After-hours/Emergency Phone: 07 889 6738

07 889 6738

Veterinary Clinic Morrinsville

Cattle Diseases

BVD disease

BVD (bovine viral diarrhoea) is a major disease in the Australasian dairy herd. It is caused by the BVD virus (BVDV). BVDV infection is extremely common, having affected 60-70% of our herds, with virus active in approximately 15% of herds at any one time. The disease is very complex, causing a variety of production limiting disease syndromes with a variety of economic outcomes. The total cost to the NZ dairy industry was estimated around $150m (average $220 per cow in infected herds) with the cost to individual beef herds around $3000-9000.

The biggest driver of BVD loss is reproductive failure. A less common result is failure to thrive, immune suppression and chronic scours in youngstock. Often the effects go undetected.

The virus can be spread in many ways. Well integrated programs are required to bring it under control, but control is possible.

Virus spread

BVDV multiplies in the white blood (immune) cells of the body, and is spread in a wide range of body fluids, including respiratory and uterine secretions, urine, milk, semen, faeces and saliva. Aerosol transmission for sneezing can happen up to 10m, allowing infection spread “across the fence” between properties.

Most BVDV infections are spread “horizontally” between  groups of “in contact” animals, but it can also be spread from dam to calf before birth. If a dam is infected prior to 150 days gestation her calf may not recognise the virus as foreign, and may become permanently infected. This calf will shed virus throughout it’s lifetime to many other cattle, and is deemed a carrier or Persistently Infected (PI) animal.

In a normal previously uninfected animal the virus spreads rapidly around the body and is shed for about 2 weeks (a transient infection, TI). Major disease seldom results and resulting immunity is lifelong.

Disease syndromes

  • The disease expressed depends on the timing of virus infection and the immune status of the animal. Prior to 40 days, a developing embryo stands no chance and dies. Slightly later in pregnancy a range of calf diseases may happen, including limb deformities and brain/balance problems. Occasionally BVD infections in later gestation calves can trigger abortion/stillbirth; mostly where there are other prenatal infections such as Neosporum operating.
  • After 150 days gestation the developing calf will mount it’s own immunity, as is the case for the rest of it’s life.
  • In growing youngstock the virus can spread rapidly through mobs of calves, causing a mild scour which does not respond to worming or antibiotics. The virus may cause immune suppression and contribute to other diseases such as respiratory infections.  PI calves can become ill thrifty and very prone to other diseases, but some progress normally.
  • Very occasionally calves and youngstock will develop intense diarrhoea, with ulcers in the mouth and gut. These cases do not survive. A genuine concern is potential confusion between this disease and catastrophic infections such as foot and mouth.
  • Transmission of the virus between mobs of heifers at grazing is significant, and if they are pregnant they can bring PI calves back to their (uninfected) herd of origin as a “Trojan Horse” calf.
  • PI bulls, or even transiently infected (TI) bulls can spread virus in an unexposed herd during mating. Infected semen causes massive infertility issues.
  • In an adult dairy herd not much disease is seen – 50% of PI animals survive beyond 2 years and many eventually underperform, eventually lining themselves up for culling. The major impacts in a dairy herd are due PI replacements spreading virus while the herd is early pregnant, resulting in poor herd reproductive performance. There can be increased time to conception, more services required and more empty cows. Immune suppression may make cows more susceptible to other disease such as mastitis.
  • Either PI dams or transiently infected cows can produce PI calves, continuing infection in to the next generation.

 

Calf Scours (diarrhoea)

Calf diarrhoea (scours) is normal. As newborn calves adjust to drinking milk (rather than being supplied food by the placenta) it is only natural that the gut should begin to function in “fits and starts”. The best assessment of whether or not scours is a problem is to look at the mob or pens of calves; not just considering the consistency of individual faeces, but viewing the whole group and the whole calf (not just the faeces).

In any given mob of calves, 10% scouring is no big deal – especially if they seem otherwise bright and energetic, and are drinking well. 30% could be a problem, and more than 50% is definitely a problem. It is also a problem if calves are lacklustre, lying down a lot and not drinking – or if you have more than 5% deaths.

Scours can come from a variety of causes. Most are not fatal by themselves, but they combine together, if the calves did not get much colostrum and if dehydration is not well managed then things can get fatal pretty quickly.

Causes of scours

The predisposing factors for scours are similar almost regardless of the cause. Some of the more common factors in outbreaks are inadequate colostrum intake, poor feeding hygiene, poor feeding routines with poor quality CMRs (calf milk replacers), inadequate housing and overcrowding.

The pathogens involved in calf scours vary from

  • None (as with smple nutritional scours)
  • Viruses
  • Protozoa
  • Bacteria.

Where there is no pathogen involved the diarrhoea is temporary and mild. This is sometimes caused “milk scours” and can be a result of a change in the milk/colostrum supply or dilution.

The main viruses are rotavirus and coronavirus, which are highly contagious. Rotavirus has a rapid incubation and can cause scours in calves just a few days old. These viruses destroy the rapidly growing cells of the intestinal tract. By themselves the effects soon pass, with very little impact on health. However if they combine with other pathogens then serious diarrhoea may result.

The protozoan organism Cryptosporidium also multiply in the gut lining cells, but eventually burst out of the cells destroying the gut lining and its absorptive function. It can take a long time to run it’s course.

Salmonella and E.coli are the big two bacteria which may be involved. They stick to intestinal cells and can both produce toxins which make calves very sick. With some strains of  E.coli calves may die even before onset of diarrhoea. Some strains (but not all) cause damage to the lining of the gut, with associated blood scours and stripping of the gut lining.  Following severe Salmonella infection, bacteria may spread to the brain, lungs and joints.

