysticercus ovis when in the muscle of sheep. It causes numerous 1-2mm diameter white cysts. The final host is the dog. The life span of the worms is about 6 months. A single infected dog spreads infection over large areas and dogs don't develop immunity. The immune response in sheep wanes over a few months in the absence of challenge. Some cysticerci survive for up to 2 years. Affects sheep of all ages.


What is taenia multiceps and how does it cause disease in sheep?

It causes coenuris cerebralis in the CNS of sheep. the final host is the dog. Oncospheres are carried in the blood to the brain or spinal cord. Large fluid filled cysts up to 5cm across with clusters of scolices on the internal wall. Causes gid in sheep - clinical signs include circling, visual defects, gait abnormalities and paralysis.


What disease does taenia hydatigena cause in sheep?

causes cysticercus tenuicollis in the abdominal cavity. The final host is the dog. the cysts are up to 8cm in diameter in the peritoneum, associated with the surface of the liver. Very common incidental finding at PPM or slaughter. Occasionally numerous 1cm greenish subcapsular nodules in the liver are associated with massive infection and daeth of developing cysticerci.


How does echinococcus granulosus cause disease in sheep?

Hydatic cysts mainly in the liver and lungs. The final host is the dog and wild canids. Cysts with diameter up to 20cm in the liver or lungs. Occasional enormous cysts in the peritoneum. Cyst capsule contains brood capsules. Sometimes cysts branch to form daughter cysts. Usually no clinical signs - only found at slaughter. is zoonotic.


What is the larval stage of taenia saginata?

Cysticercus bovis. the final host is man, site is muscle in cattle.


What are fighting teeth in camelids?

Lower canines and laterally placed upper incisors - need cutting in males.


When should crias be castrated?

From 1.5 years old.


Why are worms in alpacas/llamas a problem?

They have low resistance so small burdens are significant - beware of co grazing with sheep. may not scour even with heavy burdens as an adaption to arid climate. Severe anaemia seen with haemonchus.


What is mycoplasma haemolamae?

- a blood parasite. Healthy animals will mount a god immune response. diagnosis by fresh blood smear, will see blue organisms on RBC surface with wrights giemsa stain.


What are the most common indications for C section in sheep?

singleton lambs of pedigree meat breeds in posterior presentation, relative foetal oversize, particularly in the immature primiparous animal with a singleton foetus, incomplete cervical dilation, previous vaginal prolapse and schmallenberg virus induced deformities.


What is the aetiology of vaginal prolapses in ewes?

excess body condition, multigravid uterus, high fibre diets particularly those containing root crops, limited exercise in housed ewes, lameness leading to prolonged periods in sternal recumbency, steep fields and subclinical hypocalcaemia.


What is the treatment of a vaginal prolapse

Effective analgesia by sacrococcygeal extradural injection allows emptying of the bladder by raising the prolapse relative to the vulva in the standing ewe thereby reducing the fold in the neck of the bladder at which point urine flows from the urethral orifice.
Plastic retention devices - shaped such that the central loop is placed within the vagina which is then held within the pelvic canal by the two side arms tightly tied to the fleece of the flanks. These can cause considerable discomfort with irritation and secondary infection of the vaginal mucosa.
Harnesses or trusses - very useful in situations where farmers detect the prolapse early and there is little superficial trauma/contamination. Faecal staining of the perineum and detection of first stage labour can become problematic when harnesses or trusses are used.


describe a sacrococcygeal extradural injection

First intercoccygeal space can be identified by digital palpation during slight vertical movement of the tail. Correct position o the needle point can be determined by failure to strike bone during travel of the needle point and lack of resistance to injection of the combined lignocaine and xylazine solution. Combined extraural injection of xylazine and lignocaine at the first intercoccygeal site provides effective analgesia permitting replacement of rectal cervical or uterine prolapses after 5 minutes with analgesia persisting for 36 hours.


