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.
Sudden
Death in Store Lambs
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
–
q
redgut
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%.
PULPY
KIDNEY IS A COMMON CAUSE OF SUDDEN DEATH IN STORE LAMBS FOLLOWING A CHANGE IN
DIET
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.
REDGUT – DISPLACEMENT AND CLOCKWISE
TORSION OF THE INTESTINAL MASS
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
(Rumen acidosis)
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.
GRAIN
OVERLOAD – LAMINITIS IS OFTEN SEEN IN RECOVERING ANIMALS
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.
POLIOENCEPHALOMALACIA (cerebrocorticonecrosis,
CCN)
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.
CCN
– RECUMBENCY AND BACKWARDS FLEXION OF THE NECK
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.
ACUTE
LIVER FLUKE – SURVIVING ANIMALS OFTEN APPEAR LETHARGIC
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
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.
RAPE/KALE POISONING
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 -
q
nitrates
q
photosensitive
substances
q
haemolytic
anaemia factors
q
oxalates
q
glucosinolates
(goitrogen precursors, which can induce iodine deficiency)
q
sulphur
and molybdenum (which can induce copper deficiency)
BRASSICA
CROPS CAN CONTAIN SEVERAL TOXIC SUBSTANCES
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.
Neil Sargison BA
VetMB DSHP FRCVS
Copyright
© NADIS 2002