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Read about the conditions that can cause sudden death without any other observed signs.

Animals Found Dead

Conditions that cause sudden death without any other observed signs. When is it happening?

After a sudden change in feed

In cows around the time of calving

In young stock

Other causes

  • Acute acidosis

    Acidosis

    What to look for - ranges from serious acute disease to milder chronic form.

    Acute acidosis

    • Usually within 1 day of carbohydrate overload
    • May stop eating
    • May appear depressed
    • May be unstable if standing
    • Rumen is often distended (on left side)
    • Tapping left flank may produce splashing sounds
    • May have profuse diarrhoea with an offensive smell
    • May become dehydrated, lie down, and without prompt treatment, are likely to die

    Chronic acidosis

    • Usually a herd problem
    • Vague clinical signs Loss of appetite
    • Intermittent diarrhoea
    • Lower milk production
    • Depression

    Cause

    Excess amounts of carbohydrate-rich foods such as grains or fruit. Rumen function is overloaded leading to increased acid in the rumen. Milder forms have a slower onset, but if not managed can lead to long term changes to the rumen.

    Animals likely to be affected

    Often seen in cows in early lactation. Typically seen after calving, especially in cows that have been fed on pasture during the dry period and the rumen has not had time to adapt to concentrate feeds.

    Other diseases with similar signs

    • Acute: infections, milk fever, mastitis or displaced abomasum, other causes of scours
    • Milder chronic forms: may resemble lead poisoning, listeriosis or polioencephalomalacia

    Confirming the diagnosis

    • Recent increase in consumption of grain or fruit
    • Test rumen fluid acidity (pH)

    Treatment

    Serious cases of acidosis need rapid treatment. In severe cases your vet can operate to remove the rumen contents and provide other supportive treatments to help get the rumen operating again and prevent infection.

    Less severe cases may respond to treatment with magnesium products given by stomach tube. Afterwards it is important to feed good quality hay and ensure that animals do not have access to water until the next day.

    Animals that have mild acidosis should be fed good quality hay and reduced amounts of concentrates. Watch them closely to ensure that any animals that are not improving can be treated more intensively.

    Risk factors

    • High carbohydrate feeds are not stored securely 
    • Cattle introduced rapidly to diets containing high proportion of concentrates

    Prevention

    When introducing cattle to concentrates monitor them closely and check the consistency of their manure. 

  • Annual ryegrass toxicity

    Annual ryegrass toxicity

    Occurs in annual ryegrass pastures in South Australia and Western Australia.

    What to look for

    Ranges from mild to severe nervous signs, ie staggering, convulsions, death can occur in severe cases.

    Cause

    A bacterial toxin spread by a pasture nematode (worm). A tiny nematode invades the developing seed head in annual rye grass and turns it into an abnormal growth called a gall. The nematode carries bacteria that multiply rapidly in the gall and produce a powerful toxin that looks like yellow slime. The toxin in the gall is very persistent, so infected pastures will remain toxic until the affected plant material is removed or dies down. Hay made from toxic pastures may also cause ARGT.

    Animals likely to be affected

    All age groups of cattle are susceptible.

    Other diseases with similar clinical signs

    Lead poisoning, phalaris staggers or perennial rye grass staggers that occurs on perennial rye grass pastures.

    Confirming the diagnosis

    Finding of galls and yellow slime on annual rye grass plants. Note that rain can wash the slime off the plants.

    Spread of the disease

    The disease can be spread beyond the affected region via toxic hay, although it is not clear whether this can lead to establishment of ARGT in new regions.

    Treatment

    Any stock movement should be done carefully to avoid injuries and worsening of the clinical signs. Affected mobs should be moved quietly to a non-toxic area and supported with free access to water and high quality feed. Animals may continue to show clinical signs of ARGT for up to 10 days after being removed from the toxic pasture.

    Prevention

    If paddocks are suspected of being infected they can be sprayed out and replaced, or prevent the pasture developing seed heads by topping or hard, persistent grazing. A biological control agent called twist fungus is available commercially, which appears to be effective in reducing toxicity when it becomes established in pastures.