What is the effect of clenbuterol on the uterus?

injected prior to surgery, used by some surgeons to aid manipulation of the gravid uterus and slow the rate of uterine contraction after removal of the calf.


What is scrapie?

it is a fatal degenerative disease that affects the nervous system of sheep and goats - it is a transmissible spongiform encephalopathy, caused by a prion.


What are the clinical signs of scrapie?

Affected animals will compulsively scrape off their fleeces against trees/fences, excessive lip smacking, altered gaits, collapse, convulsions. It usually takes more than a year and a half for clinical signs to appear.


Why do serum albumin concentrations fall in late gestation?

As immunoglobulins are manufactured and accumulate in the udder. Low serum albumin concentrations in a high percentage of ewes may also indicate chronic fasciolosis.


What is the treatment for hypothermia?

In lambs 37C give a colostrum feed, warm to 39C then return to the ewe.
In lambs > 5ho, inject 20% glucose at a rate of 10ml/kg, dry thoroughly, warm to >37C, give a colostrum feed at a rate of 50ml/kg, warm to 39C, return to the ewe, monitor closely, check dam for milk supply, disease or poor maternal behaviour.


What are the clinical signs of C pavum?

Pale green coloured, watery and occasionally blood stained dairrhoea in lambs between 2 and 20 days old


What are the clinical signs of salmonella diarrhoea in lambs?

depression, profuse green/brown coloured diarrhoea with blood, variable pyrexia, dehydration, dyspnoea, rapidly progressing to recumbency and death.


What is the most common cause of joint ill (polyarthritis) in lambs?

Streptococcus dysgalactiae


What does E rhusiopathiae cause in sheep?

In neonatal lambs a bacteraemia results in organisms settling in the joints, where they cause a fibronopurulent polyarthritis in addition to osteomyelitis and in some cases endocarditis. Morbidity can reach 40% although mortality is low. Affected lambs are stiff and may be pyrexic. In the early stages, the joints are not markedly swollen. if untreated, the disease becomes chronic and results in serious ill thrift. By this stage, the joints are markedly swollen and may be ankylosed. tx is parenteral penicillin.


What are the most common causes of mastitis in ewes?

Pasteurella haemolytica (hamhemia haemolytica) and staphylococcus aureus.


What is the treatment of coccidiosis?

Decoquinate in lamb creep feed or treatment with diclazuril.


What is the causative agent of tick borne fever?

Erlichia phagocytophilia.

In most animals the primary disease is benign. but the importance is the profound effect on the immune system. The main importance is potentiation of other infections in particular louping ill and tick pyaemia. If naive and infected during pregnancy for first time then may abort.

tx - oxytetracycline


What is louping ill?

It is a difuse non suppurative meningo encephalomyelitis in sheep caused by a flavivirus. Clinical signs vary from transient ataxia to sudden death. disease usually starts with incoordination and progreses to recumbency, convulsions, coma and death within 24-48 hours.


How is louping ill transmitted?

Ixodes ricinus


What is tick pyaemia?

Intradermal innoculation of staphylococcal bacteria by ticks feeding, causes a bacteraemia and joint ill, posterior paresis de to abscesses, abscesses in other organs, potentiated by immunosuppressive effects of tick borne fever.


What is Q fever?

Caused by coxiella burnetii, rarely can be tick borne,


What are the clinical signs of babesia?

The first sign is fever (frequently ≥106°F [41°C]), which persists throughout, and is accompanied later by inappetence, increased respiratory rate, muscle tremors, anemia, jaundice, and weight loss; hemoglobinemia and hemoglobinuria occur in the final stages. CNS involvement due to adhesion of parasitized erythrocytes in brain capillaries can occur with B bovis infections. Either constipation or diarrhea may be present. Late-term pregnant cows may abort, and temporary infertility due to transient fever may be seen in bulls.


What are the clinical signs of cobalt deficiency in lambs?

Ill thrift - frequently empty, pot bellied, depressed in appearance, may have ocular watery discharge.


What is cobalt required for?

