Sheep Flashcards
0
Q
Describe the foetal development during pregnancy in relation to dietary energy supply in the second trimester
A
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.
1
Q
What are the most fundamental factors to ensure a good start for a lamb during first hourts of life?
A
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.
2
Q
What effect does under nutrition in late gestation have?
A
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.
3
Q
How can dietary energy supply relative to metabolic demands be determined in late gestation?
A
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.
4
Q
Describe what should be done on a farm visit as part of a veterinary flock health plan?
A
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.
5
Q
How should 3-OH butyrate blood samples be interpreted?
A
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.
6
Q
How can protein status be evaluated?
A
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.
7
Q
When should ewes be vaccinated?
A
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.
8
Q
How does pre partum nutrition have an effect on Perinatal lamb mortality?
A
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.
9
Q
What is the lambing percentage?
A
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.
10
Q
What events determine the lambing percentage?
A
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.
11
Q
How does dystocia cause perinatal lamb losses?
A
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.
12
Q
How much colostrum does a lamb need? What happens to lambs who do not get enough energy?
A
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.
13
Q
Describe the different possible reasons for lamb starvation?
A
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.
14
Q
Describe a PM of a lamb
A
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.
15
Q
What management practices can be utilised to minimise perinatal mortality of lambs?
A
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.
16
Q
What are the clinical signs of hypothermia
A
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.
17
Q
What is the treatment of moderate hypothermia?
A
(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.
18
Q
What is the treatment of severe hypothermia in a lamb under 5 hours old?
A
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.
19
Q
what is the treatment of hypothermic lambs over 5 hours old?
A
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.
20
Q
What is watery Mouth Disease?
A
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.
21
Q
How do viral diseases of lambs cause enteritis?
A
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.
22
Q
How does Cryptosporidiosis cause enteritis in lambs?
A
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.
23
Q
How does salmonellosis cause enteritis in lambs? how is diagnosis confirmed?
A
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.
24
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.
25
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.
26
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.
27
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.
28
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.
29
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.
30
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.
31
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.
32
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.
33
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.
34
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.
35
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.
36
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.
37
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.
38
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.
39
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.
40
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.
41
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.
42
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.
43
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.
44
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.
45
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.
46
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.
47
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.
48
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.
49
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.
50
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.
51
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.
52
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.
53
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.
54
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.
55
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.
56
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.
57
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.
58
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
59
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.
60
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.
61
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.
62
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.
63
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.
64
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.
65
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.
66
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)
67
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.
68
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.
69
What are the clinical signs and pathology of chlamydial abortion (enzootic abortion of ewes)
Agent: chlamydophila abortus. highly specialised bacterium with a unique life cycle with an infectious extracellular phase and non infective intracellular phase. Signs: rarely ay signs of impending abortion and ewes are usually unaffected unless placenta is retained and mtritis develops. abortion seen in 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 intra cotyledonary areas is classical finding. Full term delivery of moribound, stillborn or weakly lambs is also a feature. Placentitis is the major pathological component, with changes in the placenta beginning after 90 days gestation. The gut appears to be the natural habitat of C abortus, spread to placenta can happen in pregnancy. this creates a latent infection at the time of spread leading to an active Placentitis the following year when the animal becomes pregnant again.
70
How is diagnosis of chlamydial abortion made and how is it controlled and prevented?
Well preserved lambs in last 2-3 weeks of gestation and necrotic placentitis. Demonstration of large numbers of chlamydial elementary bodies in smears made from affected cotyledons. Stained by modified ziehl neelson, clusters of red bodies against blue background. Paired serology 2-4 weeks apart from aborting ewes may be useful where abortion products not available. Limit spread of infection. ewes which abortion should be isolated and clearly marked for future identification. ewe lambs from aborted females or ewe lambs fostered onto aborted ewes should not be retained for breeding as they may harbour infection until they become pregnant when they will abort. Ewes which have aborted from EAE will not abort from EAE again but remain intestinal carriers and a source of infection to rest of the flock. Treatment with long acting oxytetracycline useful in the face of an outbreak to limit severity of losses. Main effect of treatment is to suppress chlamydophila multiplication so two intramuscular injections at a two week interval are recommended. Treatment can be done strategically at 4 weeks and 2 weeks before expected lambing date. Does not eliminate the infection and the use of abx should be restricted to emergency situations and not used routinely. Vaccination with good success - live attenuated vaccine ENZOVAX and CEVAX chlamydia. Vaccination must be complete 4 weeks prior to breeding with the recommended policy being to vaccinate ewe lambs as soon as possible after 5 months of age. Vaccination has no effect on ewes/lambs already harbouring latent infection of C abortus from the previous year.
71
What is toxoplasmosis? how does it cause abortion?
A protozoan parasite toxoplasma gondi, the life cycle of toxoplasma can be divided into two parts, an asexual cycle with little host specificity and a sexual cycle confined to cats which results in the production of oocysts in cat faeces. 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 onto bedding and feed stores. signs: usually abortions or stillbirths in very late stages of pregnancy. Stillborn lambs accompanied by a mummified foetus. Ewes normally unaffected. Effects of toxoplasmosis in susceptible sheep dependent upon the stage of pregnancy at which infection occurs. Infection in early pregnancy can produce foetal resorption with a large number of ewes ending up barren, infection between about 70-120 days gives stillborn lambs/abortions/mummified foetus, infection in late pregnancy produces infected but clinically normal lambs. The main changes are in the foetal membranes with engorged, necrotic cotyledons with white speckled white necrotic foci.
72
How is diagnosis of toxoplasmosis made?
Serology is the usual method of diagnosis and gives fairly quick results. Indirect fluorescent antibody tests to detect toxoplasma antibodies in foetal fluids is most accurate, if abortion products not available, then latex agglutination test can be performed on blood from the ewe. Interpretation of titres from the latex test can be subjective - low titres can show exposure at some point whereas higher titres of >160 suggest recent exposure and likely abortion due to toxoplasmosis.
73
How is toxoplasma controlled and prevented?
Little can be done to prevent further spread in an outbreak as infection is via contaminated feed and bedding and is not thought to be sheep to sheep. Rodent and cat control on the farm should be attempted. young cats most likely to shed oocysts. By the time they are adults a large percentage of cats will have seroconverted.Keeping feedstores secure from cat entry and contamination. Feeding the coccidiostat drug decoquinate to wes during pregnancy has been shown to reduce toxoplasma related lamb mortality. Vaccination with live vaccine toxovax is best available method of control. Immunity is solid after vaccination or abortion.
74
What are the clinical signs and pathology of salmonellosis abortion in sheep?
Aerobic gram negative rods - non lactose fermenters. most commonly associated with disease in sheep are S typhimurium, S dublin S montevideo and S abortus ovis. Signs may not include general systemic signs and enteric signs as well as abortion. With S abortus ovis and S montevideo the main sign is abortion in the last 6 weeks of gestation and ewes are rarely seen ill unless metritis develops due to secondary bacterial infection. Affected ewes are sick and pyrexic and may scour profusely. May die of septicaema before they actually abort and vigorous antibiotic therapy may be required. In most cases of sallmonella abortion the foetus and placenta is moderately to severely autolysed with necrotic membranes and characteristic rotten lambing smell. lambs may be emphysematous which often makes removal difficult.
