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In the naive, non-pregnant, immunocompetent animal, BVD is normally mild: it is estimated that 70 to 90% of BVDV infections cause no clinical signs³⁰. If these subclinically affected cattle are observed closely, body temperature may marginally rise and mild leukopenia and agalactia may be seen ^{31, 32}. When clinical disease does occur in these animals, morbidity is high amongst cattle of 6-12 months of age. Following a 5-7 day incubation period, pyrexia and leukopenia is seen. Viraemia arises on days 4-5 days post-infection, and continues until around day 15³³. Although some cattle suffer diarrhoea in BVDV infection, the disease no longer seems to present as herd outbreaks of diarrhoea³⁴. Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions³⁵, with a rapid respiratory rate resembling pneumonia sometimes apparent³¹. Acutely infected, non-pregnant animals shed low concentrations of virus compared to persistently infected cattle³³, and antibodies are produced 2-4 weeks post-infection which persist for life³⁵.

In the naive, non-pregnant, immunocompetent animal, BVD is normally mild: it is estimated that 70 to 90% of BVDV infections cause no clinical signs³⁰. If these subclinically affected cattle are observed closely, body temperature may marginally rise and mild leukopenia and agalactia may be seen ^{31, 32}. When clinical disease does occur in these animals, morbidity is high amongst cattle of 6-12 months of age. Following a 5-7 day incubation period, pyrexia and leukopenia is seen. Viraemia arises on days 4-5 days post-infection, and continues until around day 15³³. Although some cattle suffer diarrhoea in BVDV infection, the disease no longer seems to present as herd outbreaks of diarrhoea³⁴. Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions³⁵, with a rapid respiratory rate resembling pneumonia sometimes apparent³¹. Acutely infected, non-pregnant animals shed low concentrations of virus compared to persistently infected cattle³³, and antibodies are produced 2-4 weeks post-infection which persist for life³⁵.

Acute BVDV infection causes a significant leukopenia, hampering the host's defences against invading pathogens. This BVDV-associated immunosupression has a particularly important role in bovine respiratory disease: an association has been demonstrated between BVDV antibody titre and treatment for respiratory disease³⁶. BVDV is the virus most frequently isolated from pneumonic lungs and is often found in association with ''Pasteurella haemolytica''³⁵, causing severe fibrino-purulent bronchopneumonia with the total lesion area increased by 35-60% to that caused by pasteurellosis alson³⁴ Synergism is also displayed with parainfluenza, bovine rhino-tracheitis and respiratory syncitial viruses.

Acute BVDV infection causes a significant leukopenia, hampering the host's defences against invading pathogens. This BVDV-associated immunosupression has a particularly important role in bovine respiratory disease: an association has been demonstrated between BVDV antibody titre and treatment for respiratory disease³⁶. BVDV is the virus most frequently isolated from pneumonic lungs and is often found in association with ''Pasteurella haemolytica''³⁵, causing severe fibrino-purulent bronchopneumonia and increasing the total lesion area by 35-60% compared ro pasteurellosis alone³⁴. Synergism is also displayed with parainfluenza, bovine rhinotracheitis and respiratory syncitial viruses.

Although BVDV infections in naive, non-pregnant animals are usually mild, outbreaks of a severe form of BVD have been known^{11, 37}. These were characterised by the acute onset of diarrhoea, pyrexia and milk drop, with some cases proving fatal. These oubtreaks were associated with genotype 2 viruses, and it transpired vaccintion with type 1 vaccines had not afforded cross-protection in these instances due to non-compliance with instructions. Generally, BVDV-2 infection is seen less frequently than disease related to type 1 virus, but is associated with haemorrhagic syndrome. Haemorrhagic syndrome is characterised by severe thrombocytopaenia leading to haematochezia, petechiation and epistaxis³⁸ and has been described in both Europe and North America. Severe disease is also possible with virulent type 1 infection, presenting as high fever, oral ulcerations, eruptive lesions of the coronary band and interdigital cleft, diarrhoea, dehydration, leukopenia, and thrombocytopenia. Thrombocytopenia may give petechiation of  the conjunctiva, sclera, nictitating membrane and the mucosal surfaces of the mouth and vulva, as well as prolonged bleeding from injection sites³⁹.

Although BVDV infections in naive, non-pregnant animals are usually mild, outbreaks of a severe form of BVD have been known^{11, 37}. These were characterised by the acute onset of diarrhoea, pyrexia and milk drop, with some cases proving fatal. These oubtreaks were associated with genotype 2 viruses, and it transpired vaccintion with type 1 vaccines had not afforded cross-protection in these instances due to non-compliance with instructions. Generally, BVDV-2 infection is seen less frequently than disease related to type 1 virus, but is associated with haemorrhagic syndrome. Haemorrhagic syndrome is characterised by severe thrombocytopaenia leading to haematochezia, petechiation and epistaxis³⁸ and has been described in both Europe and North America. Severe disease is also possible with virulent type 1 infection, presenting as high fever, oral ulcerations, eruptive lesions of the coronary band and interdigital cleft, diarrhoea, dehydration, leukopenia, and thrombocytopenia. Thrombocytopenia may give petechiation of  the conjunctiva, sclera, nictitating membrane and the mucosal surfaces of the mouth and vulva, as well as prolonged bleeding from injection sites³⁹.