    More information

    Department of Agirculture WA - Annual ryegrass toxicity in livestock

  • Anthrax

    Anthrax

      

    What to look for

    • Animals are usually found dead
    • Bloody discharge from the mouth, nostrils and anus after death
    • In the very early stages animals have a high temperature, muscle tremors, difficulty in breathing and/or convulsions.

    Cause“ a bacteria (Bacillus anthracis)

    Bacillus anthracis forms spores that allow it to persist in soil for decades. Animals become infected by eating or inhaling the anthrax bacteria from contaminated soil or water. Cases of anthrax sometimes occur after heavy rain following hot dry weather.

    Animals likely to be affected

    Ruminants (cattle, sheep and goats) and horses. Anthrax is a rare disease in dairy cattle in Australia. The disease usually causes only 1 or 2 cases on a farm (or in a district). Occasionally, larger numbers of animals will die on a farm or cases may occur on other farms in the district.

    Other diseases with similar signs

    Other causes of Sudden Death.

    Confirming the diagnosis

    • If you find an animal that has died suddenly and has blood coming from the nostrils, mouth or elsewhere, call your vet or the nearest office of the state Department of Primary Industries. It is important NOT to touch the carcase and to remove any stock from the paddock.
    • The diagnosis is confirmed by laboratory examination of a blood sample that has been carefully collected from the dead animal.

    Spread of the disease

    Contamination of food and water. Carcases of infected animals contain huge numbers of the anthrax bacteria and can be a source of future infection. Anthrax is a notifiable disease so the affected property is placed in quarantine and animal movements are restricted until deaths cease and all animals are protected by vaccination. Government animal health staff will organise carcase disposal.

    When a case occurs, the remainder of the herd will be vaccinated. Full immunity occurs 14 days after vaccination and lasts about a year. Vaccination may be extended to neighbouring herds when a number of farms are affected. Because the vaccine is alive, vaccination is carried out by veterinarians or other trained staff. Milk production may drop for a short time after vaccination.

    Anthrax in people

    People can become infected via cuts and abrasions when handling infectious material such as an animal that has died from anthrax. Carcases of dead animals should always be handled with care, using protective clothing and good personal hygiene.

    The infection usually stays localised as a pustule or œmalignant carbuncle. Seek immediate medical attention if you suspect that you have an infection. In people treatment with antibiotics is generally successful although the rarity of anthrax means that medical authorities may not make the link between œmalignant carbuncles and anthrax.

    More rarely, infection may occur from inhaling the anthrax bacteria and this can result in very severe pneumonia which can be fatal. This form of the disease was once called œwool sorter disease because it occurred in people that handled wool from dead sheep.

    Prevention

    Sites where animals have died should be thoroughly cleaned up and disinfected. 

  • Black disease

    Black disease

    What to look for

    • Animals are often found dead
    • If seen before death, animals are depressed, have reduced milk production and are not eating. After death, the animal carcase decomposes quickly, may have bloody discharges from the mouth and nose and sometimes appears black.

    Cause - a bacterium (Clostridium novyi) + liver damage

    Clostridium novyi is commonly found in soil and persists as very resistant spores. When eaten by cattle it enters the body and lodges harmlessly in the liver. If the liver is damaged it may trigger the organism to multiply and produce a fatal toxin. Liver damage is usually caused by immature fluke burrowing through the liver, so black disease generally occurs in summer and autumn when cattle are exposed to fluke infestations.

    Animals likely to be affected

    Black disease is unusual in cattle and more often seen in sheep. It usually occurs in cattle grazing damp areas.

    Other diseases with similar signs

    Can be confused with other causes of sudden death such as anthrax, grass tetany, blackleg, enterotoxaemia.

    Confirming the diagnosis

    Post mortem examination of the liver. Your vet can take samples for laboratory testing. The typical history is of sudden death of one or more animals, the farm being in a liver fluke area and animals not being vaccinated.

    Spread of the disease

    A number of animals may be affected but the disease does not spread from animal to animal.

    Risks to people

    While black disease is not a risk to people, there are other causes of sudden death in cattle, such as anthrax, which can cause serious human disease. Carcases of dead animals should always be handled with care, using protective clothing and good personal hygiene. Call your vet if you are unsure about the cause of death.