75
How is diagnosis of salmonellosis made? What are the control and prevention measures?
Isolation of the causal organisms along with gross sigs of salmonellosis if a number of ewes are sick. typical gram negative organisms are seen on direct smears of placenta and stomach contents of foetuses. Culture on desoxycholate citrate agar or maconkey agar should confirm diagnosis. Strict isolation of aborting ewes and good hygiene. Zoonotic. Limit spread by mass medication of remaining ewes to lamb eg long acting oxytetracycline. changing of lambing field or shed after a week or so of abortions may help to prevent the build up of infection. S montevideo - wild birds especially gulls have been implicated in the spread of infection from sewage outfalls to sheep water courses and feed troughs in the fields over winter time.
76
How does campylobacteriosis cause abortion?
Campylobacter fetus fetus and C jejuni. Abortion in last 6 weeks of pregnancy with a placentitis developing 7-25 days after infection. infection transmitted orally although it occurs in many closed flocks. wild life vectors such as crows and other birds implicated. diagnosis by staining with ziehl neelson smears made from cotyledons and stomach contents to observe small comma shaped bacteria. No venereal spread as seen in cattle and disease is usually self limiting from one year to the next with good immunity developing in the flock.
77
What is border disease?
A congenital virus disease caused by a pestivirus serologically related to BVD virus in cattle and swine fever in pigs. - Barre ewes, abortions, mummified foetuses, classical hairy shaker lambs, long fleeces and abnormal body tremors. Healthy adult sheep may only experience mild often inapparent disease i n the process of seroconverting. most serious consequences occur when BD infects susceptible ewes during pergnancy. before 60 days likely to result in foetal death and resorption, abortion or still birth. sme foetuses may survive and become classical hairy shakers, betweeen 600-85 days outcome is variable with some normal lambs but also some with CNS irregularities and cerebellar hypoplasia. After 85 days - competent immune system. PI - poor doers which may succumb to mucosal disease. Lab confirmation by detection of viral antigen in tissues by specific immunofluorescent staining or virus isolation from blood or tissues. sheep to sheep contact is mode of transmission.
78
What is listeriosis?
Encephalitis is the predominant form of listeriosis 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 with a ph of >5. abortions can occur at any stage but usually in the third trimester. abortions due to L monocytogenes have been reported 7 days after consuming infected silage. diagnosis relies on isolation of organism. Prevention relies on selecting best silage for feeding to sheep and avoiding silage poorly made or heavily contaminated with soil.
79
Describe polioencephalomalacia of Sheep
(PEM) It is a common acute onset neurological disease of weaned lambs that is also seen sporadically in adult sheep. Characterised by blindness, initial depression and dorsiflexion of the neck progressing rapidly to hyper excitability seizure activity and opisthotnnus. Usually affected two weeks after movement to another pasture or dietary change. Blind and becomee isolated from group and wander. When stationary there is dorsiflexion of the neck 'star gazing'
80
Describe the pathology of PEM (polioencephalomalacia). How is diagnosis made?
Affected areas of the cortex may exhibit a bright white autofluorescence when cut sections f the cerebrum are viewed under ultraviolet light. this is due to the accumulation of lipofuschin in macrophages but not all PEM cases fluoresce. Definitive diagnosis relies upon histological findings in the cortical lesions of vacuolation and cavitation of the ground substance with astrocytic swellling, neuronal shrinkage and necrosis. Diagnosis based upon clinical findings and response to parenteral administration of thiamine. Common ddx include focal symmetrical encephalomalacia in weaned lambs, pregnancy toxaemia, acute coenurosis, listeriosis in adults.
81
How is polioencephalomalacia prevented and treated?
The treatment response during the early clinical stages to high doses of thiamine administered IV for the first occasion is generally good. Successfully treated sheep are able to sand and commence eating after 24 hours although normal vision may not return for 5-7 days. Treatment should be continued for three consecutive days. the IV injection of high doses of soluble corticosteroid such as dexamethasone in the first treatment to reduce cerebral oedema remains controversial. The sporadic occurrence and good treatment response of PEM cases mean that prevention measures are rarely attempted under most grazing systems in the UK. sulphur toxicity h as been linked to PEM.
82
Describe how brain abscesses occur in ruminants?
They are rare in ruminants affecting lambs/calves 3-6 months old. clinical signs are slowly progressive and arise frmo involvement of one cerebral hemisphere with contralateral blindness and proprioceptive deficits but normal pupillary light reflexes. Depression is a fairly consistent clinical finding often with the heat turned towards the chest. There may be compulsive circling but affected animals often stand motionless or appear trapped with the head pushed into the corner of the pen. Lumbar CSF analysis may reveal a slight increase in protein and white cell concentrations. The most common differential diagnosis is coenurosis but this condition is uncommon in sheep less than 6 months old.
83
What is coenurosis?
Gid is a parasitic infection that develops in the intermediate hosts of some tapeworm infections and caused byt he coenurus the larval stage of these worms.
84
How does listeriosis occur in sheep?
Primarily but not exclusively a winter spring disease of silaged fed ruminants. The less acidic pH of spoiled silage allows multiplication of L monocytogenes. Outbreaks may ocur within 10 days of feeding poor quality silage. Removal or change of silage in the ration often halts the appearance of listeriosis but cases can still occur for a further two weeks or so. Listeria that are ingested or inhaled tend to cause septicaemia, abortion and latent infection. Those that gain entry to tissues have a predilection to localise in the intestinal wall, medulla oblongata and placenta or to cause encephalitis via minute wounds in the buccal mucosa.
85
Describe listeric encephalitis
Affects sheep, cattle goats and occasionally pigs. it is essentially a localise infection of the brainstem that occurs when L monocytogenes ascends the trigeminal n erve. Clinical signs vary according to the function of damaged cranial nerve nuclei. Signs also include depression due to involvement of the ascending reticular activating system (ARAS), circling and ipsilateral hemiparesis (damage to long tracts). The uterus is susceptible to L monocytogenes at all stages of pregnancy which can result in placentitis, metritis, fotal infection and death, abortion, stillbirths, neonatal deaths and viable carriers.
86
What are the clinical findings seen with listeric encephalitits?
May recur on the same premisis in successive years. number of naimals clinically involved in an otubreak less than 2% usually. Gimmers more commonly affected due to premolar teeth eruption predisposing to infection of buccal lesions. outbreak of listeriosis can be encountered in young lambs with access to silage. Often rapid - death may be 24-48 hours after onset of clinical signs. Recovery rate up to 30%. Lesions are localised in the brainstem and the signs indicate dysfunction of the third to seventh cranial nerves and occasionally other nerve nuclei. Anorexic, depressed, disorientated, may propel themselves into corners or lean against walls. Facial paralysis with drooping ear, deviated muzzle, flaccid lip and lowered eyelid on the affected side. unilateral lack of blink response. Profuse salivation with food material impacted in the cheek of the affected side due to trigeminal nerve paralysis which also results in loss of skin sensation of the face. Terminally, affected animals are unable to rise, lie on the same side, involuntary running movements are common. There are few gross lesions apart from some congestion of the meninges. CSf can be collected (lumbar) under local and present with elevated protein concentration and mild pleocytosis. listeriosis can be confirmed by isolation and identification of L moonocytogenes. Many healthy animals have high listeria titres on serology.