The manufacture of vitamin B12 which is required in the liver for the utilisation of rumen derived propionic acid in energy production. Vitamin b12 is also required for the metabolism of certain S amino acids which are necessary for optimum growth and wool production.


What is methylmalonic acid?

It accumulates in the plasma of cobalt deficient sheep as a result of reduced vitamin B12 co enzyme activity. Raised plasma concentrations of MMa can be used to support a diagnosis of cobalt deficiency.


What type of breeder are the sheep and the doe?

Polyoestrus short day breeders. Most breeds have a peak fertility around october/november time.


How long is the ewes oestrus?

16-17 days.


What will happen when a teaser ram is introduced to ewes?

Works in transition period
Ewes will ovulate within 2/3 days - usually non fertile/silent heat, then the CL will have a normal lifespan and ovulate again in 18-20 days OR Cl will regess prematurely at 7 days old to produce a second silent oestrus followed by luteal phase to give fertile oestrus from 24 days to 28 days. Fertile rams should replace teasers no later than 2 weeks after teasers were introduced and due to the two peaks of oestrus within a period of 10 days, a peak of lambing should be produced over a period of two and a half weeks.


How can progestagen sponges be used in sheep?

Used alone with or without injection of pregnant mares serum gonadotrophin - induciton and syncrhonisation of oestrus, spontes inserted for 12-14 days > then sudden fall in progestogen when removed which precipitates a surge of GNRH. Rams should be introduced 36-60hours later for maximal conception rates. They should then be removed 48 hours later, then returned 2 weeks later to catch any ewes which failed to conceive to the induced oestrus. ram to ewe ratio should be 10 percent.


How can melatonin be used in the alteration of breeding cycle in sheep?

Elevated plasma melatonin in winter months > stimulates secretion of GnRH, LH and FSH, which signals a peak in reproductive performance. melatonin implants (regulin) administered subcutaneously near the base of the ear. They must be kept separate from male sheep and goats, then introduce rams 35 days after implantation. 1 ram per 40 ewes. Can use tearer rams for 14 days before fertile rams to improve conception rates to first service.


You have been called to a farm to fix several rectal prolapses in a group of 60 lb pigs. The pigs are not coughing and you notice that several of the gilts in the group also have reddened and enlarged vulvas. What could be causing both problems?

The correct answer is zearalenone. This estrogenic effect of this mycotoxin causes edema of the vulva and sometimes edema of the rectum predisposing to rectal prolapses. There are some suspected genetic predispositions for rectal prolapses, but not for the enlarged reddened vulvas.

Calcium and phosphorus balance has no effects on either of the clinical presentations described. Severe diarrhea cause by salmonellosis can lead to rectal prolapses, but diarrhea or coughing (systemic manifestations) will be common.


What are the clinical signs of polioencephalomalacia in sheep?

Blindness, initial depression, dorsiflexion of the neck, hyperexcitability, seizure activity and opisthotonus. Trauma to the superficial branch of the facial nerve on the dependent site may result in ptosis and drooped ear. Dorsomedial strabismus and spontaneous horizontal nystagmus are freuqnely present in both eyes.


What are the histological findings of PEM?

Vacuolation and cavitation of the ground substance with astrocytic swelling, neuronal shrinkage and necrosis.


What are the clinical signs of listeriosis?

Winter-sprng disease of silage fed ruminants. Outbreaks may occur within 10 days of feeding poor quality silage. Listeria that are ingested or inhaled tend to cause septicaemia, abortion and latent infection. Those that gain entry during tissues cause encephalitis via minute wounds in the buccal mucosa. Signs include depression, circling, ipsilateral hemiparesis. Clinical signs vary according to the function of the damaged cranial nerve nuclei. May propel themselves into corners or lean against walls. Facial paralysis with drooping ear, deviated muzzle, flaccip lip and lowered eyelid on the affected side develops.


What is the treatment of choice with listeria?

