Sheep Flashcards
Describe the foetal development during pregnancy in relation to dietary energy supply in the second trimester
Difficult to be certain of influence because many other factors influence lamb birthweight. weather and grazing conditions need to be severe for 10-14 days to seriously impair placental development. reduced lamb birthweight can occur when placental development has been limited by the competition in the uterus for caruncles resulting in a reduced number of placentomes per foetus. Twins with disproportionate weights e.g 5.5 kg versus 2.5kg probably indicates that three embryos implanted and underwent early foetal development but one foetus failed to develop further and was resorbed and limited number of caruncles available to remaining foetus.
What are the most fundamental factors to ensure a good start for a lamb during first hourts of life?
Lamb birthweight, ewe body condition score, and colostrum accumulation at lambing. Adequate nutrition during the last six weeks of pregnancy when 75 percent of foetal growth occurs is essential to ensure appropriate lamb birthweight.
What effect does under nutrition in late gestation have?
Reduced lamb birthweight and inadequate accumulation of colostrum in the udder. Many studies have found significantly higher lamb perinatal mortality in the progeny of underfed ewes with the effects greater in triplet than twin lambs, singletons largely unaffected by dam nutritional status.
How can dietary energy supply relative to metabolic demands be determined in late gestation?
by measuring ewes serum or plasma 3-OH butyrate concentration. Increased 3-OH butyrate values reflect inefficient fatty acid utilisation caused by high glucose demand from the developing foetuses not matched by dietary proprionate or glucogenic amino acid supply.
Describe what should be done on a farm visit as part of a veterinary flock health plan?
Ewes due to lamb during the first week should be body condition scored and blood sampled four to five weeks before the start of lambing time thereby allowing sufficient time to implement dietary changes. ewe lambs and gimmers should be avoided as they have significantly more singletons and may give a skewed poplation. A random sample thereafter of 15-20 ewes should be blood sampled. if the flock has been scanned to determine foetal number an equal number of twin and triplet bearing ewes should be sampled, there is little benefit in collecting samples from ewes with singletons other than to establish reference values. Details of the diet, forage analysis and future alterations should be noted and feed allocations checked on weigh scales.
How should 3-OH butyrate blood samples be interpreted?
A range of concentrations is oftten encountered in a flock test largely in relation to foetal number, thus a more reliable interpretation of results can be afforded those flocks which have determined foetal number by prior ultrasound scanning. the average value should be determined with a target mean 3-oh butyrate concentration below 1.0mmol/l. 3-Oh butyrate concentrations above 1.6mmol/l in individual ewes represent severe energy underfeeding with the likelihood of pregnancy toxaemia developing as pregnancy advances and foetal energy requirements increase further unless dietary changes are implemented.
How can protein status be evaluated?
blood samples can be analysed for BUn which indicates short term protein intake and albumin which reflects longer term protein status. care must be exercised with interpretation of these parameters as recent feeding can increase BUN concentration and blood samples should be collected either before concentrate feeding or at least four hours to avoid post prandial increases. Low BUN concentrations indicate a shortage of rumen degradable protein. Serum albumin concentrations fall during the last month of gestation as immunoglobulins are manufactured and accumulate in the udder thus serum albumin concentrations in the region of 26-30g/l are normal during the last month of gestation. Low serum albumin concentrations in a high percentage of ewes may also indicate chronic fasciolosis.
When should ewes be vaccinated?
Ewes must be vaccinated against the clostridial diseases four weeks before lambing. it is advisable to vaccinate the flcok as two separate groups with the later lambing ewes vaccinated one week to 10 days later than those ewes lambing during the first week. The fleeces must be dry when they are vaccinated and care must be taken to ensure correct subcut injection of every ewe.
How does pre partum nutrition have an effect on Perinatal lamb mortality?
Severe maternal undernutrition during mid pregnancy results in inadequate placental development. inadequate placental development 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. Regardless of other factors, lambs born to 55-60kg ewes with birthweights below 3kg and greater than 5.5kg suffer the highest rates of perinatal mortality. optimum lamb birthweights depend on breed.
What is the lambing percentage?
The number of lams born and surviving until a definite event such as marking or weaning per 100 ewes mated. Targets vary depending on the sheep breed and production system. Optimisation is critical to the profitability of most sheep flocks irrespective of the production system.
What events determine the lambing percentage?
Oestrus behaviour, ovulation rate, fertilisation, conception, foetal development, foetal surviva/abortion, ewe deaths, perinatal lamb mortality, lamb losses from 1 week old to weaning. Perinatal lamb mortality difficult to quantify in hill and extensively managed flocks.
How does dystocia cause perinatal lamb losses?
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 occurring during parturition and subsequent infection may compromise maternal behaviour. The causes of birth stress are poor maternal pelvic conformation, foetal oversize, malpresenteed lambs, partial uterine inertia in polytocous ewes, vaginal prolapse, ringworm and unskilled shepherding.
How much colostrum does a lamb need? What happens to lambs who do not get enough energy?
Healthy lambs are born with limited energy reserves of plasma glucose and fructose, liver glycogen and brown fat. in physiologically compromised lambs these reserves are depleted or absent. starved lambs rapidly become hypoglycaemic, are weak, lethargic and unable to maintain body temperature. An average 5kg lamb requires about 1L of colostrum during its 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 disease.