87
In cattle, what is the DDx for Listeric encephalitis?
Peripheral vestibular lesions, basillar empyema (pituitary gland abscess), bovine spongiform encephalopathy, thromboembolic encephalitis, polioencephalomalacia, lead poisoning, rabies. (in lambs - should be differentiated frm brain abscess and nephrosis.
88
What is the treatment of listeric encephalitis?
Penicillion, ampicillin, ceftiofur, erythromycin and trimethoprim/sulphonamide. Penicillin drug of choice. high doses required due to achieving minimum bactericidal concentrations int he brain. No advantage of treating sheep more than 4-7 days. Injection of dexamethasone may be done at first presentation (controversial). Supportive therapy including fluids and electrolytes by orogastric tube is required for animals having difficulty eating and drinking. In an outbreak afected animals should be segregated. Use of that particular silage should be discontinued. Spoiled silage should be discarded routinely. L monocytogenes is Zoonotic. (little risk if just in brain).
89
Describe how vestibular lesions present in sheep and cattle
Clinical signs depend on whether there is unilateral or bilateral involvement and if the disease process involves the peripheral or central components of the vestibular system. Unilateral peripheral vestibular lesions are commonly associated with otitis media and ascending infection of the Eustachian tube is not uncommon in growing lambs. Sheep with unilateral vestibular disease present with a head tilt towards the affected side and a horizontal nystagmus with the fast phase directed away from the side of the lesion although the nystagmus may regress with time. Circling behaviour towards the affected side may be present. Eye droop on the affected side is usually present. ipsilateral facial nerve paralysis frequently results from otitis media causing ptosis and drooping of the ear.
90
What is the treatment for vestibular lesions in sheep?
Pasteurella, streptococcus and trueperella have been isolated from infected lesions. a good treatment response has been achieved with 5 consecutive days treatment with procaine penicillin when disease is recognised during the early stages.
91
How can sarcocystis cause neurological disease in sheep?
All ages of sheep may be affected but neurological signs have been more commonly observed in 6-12 month old lambs introduced onto highly contaminated pasture. Pelvic limb ataxia an paresis have been described with affected sheep adopting a dog sitting posture. some sheep may die without premonitory signs whilst less severely affected sheep may recover with supportive care. Diagnosis is difficult because compressive spinal cord lesions and delayed swaybcak present with similar neurological findings. Serology not helpful. Confirm by demonstration of characteristic histological lesions in the CNS.
92
What is cerebellar abiotrophy?
A familial syndrome described in 3-4mth old charolllais lambs and holstein calves. The clinical signs include lowered head carriage, intention tremors, a wide based stance, ataxia but wih preservation of strength and dysmetria. The pelvic ataxia may result in falling over. The cliincal diagnosis is based upon the history of progressive deterioriation in neurological function with signs indicative of a cerebellar lesion. in utero infections causin cerebellar dysplasia such as border disease virus and BVD present with neurological signs at birth. confirmation of diagnosis of cerebellar abiotrophy requires histological demonstration of widespread purkiinje cell degeneration in the cerebellum. the possible inherited nature of this metabolic defect stresses the importance of an accurate diagnosis especially in a stud ram.
93
What are the clinical signs of Scrapie?
Fleece on poor condition with wool loss over flanks and tail head caused by rubbing. regrowth of fleece with hyperpigmentation can occur. Cutaneous stimulation of the skin over the dorsal sacral area elicitis a nibble response in the majority of sheep including manic lip smacking and swaying of the hindquarters. (provocative scrapie test). The neurolgical findings can be attributed to cerebral and cerebellar ysfunction. cerebral dysfunction is indicated by an altered mental state with depression and a vacant detached appearance but hyperaesthesia to visual auditory and tactile stimuli. Vision and pupillary light reflexes are normal. In early stages affecteed ewes when stressed such as gathering collapse into sternal recumbency with the neck extended. Cerebellar dysfunctioin is indicated by postural and gait abnormalities, namely pelvic limb ataxia but with preservation of muscle strength, dysmetria, most commonly hypermetia of the thoracic limbs and a wide based stance. Gait abnormalities are most obvious when the animal is made to trot downhill or turn acute angles when hoping with both pelvic limbs . Signs indicative of a brainstem or vestibular lesion are not detected in scrapie. Lack of inflammatory reaction, despite extensive CNS histopathologicaal change in scrapie allows many common CNS system diseases which evoke inflammatory changes in CSF t be elminated.
94
What is the brain form of Visna?
Visna is an uncommon manifestation of MVV infection . Uncommon brain form which manifests clinically as a head tilt, circling behaviour and ataxia and a spinal form which presents initially as unilateral Pelvic limb conscious proprioceptive deficit progressing to pelvic limb paresis. The neurological signs present as a head tilt, approx 5-10 degrees from the vertical plane and circling towards the affected side. these clinical signs result from lesions within the lateral ventricles. Some affected animals may display hypermetria and pelvic limb ataxia. In spinal cord form the initial neurological signs are hypometria with reduced flexion of the distal limb joints, conscious proprioceptive deficits and reduced weight bearing affecting one pelvic limb.
95
How can CSF be collected?
Mid point of the lumbosacral space which can be identiified as the midline depression between the last palpable dorsal lumbar spine and the first palpable sacral dorasl spine. site must be clipped surgically prepared and between 1-2mls of local injected subcutaneously. Slowly advanced at a right angle to the plane of the vertebral column. Once the needle point has penetrated the dorsal subarachnoid space the CSF will well up in between the needle hub within 2-3 seconds. 1-2 mls of CSF is sufficient for laboratory analysis and while the sample can be collected by free flow it is more convenient to employ gentle syringe aspiration over 10 to 30 seconds. Normal range for CSf protein concentration is <0.3g/l. RBCS may be present in the CSF following pathological haemorrhage into subarachnoid space but more commonly result from needle puncture of blood vessels on the dura particularly the leptmeninges.
96
What are the main problems in diagnosis of respiratory disease in sheep?
An accurate history often not available due to problems with frequency of observation and identification of individual animals. Signs usually used for the identification of respiratory disease in other species are unreliable in sheep i. rectal temperature variable up to 40C, abdominal breathing is normal, respiratory rate variable, auscultation is limited by fleece and relatively harsh lung sounds are noraml. All these factors shoudl be considered with reference to others in the same group, environmental conditions, activity, stage of pregnancy etc. A debilitated sheep will often show a scant nasal discharge of ruminal contents and this should not be interpreted as a sign of respiratory dsiease. Coughing, nasal discharge (mucopus, blood or copious serous) and dyspnoea are significant, as are adventitious sounds such as crackles and wheezes if identified.
97
Describe Parainfluenza infection in sheep
Ovine Parainfluenza virus is related to but distinct from bovine parainfluenza. Most infections appear subclinical or mild but acute, high morbidity outbreaks of respiratory disease have been recrded and attributed to PI3. Specific diagnosis of Pi3 involvement rarely atetmpted but may include virus isolation from swabs or tissue, FAT of tisue, paired serology etc. Antibodies to Pi3 are found widely in both healthy and pneumonic sheep. most have been infected by 12 months old. flock infections maintained by transient or persistent infections in immune animals. Infection with Pi3 predisposes lambs to infection with manheimia haemolytica. Intranasal Pi3 vaccine trials have demonstrated a reduction in the prevalence of pneumonia. half the cattle dose of imuresp given to ewes before tupping and lambs a 6 weeks old apparently gave good results. Parenteral administration has also been shown to stimulate immunity.