Penicillin, ampicillin, ceftiofur, erythromycin. drug ofchoice is penicililn.


What are the clinical signs of sarcocystis in sheep?

Pelvic limb ataxia and paresis with sheep adopting a dog sitting posture. Compressive spinal cord lesion.


What is cerebellar abiotrophy?

A familial syndrome described in 3 -4 month old charolais lambs and holstein calves. the clinical signs include lowered head carriage, intention tremors, a wide base stanced, ataxia but with preservation of strength, dysmetria. The clinical signs are progressive deterioration in neurological function with signs indicative of a cerebellar lesion.


what are the clinical signs of scrapie?

Fleece in poor condition, wool loss over flanks and tail head caused by rubbing. Cutaneous stimulation of skin over dorsal sacral area elicits a nibble response including manic lip smacking and swaying. Depression, vacant, detached appearance due to cerebral dysfunction, but with hyperaesthesia to visual, adutiroy and tactile stimuli. vision and pupillary ligh reflexes are normal. When gathered with sheepdog - affected ewes appear to collapse. Cerebellar dysfunction is indicated by postural and gait abnormalities, namely pelvic limb ataxia, hypermetria in the thoracic limbs and wide base stance.


What are the clinical signs of Visna?

Two forms - a brain form which manifests clinically as a head tilt, circling and ataxia and a spinal form which presents initially as unilateral pelvic limb consicous proprioceptive deficit.


What is the normal protein range for CSF?



What does pasteurella trehalosi cause in sheep?

Septicaemia in 6-10 month old lambs.


What are the clinical signs of pneumonic pasteurellosis?

sudden death,
dyspnoea, tachypnoea
serous ocular and nasal discharges,
frothy fluid at the mouth in the temrinal stages.
Most common to see outbreaks in May-july.
There are ecchymotic haemorrhages over the throat and over the ribs. The lungs are swollen and purple-red in hyperacute cases, and the airways contain pink stained froth.


What are the cliincal signs of mycoplasma ovipneumoniae infection?

A chronic soft cough with some mucopus nasal discharge that spreads slowly through a group of lambs. some dullness, tachypnoea, growth rates are affected


what are the clinical signs of OPA? (jaagsiekte, spa)

Loss of body condition, exercise intolerance, serous nasal discharge, afebrile, episodes of mouth breathing, then dyspnoea, tachynpoea, increased abdominal effort, fluid fathers in respiratory tract, soft cough. Tumours in lungs are enlarged and heavy, solid and grey and well demarcated. Bronchi and trachea contain copioius frothy fluid.


What are the clinical signs of maedi?

Exercise intolerance
Usually in sheep over 3yo
Neck extended, increased resp rate, flared nostrils
Dsypnoea, weight loss.
A large no of sheep also have an indurative mastitis.


What is the difference between toxoplasma infection in sheep and goats?

Goats remain infected for life and unike sheep they may abort in subsequent pregnancies so culling of infected does is advisable. chemoprophylaxis is likely to be of limited value. The toxoplasma tachyzoites are passed in milk of infected does therefore public health risk where they are dairy goats.


What is beta mannosdiosis?

an autosomal recessive lysosomal storage disease of anglo nubians. Usually bright and alert and able to suck, but often unable to stand. Head & neck tremor, nystagmus and deafness, dome shaped skull, carpal contracture, fetlock hyperextension, thickened skin.


What is the cause of coenurosis cerebralis?

Conurosis cerebralis is the cystic stage of taenia multiceps.


Which mastitis pathogens commonly affect goats?

Staph aureus, strep uberis, E coli, Coagulase positive stpahylococci most common cause of peracute mastitis.


Which goats are prone to gynaecomastia?

British saanen and saanen males.


What is caseous lymphadenitis?