Describe the different possible reasons for lamb starvation?
Genotype, inexperienced mother, undernutrition of ewe, dystocia, concurrent diseases of ewe, mastitis, multiple births. Lamb - genotype, multiple litters, birth stress, prenatal malnutrition, hypthermia, infectious disease. Extrinsic reasons - high stocking density of lambing ewes, disturbance of lambing or newly lambed ewes, human interference, poor pasture availability near to the lambing site, exposure. Different factors may be important in different flocks and different seasons all with the same results.
Describe a PM of a lamb
weigh lambs, examine feet, umbilical cord, check for meconium staining, trauma, swellings, other physical abnormalities, examine brown fat, clotted milk in the abomasum, note blood in the peritoneum and liver capsule rupture, examine lungs to determine if they are inflated or not, look for submandibular or other subcutaneous oedema, examine and weigh thyroid glands, note evidence of sepsis or inflammation.
What management practices can be utilised to minimise perinatal mortality of lambs?
Adequate maternal nutrition - correct feeding of the dam throughout pregnancy. Dystocia - selection of replacement ewes, permanent marking and culling of problem ewes, selection of terminal sires, use of ram harnesses, weighing/body condition scoring and ultrasound scanning, careful shepherding, employment of sufficient skilled labour. Adequate early lamb nutrition - management practices aimed at ensuring adequate nutrition of the pregnant ewe and prevention of dystocia, selection for mothering ability, inexperience in ewe lambs or gimmes, skilled labour, essential lambing kit. When provided when adequate neonatal care, even lambs suffering from mild birth stress or pre partum undernutrition can survive. the provision of adequate shelter is an essential component of such care on all farms.
What are the clinical signs of hypothermia
Rectal temperature 39-40 - healthy lamb exhibiting normal suckling behaviour.
Rectal temp 37-39 - weak, still capable of following the dam and suckling.
<37 - ambulatory, weak and depressed, may stand with an arched back, hollow flanks and lowered head, sometimes sheltering close to the ewes udder but is unable to suckle. clinical signs rapidly progress to recumbency coma and death.
What is the treatment of moderate hypothermia?
(37-39) - dry thoroughly,ensure a colostrum or milk feed, return o ewe, supervise closely. lambing buildings should be draught free and all round shelter should always be available in outdoor lambing fields.
What is the treatment of severe hypothermia in a lamb under 5 hours old?
dry thoroughly, warm to >37, give a colostrum feed at 50ml/kg , warm to 39C, return to the ewe, monitor closely and check dam for milk supply, disease or poor maternal behaviour.
what is the treatment of hypothermic lambs over 5 hours 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 disease or poor maternal behaviour. variations of moredun type lamb heater are preferable to heat lamps for warming lambs. Severely hypothermic lambs over 5 hours old are hypglycaemic. warming results in increased cerebral metabolism which rapidly leads to convulsions coma and death if the hypgoclyaemia is not first corrected by Intraperitoneal administration of glucose. oral administration of fluids to hypothermic lambs causes regurgitation and inhalation asphyxia or pneumonia.
What is watery Mouth Disease?
A disease of lambs 1-3 days old characterised by lethargy, profus salivation and abdominal distension. Poor treatment response in advanced cases. Disease is seen under all management systems but morbidity rates highest in intensive indoor lambing flocks of prolific ewes. Triplets more likely to be affected. Watery mouth follows reduced or delayed colostrum intake and is essentially a generalised endotoxaemia. The mouth is cold and the commissures of the lips and lower jaw wet due to drooling of the saliva. Frequently dehydrated with abdominal distension. Rectal temperature may be normal but extremities often cold. Usually no faeces in distal rectom. Treat with Iv fluniixin, oral dextrose electrolyte solution, enemas, metoclopramide, broad spectrum systemic antibiotics. Prevention - coorrect nutrition of the pregnant ewe, management of abortion and dystocia, adequate supervision to ensure all lambs suckle or receive 50ml/kg of colostrum in first hour, maintenance of a clean lambing environment, prophylactic use of oral aminoglycoside antibiotics administered to all lambs within 15 minutes of birth.
How do viral diseases of lambs cause enteritis?
Enteric viruses do not appear to cause primary disease in lambs, although lambs may be infected during the first week of life. They iinvade small intestinal villous epithelial cells causing villous atrophy and compensatory crypt cell proliferation, resulting in decreased absorption and increased secretion. The main pathogenic role of enteric viruses is to enable the establishment of other enteric infections.
How does Cryptosporidiosis cause enteritis in lambs?
Cryptosporidium parvum is not species specific and hence potentially zoonotic. C parvum infection causes villous atrophy of the distal small intestine leading to malabsorption, secondary fermentation and diarrhoea. C parvum alone seldom causes severe disease in lambs however if environmental oocyst contamination is high or if the lambs are otherwise compromised or stressed the organism may cause acute onset, pale green coloured, watery and occasionally blood stained diarrhoea in lambs between 2 and 20 days old. Treatment is based on oral fluid therapy. Control depends on hygiene and the regular movement of susceptible lambs to a cleaner environment.