98
Describe adenovirus infection in sheep
Infection appears commonly in young lambs, most causing transient or persistent inapparent infection. may also cause enteritis. vaccination practised in hungary where adenoviruses important pathogens.
99
What is pasteurellosis?
Manheimia haemolytica of considerable economic importance. causes septicaemia in young lambs, pneumonia in growing lambs and mastitis in ewes. serotype 2 is the most commonly diagnosed. pasteurella trehalosi causes septicaemia in 6-10 month old lambs. serotype 10 is the most commonly diagnosed. Pasteurella multocida only rarely causes disease. Manheimia haemolytica and pasteurella trehalosi can be isolated from nasopharynx and tonsils of healthy sheep.
100
What are the clinical signs of pneumonic pasteurellosis?
Hyperacute - sudden death
Acute - sudden onset anorexia and dullness
Pyrexia
Hyperpnoea/dyspnoea
Serous ocular and nasal discharges
Frothy fluid at the mouth in the terminal stages.
Subacute and chronic presentations - as above but more transient/ milder, may lead to ill thrift. 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. cases of longer duration show cranioventral consolidation and pleurisy.
101
What are the clinical signs of septicaemic pasteurellosis?
An important cause of sudden death in lambs up to 12 weeks old. Affected lambs are depressed, easily caught, injected mucous membranes and marked dyspnoea. most lambs are pyrexic >40C. there is pleurisy and pericrditis with petechiae in the myocardium, spleen, liver and kidney, enlarged LNs and hepatic fatty change.
102
How is M haemolytica diagnosed?
nasal swabs and serology are of no use. Diagnosis is based on clinical signs and post mortem findings including bacteriology from untreated cases. (lung, liver, kidney, spleen, thoracic fluid, heart, blood). COngestion without consolidation in hyperacute cases resembles clostridial disease, autolysis etc.)
103
Describe the epidemiology of M haemolytica?
the condition occurs sporaically or as a flock outbreak. ewes and lambs may be affected. sudden deaths often seen first, teh septicaemic form in young lambs or the hyperacute pneumonic form in older lambs. Other animals when noticed with signs of pneumoniia. Most common in late spring/early summer. Mortality is variable at 2%. As P haemolytica is an inhabitant of the nasopharynx of healthy sheep, predisposing factors play a role in triggering clinical diseae. These can include environmental conditions; extremes of temperature, wet weather, handling stress, Pi3 virus - creates an ideal microcilmate and suppresses local immunity, SPA, mycoplasma/bordetella.
104
What is the treatment of M haemolytica?
clinical cases - oxytetracycine, NSAId, (rimadyl or finadyne). A decision must be made whether to gather and treat the lambs during an outbreak. handling for treatment may trigger further deaths/disease. most acute mortality often occurs in the first day or two of the outbreak. In vitro produced serotype a2 antigens are poorly immunogenic so afford poor protection. newer vaccines based on cells of major serotypes of M haemolytica and P trehalosi grown under conditions of iron limitation are more effective.
105
Describe disease caused by pasteurella trehalosi in sheep
Systemic pasteurellosis caused by P trehalosi is the most commonly diagnosed cause of sudden death in lambs between july and december. those seen alive are depressed, dyspnoeic, recumbent and frothing at the mouth. Haemorrhages over neck and thorax, pleua, diaphragm and epicardium. swollen lungs with haemorrhages and blood stained froth in airways, necrotic erosions in pharynx around tonsils, nasal mucosae and upper alimentary tract. liver congestion with necrotic infarcts in lier, kidney and spleen. The signs need to be differentiated from other peracute septicaemic toxic orr stress induced coonditions. Causes of sudden death include; clostridial disease, ruminal acidosis, redgut, acute fluke ,brassica poisoning, nitrite poisoning, dog worry, phenolic dip aspiration, rhododendron poisoning. confirmation is byt he isolation of large numbers of P trehalosi from the liver lung or spleen. Most common in lambs from october november and december. frequently follows movement of lambs onto rape, turnips or improved pastues. GI erosions and ulcers caused by dietary cahgne seem to be the port of entry for the normally commensal bacteria leading to septicaemic disease. Stress is a major component in the epidemiology of systemic pasteurellosis which must be considered when making a decision to gather a flock in order to administer long abx such as oxytetracycline. Control is by vaccination.
106
What is atypical pneumonia in sheep?
A non progressive chronic pneumonia of housed sheep under a year old caused by mycoplasma ovipneumooniae and possibly chlamydia psittaci. Predisposing factors include PI3 and M haemolytica. there is 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. som lambs may develop a secondary pasteurellosis. Red brown or grey consolidated then later collapsed areas in the apical and cardiac lobes. histology shows a lymphocytic cuffing pneumonia with pseudoepithelialisation of the alveoli and hyperplasia of the bronchial epithelium. Diagnosis is on clinical signs in housed or hevily stocked labs, confirmation at PM. age pattern and histology will differentiate from maedi and SPA. bacteriology useful but nto conclusive. serology possible. Oxytetracycline or a macrolide antibiotic may be given to sick lambs. control is by improving ventilation, reducing stocking densities, avoiding sharing an airspace with older sheep, isolation of purchased lambs, vaccination against pasteurellosis.
107
What is parasitic bronchitis? What parasites cause this?
Dictyocaulus filaria infection most common lungworm in sheep. May cause outbreaks of coughing and weight loss in the late autumn/early winter. Infection may trigger secondary pasteurellosis. Protostrongylus rufescens - only problem if very heavy infestation. Muelleris capillaris more common but no clinical significance. The life cycle of dictyocaulus filaria is similar to D viviparus. first stage larvae are passed in faeces which develop into infective L3 on pasture, spring pastures are infected by overwintered larvae or via faeces of ewes or hoggs. Clinical disease is seen in the autumnw ith adult worms in the bronchi. PRotostrongylus rufescens and muelleris capillaris require land snail intermediate hosts. M capillaris inhabits the alveoli causing green/grey sub pleural nodules in the caudal lung lobes while P rufescens inhabits the bronchioles casing small yellow/grey granulomas also in the caudal lobes. Diagnosis is by history clinical signs Pm and demonstration of L1 in faeces using the baermann technique. GI nematode control programmes should control parasitic bronchitis although clinical disease may occur if dosing is stopped in autumn or winter. all common anthelmintics should be effective.
108
What is chronic suppurative pneumonia?
This follows pneumonic pasteurellosis and occurs when pockets of bacterial infection persist and are walled off as chronic absceses in the lung tissue or pleural space. It may also be caused by bacteraemic spread frmo a spetic focus. bacteria involved may include manhaemia haemolytica, arcanobacterium pyogenes, pasteurella multocida and E. coli. Other causes of lung abscesses may include Coryne bacterium pseudotuberculosis and tuberculosis. The clinica signs are weight loss/ill thrift, mild fluctuating pyrexia or normal temperature dyspnoea, purulent nasal discharge, muffling on thoracic auscultation. Hyperglobulinaemia >50g/l, PM examination. Treatment - 4 weeks procaine penicillin.
