Sudden death in lambs
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NADIS disease bulletins are written specifically for farmers, to increase awareness of prevalent conditions and promote disease prevention and control, in order to benefit animal health and welfare. Farmers are advised to discuss their individual farm circumstances with their veterinary surgeon.
NADIS Sheep Disease Focus – September 2005
Sudden deaths often occur in store lambs following movement onto stubbles, forage crops or lush aftermath pastures during the autumn. The common causes of sudden death associated with stressful husbandry, feed changes or toxic substances in forage crops are –
- clostridial diseases
- redgut
- systemic pasteurellosis
- grain overload
- acute liver fluke
- nitrate poisoning
- Brassica poisoning
Different practices are required for the prevention and management of these diseases, so it is important that the cause of unusually high losses is investigated. The diagnosis is usually based on the flock management history and post mortem findings from dead lambs. Most of the common causes of sudden death are associated with specific post mortem signs, although in some cases appropriate samples may have to be submitted for further laboratory tests. Sometimes losses are occur as a result of more than one cause, so as many dead lambs as possible should be examined.
The various clostridial bacteria associated with disease in sheep are anaerobic, spore-forming, toxin-producing organisms, which are normally present in soil, faeces or intestinal contents. Most 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. Most of the clostridial diseases are characterised by peracute fatal illness. Sheep farming had become untenable in many parts of Britain before the development in the 1950s of the first multi-component clostridial vaccines. While modern vaccines provide excellent protection against the important clostridial diseases of sheep, many flocks are improperly vaccinated or not vaccinated at all, sometimes in an ill-advised attempt to reduce production costs. Clostridial diseases of sheep are, therefore, endemic throughout Britain. The clostridial bacteria are ubiquitous, so eradication of clostridial diseases is impossible, but good control can be achieved by vaccination.
Pulpy kidney
Pulpy kidney is a common and usually fatal disease of sheep of all ages caused by the epsilon toxin of Clostridium perfringens type D. The disease is often seen in fattening lambs between 6 months and 1 year old, associated with a change in diet such as movement onto silage aftermath or Brassica crops. Following a feed change, partially digested food containing carbohydrate can escape to the small intestine where it can multiply and produce toxins. This risk persists until the ruminal microflora adapt to the improved diet.
Most cases present as sudden death, but animals are occasionally seen alive with non-specific neurological signs and diarrhoea. In extreme cases, losses of between 10 and 15% have been reported.
The initial diagnosis of pulpy kidney is made on the basis of history of sudden deaths in well-grown, unvaccinated lambs fed on a carbohydrate rich diet. However confirmation of this diagnosis depends on post mortem findings, supported by laboratory tests for the presence of epsilon toxin.
Other clostridial diseases
Blackleg occasionally causes high losses in wintering hoggs on root crops.
Braxy is a rare peracute disease of hoggs which occurs during late autumn when the first severe frosts occur. Ingestion of frosted food, such as turnips, is believed to provide a suitable environment in the abomasum for multiplication of the clostridial organism, invasion of tissues and production of toxin. Affected sheep are seldom seen alive.
Black disease and redwater are fatal diseases which occur when migrating liver fluke larvae provide suitable conditions for clostridial multiplication and toxin production. Losses can occur throughout the high-risk period of liver fluke larval migration, which often amount to 5% and occasionally reach 30%.
Prevention of clostridial diseases in sheep
Clostridial diseases can be effectively prevented through vaccination. Previously unvaccinated ewes should be given an initial course of two vaccine injections 4 – 6 weeks apart when they enter the breeding flock, followed by an annual booster about 6 weeks before lambing. This pre lambing booster with a multi-component vaccine also ensures transfer to lambs of passive protection against pulpy kidney, which lasts up to 16 weeks of age. Lambs born to vaccinated dams should receive a first sensitiser dose at about 8 – 12 weeks old, followed by a second booster at least 4 weeks later. While an interval between sensitiser and booster of 4 – 6 weeks is recommended, an immediate response to booster vaccination has been shown in sheep sensitised as long as 18 months previously.
Vaccination should be combined with good stock husbandry, including careful introduction to improved planes of nutrition.
Management of disease outbreaks
Many British sheep are inadequately vaccinated against clostridial diseases and severe outbreaks of pulpy kidney occur sporadically. In these cases it is important to immediately instigate a vaccination programme. Where a sensitiser, but no booster dose of vaccine has been previously used, a single injection of vaccine in the face of an outbreak usually provides immediate protection.