How does salmonellosis cause enteritis in lambs? how is diagnosis confirmed?
Outbreaks in lambs are rare and usually follow the purchase of infected carrier sheep or calves. Mot cases are caused by salmonella typhimurium or salmonella dublin although outbreaks associated with exotic salmonellae have been reported. Salmonella spp cause severe intestinal inflammation, destroying the absorptive capacity and stimulating secretion. Salmonella spp are also invasive leading to bacteraemia and infection of other organs. Endotoxins are released into the systemic circulation on bacterial death further resulting in depreession, circulatory failure and collapse. Profuse green/brown coloured blood stained diarrhoea with variable pyrexia, dehydration and dyspnoea, rapidly progressing to recumbency and death. Diagnosis is confirmed by faecal culture or culture from liver, gall bladder small intestine and mesenteric lymph nodes at PM examination. Treatment success with intensive fluid therapy, broad spectrum systemic antibiotics and flunixin meglumine is variable and lambs which recover are ill thriven and may be carriers.
How does enterotoxigenic E. coli cause Enteritis in lambs?
E. coli possess K99 Adherence pilli 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. Control and prevention depend on strict hygiene, ensuring adequate colostrum status and immediate isolation of sick lambs. to control the disease ewes can be immunised using a vaccine containing k99 E. coli, aministered at the same time as clostridial vaccine.
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 multiiplication in other organ systems and subsequent polyarthritis, omphalophlebitis, endocarditis or meningitis.
How does meningitis affect lambs?
Bacterial meningitis occurs most commonly in lambs 2-4 weeks old. the clinical signs are isolation from the dam and failure to suckle with episcleral 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 are the clinical signs of joint ill? (polyarthritis)
polyarthritis may occur in lambs as young as 5 days old and is characterised by sudden onset lameness with pain, heat and fluctuating swelling of several limb joints, leading to poor suckling behaviour and ill thrift. At PM, incised joints contain pus, synovial membranes are thickened and congested and articular surfaces are eroded. Streptococcus dysgalactiae has been identified as an important cause of polyarthritis in lowland flocks. Infection may be acquired from the dams teats or milk and morbidity rates can be high, despite good hygiene and colostrum management. In many flocks the disease recurs in subsequent yeras.
What is navel ill?
Omphalophlebitis may follow bacteraemia or infection of the umbilical vessels and urachus from a contaminated environment. Affected lambs may adopt a hunched back stance with poor body condition ahd holow flanks due to poor suckling behaviour. The navel is moist, swollen and painful and may exude purulent material. swelling may continue internally along the round ligament of the bladder or along the falciform ligament to the liver, detected by pain on palpation. Concurrent signs of systemic infection may also be noted.
Describe management practices to prevent meningitis, joint ill and navel ill?
Correct maternal nutition, control of abortion and prevention of dystocia are essential to ensure optimal physiological adaptation to extra uterine life. to further minimise the prevalence of infectious diseases - employ sufficient skilled assistants, install good access to lambing pens and good lighting, aim for a compact lambing period, maintain strict hygiene of lambing accommodation - stocking rate and pens. dip all lambs navels in strong iodine solution at birth. ensure that all lambs receive adequate colostrum within first 4 hours of life, hot water and a full clean laming kit should be easily available, check all penned lambs regularly for signs of brightness and full stomachs.
How does erysipelothrix rhusiopathiae infection affect lambs?
E rhusiopathiae 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 as they acquire other forms of joint ill. Older lambs usually becoe infected via docking or castration wounds. A bacteraemia in neonatal lambs results in organisms settlingi n the joints where they cause a fibriinopurulent polyarthrtis in addition to osteomyelitis and sometimes endocarditis. Affected lambs are stiff and pyrexic. Joints are not markedly swollen in early stages. If untreated becomes chronic and results in serious ill thrift. Joints then become markedly swollen and may be ankylosed. Treatment with parenteral penicillin high doses in early stages is effective. Control requires good husbandry and management. Vaccination in problem flocks with two doses of bacterin, 4-6 weeks apart in the first year and one booster 3-4 weeks before lambing in subsquent years is effective.
What bacterium may cause liver abscessation?
Navel infection with fusobacterium necrophorum can result in the formation of characteristic white spot, 2-10m diameter, abscesses in the liver and secondary spread to joints and lungs. Necrobacillosis is usually associated with poor environmental hygiene and poor passive immunity.
What are the clinical signs of iodine deficiency in lambs? How is diagnosis made?
Goitre in newborn lambs. Lambs with congenital goitre may be pot bellid in appearance and wool is scant and lacks crimp. lambs from same litter can be affected to different extremes. animals with severe goiter usually die son after birth. high lamb losses occur duing adverse weather conditions due to starvation/hypothermia or stillbiths where the foetal membranes still cover the lambs nose. This is due to the role of iodine iin thyroid hormones in foetal maturation and thermoregulation. Severe goitre is confirmed at PM and by histological examination of the thyroid gland. Production responses, have been recorded in flocks wwith no clinical evidence of goitre. when thyroid:body weights of newborn lambs exceeds 0.4g/kg - likely to benefit from supplementation of iodine. Pasture iodiine concentrations unhelpful due to role of goitrogens in inducing deficiency. Controlled supplementation trials provide accurate information about flock iodine status but are not always a practical diagnostic method. Iodine deficiency can be prevented by injecting ewes before mating with an intramuscular injection of iodised oil, although such supplementation is expensive and laborious due to high viscosity of the product.