109
What is Jaagsiekte / Sheep pulmonary adenomatosis?
an infectious tumour condition resulting from infection with a lentivirus (jaagsiekte retrovirus JSRV). A herpes virus is also involved the lesions. Incubation period is several months. Disease in 2-4 old sheep, occasionally in the yearling lambs of infected dams. Loss of body condition, exercise intolerance, serous nasal discharge, episodes of mouth breathing, appetite OK, afebrile, then develops into dyspnoea, tachypnoea, increased abdominal effort, fluid gathers in respiratory tract, may flow freely from the nostrils when the head is lowered, soft cough, fluid sounds may be heard on auscultation, ventral and cranial. Death frequently foollows secondary infection with pasteurella haemolytica. The lungs are enlarged and heavy. Tumours 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. The brnchi and trachea contain copious frothy fluid.
110
How is diagnosis of SPA/jaagsiekte made? what is the treatment and how can it be controlled?
No diagnostic test. an afebrile wasting respiratory condition with free fluid running from nostrils when head is lowered gives a good indication of disease presence. real time ultrasonic imaging of the lung fields behind the shoulder in the standing animal demonstrates the severe ventral consolidation caused by the tumour tissue, aiding in the differentiation of SPA fom other chronic pneumonias. the main route of infection is by respiratory aerosol. close confinement during housing or trough feeding increases the rate of spread of infection. No recognised effective control method. prompt culling of lean or dyspnoeic sheep may slow the spread of infection. the offspring of affected sheep frequently also develop SPA so should not be retained as replacements. Maintaining sheep of different age groups separately will reduce clinical disease.
111
What is Maedi in sheep?
A lentivirus infection causing respiratory disease (maedi), nervous disease (visna), mastitis and arhtritis. Maedi - clinical signs occur in sheep over three years old. The earliest sign of maedi is exercise intolerance, noted at gathering. AFfected sheep stand with neck extended, increased resp rate, flored nostrils and an abdominal component to the breathing. Wasting occurs and dyspnoea becomes obvious even at rest. any exercise results in tachypnoea and mouth breathing and if severely stresse, cyanosis and collapse may ensue. sheep remain bright and continue to eat. Visna less common, nervous signs include gait abnormalities eg dragging a hiind limb, knuckling, ataxia, incoordination, collapse and death. on PM - the lungs are firm rubbery and heavy.
112
How is maedi visna diagnosed? How is maedi visna treated?
Diagnosis may be masked at PM by pneumonic pasteurellosis or pulmonary adenomatosis. Lesions not pathognomic at histological diagnosis.DDx - lungworm infection, infestation and lymphoid infiltration with mycoplasa and chlamydial infection. Diagnosis relies on detecting antibody to virus by Agar gel diffusion test AGID. Some animals never develop antibodies so test not particularly sensitive. Most important route of transmission of the virus is from mother to offspring in colostrum and milk . Virus establishes infections in the lungs udder CNS and haemopoeitc organs. Vaccination unlikely to ever be a control option due to virus ability to mutate. prevention through adequate biosecurity measures and purchase of MV free stock. Control can be attempted by serological testing and culling of seropostiive sheep and removal of their offspring.
113
why do helmminth parasites cause economic losses?
Poor growth rates, lower carcase values, ill thrift in adult animals, deaths, treatment and management costs.
114
Describe the life cycle of ostertagia ostertagi
Adults in lumen of the gut, eggs shed in faeces, L1 development in daeces, 2 development in faecest, L3 infective larvae on herbage, L3 enter gastric glands, L4 emerge onto gut mucosa. Eggs and L3 survive best at temperatures 18-26C. a higher temperatures larvae develop faster but deplete energy - mortality increases. At 80%. Humidity in faeces/grass allows development when dry. Dessication kills L3. Larvae develop in and disrupt abomasal glands. adults emerge after about 18 days after infection. severe pathology is associated with emergence of adults. pH of abomasum rises due to replacement of HCl secreting cells with undifferentiated cells. Pepsin digestion of protein is inhibited. substantial albumin leakage through the abomasal mucosa occurs. Bacterial overgrowth in abomasum occurs.
115
What are the parasites which commonly affect cattle in the UK?
Abomasum - ostertagia ostertagi, haemonchus contortus, trichostrongylus axei.
Small intestine - cooperia, strongyloides, nematodirus helvetianus, trichostrongylus spp.
Large intestine - trichuris, oesophagostomum radiatum.
Lungs - dictyocaulus viviparus.
116
Describe the common parasites which affect sheep in the UK
Abomasum - teladorsagia circumcinta, haemonchus contortus
Small intestine - trichostrongylus vitrinus, nematodirus battus, cooperia, strongyloides papillosus
Large ingestine - oesophagostomum venulosum, trichuris
Lungs - dictyocaulus filaria, mueleris caillaris, protostrongylus rufescens.
117
Describe Teladorsagia circumcincta?
An abomasal parasite (brown stomach worm) about 1.5cm long and hair like. 5000 or more worms can cause severe clinical disease. Disease is seen during the summer and autumn months. Watery diarrhoea, loss of appetite and weight loss. There is hyeprplastic inflammation of the abomasal mucosa. Replacement of gastric secretory cells by unfunctional cells. Hypoproteinaemia due to leakage across damaged mucosa. Impaired abomasal function associated with alteration in pH.
118
Describe haemonchus contortus?
An abomasal parasite, which feeds on blood and causes anaemia and hypoproteinaemia. Disease is usually seen in lambs during late summer. Can occur in naive untreated adults at any time of the year. As few as 500 worms can result in clinical disease; anaemia, submandibular oedema, ascites, ill thrift, death, scour is seldom present.
119
What is trichostrongylus vitrinus?
Black scour worm - in proximal small intestine. about 1.5cm long white and hair like. 5000 worms or more can cause clinical disease. Villous atrophy caused by trichostrongylus vitrinus burrowing under the mucosa. Mucosal hypertrophy and villous atrophy. protein leakage, electrolyte and mineral imbalance. Disease usually seen during autumn and early winter months. anorexia, dark coloured scour, poor skeletal growth and wool quality.
120
What is nematodirus battus?
A small intestinal parasite. 2-3 cm long white worms coiled around the villi. Catarrhal inflammation of the small intestine. Disease of young lambs between 6-12 weeks old during may/June. 2000 worms can result in severe disease; acute onset diarrhoea, lethargy, abdominal pain, rapid weight loss, dehydration, sudden deaths.
121
How can infection with teladorsagia cause infection with other worms?
Host protective immune responses to teladorsagia in the abomasum alter the environment in the proximal small intestine, enabling the establishment of trichostrongylus in the autumn as the size of the teladorsagia population falls. Similar relationship between ostertagia and cooperia in cattle.
122
Which animals are parasitic nematodes most important in affecting?
Naive lamb and calves. naive animals moved from extensive grazing to contaminated lowground pasture, animals with compromised immunity - poor body condition, concurrent disease, lactation.
123
How long before egg shedding and infective larvae on pasture?
Under optimal conditions the period between egg shedding and maximum number of infective larvae on pasture is 3-6 weeks. Early larval stages are easily killed by dessication but survive well given wet conditions. Most infective third stage larvae survive on pasture for 10-12 weeks. Infective larvae can survive frosts and when cool and damp condtions persist can survie for up to 12 months.
