Rural veterinary practice
Overlaying of piglets
Delivery of a goat
Foot and Mouth Disease
Bovine Virus Diarrhoea
20. Bovine Virus Diarrhoea (immune deficiency)
Mucosal lesions in the mouth and throat of cattle are not only caused by diphtheria or foot and mouth disease, but also by an infection named mucosal disease. That disorder makes up part of a disease complex referred to as Bovine Viral Diarrhoea (BVD). Which is a viral infection in cattle that occurs on an extensive scale in the Netherlands. It generally causes little damage because the majority of the cattle has antibodies to counteract the virus. Only a small part of the infected animals develops a fatal diarrhoea due to an inflammation of all mucosal membranes including mouth, throat and guts. Which is why that specific disorder is called mucosal disease.
In a pregnant cow or heifer that lacks antibodies to counteract the BVD-virus and that becomes infected, the virus penetrates in the uterus and infects the unborn calf. If the infection comes about in the first four months of carrying, when the immune system of the embryo is still developing, then the virus is not recognised as being foreign to the body and it can stay in the calf undetected. After birth the animal will then secrete BVD-virus in its manure and urine for the rest of its life; in its runny nose and tear-water, and, later on, in the milk if the calf concerned is female or in the sperm if it is a male calf. In this way, these so-called permanent virus secretors infect all of the cattle with which they come into contact. But their immune system is not functioning properly: through causes unknown, all of the mucosa in their gastrointestinal tract can become seriously inflamed sooner or later, from the mouth to the anus. The result is untreatable diarrhoea and ultimately death. That is the classic clinical picture of mucosal disease. Only approx. 10% of the permanent virus-secretors reach maturity. They appear to be healthy but they continue to secrete the virus for the rest of their lives. Fortunately, humans cannot become infected with the BVD-virus.
If the infection of the unprotected mother (without antibodies) occurs after the fourth month of gestation (the gestation of a cow is nine months), then the calf in the uterus usually dies and is rejected. But the BVD-virus does not only impair the immune system of unborn calves; the infection in unprotected animals causes an immune deficiency in cattle of all ages. This lowers their resistance, making them susceptible to all kinds of infections. Which disease then manifests itself depends upon which infectious virus or bacterium is most viable in their environment. For example, unprotected calves that become infected with the BVD-virus will often develop an infection of the bronchial tubes and lungs; for example, a deep bronchitis by a BRSV infection (Bovine Respiratory Syncytial Virus) or a pneumonia by pasteurellosis. Cows infected with the BVD-virus may develop acute udder infections on one farm; on another farm a BVD infection may result in seriously crippled cattle as a result of panaritium (interdigital phlegmon) affecting almost half of the dairy cows. And in patients with a poorly functioning immune system, the result of any treatment will disappoint. This increased susceptibility to all kinds of infections can be compared to AIDS in humans. In these patients the immune deficiency is caused by the HIV (Human Immunodeficiency Virus). As a result, a variety of infections may occur which are difficult to treat. It would therefore be more accurate to call the cause of this immune deficiency in cattle BIV (Bovine Immunodeficiency Virus) instead of BVD-virus.
At the beginning of 1988, there was a serious outbreak of BRSV with deep bronchitis among young cattle on a large sized cattle farm in Rosmalen The sick calves and yearlings (ranging from three months up to two years) were treated with injections of doxycycline (an antibiotic) and meloxicam (an anti-inflammatory agent) for a course of three days. Still, fifteen animals died. A few of the dead animals were transported to the Health Service for Animals (GD) for an autopsy. BRSV was found to be the cause of death. But the young cattle on the farm had been systematically vaccinated against this virus for years. And there had been no breakthrough infections on any other farms where I had used the same vaccine. Blood tests were conducted on seven ill animals that were yet to be treated. In the blood smears the white blood cells indicated for acute inflammation. And a low zinc concentration was found in all seven samples. The inflammation was undoubtedly result of the BRSV infection. But at that time, there was no explanation available for the zinc shortage in the blood. In retrospect, it seems to be an indication for malfunctioning of the immune system. Treating the ill animals with injections of trimethoprim sulfa (a chemotherapeutic agent) and flunixin (an anti-inflammatory agent) was not that successful either: an additional five calves died. Somewhat later, a GD-specialist measured the climate in the barn of the young cattle by means of smoke tests. The tests showed the presence of draft and cold air rising from the manure drain. Screens to prevent draft were installed, along with rubber mats to cover the grids above the manure drain. But that didn’t help either. It was not until in the course of May that the calves began to improve and the problems appeared to be finally over. The surviving youngsters were meanwhile lagging considerably behind in terms of growth.