Describe Mastitis infection in ewes and the clinical signs?
Bacterial infection of the udder by bacteria staphylococcus aureus or pasteurella haemolytica. S aureus present on the teats of all ewes and P haemolytica found in mouths of most young lambs. Mastitis occurs when these bacteria have the opportunity to enter the normally protective teat canal. This can occur when the ewes milk supply is insufficient, resulting in excessive suckling and teat injry, orf lesions or exposure to cold winds. Treatment seldom Successful in cases where udder is purple coloured and cold. In survivors - ill thrifty and skin of udder may slough, revealing raw glandular tissue. Susceptible to flystrike. humane destruction recommended. Less severe cases respond to abx treatment but subsequently require culling. prevention depends on identifying predisposing factors - poor milk production, body condition and protein nutrition of ewes during the last third of pregnancy. orf can be controlled by vaccination. mastitis may go unrecognised during the acute stages of the disease, but is later identified by the presence of hard swellings within the udder. Prevent with dry ewe mastitis tubes/tilmicosin iinjections.
Describe coccidiosis in sheep
Outbreaks are caused by Eimeria crandallis and E ovinoidalis. Most outbreaks occur in 4-8 week old lambs or older naive animals weaned onto heavily contaminated small paddocks. Characterised by acute onset diarrhoea, dullness, anorexia, dehydration and weight loss affecting a high proportion of the lamb flock. Following ingstion 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. Oocysts are shed in faeces, further contaminating the environment. Under cool moist conditions many oocysts survive over winter in buildings and on pasture. oocyst shedding by healthy ewes also contributes to the environmental contamination. Severity of disease is proportional to the level of environmental oocyst contamination. Early born lambs may not ingest sufficient oocysts to become clinically affected and develop immunity, but contribute significantly to the contamination of the environment and disease in later born lambs. Diagnosis based on history of intensive lamb management and clinical signs, faecal oocyst counts, (may be present without causing disease). diagnosis usually confirmed by PM findings. Outbreaks usually managed by whole flock treatment with sulphonamide drugs and avoidance of intensive grazing. 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.
Describe Urolithiasis In adult sheep. What is the cause of urolithiasis and the prognosis?
disease of feeding wether lambs, associated with precipitation of solutes from urine to form a sludge which results in blockage of the urethra. usual sites of obstruction are the vermiform appendage and sigmoid flexure. Most outbreaks are associatd with intensive concentrate feeding and are due to combinations of calcium magnesium phosphate and magnesium ammonium phosphate calculi. Cereal diets and beet pulp are low in calcium and high in phosphorus cause increased urinary output of phosphorus. the problem is compounded by addition of magnesium to the diet, so ewe rations should never be fed to housed wether lambs. Clinical signs - anorexia, discomfort, frequent straining and dribbling small amounts of urine. Abdomen and prepuce become swollen ddue to leakage of urine into subcutaneous tissues which eventually slough. Calculi at the vermiform appendage are clinically obvious. Sevrely affected cases can be treated in the short term by amputation of the urethral process or by pelvic urethrotomy but long term prognosis is poor because of hydronephrosis The most important consideration should be prevention of further cases. Ration should be checked for phosphate and magnesium levels and altered accordingly. acidification of the urine by feed withdrawal for 24 hours and daily dosing with 7-10g of ammonium chloride in solution reduces likelihood of calculus foormation.
What is tick borne fever?
Caused by erlichia phagocytophilia. In most animals the primary disease is benign, the importance of the disease is its profound effect on the immune system. The disease begins with a sudden high fever of 4-22 days duration, but the most important effect is intracellular infection of white blood cells. most infected animals become carriers and suffer periodic spontaneous relapses. 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 of tick borne fever is potentiation of other infections in particular louping ill and tick pyaemia. the two groups of sheep at greatest risk are new born lambs and bought in pregnant ewes. Most young lambs are infected within the first two weeks of life. Diagnosis of tick borne fever edpends on knowledge of tick activity and the identification of rickettsias in gimesa stained blood smears. Positive serology indicates exposure. PRevention is by dipping - not advised - or applying back line pour on treatments of flumethrin or high cis cypermethrin when new born lambs are introduced to the hill. Anaplasma phagocytophilia is sensitive to oxytetracycline and some hill farmers combine pour on treatment with a single prophylactic injection of long acting oxytetracycline.
What is louping ill?