    Treatment

    If animals are found in an early stage of the disease they may respond to antibiotics.

    Risk factors

    • Failure to vaccinate stock with Clostridial vaccines that include black disease
    • Failure to control liver fluke 

  • Blackleg

    Blackleg

    What to look for

    Animals are usually found dead
    If animals are observed before death they may:

    • Be very depressed and have a high fever
    • Have difficulty walking 
    • Have swelling in the major muscles of the leg or neck
    • Have pockets of gas that may be felt in the affected tissues

    Cause

    A bacterial infection (Clostridium chauvoei).This bacteria is widespread and can form highly resistant spores that persist in the environment. Animals pick up the bacteria from pasture and it lodges in their muscle tissues. If the muscle is wounded or bruised, this triggers the organism to start to proliferate and produce a lethal toxin.

    Animals likely to be affected

    Cattle 6-24 months of age, grazing on good quality pastures and in good condition.

    Other diseases with similar signs

    Enterotoxaemia, bloat, anthraxgrass tetany or some types of poisoning.

    Confirming the diagnosis

    Changes in muscle tissue at post-mortem.

    Spread of the disease

    Not spread from animal to animal. Several animals may be affected at the same time which may mean they have had a common exposure to the same trigger from handling or transport.

    Risks to people

    While blackleg is not a risk to people, other causes of sudden death in cattle, such as anthrax, can cause serious human disease. Dead animals should be handled with care, using protective clothing and good personal hygiene. Call your vet if you are unsure about the cause of death.

    Treatment

    Usually too late to treat. The most effective action is to remove the herd to another paddock and to vaccinate all stock against the common Clostridial diseases.

    Risk factors

    • Failure to vaccinate young stock
    • Rough handling of stock in yards or during transport

    Prevention

    Give in "5 in 1", "7 in 1" or "8 in 1" Âclostridial vaccine according to the label recommendations.

  • Bloat

    Bloat (frothy)

    What to look for

    • Animals are often found dead with a very distended abdomen
    • If found before death: distended abdomen on the left side between the last rib and the hip bone very distressed, difficulty breathing if untreated, may die quickly
    • Cows can also have less severe forms of bloat that may depress milk production

    Cause

    Consumption of young, rapidly growing legumes, clover or lucerne. Bloat is usually caused by eating pasture species that are growing quickly and contain low fibre levels. Consequently, animals produce less saliva production which makes them more susceptible to bloat. Under certain circumstances, feeding on these pastures can lead to build up of foam in the rumen that prevents animals burping to remove the gas produced in the rumen.

    Animals likely to be affected

    Heifers are more likely to die of bloat than older cows. There may be breed differences in susceptibility, with Jerseys and crossbred cattle being more susceptible.

    Other diseases with similar signs

    Other causes of sudden death.

    Confirming the diagnosis

    • Sudden death of animals with very distended abdomens (this is only useful in diagnosis if the animal has died recently because all animals will œblow up after death)
    • Recently introduced to pastures with a high clover or lucerne content
    • Characteristic foam in the rumen (but this only lasts for a few hours after death)

    Treatment

    Move animals from the toxic pasture to a pasture with lower levels of clover or lucerne
    Provide supplementary feed such as hay or silage
    Animals that are mildly affected can be treated with a bloat drench. In advanced cases of bloat it is often difficult to administer treatments that will reduce foam in the rumen.
    Seriously affected animals (having difficulty breathing, open mouth, tongue out) need immediate assistance to either reduce the foam or remove it. As a last resort, an incision can be made in the upper left flank to allow the foam to escape. While this approach may save the bloated animal it is essential to call your vet immediately to repair the wound and administer antibiotics to counter infection.

    Risk factors

    Overconsumption of young, rapidly growing legumes, clover or lucerne pastures

    Prevention

    Only introduce animals when their appetite has been partially satisfied with safe pastures, hay or silage. Limit grazing time and observe cattle closely to assess the risk and act quickly if animals start to show signs of bloat.

