Sudden death of animals
Conditions that cause sudden death without any other observed signs.
When is it happening?
Understand the conditions that can cause sudden death without any other observed signs.
Conditions that cause sudden death without any other observed signs.
When is it happening?
What to look for - ranges from serious acute disease to milder chronic form.
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.
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.
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.
When introducing cattle to concentrates monitor them closely and check the consistency of their manure.
Occurs in annual ryegrass pastures in South Australia and Western Australia.
Ranges from mild to severe nervous signs, ie staggering, convulsions, death can occur in severe cases.
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.
All age groups of cattle are susceptible.
Lead poisoning, phalaris staggers or perennial rye grass staggers that occurs on perennial rye grass pastures.
Finding of galls and yellow slime on annual rye grass plants. Note that rain can wash the slime off the plants.
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.
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.
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.
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.
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.
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 carcass 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.
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 malignant 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 malignant 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 wool sorter disease because it occurred in people that handled wool from dead sheep.
Sites where animals have died should be thoroughly cleaned up and disinfected.
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.
Black disease is unusual in cattle and more often seen in sheep. It usually occurs in cattle grazing damp areas.
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.
A number of animals may be affected but the disease does not spread from animal to animal.
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.
If animals are found in an early stage of the disease they may respond to antibiotics.
Animals are usually found dead. If animals are observed before death they may:
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.
Cattle 6-24 months of age, grazing on good quality pastures and in good condition.
Changes in muscle tissue at post-mortem.
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.
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.
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.
Give in "5 in 1", "7 in 1" or "8 in 1" clostridial vaccine according to the label recommendations.
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.
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 causes of sudden death.
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.
Over consumption of young, rapidly growing legumes, clover or lucerne pastures
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:
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
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 of any age.
Other causes of sudden death. May be confused with calving paralysis.
Identify the toxin in the gut contents of affected animals and/or in material that is suspected of causing the disease.
Does not spread from animal to animal but multiple cases may occur if a group of animals access toxic material.
People do not contract botulism from cattle and the toxin does not pass into their milk.
Nursing of mild cases can be effective.
In regions where botulism occurs, vaccinate animals that may be exposed to toxic material.
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.
Young cattle that are in good condition and on very good feed
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.
Enterotoxaemia does not spread from animal to animal.
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.
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.
Failure to fully vaccinate young stock with clostridial vaccines (5 in 1, 7 in 1 or 8 in 1)
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.
Dairy cattle within the first 6 weeks after calving. Susceptibility increases with age. Grass tetany is generally a herd problem.
Other causes of sudden death:
Diseases causing nervous signs:
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.
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.
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.
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:
In the more chronic form:
Ingestion of toxic amounts of lead
Most often seen in younger animals. Calves tend to be more curious and are more susceptible to poisoning, especially when on milk based diets.
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.
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.
Animals may recover from lead poisoning if they receive veterinary treatment at an early stage. Young animals are less likely to respond to treatment.
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.
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.
Causes of sudden death such as:
Causes of downer cows such as calving paralysis, lameness, injury, acute cases of mastitis
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.
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.
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.
Transition feeding with limited effective fibre (PDF, 281KB)
Learn how a pre-calving diet sets up cows for lactation:
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:
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.
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.
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.
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 that cause nervous signs in animals include:
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.
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.
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.
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.
Cattle of any age.
Other diseases that cause sudden death. Young animals seen in the early stages of the disease might show similar signs to animals with polioencephalomalacia.
The tetanic muscle spasms are usually characteristic enough to diagnose tetanus especially if there is a history of a deep wound in the last few weeks.
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.
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.
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.
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.
Our Farm, Our Plan is a new program designed to equip farmers to clarify their long term goals, identify the actions needed and to manage uncertainty and risk.
The hay and grain report is commissioned by Dairy Australia to provide an independent and timely assessment of hay and grain markets in each dairying region. The report is updated 40 weeks per year.