An important diffuse non suppurative meningoencephalomyelitis in sheep caused by a flavivirus. Clinical signs vary from transient ataxia to sudden death. Disease usually starts with incoordination and progresses to recumbency, convulsions, coma and death within 24-48 hours. In some non fatal cases, residual torticollis or posterior paralysis may remain for several months. Transmission of louping ill is dependent on ixodes ricinus and is linked to the annual periodicity of ick feeding activity. In endemic louping ill areas, losses are principally in lambs and replacement breeding stock. older sheep are immune. colostrum derived antibodies provide good protection in lambs born to immune ewes so only lambs acquiring insufficient colostral antibody die in their first spring. Lambs protected by colostral antibodies are fully susceptible during their second spring, most losses are in ewe lambs retained for breeding. When sheep are concurrently affected by tick borne fever the disease is much more severe, mortality sometimes being 100%. In addition to the nervous sigs these sheep may also show signs of dysentery due to superinfection with fungi. Diagnosis based on clinical signs, knowledge of infected tick activity or recent transportation from an infected area. Histological examination of the brain and virus isolation from brain tissue can be used to confirm the diagnosis. Serum can be submitted to veterinary laboratory for an ELISA test and positive result indicates exposure. Vaccine - in autumn or following spring before ticks become active. All purchased sheep are vaccinated once at least 28 days before exposure to the tick infested pasture. human infection can result from contact between skin cuts and blood from viraemic animals so care should be taken when handling suspected clinical cases. human infection can also be via the oral route and might occur through ingestion of uncooked meat.
What is tick pyaemia?
Intradermal nnoculation nof staphylococcus aureus a commensal on the skin surface, causes a bacteraemia and joint ill which results from feeding activity of Ixodes ricinus. The disease is potentiated by the effect of E phagocytophilia. Spinal abscesses, leading to osterior paresis are common. Abscessation of other internal organs may also occur.
What are clostridial bacteria? what diseases do they cause?
Anaerobic, spore forming, toxin producing organisms which are normally present in soil, faeces or intestinal contents. with the exceptioin of botulism, clostridial diseases result from toxin production following the opportunistic, rapid multiplication of bacteria in the animal. A variety of management and other factors enable such rapid clostridial multiplication.
How do Clostridium perfringens cause entertoxaemias?
Normally present in the intestinal contents of sheep, under certain conditions can cause enterotoxaemias. In healthy animals a balance exists between multiplication and passage into faeces, maintaining a low level of infection. C perfringens is saccharolytic and can multiply rapidly when the anaerobic conditions in the abomasum and small intestine are combined with the presence of large quantities of fermentable carbohydrate. These conditions occur when sudden changes in diet enable the overflow of undigested feed into the small intestine. conditions which result in gut stasis, eg insuffcient dietary fibre or severe GI parasitism may also contribute to build up of toxins in the intestine. C Perfringens bacteria produce non toxic prototoxins which are converted to toxins by the action of digestive enzymes and the pathology of entertoxaemia is determined by the combination and amounts of these toxins.
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. 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.
What is pulpy kidney?
A common peracute and usually fatal dsiease 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 between 6 months and 1 year old. associated with a change in the diet. animals are occasionally seen alive with Hyperaesthesia and ataxia, which progresses rapidly to recumbency, opistotonus, convulsions and death, signs associated with focal symmetrical encephalomalacia and diarrhoea are seen in lambs which live longer. in extreme cases, losses of between 10-15% have been reported.
What is struck? How is diagnosis of enterotoxaemia made?
A rare peracute disease of adult shepe, caused by a beta toxin of clostridium perfringens type C. Causes enteritis , peritonitis and sudden death. The initial diagnosis of enterotoxaemia is made on basis of history of sudden death in well grown unvaccinated lambs fed on carbohydrate rich diet, supported by PM findings. positive test results for ELISA for identification of toxins in intestinal contents or peritoneal fluid support but do not confirm the diagnosis because immune animals may have high concentrations of toxin but not suffer from its effect. diagnosis confirmed by brain histopathology.
How can enterotoxaemia be prevented?
Achieved through vaccination. 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. This pre lambing booster also ensures passive protection of lambs up to 16 weeks of age. lambs born to vaccinated dams should receive a first sensitiser dose about 8-12 weeks old followed by a second booster at least 4 weeks later. Vaccination should be combined with good stock husbandry including good hygiene at lambing, the insurance of adequate early colostrum intake and careful introduction to improved planes of nutrition.
What is blackleg?
It is caused by toxins produced by clostridium chauvoei which survive in soil for many yeras. outbreaks usually require predisposing factor such as docking, castration, shearing under dirty conditions, using dirty needles for routine vaccination or wintering hoggs on route crops. IN ewes often associated with poor lambing hygiene and dystocia. Clinical signs depend on site of infection - when limbs are involved sheep become stiff and unable to move. there is subcut oedema and gas production but these signs can be difficult to determine because of the presence of the fleece. Cases associated with parturition injury are characterised by the erosion of the vulval mucosa and vulval and perineal oedema with dark red and gassy necrosis extending to adjacent muscles. Blood stained droplets may ooze from the skin. Blackquarter metritis occasionally occurs before lambing in which case the entire uterus may be oedematous and foetus dead and anasarcous. When the head is affected, as some times occurs in rams during the autumn following fighting the whole face may swell. Such cases may bleed from the onse and are referred to as malignant oedema. The gross PM signs of blackleg in freshly dead animals are characteristic but when animals have been dead for a few hours the signs may become difficult to interpret due to post portem autolysis. confirmation of the diagnosis can be gained frmo histopathology of the formalin fixe sections from the edge of the lesions or from positive fluorescent antibody tests on smears of unfixed tissue from the periphery of lesions.