Even when no vaccine has been used, a single injection of vaccine offers significant protection within 48 hours, probably because most animals are naturally sensitised by the presence of small amounts of toxin in their intestines. Yarding of animals for vaccination and restricted feeding usually halt the progress of the disease until the vaccine is effective.
Administration of clostridial vaccines
The recommended dose of vaccine should be administered under the skin over the neck. Clean needles should be used and regularly changed. Vaccines should be correctly stored in a dark place at about 5oC, but protected from freezing. Vaccines should be used before their expiry date and as a general rule, partially used packs should be discarded at the end of the day.
Eight of 400 Suffolk cross lambs were found dead about 3 weeks after introduction to a forage rape crop. Post mortem examination showed the cause of death to be torsion of the small intestine, commonly referred to as redgut.
Redgut is a colloquial term, which is used to describe intestinal displacement and torsion of sheep. The condition is characterised by sudden death and occurs most commonly when weaned lambs have been fed fast-growing lush pasture for a period of three weeks or more. Sporadic losses of 1 – 2% can occur.
The most plausible hypothesis for the cause of redgut is that the feeding of a highly digestible feed promotes a rapid rate of passage of digesta through the forestomach. After a period of about three weeks on such diets, the animal’s rumen volume is reduced. Furthermore, significant amounts of fermentable carbohydrates remain in the digesta which leaves the forestomach. In the large intestine, fermentation and the production of volatile fatty acids result in reduced gut motility and gut distension. The net effect is a reduction in rumen volume, accompanied by an increase in large intestinal volume. It has been speculated that these unstable conditions enable displacement of the abdominal contents and in extreme cases, cause intestinal torsion.
The post mortem examination of freshly dead lambs is required to differentiate redgut from other causes of sudden death such as clostridial diseases. In cases of redgut, the displaced intestine is seen immediately on opening the abdominal cavity. The displaced intestine is bright red and distended from the duodenum to the terminal colon. In most cases a clockwise torsion of the intestinal mass can be determined.
Where there is a commercial requirement to feed lambs on fast growing leguminous crops, roughage supplementation in the form of ad libitum hay can reduce the incidence of redgut. Anecdotal evidence suggests that a five-day lush pasture and two-day rough pasture feeding cycle effectively prevents deaths from redgut.
25 of 450 Scottish Blackface ewe lambs were found dead in October 2001 within 2 weeks of a move from hill to lush dairy cattle aftermath pasture. Systemic pasteurellosis was confirmed as the cause of the problem by post mortem examination of several dead lambs.
Systemic pasteurellosis is the most commonly diagnosed cause of sudden death in store lambs between October and December. Mortality rates of 20% have been reported, but losses of about 2% are more commonplace.
Systemic pasteurellosis is caused by the bacterium Pasteurella trehalosi, but the reasons for disease outbreaks are not fully understood. Outbreaks frequently follow movement of lambs onto rape, turnips or improved pastures. Wet and cold weather has also been implicated. P. trehalosi is found in the tonsils and upper gastro-intestinal tract of healthy sheep and it has been suggested that under certain stressful conditions, the bacteria multiply and spread rapidly to the lungs and other organs. Concurrent diseases such as cobalt deficiency or tick borne fever may also predispose to outbreaks of the disease.
Cases of systemic pasteurellosis are seldom seen alive. The first signs of the disease are sudden onset dullness, recumbency, respiratory distress and frothing at the mouth, which usually progress to death within a few hours.
In the face of an outbreak of systemic pasteurellosis, whole flock treatment with a single injection of long-acting antibiotic may help to prevent further losses, although the stress of gathering and injecting the lambs may itself precipitate some deaths. It is, therefore, impossible to determine the effectiveness of this strategy and the decision to treat or not is based on individual flock circumstances.
Prevention of systemic pasteurellosis is also problematic. Avoidance of nutritional stress and wet weather conditions, which predispose to the disease, is difficult and pasteurella vaccines only afford variable short-lasting protection.
Grain overload is associated with sudden increases in the level of concentrate feeding. The problem is common in late pregnant ewes and intensive grain-fed finishing lambs, and is occasionally seen in sheep grazing stubbles where piles of grain have been left.
Fermentation rather than digestion of grain in the rumen results in production of large amounts of lactic acid and other toxins, which when absorbed into the circulation result in acidosis and endotoxic shock. Large quantities of lactic acid decrease the pH of the rumen and kill the normal flora of bacteria and protozoa. Water is drawn from the circulation into the rumen resulting in dehydration.