A chronic contagious disease, mainly in sheep and goats, caused by corynebacterium pseudotuberculosis. entry via cuts/abrasians with incubation of 2-6 month before abscesses noted in superficial LNs. Abscesses may rupture spontaneously and shed infection to others. Abscesses especially in parotid, prescapular and mandibular LNs. Internal abscesses may develop especially in the lungs, leading to signs of respiratory disease and weight loss. Diagnosis by culture of organism via sterile aspirate of abscess. New ELISA to detect serum antibodies against PLD in sheep.


What is goat pox?

Staphylococcal dermatitis - small pustules and eruptions over the body and back and on th udder. infection associated with staphylococcus aureus. Tx with penicillin.


What is Caprine arthritis encephalitis?

A lentivirus closely related to maedi visna virus in sheep.
Milk is the major mode of transmission but also direct contact. Arthritis is the most common form seen in yearlings to adults, chronic progressive synovitis in joints, afebrile, bright, good appetite, gradual loss of condition to emaciation. Encephalitis not seen in the UK yet. Signs - knuckling of fetlocks, circling, paresis, hyperaesthesia, blindness.
also causes pneumonia and hard udder.


What type of poisoning are goats susceptible to?

Rhododendron poisoning. Clinical signs include abdominal pain, depression, projectile vomiting and regurgitation.


What is the cause of sheep scab?

Psoroptes ovis. The scab mite causes a hypersensitivity as the animal exudes protein rich fluid. Mite mouth parts do not abrade the skin but feed on the surface and are highly pruritic. Sheep exhibit abnormal behaviour due to pruritus and discomfort.


How can sheep scab be controlled?

One off autumn acaricide treatment is required. Doramecin is siutable. handling pens and fields should be considered as a source of re infection for at least 17 days after removal of untreated sheep. Ideally they should be treated and quarantined to ensure that any scab mites are killed before returning. Plunge dipping in pyrethryoid based solutions is proven method of treatment. pour ons/showers are ineffective for the treatment and control of sheep scab. Two subcut injections of invermectin or a single im injection of doramectin are best, but neither provide residual infection.
a single subcut injection of moxidectin provides residual protection against sheep scab for atleast 28 days but two injections 10 days apart are recommended for the treatment of scab outbreaks.


How can blowfly strike be controlled?

Control of parasites and footrot
Baited fly traps
Plunge dipping in organophosphates or cypermethrin


What is footrot in sheep?

F necrophorum penetrates stratum corneum, then D nodosus proteases cause hoof separation and alow deeper penetration of F necrophorum.


What is the cause of scald?

It is the first stage in the pathogenesis of footrot. caused by F necrophorum infection alone, and does not require Dnodosus. it is clinicaly indistinguishable from benign footrot and early virulent footrot.


What are the clinical signs of scald?

The interdigital skin is inflamed and swollen with white necrotc material and may progress to erosions. there is no under running of horn and no smell. tx with 10% zinc sulphate solution footbath.


What is the cause of ovine digital dermatitis?

A new varient footrot - associated with a spirochaete, severe lameness, full thickness skin ucleration at the coronary band, hoof wall under run from coronary band and often shed to expose the sensitive laminae. Footbathing with tylosin or lincomycin appears to be effective for prevention and treatment.


What is shelly toe?

Separation ofthe superficial hoof wall close to the white line at the toe. commonly seen in sheep grazing on lush pasture. lameness when impacted with soil and faecal material.


What are the clinical signs of new varient footrot?

Severe lameness, full thickness skin ulceration at the coronary band, hoof wall under run from coronary band, often shed to expose the sensitive laminae.


How many chambers do alpacas have in the stomach?

3 - c1 rumen, c2 reticulum, c3 - only caudal 20% acidic, glandular stomach. they are foregut fermenters.


How long is the gestation of a camelid?

approx 340 days +- 25 days.


How can you terminate a pregnancy in a camelid?

PGF2a from 6-100 days. or PGF2a within 10 days of due date for induction of parturition.


What is mycoplasma haemolamnae?

A blood parasite of camelids. Seen as blue organisms on RBC surface, on a wright geimsa stain. they cause anaemia but healthy animals mount a good immune response. tx oxytetracycline.