Describe blackleg disease in cattle
Disease occurs sporadically as well as associated with predisposing factors such as rough handling in dirty yards. If seen alive affected cattle may be pyrexic, depressed, tachypnoeic and anorexic. They are stiff and lame in one or more limbs and there is swelling and pain at the site of infection. any skeletal muscle mass can be affected althought the most common sites are the upper limbs and spinal muscles. Occasionally the vulva and perineal region is affected. wounds may discharge rancid smelling serosanguinous fluid. over a period of 12 -24 hours the disease progresses with the development of tremors, ataxia, recumbency coma and death. Treatment of early cases involves cleaning and surgical debridement of any obvious wound, high doses of penicillin, supportive fluid therapy and high doses of corticosteroids but is seldom effective. Control is achieved by vaccination with a formalin killed bacteria and toxoid. These are administered to cattle as a single vaccine but in sheep are usually included in a multi component vaccine along with other clostridial oxoids. Additional hygiene precuations 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 hseep intestinal contents. Under anaerobic conditions the bacteria become motile and it is believed that some pass through the intestinal wall and become lodged as spores in the livers of healthy animals. liver fluke larvae 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. Other forms of liver damage may also trigger black disease. Characterised by sudden deaths following a short incubatiion period. losses can occur throughout the high risk period of liver fluke larval migration which often amount to 5% and occasionally reach 30%. diagnosis based on history and knowledge of migrating liver fluke larvae and PM findings. Carcases uatolyse very rapidly. Subcut blood vesels are engorged giving the characteristic black colour, liver is dark and contains distinct paler areas of necrosis. Usually evidence of recent migration of liver fluke larvae. Diagnosis supported by identification of large gram positive rods in smears of cut liver tissue and positive fluorescent antibody test results from fresh air dried smears of liver tissue. PM invasion of Csepticum often overgrows C novyi. Control by vaccination.
What is tetanus? What are the clinical signs?
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 the soil and causes disease when spores in the environment enter deep wounds with devitalised tissue. in sheep the disease is commonly associated iwht docking wounds, especially following the use of rubber rings. 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. Animals become laterally recumbent with saw horse apperance due to extension of neck, thoracic and pelvic limbs. Extremely painful disease, humane destruction recommended. Eventually die fmor asphyxiation due to paralysis of respiratory muscles. No specific gross PM signs so diagnosis of tetanus depends on interpretation of history and clinical signs. early cases can be succesfully treated with tetanus antitoxin, abx and anti inflammatory drugs, prognosis is always guarded and treatment is expensive. outbreaks of tetanus in lambs usually triggered by a specific event such as docking and incubation period is 1-3 weeks. Tetanus antitoxin can provide immediate protection of lambs for about 3 weeks - in face of outbreak. PRevention is by vaccination. it is important that ewes are vaccinated to ensure passive protection of their lambs. in problem flocks the method of docking could be changed or the routine use of tetanus antitoxin at docking might be considered.
What are the common causes of ill thrift in weaned lambs? How can ill thrift be investigated?
Determination of the causes of ill thrift in lambs begins with a relevant history, focussed on important common causes of ill thrift in lambs. Common causes; Poor nutrition, parasitic gastroenteritis, cobalt deficiency, selenium deficiiency, liver fluke, respiratory disease lameness, sheep scab, coccidiosis, border disease. Basic history should include farming system, feed management, times of lambing and weaning, worming regime and anthelmintic used, previous trace element problems and supplements used, observations of scouring, coughing, lameness and skin disease, weather conditions. Clinical examination must be focussed on the whole flock rather than solely on the detailed examination of a few ill thrifty individuals which may not be representative of the overall problem. Examination of the flock should include careful observations of pasture and feed availability over the whole farm, variation in size and weight within the group, body condition scores across the group, size variations within the group, ameness, coughing, scouring, ocular disease and pruritis. Having appraised the group as a whole it may be appropriate to perform a detailed clinical examination on one or two of the worst affected animals. This basic process will identify the presence of specific problems such as enzootic pneumoniia, footrot and sheep scab. Faecal samples should be collected for worm egg counts, coccidia oocyst counts or identification of fluke eggs, serum and blood samples should be taken for vitamin B12 and glutathione peroxidase assays.
Describe the clinical signs of cobalt deficiency
A frequently diagnosed cause of ill thrift in weaned, growing lambs. severe deficiency in pregnant ewes has been associated with poor reproductive performance, poor milk production and high perinatal lamb mortality rates. The principal sign is ill thrift. affected lambs are frequently empty, pot bellied and depressed in appearance. A watery ocular discharge associated with a low grade conjunctivitis is often present. Severely affected animals are pale and anaemic, although in these cases the DDx haemonchosis should be investigated. high perinatal mortality rates and susceptibility to infection have been reported in lambs born to cobalt deficient ewes. Fatty infiltration of the liver has been associated with low vitamin b12 status of lambs.