    Administer anti-foaming chemicals:

    • detergents such as the teric group of chemicals
    • anti-foaming agents (bloat oils) such as paraffin oil and tallow
    • rumen modifiers such as monensin

    Most anti-foaming chemicals are only effective for a relatively short time. The major challenge is to ensure that animals have a continual supply of the chemical in their rumen. Systems for maintaining a safe level of chemical in the rumen include: drench twice a day

    • spray pastures with oil
    • mix the medication with feeds that delivered in the bail during milking
    • flank application of bloat oil - some animals do not lick the oil and are not protected
    • add detergents to drinking troughs
    • bloat blocks limited success because not all animals will lick the blocks
    • bloat capsules - designed to stay in the rumen and slowly release monensin for ~ 3 months

  • Botulism

    Botulism

    What to look for

    • Animals are found dead or paralysed
    • Paralysis usually affects the muscles of the legs, tongue, jaw and throat
    • Affected animals stumble, lie down and are unable to eat, but usually remain upright
    • Characteristic weakness and paralysis of the legs and head
    • Mildly affected cattle may recover over several weeks

    Cause

    A toxin produced by bacteria (Clostridium botulinum). This bacteria grows only in environments low in oxygen such as inside rotting carcases. Clostridium botulinum produces spores that can last many years in the soil. Cattle are very sensitive to fatal poisoning by the botulism toxin. Exposure most often occurs via rotting carcases of cattle in water courses, carcases of rodents, snakes or possums trapped during hay or silage production, or in rotted food by-products such as brewer's grains, citrus pulp and cannery waste. Outbreaks have occurred in cattle with access to poultry manure that contained poultry carcases.

    Animals likely to be affected

    Animals of any age.

    Other diseases with similar signs

    Other causes of sudden death. May be confused with calving paralysis.

    Confirming the diagnosis

    Identify the toxin in the gut contents of affected animals and/or in material that is suspected of causing the disease.

    Spread of the disease

    Does not spread from animal to animal but multiple cases may occur if a group of animals access toxic material.

    Risks to people

    People do not contract botulism from cattle and the toxin does not pass into their milk.

    Treatment

    Nursing of mild cases can be effective.

    Risk factors

    • Cattle have access to toxic material e.g. dead animals in watercourse
    • Feeding poorly made hay or silage that may contain animal carcases Failure to vaccinate in high risk regions

    Prevention

    In regions where botulism occurs, vaccinate animals that may be exposed to toxic material.

  • Enterotoxaemia

    Enterotoxaemia

    Clinical signs

    • Sudden death
    • Young animals may be found lying down having convulsions
    • Older animals may have a longer illness, and appear depressed, bloated and have no appetite
    • Some animals will have nervous signs such as aimless wandering

    Cause - a bacterial infection (Clostridium perfringens)

    This organism is normally found in the gut of healthy animals and only causes disease under exceptional conditions which allow it to multiply and produce a lethal toxin. This toxin is absorbed by the animal and causes damage to the lining of blood vessels. Enterotoxaemia also occurs in sheep and goats and in these species it is usually referred to as pulpy kidney.

    Animals likely to be affected

    Young cattle that are in good condition and on very good feed

    Other diseases with similar signs

    Any other diseases that cause sudden death and or nervous signs for example, anthraxgrass tetany or poisoning (lead or other toxic substances or plant toxins)

    Confirming the diagnosis

    The history of sudden death in young animals that are on good feed, and in good condition, suggests a diagnosis of enterotoxaemia. Laboratory examination of intestinal contents and blood can confirm the diagnosis.

    Spread of the disease

    Enterotoxaemia does not spread from animal to animal.

    Risks to people

    Enterotoxaemia in cattle is not a public health risk, but it is always important to be careful about personal hygienic when handling the carcase of an animal that has died suddenly, as it could be a disease such as anthrax that can infect people.

    Treatment

    Even if animals are found alive they usually do not respond to treatment. The most effective action is to remove the herd to another paddock where the feed is less lush and to vaccinate with a clostridial vaccine.