124
When does faecal T circumcinta egg output rise in ewes?
Periparturient rise - increase in FEC around parturition and early lactation. Due to competition between immune system requirements and of pregnancy/ early lactation. EWes play an important role in the epidemiology of teladorsagiosis.
125
What is the Disease risk for teladorsagiosis, trichostrongylosis and haemonchosis associated with?
Overwintered L3 populations
Ewe faecal egg output - (use of persistent products, nutrition)
Autoinfection (suppressive anthelmintic treatments, nutrition.)
126
Describe the epidemiology of ostertagiosis
L3 overwinter -die by mid summer. cycled by calves - spring/early summer. Egg to L3 faster as temperature increases. L3 peak towards mid summer. Eggs to L3 slows/stops in autumn. Overwintered L3 ingested early in the grazing season develop to aults which are hte major source of subsequent pasture larval contamination infection. The rate of pasture larval contamination is most rapid in mid summer as temperatures increase so the majority of eggs deposited during april, may and june all reach the infective L3 stage from late summer. - environment within the faeces. Ingestion of large umbers of L3 causes type I disease. In spring and beef cattle - most of the overwintered 3 are ingested and killed in immune cows. overwintered L3 which remain on the pasture mostly die before calves are old enough to ingest significant amounts of herbage. Level of pasture L3 contamination in late summer and autumn is usually low. Calves susceptible to parasitic gastroenteritis during their second grazing season.
127
Describe type II ostertagiosis
Low autumn temperatures condition a proportion of ingested L3 to become inhibited/arrested at the early L4 stage in the abomasal glands. The presence of arrested El4 in the abomasum is usually asymptomatic. disease occurs in late winter when arrested EL4 simultaneously complete their development and emerge as adults. the risk of type II disease is increased by dry summers, followed by autumn rains, or any pasture management practices which delay the exposure of susceptible calves to high levels of pasture L3 contamination.
128
How does nematodirus battus differ from the other nematode parasites?
DEvelopment to L3 occurs within the egg. L3 in eggs can survive freezing and very low temperatures for up to 2 years. Hatching and release of L3 only occurs after a period of cold exposure followed by daily maximum temperatures above 10C. Eggs passed one year, hatch the following year. Hatching en masse usually occurs during may and june. Hatching en masse usually occurs during may and june. acute disease is seen when the hatch coincides with the presence of susceptible grazing lambs. Severe disease is not seen during seasons when the hatch occurs befre lambs are able to garze pasture or after they have reached 3 months old. The life cycle essentially only involves lambs. accumulation of inection on pasture takes place over a period of several years.
129
Describe the epidemiology of cattle lungworm
Adult dictyocaulus viviparus in the trachea and bronchi lay eggs which contain L1. L1 hatch quickly, are coughed up, swallowed and passed in faeces. Development to infective L3 can take as little as 5 days. development to L3 in faeces is fastest during warm weather and escape of L3 to herbage is moisture dependent. L3 are ingested with the grass and penetrate the intestinal mucosa. Moulting to L4 occurs in the mesenteric lymph nodes followed by migration to the ventral parts of the caudal lobes of the lungs via lymphatics and blood. L4 enter alveoli where they moult to L5. The prepatent period is 21-28 days. Severity of lungworm disease depends on the number of laevae ingested and on the hosts immunity. the bionomics of lungworm are complex and infection less predictable than gastroenteritis. Some L3 overwinter on pasture and some adult parasites or inhibited L5 survive in carrier animals. in wet weather pilobolus fungi facilitate airborne spread of L3 to other pastures. The infectious dose of L3 to induce disease is small. Primarily infection of previously unexposed cattle. Or reinfection of previously exposd cattle following massive challenge.
130
Describe the lifecycle of muelleris capillaris?
Lifecycle involves an intermediate mollusc host. sheep become infected when they eat the mollusc host with herbage. Adult worms are present in the alveoli. multifocal 2mm diameter, greyish subpleural nodules mostly in the caudal lung lobes
131
Describe the lifecycle of protostrongylus rufescens.
Lifecycle involves an intermediate mollusc host. sheep become infected when they eat the mollusc host with herbage. slender red 1.5cm-3.5cm adult worms in the small bronchioles.
132
Why do subclinical infections occur in sheep and cattle with nematode infections?
sub clinical production losses arise from continuous low level exposure of susceptible animals to infective nematode larvae. Lambs can still perform when challenged with small/moderate numbers of Infective L3. Compensatory growth is unlikely once lambs have had a check in growth so they will finish later.
133
What are the aims of nematode control?
To limit the host challenge to a level which does not compromise performance or welfare while at the same time enabling the development of immunity. Sustainable control programmes in individual flocks or herds are based on the common sense application of knowledge of the farming system and of the relationship between pasture contamination and the availability of infective larvae on pasture and build up of infection in animals
134
What are the principle control methods for nematodes parasites?
Finish lambs quickly before pasture larval burdens become production limiting. only graze susceptible sheep on safe pasture. suppression of pasture larval contamination using anthelmintics. A combination of these - integrated control.
135
How can 'safe' pasture be provided?
Interchange grazing management - annual rotation of grazing by cattle and sheep/goats. Use cereal crops, brassicas or silage, hay or silage aftermaths or mixed grazing of lambs with cattle. Few commercial sheep farms are able to provide sufficient safe pasture for the purpose of nematode parasite control in sheep without compromising the efficiency of crop or cattle production.
136
When should suppressive anthelmintic treatments be given?
Dose ewes at lambing to prevent them from multiplying larvae which overwintered on pasture during their post lambing period of relaxation in immunity. DOse lambs before weaning for nematodirus control. Suppressive anthelmintic treatment of lambs throughout summer.
137
What are the different anthelmintic drug groups?
Tubulin binding drugs - benzimidazoes and pro benzimidazoles.
Ganglion blocking agents - levamisole and moreantel
Macrocyclic lactones - avermectins and milbemycin
Aminoacetonitrile derivates - monepantel
Spiroindole/abamectin combination.
choice of anthelmintic drug is based on efficacy against the parasites present, persistence of action, preferred method of administation, meat withdrawal period, cost. Provided that anthelmintic resistance is not present, any of the licensed anthelmintics can be used. lambs often fail to achieve satisfactory weight gains when returned to heavily contaminated pastures after treatment.
138
When should calves be dosed with anthelmintic to provide suppressive anthelmintic control of parasitic gastroenteritis?
Dairy calves - anthelmintic treatments during first grazing season
spring beef calves - single treatment at first housing and anthelmintic treatments during second grazing season
Autumn beef calves- anthelmintic treatments during first grazing season.
Calves may not acquire immunity so they may remain susceptible to disease during the following grazing season. need to permit sufficient exposure to L3 to stimulate immunity without causing loss of production.
139
How is a diagnosis of parasitic gastroenteritis made?
Clinical signs, faecal worm egg counts, PM examination - gross findings, total worm egg counts, histopathology, plasma pepsinogen.
Egg counts - recent samples from 10 animals. reasonable estimate. variations - genera, breed, aage, reproductive status, length of time off pasture, DM content on faeces. Only indicates presence of adult worms. FWECS should be interpreted in conjunction with knowledge of general farm management, parasite control practices climate and time of yaer. each egg seen - 50 eggs per gram.