Meanwhile in the cow shed four of the cows in calf had rejected their calves during that same period (beginning of ’88). Seeing that the herd counted a total of ninety dairy cows, this was not considered alarming, as the average percentage of abortions per year on Dutch dairy farms was 3 percent at the time. Furthermore, the cows and heifers showed no symptoms of illness and the milk production was normal. The standard blood test for brucellosis was negative for the animals that had aborted their young. But in May, the number of abortions had increased to seven. No cause could be found. After that, there were no new cases of abortion. For the next eight months things got back to normal.
But in the beginning of 1989, an epidemic of pneumonia once again struck the herd of young cattle. Twenty-five calves died within a few weeks. This time the autopsy showed: BVD. One calf proved to be a carrier of the virus. The animal was a permanent virus-secretor.
farmer and researcher
The blood of the approx. 275 animals on the farm was subsequently tested for antibodies for the BVD-virus. Antibodies were found in all of the heifers and cows in the dairy cow barn and in most of the calves and yearlings in the barn for young cattle. Which means that these animals had experienced an infection. The blood of the youngsters without antibodies was subsequently tested for the presence of the virus. Fifteen of the calves concerned were found to have the BVD-virus in their blood. The tests were repeated three weeks later to exclude a coincidental acute infection. Again, all fifteen were positive for the BVD-virus; and so they were all permanent virus-secretors.
The initial wave of infection with the BVD-virus struck the entire farm at the beginning of 1988. Its cause could not be determined. At that time, twenty-three cows in calf in the dairy cow barn became infected: seven of these in an advanced stage of gestation (more than four months) rejected their calves. The embryos of the other sixteen (less than four months of gestation) became infected in the uterus. These calves were born as permanent virus-secretors about six months later. The initial infection wave subsided and all was going back to normal on the farm. The entire herd had become immune for the BVD-virus thanks to the generation of antibodies. These antibodies are extremely persistent and possibly effective for the rest of a cow’s life. So the sixteen young permanent virus-secretors could not, at first, cause any harm. All of the cows and heifers in the dairy cow barn had antibodies. So the subsequent births concerned normal calves. But when these calves were moved to the young cattle barn at the age of approx. three months, they lacked antibodies while they were being exposed there to sixteen yearlings that permanently secreted the BVD-virus. That infection rendered the immune system of these calves deficient and they were subsequently the victim of the BRSV circulating in the barn. Thus the second wave of the BVD-virus in the barn with young cattle proved fatal for twenty-five calves. Meanwhile, also one of the permanent virus-secretors died (the ‘indicator-animal’ in autopsy).
The insurance company covered all of the direct losses: seven cows that had rejected their calves and that were disposed of; twenty calves and yearlings that died during the first wave and twenty-five calves that were a victim of the second infection wave, plus sixteen virus-carriers. The costs of the blood tests and the autopsies were covered as well. All in all a considerable amount. But the consequential loss that the insurance did not cover was much greater. Because of the lag in growth of the young cattle, the bulls had to be fattened up for an additional three months in order to reach the appropriate weight for slaughtering. The heifers also lagged behind in size and they did not produce enough milk. They, approx. 40 in all, were disposed of for that reason following a single lactation period. This made it impossible to meet the milk quotum. The consequential losses are estimated at one hundred and fifty thousand.
A BVD-virus infection can cause huge losses in an unprotected herd of cattle (lacking antibodies).
© Leo Rogier Verberne