The severity of the disease depends on the amount of grain eaten, the physical state of the grain (bruised grain ferments more rapidly in the rumen than whole grain) and previous adaptation to grain feeding. In the early stages of the disease, animals may show signs of mild colic and tooth grinding, progressing in severely affected animals to a staggering gait, apparent blindness and stupor. Severely affected animals may become recumbent and die within 24 hours of grain engorgement.
Recovery in many cases is slow because the rumen becomes inflamed due to secondary fungal and bacterial infections. Lameness is often seen in recovering animals due to laminitis.
The diagnosis of grain overload is based on the feeding history and clinical signs. Post mortem examination of dead lambs is often unrewarding, although the presence of partially digested grain in the rumen of a dehydrated and congested carcase may support the diagnosis.
When grain overload is suspected, animals should be removed from the source of grain and provided with good quality roughage. Affected animals can be treated orally with 30 ml of milk of magnesia (magnesium hydroxide) and given multivitamin injections, but the prognosis is poor in advanced cases.
Several cases of poiliencephalomalacia in lambs were reported during autumn 2001. The early signs of the disease are blindness, isolation from the rest of the flock and aimless wandering. As the disease progresses over a period of 12 – 24 hours, sheep become recumbent and periodically flex their neck backwards and ‘stargaze’. Untreated animals die within a few days.
In most cases, the disease is due to necrosis of the superficial tissue of the brain associated with an induced deficiency of vitamin B1 (thiamine). Thiamine is normally synthesized in the rumen, but overgrowth of thiaminase-producing bacteria in the rumen following a change of diet destroys the vitamin. Bracken contains high concentrations of thiaminase enzymes which may be responsible for some outbreaks of CCN and some cases are associated with dietary sulphur toxicity.
Most cases occur about 2 weeks after movement to lush pasture or other dietary change such as overnight yarding before anthelmintic drenching. The treatment response to intravenous vitamin B1 and corticosteroids is good, provided that affected animals are identified promptly. Further subcutaneous injections of vitamin B1 are usually given. Your vet can provide further specific advice on the diagnosis and treatment of CCN.
Four of about 200 Suffolk cross lambs were found dead at the end of October 2001, a few days after handling to draw finished lambs. Surviving lambs were reported to be dull and lethargic. Post mortem examination of the dead lambs revealed extensive peritionits, and haemorrhagic tracts throughout a pale and mottled liver. These findings are consistent with acute liver fluke infection. This particular outbreak occurred in a part of south-east Scotland which is not recognised as a high fluke-risk area.
Liver fluke is an important annual cause of ill thrift and deaths of ewes and lambs in wet parts of western Britain during autumn and early winter. In some years following prolonged wet weather, the disease also occurs in normally drier eastern areas where it may be unrecognised and cause significant losses.
Acute liver fluke disease is caused by massive liver damage due to the presence of up to 1000 migrating immature flukes and is characterised by lethargy, pallor, laboured breathing and deaths of sheep of all ages from September to December. Sudden deaths may occur when animals are handled, as a result of liver rupture. Sudden deaths from black disease or redwater may occur in unvaccinated sheep.
Liver fluke disease in sheep and cattle is caused by the trematode parasite Fasciola hepatica. F. hepatica has a two host life cycle involving Lymnea truncatula snails and a variety of mammalian species including sheep, cattle, goats, deer and rabbits. The seasonal appearance of liver fluke disease is determined by the effects of moisture and temperature on the snail populations and free-living stages of F. hepatica. Under typical British conditions, the only time when temperatures and moisture are adequate for both snails and fluke is between April and November. Typically, snails are infected in late spring, giving rise to metacercariae, capable of infecting sheep or cattle in late summer and autumn.
The diagnosis of acute liver fluke disease in based on the history of sudden deaths in recognised fluke areas at the relevant times of year. The diagnosis is confirmed by the characteristic post mortem findings. Elevated serum concentrations of the liver enzymes in surviving lambs can support the diagnosis of acute liver fluke disease.
Treatment and control of liver fluke
The flukicides which are available in Britain differ in their efficacy against immature and adult F. hepatica. For the treatment of acute liver fluke disease it is necessary to use triclabendazole which has good efficacy against early immature flukes. When “safe” dry pasture is available, a single treatment is given before moving the sheep. “Safe” pasture is seldom available on typical hill farms in fluke areas, so repeated treatments at 3 week intervals are required throughout the high risk period of autumn and early winter. Careful animal handling is necessary and some deaths may occur despite treatment. After treatment animals should be provided with good quality nutrition. Triclabendazole has a meat withdrawal period of 56 or 28 days, depending on the product used.