    Risk factors

    Failure to fully vaccinate young stock with clostridial vaccines (5 in 1, 7 in 1 or 8 in 1)

  • Grass tetany

    Grass tetany

    What to look for:

    • Can range from mild signs to a rapidly fatal illness:
    • Sudden death
    • Strange behaviour or aggression
    • Convulsions and muscle spasms
    • Over reaction to sounds or movement
    • Collapse
    • Milder cases show poor appetite, slight agitation and reduced milk production

    Cause - low magnesium intake

    Cattle cannot store magnesium so require a daily intake to maintain adequate blood levels. Symptoms occur when the cow'™s magnesium levels drop below a threshold level. Animals are most at risk when grazing lush pasture especially if it has been fertilized with nitrogen or potash. Outbreaks of grass tetany may be set off by a sudden change of pasture or by bad weather that reduces grazing time.

    Animals likely to be affected

    Dairy cattle within the first 6 weeks after calving. Susceptibility increases with age. Grass tetany is generally a herd problem.

    Other diseases with similar signs

    Other causes of sudden death:

    • Milk fever
    • Anthrax
    • Nitrate poisoning
    • Clostridial diseases

    Diseases causing nervous signs:

    • Nervous
    • ketosis
    • Lead poisoning
    • Urea poisoning
    • Listeriosis (usually a single animal)
    • Polioencephalomalacia (usually young animals)

    Confirming the diagnosis

    Blood magnesium levels are not a reliable diagnostic test in dead animals, so your vet may take a fluid sample from the back chamber of the eye.

    Treatment

    The aim is to increase blood levels of magnesium as quickly as possible without damaging the heart. Intravenous administration of a magnesium solution is difficult in an animal with convulsions and is best done by your vet. Additional treatment involves injecting magnesium solution under the skin and allowing the animal to recover in a quiet environment.

    Risk factors

    • Grazing on lush pasture, especially if it has been fertilized with nitrogen or potash
    • Cows in early lactation
    • Bad weather or sudden change in pasture

    Prevention

    Magnesium compounds are effective but require daily administration e.g. daily drenching, adding the treatment to feed in the bail, spraying it on to hay, adding it to water or using magnesium blocks.

  • Lead poisoning

    Lead poisoning

      

    What to look for

    Ranges from sudden death to nervous signs, weight loss and weakness. Signs depend on the amount and form of lead eaten by the animal

    In the more acute form:

    • Staggering, depression, blindness
    • Failure to eat, changed behaviour and convulsions

    In the more chronic form:

    • Weight loss, poor appetite
    • Depression and a range of nervous signs

    Cause

    Ingestion of toxic amounts of lead

    Animals likely to be affected

    Most often seen in younger animals. Calves tend to be more curious and are more susceptible to poisoning, especially when on milk based diets.

    Other diseases with similar signs

    Can be confused with other causes of sudden death and also diseases that cause nervous signs such as grass tetany, listeriosispolioencephalomalacia or ketosis.

    Confirming the diagnosis

    Lead poisoning may be confirmed by blood tests but these are not very reliable. In dead animals the lead levels in tissues can be determined and, in some cases, it may be possible to find lead particles in the rumen or reticulum.

    Risks to people

    People are also vulnerable to lead poisoning and care always needs to taken in handling lead sources especially in old buildings where lead-based paints may have been used.

    Treatment

    Animals may recover from lead poisoning if they receive veterinary treatment at an early stage. Young animals are less likely to respond to treatment.

    Risk factors

    • Animals have access to sources of lead e.g. discarded car batteries, lead flashing or pipes
    • Housing calves in buildings with walls or woodwork painted with old lead-based paints

  • Milk fever

    Milk fever

    What to look for

    • Downer cow shortly before or after calving
    • Most often found lying down, resting upright on the sternum with the head erect
    • Progresses to lying on their side If not treated, will become unconscious and die within a few hours
    • In the early stages cows may be excitable and appear unstable when standing and walking

    Cause

    Low blood calcium level. Around calving time, cows need to mobilise large amounts of calcium from body stores such as bone. If this occurs too slowly the amount of calcium in the blood may fall below optimal levels resulting in milk fever.

    Animals likely to be affected

    Older, high producing cows in good body condition, shortly before or after calving. Occasionally occurs a few weeks after calving when cows are in oestrus.

