Changes

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 is particularly important role in bovine respiratory disease, with an association between BVDV antibody titre and respiratory disease treatment being demonstrated (Martin and Bohac, 1986). BVDV is the virus most frequently isolated from pneumonic lungs, often found in association with Pasteurella haemolytica (described by Baker, 1995). This pathogen combination causes severe fibrino-purulent bronchopneumonia, with the area of pneumonic lesions increasing by 35-60% compared to that caused by Pasteurella infection alone (Brownlie, 1985). 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 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.

 

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 epistaxis</sup>38</sup> and has been described in both Europe and North America.

Although BVDV infections in naive, non-pregnant animals are usually mild, outbreaks of a severe form of BVD have been known^{11, 36}. These were characterised by acute onset of diarrhoea, pyrexia and milk drop and decreased milk production, sometimes proving fatal. Non-cytopathic, type 2 viruses were implicated in these cases, raising the issue of the degree of cross protection afforded by type 1 vaccines. However, severe disease was only seen in cattle where vaccine manufacturers’ instructions had not been followed, implying protection is usually given.

 

BVDV2 infection may also result in haemorrhagic syndrome (HS), reported in both North America (Perdrizet et. al, 1987; Rebhun et.al, 1989) and Europe. This is characterised by significant thrombocytopaenia, giving rise to bloody diarrhoea, petechial haemorrhages of mucous membranes and epistaxis (Rebhun et. al, 1989). Fever and leucopaenia are also seen.

====Acute Infections: Pregnant Animals====

====Acute Infections: Pregnant Animals====