The risk of fascioliasis can be predicted using knowledge of lifecycle and weather conditions and local knowledge of the disease. In normal years all at-risk sheep are strategically treated with an appropriate flukicide in late spring (to remove adult flukes), in October (to remove immature flukes) and in January (to remove immature and adult flukes). In years when a high risk of fascioliasis is forecast, extra strategic treatments are given 4 – 6 weeks after the standard treatments. The national liver fluke risk this year is currently believed to be ‘normal’. However, your vet can provide more specific information about the disease risk in your area.
Where possible sheep should be grazed away wet areas during high risk periods. Drainage and fencing off wet and boggy areas may help, but is often impractical.
Nitrate poisoning is an uncommon cause of death in store lambs. However, when the problem occurs, lamb losses can be high. The disease results from the ingestion of large amounts or nitrates, either directly following access to nitrogenous fertiliser or through nitrate containing plants such as clover or Brassica crops. Occasionally, when rapid growth occurs in heavily fertilised pastures due to rainfall after a prolonged dry period, normally safe grazing can contain high concentrations of nitrates.
Nitrates are metabolised in the rumen to harmful nitrites, which when absorbed, combine with haemoglobin in the blood to form methaemoglobin. Methaemoglobin is incapable of transporting oxygen, so affected animals are weak and lethargic, with a rapid pulse and shallow breathing. The skin and mucous membranes around the mouth and vulva of female animals become brown-coloured and eventually cyanotic in appearance.
The diagnosis of nitrate poisoning is based on the grazing history, clinical signs and post mortem findings. In affected animals, blood is chocolate-coloured and opaque. The percentage of methaemoglobin in the blood can be determined, but this is usually unnecessary.
The treatment response to intravenous infusion of methylene blue is usually good, although this chemical is seldom immediately available. Animals should be removed slowly from the source of nitrates and if necessary only reintroduced gradually.
Brassica crops provide a balanced source of carbohydrate, protein, fibre and minerals and are a very useful sheep feed. However, when fed exclusively, lambs seldom achieve growth rates which would be predicted on the basis of the feed analysis. This is because Brassica crops also contain several important toxic substances which cause depressed appetite. The list of toxic substances includes –
- nitrates
- photosensitive substances
- haemolytic anaemia factors
- oxalates
- glucosinolates (goitrogen precursors, which can induce iodine deficiency)
- sulphur and molybdenum (which can induce copper deficiency)
Haemolytic anaemia
One particularly important toxic substance is a haemolytic anaemia factor, S-methylcysteine sulfoxide (SMCO). SMCO is converted by bacterial fermentation in the rumen to dimethyl disulfide, which causes haemolysis (red blood cell destruction).
Severity of the disease is proportional to the SMCO content of the crop. When present in small amounts, the toxin results in poor growth rates. However, when SMCO is present in high concentrations, lambs become anaemic with haemoglobinuria (red urine), progressing rapidly to death.
SMCO concentrations in plants can be analysed and Brassica crops categorised as low or high potential risk. However, SMCO increases with the age of the crop, so even low risk varieties can become potentially hazardous as they reach maturity or if they are fed to excess. To avoid these risks, long-keep store lambs should not be grazed on Brassica crops for prolonged periods and animals should be provided with a pasture run-off or supplementary feed.
The diagnosis of haemolytic anaemia is based on the history of grazing potentially high-risk Brassica crops, clinical signs in affected animals and post mortem findings from freshly dead animals of jaundice, haemoglobinuria and anaemia, with congestion of the internal organs. Blood samples from sick animals are dark red and watery.
When the disease is suspected, animals should be removed from the crop and carefully introduced to supplementary feed.
The list of causes of sudden death described in this NADIS Sheep Disease Focus is by no means comprehensive. For example, louping ill should be considered when losses occur in naïve animals introduced to tick areas. Your vet can provide specific advice about the diagnosis, management and prevention of sudden death problems in your flock.
Copyright © NADIS 2005
www.nadis.org.uk
While every effort is made to ensure that the content of this forecast is accurate at the time of publication, NADIS cannot accept responsibility for errors or omissions. All information is general and will need to be adapted in the light of individual farm circumstances in consultation with your veterinary surgeon.
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