On farm pm - swirling movement of the diesta, identification of H contortus & O circumcincta, thickening of mucoa, pallor, ascites.
140
What factors influence faecal helminth egg counts?
Variation in egg production between genera - consider which helminth are likely to be present. Influences of hosts immune status - effects of sheep breed, age, reproductive status, management. Knowledge of scour or pelleted faeces - effects on fecal dry matter. positive counts only seen with patent infections.
141
What are the possible reasons for poor anthelmintic efficacy?
Underdosing - underestimation of lamb weights, inaccurate dosing guns, mathematical calculation errors, poor drenching technique.
Poor anthelmintic efficacy - out of date, poor product storage, poor quality product.
Anthelmintic resistance.
142
What are the different types of tests for anthelmintic efficacy?
```
drench check
Egg hatch assay
Larval development test
LArval migration inhibition assay - highly sensitive to complex extrinsic factors, differences in discrimatory doses between sensitive and resistant populations are small, target mechanisms may differ from those within the sheep.
Adult motility assay
LArval feeding inhibition assay
Molecular markers - BZ - many species
```
143
Why is anthelmintic resistance important?
selection for resistance is an inevitable consequence of good worm control. resistant worms cause no more serious disease than non resistant worms. Once resistance has emerged, worms can no longer be controlled using that anthelmintic group. In most flocks, worms can still be adequately controlled when resistance is present. In the absence of effective vaccines that might enable adequate production and protect animal welfare in the face of a low level of challenge, the guaranteed availability of conventional medicines is paramount.
144
Why is selection for anthelmintic resistance an inevitable consequence of good worm control?
The proportion of the total helminth population not exposed to anthelmintics is said to b e in refugia. In typical UK conditions the majority of helminth populations is in refugia. the larger the in refugia population the lower the selection pressure by anthelmintic treatment. The aim of helminth control is to limit exposure of susceptible sheep to infective larvae on pasture.
145
How can effective flock worm control be implemented while preserving the efficacy of the current remaining anthelmintics?
Always dose for the heaviest weight in the group. - Reduce feed intake by yarding sheep for 24 hours before oral dosing with BZ or ML anthelmintics. avoid keeping sheep and goats on the same farm. do not use inferior or poorly stored products. Weigh sheep accuratey. calculate correct dose volume. drench carefully to back of the mouth, calibrate drenching guns.
Avoid grazing sheep and goats on the same pasture - sheep and goats share many of the same nematode parasites. intrinsic differences exist between pharmacokinetic of anthelmintic drug absorption and elimination. goats metabolise drugs more rapidly. goats have a higher incidence of ruminoreticulum bypass. adult goats do not become fully immune. Underdosing selects for resistance if heterozygous nematodes survive. sheedding of nematode egs during prepatent period provides evidence of underexposure of female nematodes within their cattle hosts. RR survive full therapeutic dose. SS killed by full therapeutic odse.. RS killed by full therapeutic dose but survive underdosing.
Ensure maximum pharmacokinetic efficacy - unintelligible instructions, out of date products, poor storage, interior copies/generics. Practical inefficacy of an anthelmintic drug group due to nematode resistance might arise on a sheep farm in one or more ways - by gene flow with introduced animals, following repeated exposure of nematodes to subtherapeutic drug concentrations, by recurrent mutations after the onset of selection, by selection of preexisting resistant nematodes by affording them a competitive advantage over susceptible nematode. Major challenge is to avoid further selection by affording the resistant nematodes a compeititive advantage over susceptible nematodes.
Avoid unnecessary anthelmintic usage. - adult/immune sheep, extend the suppressive dosing interval, safe grazing targeted anthelmintic treatments.
maintain a susceptible worm population in refugia. - leave a proportion of the sheep untreated, return to contaminated pasture after dosing, dont dose before moving. Liit use of safe grazing to finishing lambs or dont use the pasture for sheep during the following year.
SHould ewes be dosed before mating ? probably selects for anthelmintic resistance and exposes worms to an anthelmintic at a time when they are in a hard to kill inhibited state. Frequent anthelmintic treatments select for resistance because they result in small numbers of nematodes in refugia and frequent exposure of a large proportion of the total nematode population to the drug.
Treat all introduced animals on arrival.
Routine drench checks.
146
What is safe grazing?
Pasture Which has not been grazed by sheep or goats during the previous 12 months
147
How do you control the periparturient rise in faecal egg output by ewes?
If safe grazing available - a single shot acting anthelmintic treatment around lambing when the ewes are turned onto safe pasture will remove arrested larvae and adult worms from the ewe. When clean pastre not available - conventional anthelmintic dosing of periparturient ewes needs to b e repeated at 3 weekly intervals or a peristent acting anthelmintic used. When safe grazing is available it is usually only necessary to worm lambs with an effeective wormer and yard or return them to their original pasture for 24 hours before moving. further worming is not usually required until autumn by which time many lambs have been sold. when clean grazing is unavailable, anthelmintic treatments are required throughout the summer months to suppress pasture larval contamination at usually 4 week intervals.
148
What is the predominant parasite species in the summer and autumn months?
T circumcincta in summer, T vitrinus in autumn.
149
Resistance to what anthelmintics is present in the UK?
Predominantly T circumcinta, BZ resistance is present in about 80% of lowground flocks. resistance to both BZ and LEv is seen.
150
Describe the strategies which may reduce the rate of development of anthelmintic resistance?
Quarantine treatments - full dose combinations
Reduction in anthelmintic usage - doosing ewes, clean grazing
Dose correctly for weight of heaviest in group - weight sheep
Annual drench rotation
Periodic use of narrow spectrum anthelmintics
Prolongation of anthelmintic activity - yarding for 24 hours, repeat dosing, anthelmintic capsules.
Drench checks
151
What is type I ostertagiosis?
Type I disease is seen in young cattle during late summer and autumn of their first grazing season. Ingestion of large numbres of L3 results in clinical type I disease after about 18 days.
152
What is type II ostertagiosis?
Type II disease is occasionally sene in yearling cattle in late winter or spring following their first grazing season. Low environmental temperatures duing autumn condition a proportion of ingested L3 to become inhibited/arrested at the early l4 stage in the abomasal glands. the presence of L4 in the abomasum is usually asymptomatic until late winter to spring when they simultaneously complete their development and emerge as adults. dry summers followed by autumn rains or any pasture management practices which delay the exposure of susceptible calves to high levels of pasture L3 contamination increase the risk of type II disease.
153
Describe fasciolosis in sheep?
An important annual cause of deaths and ill thrifts. traditionally seen in wet parts of western UK during autumn and early winter. during the past decade sub acute liver fluke has been a serious problem in normally drier eastern areas. It has a two host life cycle involving lymnea truncatula snails and a variety of mammalian species including sheep, cattle, goats, deer and rabbits. Sheep final host. mature flukes in bile ducts lay up to 5000 eggs per day. miracidia develop within the egg. Miracidia swim until they find a snail host. each miracidium multiplies asexually through sporocysts and redia to several hundred cercariae. cercariae swim and encyst as metacercariae on vegetation. metacercariae ingested by final host. Miracidia only develop within the fluke egg when temperatures are above 10C. Miracidia hatch about 6 weeks after eggs are shed when the temperature is 15C. At temperatures above 22C hatching can occur after only 10 days. Under suitable moist conditions most hatching usually occurs en masse. Miracidia must find a snail host within 3 hours of hatching. Galba truncatula inhabits ponds and slightly acidic marshy areas. Areas trampled by cattle provide ideal snail habitats. Most snails die during the winter but populations rapidly multiply in spring 15C-26C.