    Other diseases with similar signs

    Causes of sudden death such as:

    • bloat
    • anthrax
    • grass tetany

    Causes of downer cows such as calving paralysis, lameness, injury, acute cases of mastitis

    Confirming the diagnosis

    Milk fever is usually diagnosed by the cow'™s history and her response to treatment. If the cow is found dead, laboratory testing can help rule out other possible causes of sudden death.

    Treatment

    Cows with milk fever need an injection of calcium (usually calcium borogluconate solution) preferably early in the course of the disease. There is little evidence that milk fever treatments containing additional minerals are any more effective than straight calcium products. If the cow is found early, oral calcium supplements or a calcium injection under the skin can be very effective. Injections under the skin can cause problems such as swelling and infection. Your vet may need to give a treatment into the vein but this requires careful monitoring to prevent heart failure.

    Cows need to be watched after treatment because they can appear to recover and then have a relapse some time later. If a cow responds to treatment but is reluctant to get to its feet, it should be encouraged to rise as lying down for long periods can lead to further complications.

    Risk factors

    • Cows calving in good or fat condition
    • Jersey breed
    • Cows with history of milk fever
    • High green feed diet during the transition period
    • Feeds that have had recent application of potash

    Prevention

    Changing the cow'™s diet during the transition period (from 4 weeks before calving until 4 weeks after calving) can reduce the occurrence of milk fever and other metabolic diseases, and optimise production and fertility. The simplest approach is to restrict the amount of green feed in the last 2 weeks of pregnancy and provide hay from sources that not recently been treated with potash fertilisers. At the other end of the scale cows may be fed a total mixed ration that includes a balance of dietary cations and anions.

    More information

    Transition feeding with limited effective fibre (PDF, 281KB)

    Learn how a pre-calving diet sets up cows for lactation:

    1. Meet her nutritional requirements, not just for maintenance, but also for final development of her foetal calf, and development of her udder.
    2. Give her rumen microbes time to gradually adapt to the milker diet they will need to handle once she calves.
    3. Reduce the chances of her suffering metabolic disorders and other health problems around calving, such as milk fever, grass tetany, ketosis, twisted stomach (displaced abomasum or DA) and retained foetal membranes (RFMs).
    4. Enable her to eat more in the first few critical weeks of her lactation, and thereby lose less body condition and produce more milk.

  • Nitrate poisoning

    Nitrate poisoning

    What to look for

    • Sudden death in a number of animals
    • Animals found alive are depressed, have difficulty breathing and are uncoordinated
    • Abortion may occur in pregnant cows weeks after they are exposed to toxic levels of nitrate
    • The blood of recently dead animals is a brownish colour

    Cause - rapid build up of nitrate in the rumen

    Nitrate is a normal component of plants and is usually converted in the rumen to nitrite which is, in turn, changed to ammonia. If nitrate levels in plants are higher than usual and/or the conversion of nitrite in the rumen is too slow, nitrate concentrations in the rumen can build up to toxic levels. Excess nitrate is absorbed into the bloodstream where it binds with haemoglobin and reduces the ability of the blood to carry oxygen.

    Nitrate can build up in many plants including pasture species such as rye grass, fodder crops such as millet or brassica, or weeds such as capeweed.

    Build up is most likely to occur when:

    • the weather is overcast
    • plants are having a spurt of growth following a period of stress if nitrogenous fertilizers have recently been spread on the pasture
    • Animals appear to be able to adapt to higher levels of nitrate and this can be assisted by providing some roughage such as hay when animals are grazing lush pastures.

    Other diseases with similar signs

    Any disease that causes sudden death such as anthrax, bloatenterotoxaemia (pulpy kidney) or milk fever can be confused with nitrate poisoning.

    Confirming the diagnosis

    Consider nitrate poisoning when the disease outbreak involves a number of animals that have been on potentially toxic pastures, and the blood of recently dead animals is a brownish colour. Your vet can test blood, urine or fluid from inside the eye for the presence of methaemoglobin. Plants can also be tested for nitrate, but care is needed to interpret the results.

    Treatment

    If you suspect nitrate poisoning quietly move the remainder of the mob to a paddock that has less toxic pasture and provide alternative feed such as hay or silage. If sick animals are identified early it is possible for your vet to treat them with methylene blue injections.