Management of Scours

Diagnosis of the infectious agent is very useful, as it can influence both prevention and treatment. This may be achieved by stool samples but post-mortem tissues might be necessary as well. Postmortem exams and examination of the scene by an experienced vet can be very insightful.

Treatment of scours is based on the following;

Good fluid therapy

In mild cases oral therapy is sufficient, but if severely dehydrated (assessed by eyeball sunkenness and skin tenting) intravenous therapy is essential. Milk may be discontinued for a short period, but should be reinstated as soon as possible to provide energy, even if it makes the calves a little loose.

Balanced fluid therapy not only corrects water deficits, but also corrects  electrolyte, acidosis and energy deficits as well. This is the cornerstone of survival and recovery.

Antimicrobial therapy

The use of very broad spectrum such as Bivatop is wise as we may not know the cause, and damage to the gut lining can allow all sorts of bacteria to enter the bloodstream. Injectable is best, so all tissues are reached.

Pain relief.

This can be a dramatic help, as pain free calves will suckle better and rehydrate themselves. Metacam 20 has an outstanding reputation and scientific backing for this purpose.

Prevention and control of calf scours is best achieved in shed by patience, cleanliness and attention to detail. Provision of high quality feeds, good hygiene, careful observation and prompt/vigorous treatment of calves is recommended. 

Setting up the calf shed with batch management (all in, all out) and vaccination of dams against E.coli, Salmonella and rota/corona viruses can be very helpful, provided the calves are fed adequate colostrum!

Give us a call if you have any questions about setting up calf sheds, establishing treatment protocols or training staff.

Clostridial Disease

Clostridial diseases are caused by a family of bacteria recognised for rapid growth and overwhelming blood poisoning. They can cause some very nasty tissue swelling and death is a common outcome. Species other than cattle can be affected, and some diseases (eg Tetanus) are caused by the same bacteria in many species, including man. If cases are treated early they may respond to high doses of penicllin, but usually it is too late by the time they are noticed. The most fortunate thing about them is that we can vaccinate, and vaccination lasts for life.

Clostridial organisms are commonly found in soil, water and rotting plant/animal material. Animals dying of clostridial diseases often swell up and rot very quickly. Diagnosis is usually at post mortem. The bacteria are not contagious and clostridial diseases generally occur in small numbers. Animals are frequently in good condition and well fed. Clostridia have a hardy spore forming capability which means they can survive in the soil for decades and recur in certain properties. In Australasia the diseases are, in order of importance:

  1. Blackleg - Animals eat the spores of Clostridium chauvoei, which enter via the gut and lodge in the muscles with no ill effects. Sometime later if the animal gets bruised (often in the leg, but also in the back, tongue or jaw), the spores come to life in the anaerobic muscle. They multiply rapidly, rotting the muscle and their toxins kill more muscle tissue and eventually affect the whole animal.
    The animal may be lame for a few hours in the affected leg, but usually dies quickly and the post-mortem shows black muscle tissue where the bruise was.If there is a traumatic event such as yarding this may cause outbreaks of blackleg, but otherwise there are only a few animals affected.
  2. Malignant Oedema - MO is very similar to blackleg, but is associated with a history of recent deep penetrating wounds such as vaccination, castration and calving. Rather than a discrete area of muscle affected, swelling, gas and oozing bloody fluid spreads rapidly around body connective tissue
  3. Sudden Death Syndrome - A recent syndrome, studied in New Zealand where rapidly growing, very well fed young (mainly beef) cattle have died have been put down to Clostridium sordellii. It is believed the bacteria multiply rapidly in the rich environment of the gut, leaking in to the tissues and multiplying from there. The disease can be confused with bloat, so a careful post mortem is advisable.
  4. Black disease - Clostridium novyi spores lodged in the liver are triggered to start multiplying by liver fluke damage. Affected animals die rapidly from liver failure, peritonitis and heart infection. After death the whole carcase may appear black. This disease is more common in Australia than New Zealand. Unlike other clostridial disease, annual booster vaccinations are recommended if the disease is common.
  5. Enterotoxaemia - Similar to the disease pulpy kidney in sheep, well fed rapidly growing young animals get a gut infection of Clostridium perfringens. Large amounts of the toxin spread to the kidney and heart. At post-mortem there is haemorrhage in the abomasums (4th stomach) and small intestine, with small amounts of creamy feed mix.
  6. Tetanus - Tetanus is not so much a cause of sudden death, but of muscular stiffness, lockjaw and bloat (spasm of the rumen). It takes some days to develop, and is not necessarily fatal. Caught early, cases will respond to penicillin and supportive treatment.
    Small wounds, such as castration, docking and dehorning which get contaminated with spores from the soil are the inciting cause.
  7. Botulism - The bacteria Clostridium botulinum causes a flaccid “flat” paralysis of muscles due to a nerve toxin. Unlike the other clostridial diseases, it results from eating toxic material. This may be feedstuffs with rotting plant or animal material or contaminated water. Outbreaks can occur in phosphorus deficient environments where cattle are prone to chewing bones, and around waterholes where dead wildlife may contaminate.
    Botulism may cause sudden death where large doses of the toxin are ingested, but where smaller doses are taken the clinical signs mimic milk fever. Outbreaks may have high numbers of deaths initially but sublethal cases continue for weeks afterwards. The sublethal form produces a creeping paralysis, initially of the hind legs, but then the front legs. The tongue may protrude, with drooling and inability to swallow. Many animals eventually die, but some survive with supportive treatment.Botulism can be prevented by vaccination and/or preventing contamination of feed and water. It is particularly important to keep the bones of dead animals and chicken litter out of feed. Supplementary feed with clean sources of protein and phosphorus if the diet is deficient. 

 

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