154
When does fluke infection usually occur?
The main time in the Uk when temperatures and moisture are adequate for both snails and fluke is between april and november. typically snails are infected in late spring and early summer by miracidia hatched from eggs deposited during the previous autumn and winter. Cercariae from this infection encyst as metacercariae in late summer and autumn.
155
What is acute fasciolosis due to?
Massive liver parenchymal damage due to the presence of up to 1000 migrating immature flukes. usually seen in sheep of all ages from september to december. clinical signs; lethargy, pallor, dyspnoea, death. The liver is friable and has a mottled apperance. Haemorrhagic tracts are present throughout the liver parenchyma. Blood stained fluid is present in the peritoneal cavity. may be extensive severe peritonitis.
156
What is black disease?
A fatal peracute infection of sheep of all ages due to alpha and beta toxins of clostridium novyi type B. it is triggered by migrating fasciola larvae.
157
Describe the clinical signs of chronic fasciolosis?
Adult flukes in the bile ducts. Usually see in february and march. Also seen in the summer associated with winter infection of snails or previously missed infection. Clinical signs; poor body condition, anorexia, anaemia, ascites and submandibular oedema, death. There are varying degrees of hepatic fibrosis and mature flukes are found within the bile ducts. Raised areas of fibrosis around the bile ducts may be seen on the surface of the liver. The liver may b e irregularly shaped due to compensatory hypertrophy of less affected areas. Infection occurs as a continuum hence changes due to subacute and chronic fasciolosis are often seen together.
158
How does fasciolosis present in cattle usually?
Clinical signs of subacute fasciolosis are seldom seeen. Ill thrift, submandibular oedema and pallor are seen due to chronic disease. It is associated with poor reproductive performance. There is an association with reduced milk yields. Disease is exacerbated by poor nutrition or gastrointestinal parasitism.
159
What are fasciola gigantica?
A tropical large liver fluke. Life cycle and snail hosts similar to F hepatica. Pathogenesis and control as for F hepatica.
160
What is fascioloides magna?
Parasite predominantly of deer, intermediate host is freshwater snails, particularly pathogenic in sheep due to persistent migration through liver parenchyma and no encapsulation. Seen in N america and Europe but not UK.
161
Describe the life cycle of dicrocoelium dendriticum?
Adult flukes in the bile ducts of mammalian hosts lay eggs, containing miricidia. Eggs hatch after ingestion by land snails. Two generations of sporocytsts develop in the snails. Cercariae are extruded int he slime that adheres to vegetation. slime balls are ingested by formica ants. Metacercariae develop in the ant body cavity and brain. Brain lesions induce ants to climb to the tip of the herbage. Ants are ingested by ruminants. Metacercariae hatch in the small intestine of the final host. Immature flukes migrate along the main bile duct to the liver. No parenchymal migration. Adult flukes in bile ducts survive manly years. Clinical signs only in heavy infestatinos.
162
What are paramphistomes?
Rumen flukes. Calicophoron daubneyii. Clinical significance unknown - transient diarrhoea. Similar free living and intermediate host stage life cycle to F hepatica. Planorbis and bulinus water snails are known to be intermediate hosts for Daubneyi in mainland europe. Metacercariae excyst in the duodenum. Immature flukes attach and plug feed for about 6 weks. young flukes migrate to the forestomach where they mature. Adult flukes attach to the forestomach wall using their sucker and feed on blood.
163
What is a suitable treatment for fasciolosis?
Triclabendazole - kills all stages in sheep and cows
Closantel - kills 6 week immature to adult
Nitroxynil - kills 6 week immature to adult
Albendazole, clorsulon - only removes adults.
164
What is the aim of F hepatica control?
Too minimise the metacrecarial challenge to susceptible final hosts. Use of anthelmintic dugs to suppress fluke egg output and pasture metacercarial challenge, drainage to reduce rate of egg hatching and survival of free living stages of F hepatica and to prevent the establihsment of adult snail populations. Grazing management srategies to avoid contact between metacarcariae and susceptible final hosts.
165
When should anthelmintic drugs be used to suppress fluke egg output and pasture metacercarial challenge?
Timing of anthelmintic treatments must be carefully tailored to match the epidemiology of liver fluke on a specific farm. Timing of first winter treatment is critical. delay can lead to clinical disease. unnecesasry advance is wasteful. use of forecasts of the effects of summer temperature and rainfall on - rate of fluke development., availability of snail intermediate hosts.
166
Why should cattle b included in a F hepatica control programme for sheep?
Cattle are important maintenance hosts because their grazing behaviour on we farms tends to create snail habitats ensuring that small numbers of miracidia that hatch from eggs shed by cattle efficiently find snails in which the developmental stages can multiply. Treat in late autumn/early winter with triclabendazole to reduce liver parenchymal damage. Growing animals may be dosed after housing with a flukicide effective against adult and later immature flukes. Outwintered cattle may be treated with a flukicide in spring to remove adult flukes and reduce the level of egg contamination of the environment. Most have long milk withdrawal period/cant bee used - treatment of cows at beginning of ddry period may not fit epidemiological pattern.
167
Describe different principles of management of fluke disease rather than reliance on chemotherapy?
Installation of clean water to prevent livestock from drinking from cercarial or metacercarial contaminated water.
168
How can subacute fasciolosis be diagnosed?
History
ULtrasonography - accumulation of peritoneal exudate, adhesions, liver enlarged.
PM findings - liver pathology, Identification of occasional fluke eggs in faeces.
Serum protein concentrations - albumin low, globulin high.
Serum GLDH concentrations
Coproantigen ELISA
169
How can rumen fluke calicophoron duabneyi be diagnosed?
Sediment method - place faeces in sieve & add water, leave to stand and sediment, discard water, repeat, examine sediment under microscopy for presence of fluke eggs.
170
Which cestodes are common in UK sheep and cattle?
definitive host as sheep - monezia expansa
Sheep as intermediate host - taenia hydatigena, taenia multiceps, taenia ovis, echinococcus granulosus.
Cattle as intermediate host - taenia saginata.
Sheep are infected when they ingest oncospheres from pasture contaminated by canid faeces. oncospheres penetrate the gut wall and travel to target organs in the circulation. Development to second stage larval cysts. Canids are infected when they scavenge sheep carcases.
171
Describe taenia saginata (cysticercus bovis)
The definitive hosts are hmans. little pathogenic significance. Typically calves are infected with eggs on the hand of stockpersons or eggs from the environment. associated with poor human sanitation. oncospheres travel to striated muscle once ingested by cattle. Humans become infected by eating raw or inadequately cooked meat. Usually linked to broken sewage pipes or flooding allowing raw sewage onto ground grazed by cattle.
172
Describe how the pet passport scheme restricts cestode infections?
Dogs must be treated for tapeworm between 1 and 5 days before arrival in the UK. treamtnet must have praziquantal or equivalent as its active ingredient. Treatment details must be reported in dogs passport.