    Risk factors

    • Grazing of lush pastures, especially, if cattle have access first thing in the morning or the conditions are overcast
    • Introducing hungry animals to rich pastures without access to roughage, particularly following a period of stress
    • Recent application of nitrogenous fertilizers

    Prevention

    • Check pasture nitrogen levels before grazing
    • Strip graze high risk pastures
    • Pre-feed hungry cattle with hay prior to grazing high risk pastures
    • Wait for sunny conditions to reduce pasture nitrate levels 

  • Polioencepholomalacia

    Polioencepholomalacia

      

    What to look for

    • Depression
    • A range of nervous signs - blindness, wandering aimlessly, excessive salivation and head pressing
    • A fine tremor of muscles may progress to convulsions
    • Death

    Cause - Thiamine deficiency

    Thiamine (vitamin B1) is usually produced in the rumen, but sometimes chemicals (known as thiaminases) break down the thiamine in the rumen. Thiaminases can arise from microorganisms that live in the rumen and it is also believed that ingestion of some plants may contribute to the problem. In some cases it is thought that an excessive amount of sulphur in the diet can cause changes in the rumen that limit thiamine production or availability.

    Animals likely to be affected

    Young animals between 6 - 18 months of age. Most cases involve recently weaned calves during the early summer months. Occasionally, adult animals are affected.

    Other diseases with similar signs

    Other diseases that cause nervous signs in animals include:

    Confirming the diagnosis

    Diagnosis is made on the history of the outbreak, the clinical signs in affected animals and their response to thiamine. There are no routine laboratory tests for use in live animals but, if an animal dies, a post-mortem examination will reveal distinctive changes in the brain.

    Treatment

    Animals suspected of having PEM should be promptly treated by thiamine injections into the vein. The effect of this treatment is relatively short-lived and it needs to be repeated every few hours and followed up by treatment over the next few days. Animals treated early in the course of the disease have a reasonable chance of recovery but treatment of seriously affected animals is unlikely to be successful.

    Prevention

    PEM is not often seen and there is little that can be done to anticipate or prevent cases. If your farm is in an area where PEM occurs more often there may be some local information on plants that could be sources of thiaminases. If so, it may be worthwhile restricting access of susceptible animals to these plants.

  • Tetanus

    Tetanus

      

    What to look for

    • Stiff movement
    • Over-reaction to sudden sounds or movements
    • Muscle spasms
    • Sudden death

    Cause - a bacterial infection (Clostridium tetani)

    This organism is widespread in the environment but only rarely causes disease in cattle. Tetanus usually occurs when an animal has had a penetrating wound, has been castrated or tail docked, or had a difficult calving. It can take days to weeks from receiving the original wound until the appearance of tetanus. The tetanus organism must enter the wound and be sealed off from the air before it can multiply. It then produces a powerful toxin that targets the nerves responsible for muscle movements.

    Animals likely to be affected

    Cattle of any age.

    Other diseases with similar signs

    Other diseases that cause sudden death. Young animals seen in the early stages of the disease might show similar signs to animals with polioencephalomalacia.

    Confirming the diagnosis

    The œtetanic muscle spasms are usually characteristic enough to diagnose tetanus especially if there is a history of a deep wound in the last few weeks.

    Spread of the disease

    The disease does not spread from animal to animal but sometimes a number of animals may develop tetanus at the same time. This is usually because the animals have become infected at the same time following a procedure such as castration.

    Risks to people

    Take care when handling animals that are experiencing muscle spasms. People cannot get tetanus from direct contact with cattle, but are susceptible to infection with the tetanus organism through a penetrating wound. It is also important for all people that handle livestock to make sure that their tetanus vaccinations are up to date.

    Treatment

    If animals are seen early in the course of the disease and are particularly valuable, your vet may administer an antitoxin and recommend other measures that will save some animals. Treatment is not effective if animals are in an advanced stage of the disease.

    Prevention

    Ensure that all calves are protected against tetanus with a clostridial vaccine (5 in 1, 7 in 1 or 8 in 1). Use high levels of hygiene when performing procedures such as castration and dehorning.  

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