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BVD in the UK 2006

Gina Bromage

The research carried out by veterinarian Gina Bromage and referred to in this article was made possible by a grant from British Camelidsí Trust and assistance from the State Veterinary Service.

Bovine Viral Diarrhoea is primarily a cattle virus, causing in cattle a variety of signs, including diarrhoea, but also pneumonia, stillbirth, abortion, embryonic death and infertility, weakness, nervous signs and poor immunity in newborn animals. In its chronic (long term) form it causes Mucosal Disease, a fatal ulcerating condition of the mouth, but including digestive problems, intermittent diarrhoea and eventual wasting and death. Skin lesions that fail to heal are also a feature of the chronic disease in cattle. Sheep can also be infected and may show some of the same signs. Infection of the pregnant cow can result in birth of live offspring which possess permanent tolerance of virus, and which shed large amounts of virus throughout life, the so-called PI (Persistently Infected) individual. These individual animals are an important source of infection in the population as a whole, because they can spread it to new animals over a long period of time.

Although there can be widespread disease in cattle herds with no immunity to the virus, survivors usually seem to develop a solid protection and once a herd has become infected, the disease almost disappears until a generation with no exposure to the virus is born. This new generation will show disease and the cycle begins again, with a more sporadic occurrence, because at any one time most individuals may have some immunity.

Disease caused by BVD virus has been reported in camelids in the US and the UK.

In the US it was found in one herd, where 14% animals responded with antibodies to infection, but the rest did not. The virus was associated with respiratory disease, abortion, weight loss, diarrhoea and general ill thrift in llamas.

BVD disease has been described in the last 18 months in UK alpacas. In the first case, a seven month old female had swollen joints, diarrhoea and chronic ill thrift. Post mortem examination yielded a positive PCR. An eight month old in contact animal was transiently PCR postive but then became negative.

A second case from the same farm was sold on, and at twenty two months of age, was treated for a dental abscess for four months, then developed diarrhoea and died. Others sold with it were all normal. The one that died was PCR positive.

There was a third case from same herd. It was two months old, had had diarrhoea at one month that had responded to antibiotics, then relapsed and deteriorated rapidly. It was also PCR positive.

The virus identified was Subtype 1b (Subtype 1a is more common in UK cattle).

A further UK outbreak was investigated by the author with support from the British Camelidsí Trust.

The herd concerned comprised twenty adult females, three adult males, plus six juveniles, four female and two male. The animals had been moved from an original farm to two different farms before going to their final destination. Some had been to both of the interim farms, some to only one of them.

The first disease observed was pneumonia on 19/10/05 in an adult female who was three months pregnant. She subsequently gave birth at term to a small cria with a stringy hairy coat that is positive for virus on PCR and negative for antibody, therefore presumed to be a PI.

There followed a cluster of six pneumonia cases in the females from February 2006 to July 2006. Apart from the maiden female amongst the affected animals, the crias of all but one of them died, some born prematurely, others at term showing nervous signs. The surviving cria was born at 339 days of gestation to a mother who had shown signs of pneumonia three months before. The cria was PCR negative, but seropositive (titre 120). The female was PCR negative, but seropositive with a titre of 480.

There were four abortions in the group, three from females who had not shown illness, and the fourth following pneumonia by a week. The aborted females were all PCR negative with one seronegative and three weakly seropositive (80 titres).

When blood was sampled on 31/7/06, none of the pneumonia cases were PCR positive, but all were seropositive, some only weakly so.

Three adult females were PCR positive, none of which had shown visible disease, although one gave birth to a deformed (undershot mandible) cria that died. The crias of the other two were, and remain, PCR positive.

One cria was born PCR positive to a PCR negative mother, and remained PCR positive at a second sampling two months later. However it had seroconverted at the second sampling, showing a very large immune response.


These comprised three adult females and four crias. When re sampled two months later, only one female had become PCR negative. Of the four crias, at second sampling, three had mounted very large antibody response, and one, (the one born stunted with a stringy fleece), had not. This cria did, however, thrive, but remains slightly small for its age. The three with antibodies have gone on to grow well, although one had a bout of illness which responded to antibiotic treatment.


Only one of the males was seropositive, and strongly so. He was a juvenile who had been at foot to a female who had shown pneumonia and then gone on to give birth to the stunted PI cria with the stringy fleece. None of the other males showed virus on PCR, or antibodies.


When the outbreak was first diagnosed, some of the herd had been dispersed to two stud farms and run with other animals there. PCR and serology on ten contacts from those two farms failed to find evidence of infection in these contact animals, although a single female was weakly antibody positive, but PCR negative.


Even in a naive herd not all animals will show disease, of those which donít, some may seroconvert in any case.

Clinical signs appear not to include diarhoea, but rather malaise, inappetance, pneumonia, abortion and sick, non viable crias.

Even animals that should not in theory be PI, because of a strong antibody response, will take some months to become negative for viral antigen.

The PI cria appears to be growing, vigorous and healthy at five months of age, despite its slightly strange appearance. It remains to be seen whether this continues to be the case.

The best way of preventing spread of this disease would seem to be pre movement blood testing of animals for PCR, especially crias at foot of their dams, to prevent the most infectious animals from moving on to new premises.


PCR Polymerase Chain Reaction. This test is very sensitive and detects virus itself, or bits of virus (so called viral antigen). It indicates the presence or very recent presence of actual virus, and therefore of possible infectiousness. Carried out on blood samples or on tissue samples.

Serology/Antibody Test/ SNA (serum neutralizing antibody). (All of these terms may be used for the same test) This detects antibody to the virus. If positive, it indicates that the individual has been exposed to infection and mounted an immune response to it. It remains positive for a long time after the infection is gone, and is useful to demonstrate past exposure in healthy animals, which may well never have shown signs of disease. If negative, it indicates either that the individual has not been exposed to infection (and would have a corresponding negative PCR test) or that it has failed to mount an immune response, in which case, a positive PCR test would be expected. An animal which is positive to this test is said to be seropositive. One which is negative is said to be seronegative. The process of developing an immune response which results in becoming seropositive is called seroconversion.

ELISA (Enzyme Linked Immunosorbent Assay) One of the more common tests for BVD in cattle, it does not appear to detect BVD in camelids. Carried out on blood samples.

Immunohistochemistry. Performed on tissue samples it involves special stains which should show up BVD. It seems to be unreliable or useless in camelids at present in the UK.