What is the cause of alpaca fever?

Streptococcus equi subsp zooepidemicus. Causes anorexia, recumbency, pyrexia, sudden death, colic.


Which species parasitise the abomasum in cattle?

Ostertagia ostertagi
Haemonchus contortus


Which species parasitise the small intestine in cattle?

Cooperia spp, trichostrongylus, nematodirus helvetianus


What is the life cycle of ostertagia ostertagi?

Larvae develop in and disrupt the abomasal gastric glands. The prepatent period is about 18 days after which the adults emerge and pathology occurs. the Ph of the abomasum rises as the hcl secreting cells are replaced by undifferentiated cells. There is albumin leakage through the amomasal mucosa resulting in hypoproteinaemia. Clinical signs include scour, ill thrift, suboptimal weight gains and reduced milk yield. Eggs are shed in faeces > L1 develop in faeces > L2 develop in faeces > L3 are infective larvae on herbage > L3 enter gastric glands.


What is the life cycle of teldorsagia circumcinta (the brown stomach worm) in sheep?

Abomasal parasites that act similarly to O ostertagia. the are about 1.5cm long and hair like. Disease is seen in summer & autumn months. T circumcinta causes hyperplastic inflammation of the abomasal mucosa causing replacement of the Hcl secreting cells. Clinical signs - watery diarrhoea, loss of appetite, weight loss.


What is the difference between type I and II ostertagiosis?

I - occurs when there is ingestion of large numbers of L3.
II - Occurs when low autumn temperatures allow a proportion of ingested L3 to become arrested in L4 form in the abomasal glands. this process is normally asymptomatic. Disease occurs then in late winter/early spring when the aarrested L4 simultaneously emerge as adults. Type II disease increases when there is a dry summer followed by autumn rains.


How does the epidemiology of nematodirus battus differ?

Development of L3 occurs within he egg, therefore the L3 can survive freezing and very low temperatures as it is still inside the egg. Hatching and release of L3 only occurs after a period of cold exposure followed by daily max temp above 10 degrees. therefore eggs that are shed one year will hatch the following year. Hatching normally occurs en masse during may- june. Acute disease is seen when the hatch coincides with the presence of susceptible grazing lambs. therefore the life cycle only involves lambs essentially.


What technique can be used to detect dictyocaulus vivparus?

L1 are shed in the faeces not eggs - so use baerman's.


What is the life cycle of Dictyocaulus viviparus?

Adults in trachea and bronchi > lay eggs which contain L1, which hatch and are then coughed up swallowed and passed in faeces > develop to L3 > ingested and penetrate mucosa >migrate to LN > develop to L4 > migrate via lymphatics via lungs. Prepatent periods is 21-28 days. L3 may be spread by earthworms.


When should you dose sheep and lambs with suppressive anthelmintic treatments?

Ewes should be dosed at lambing to prevent them from multiplying overwintered larvae during peripartruient rise.
lambs should be dosed before weaning for nematodirus control.
Lambs should be treated regularly throughout the summer to reduce amount of shedding.


What wormer should be used to treat severe cases of lungworm in cattle?

Levamisole - this paralyzes the worms rather than killing them immediately


What is best to worm sheep with before quarantining as new arrivals?

A combination of a macrocyclic lactone and monepantel


Describe the life cycle of the fluke fasciola hepatica?

Mature flukes in bile ducts lay up to 5000 eggs. > miracidia develop in the egg which requires temperatures >10C > miracidia swim until they find a snail host > the mud snail galba truncatula > Each miracidium multiplies asexually through sporocysts and redia to several hundred cerceriae > cercariae swim and encyst as metacercariae on vegetation > Metacercariae are ingested by the final host.


Which anthelmintis treat fluke?

Triclabendazole - kills all stages
Closantel - kills 6 week immature - adult fluke in sheep
Nitroxynil - kills 6 week immature - adult fluke
Oxyclozanide - only removes adults.