Describe the animal requirements for Cobalt? what is it required for
Cobalt is 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. poor utilisation of propionic acid results in reduced dry matter intakes, therefore the principal clinical sign is ill thrift. Sheep have higher requirement than cattle. Growing animals have a higher requirement than adults. Requirements of pre ruminant animals are low. Pre ruminant lambs rely mainly on glucose as an energy source, whilst most energy in ruminants is derived by vitamin B12 dependent gluconeogenesis from propionic acid. Vitamin B12 readily croosses the placenta and is stored in the foetal liver. Concentrations in milk and colostrum are also high. Pasture cobalt concentrations vary throughout the year, and are generally lowest during spring and highest during the winter. Consequently clinical signs are most commonly reported in weaned lambs during the summer and in newborn lambs of deficient dams during the spring.
Can soil levels of cobalt be used to diagnose cobalt deficiency? How do pasture levels differ to soil levels?
No. Soils derived from acid igneous rocks such as granite are low in cobalt. The relationship between soil, plant and animal cobalt status is complex and soil cobalt concentrations are a poor index of deficiency. other elements can interfere with cobalt uptakes by plants for example manganese, iron and nickel. Soil pH above the optimum range of 5.8-6.3 can affect cobalt availability and soil compaction associated with rotational grazing may reduce pasture uptake of cobalt. 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 level than pasture grown on well drained soils. Plants differ in their ability to accumulate cobalt, although when soil cobalt is low the concentrations in all plant species are low. The cobalt content of clover is greater than that of other pasture species. pasture cobalt concentrations are more useful than those of soil but cannot be used alone to diagnose deficiency in animals.
What is a dose response trial?
Comparing growth rates of supplemented animals with un supplemented controls. The two groups need to be grazed and managed under the same conditions. such an approach is not always practical or appropriate.
How do blood and vitamin B12 levels provide a guide to cobalt intake?
Blood levels reflect immediate dietary cobalt intake whilst liver vitamin B12 conentrations provide a guide to the 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. Unless severely deficient the individual variation in serum vitamin B12 concentrations is high and it is recommended that a minimum of 10 samples be collected. Less variation in liver vitamin B12 concentrations and 3 samples are adequate.
What is methylmalonic acid?
IT accumulates in the plasma of cobalt deficient sheep as a result of reduced Vitamin B12 coenzyme activity. Raised plasma concentrations of MMA can 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 short term cobalt supplementation be provided?
Through oral drenching of weaned lambs with cobalt sulphate, foliar spraying with cobalt sulphate or vitamin B12 injections. oral drenching with cobalt sulphate provides an effective supplement for about 7 days. However, weekly drenching is required to provide adequate supplementation which is not practical in most sheep flocks. mineralised anthelmintic drenches probably dont provide enough cobalt to be worthwhile in most flocks. foliar liquid application at a rate of 175-350g per hectare can raise pasture cobalt levels for about 6 weeks. Selected paddocks can be sprayed before lambs and adult sheep graze. Silage paddocks can als be sprayed at the early growht stage to raise the cobalt content of the stored feed. On many farms vitamin B12 injections are considered to be a practical and cost effective method of short term supplementation for fattening lambs. 1-2mg injections of vitamin B12 raise serum and liver vitamin b12 concentrations of 15-30kg lambs for 1-4 weeks. Where repeated vitamin b12 injections are required supplementation becomes expensive in terms of labour and the cost of the drug.
How can long term cobalt supplementation be implemented??
Of replacement ewe lambs or long keep store lambs can be achieved using intra ruminal cobalt bullets or by pasture top dressing with cobalt sulphase. (not currently cost effective on most farms). Overseas long acting Vitamin B1 injections are available. Intraruminal cobalt bullets raise vitamin B12 levels for over one year.
Describe reproductive behaviour in the ewe and doe?
Seasonal polyoestrus short day breeders. Sexual activity is controlled by the hormone melatonin which is secreted by the pineal gland in the brain. In the temperate regions as the day length shortens, increasing amounts of melatonin is secreted and sexual activity increases. Onset of activity is breed dependent eg dorset horn is capable of lambing all year rounds but mountain breeds like blackface have a short breeding season of around 4 months and crossbreeds like greyface are somewhere inbetween. Most breeds have a peak fertility around october/november time.
Breeding season - late summer to early spring
Lambing season - march - April - may
What are the potential benefits of altering the ewes natural breeding cycle?
Synchronisation - compact lambing with better utilisation of labour, more accurate feeding and ration control, even batches of lambs, use of AI programmes. Advanced breeding - better prices for new season lamb around easter, growth of pedigree lambs for autumn sales, 3 crops in 2 years systems can be run. breeding outside of the natural season is likely to result in lower fertility and lower prolificacy.
Describe the oestrus cycle of the sheep
averages 16-17 days, (doe 19-20days). Thirteen to fourteen days taken up by luteal phase, follicular phase 3-4 days, follicular phase is characterised by exhibition of oestrus behaviour, LH surge, ovulation. Transition from follicular to luteal phase is marked by ovulation and formation of a corpus luteum which persists throughout pregnancy. If does not conceive - then from around day 12 of the cycle, the CL fades and progeterone levels fall. PGF2a which is secreted by the uterus brings about this process of luteolysis. Maintenance of pregnancy is dependent throughout the entire gestation on the production of progesterone from the CL. In the ewe, the supply of progesterone for maintenance of the pregnancy comes primarily from the placenta and not the CL. this difference in reliance is important for inducing lambing.
Define the different stages of the reproductive year in a sheep flock?
Anoestrum (mid december to mid june is the period when no ewes are ovulating or exhibiting behavioural oestrus. Transition - approx mid june to mid september is the period when a proportion of the flock are ovulating with or without behavioural oestrus. breeding season - mid september to mid december is the period when the greater proportion for ewes are ovulating and exhibiting behavioural oestrus.
What is the ram/teaser effect?
A non chemical method most successfully employed in the transition period. Although it can be used in anoestrus the results are not so good and unless teasing is maintained the day length will cause the ewes to decline into anoestrus once teasing stops. The method can therefore be used to encourage ewes to cycle a few weeks earlier than the breed would do naturally. The ideal teaser is a fit and healthy, virile ram which can be vasectomised by simple surgery. Provided ewes have been kept separate from males for several weeks previously, the introduction of a teaser will cause ewes to ovulate within 2/3 days of introduction. Usually this heat is a non fertile and silent heat and following this ewes will respond in one of two ways:
The CL will have a normal lifespan with the ewes ovulating and showing a fertile behavioural oestrus around 1-20 days after teaser introduction. OR the CL regresses prematurely when approximately 7 days old. This produces a second silent oestrus followed by a luteal phase of normal length to give a fertile oestrus from days 24 to 28. 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. Fertile rams shoudl be used at a ratio of approx 20-30 ewes.
How can progestagen sponges be used to synchronise oestrus in sheep and goats?
Intravaginal progestagen impregnated sponges used either with or without an injection of pregnant mares serum gonadotrophin (PMSG) - most widely used products used for induction and synchronisation of oestrus in sheep and goats. Sponges are inserted for 12 to 14 days to provide a period of progesterone priming, when sponges are removed, the sudden fall in progesterone levels precipitates a surge of gonadotrophin hormones that leads to oestrus activity. If used for synchronisation within the breeding season, PMSG is not generally required unless in AI programmes, whereas ewes in the transitional period or anoestrus will require a certain dose of PMSG at the time of sponge removal to stimulate follicular activity. Sponges should be inserted 2 weeks before mating is required to begin. After 12-14 days sponges should be removed and PMSG given by IM injection. Timing of fertile ram introduction following sponge removal is crucial - 36-48 hours to come into season post sponge removal so rams should be introduced at 36-40 hours for maximal conception rates. Rams should be removed after 48 hours and fed well to maintain condition. they are returned to the ewes 2 weeks later to catch any ewes which failed to conceive to the induced oestrus.
What is the role of melatonin in breeding seasonality?
Melatonin is secreted by the pineal gland in increasing amounts in response to increasing hours of darkness. these elevating plasma melatonin levels in winter months, feed back to the hypothalamus and pituitary to stimulate secretion of GNRH, LH and FSH. This signals increased reproductive system activity, producing a natural peak in breeding performance in the autumn. This effect can be mimicked by the use of slow releasing melatonin implants, eg regulin, improves performance of sheep to be mated early in the season before the usual peak of reproductive activity. one implant per ewe administered subcut near base of ear. keep separate from al male sheep and goats.
describe the treatment regime of regulin and its advantages?
Day 1 - 30 weeks before intended date of lambing - remove all male animals from contact
Day 7 - implant ewes
Day 42- introduce rams. Period between implantation and ram intro must be 30-40 days. vasectomised rams may be used for approx 14 days before fertile rams to improve conception rates to first service. Expect a delay of 14-21 days before mating activity commences. Peak of mating activity will occur 25-35 days after introducing the rams. Advantages - increase reproductive output, increase conception rates to first mating, only 1 ram per 40 ewes required.
How can prostaglandin in sheep be used for synchronising sexually active ewes?
Mode of action is to cause regression of the CL - it has no use for out of season breeding programmes. but can be used to synchronise groups of sexually active ewes. the CL is responsive to PG days 4-14 of the cycle, similar to cattle. there is debate regarding interval between injections but intervals between 9-15 days are recorded. oestrus occurs approx 40 hours after PG with ovulation 30 hours later. Results much more variable than sponging. (cloprostenol)
How can parturition be induced in ewes?
16mg betamethasone given IM will induce lambing in 26-60 hours in most cases. 15-20mg oestradiol benzoate can also be used. Prostaglandins are not effective in sheep because maintenance of pregnancy is not dependent on a viable corpus luteum. In does- synthetic PGF2a given i/m is effective in inducing parturition as maintenance of pregnancy is dependent on progesterone secretion from the CL.
What is your advice to a farmer after an abortion occurs in one of his sheep?
Isolate any aborting/aborted ewes and dispose of any abortion products by incineration or deep burial. Observe strict personal hygiene to prevent risk of zoonoses especially women with regard to EAE and toxoplasmosis. Pregnant women should have no contact with lambing ewes at all. submit several sets of aborted foetuses complete with placenta for accurate diagnosis of abortifactive agents. Take appropriate action fi a specific agent is identified.
