Changes

===Clinical Signs===

===Clinical Signs===

 

The disease caused by bovine viral diarrhoea virus is known as bovine viral diarrhoea. It might be expected from this nomenclature that diarrhoea is a key clinical feature in BVDV infection, but disease can actually manifest in a variety of ways, ranging from subclinical disease to muscosal disease. Virulence factors related to genotype and strain are partially responsible for these variations, but host factors are also important. Pregnancy status, stage of gestation, immunity and the level of develoment of the foetal immune system all contribute to the outcome of BVDV infection.

The disease caused by bovine viral diarrhoea virus is known as bovine viral diarrhoea. It might be expected from this nomenclature that diarrhoea is a key clinical feature in BVDV infection, but disease can actually manifest in a variety of ways, ranging from subclinical disease to muscosal disease. Virulence factors related to genotype and strain are partially responsible for these variations, but host factors are also important. Pregnancy status, stage of gestation, immunity and the level of develoment of the foetal immune system all contribute to the outcome of BVDV infection.

In the naive, non-pregnant, immunocompetent animal, BVD is normally mild: it is estimated that 70 to 90% of BVDV infections cause no clinical signs²⁸. If these subclinically affected cattle are observed closely, body temperature may marginally rise and mild leukopenia and agalactia may be seen ^{29, 30}. 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 15³¹. Although some cattle suffer diarrhoea in BVDV infection, the disease no longer seems to present as herd outbreaks of diarrhoea³². Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions³³, with a rapid respiratory rate resembling pneumonia sometimes apparent²⁹.

In the naive, non-pregnant, immunocompetent animal, BVD is normally mild: it is estimated that 70 to 90% of BVDV infections cause no clinical signs²⁸. If these subclinically affected cattle are observed closely, body temperature may marginally rise and mild leukopenia and agalactia may be seen ^{29, 30}. 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 15³¹. Although some cattle suffer diarrhoea in BVDV infection, the disease no longer seems to present as herd outbreaks of diarrhoea³². Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions³³, with a rapid respiratory rate resembling pneumonia sometimes apparent²⁹. Acutely infected, non-pregnant animals shed low concentrations of virus compared to persistently infected cattle³¹, and antibodies are produced 2-4 weeks post-infection which persist for life³³.

 

Acutely infected non-pregnant animals shed low concentrations of virus compared to persistently infected cattle (Duffell and Harkness, 1985). Animals produce antibodies to BVDV 2 to 4 weeks after infection (Baker, 1995), which persist for life.

“Severe BVD” also exists, seen in the UK in 1992-1993 (Hibberd and Turkington, 1993), and in herd outbreaks between 1993 and 1995 in Ontario (Carman et. al, 1998). Infected animals showed acute onset of diarrhoea, fever 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.

Although BVDV infections in naive, non-pregnant animals are usually mild, outbreaks of a severe form of BVD have been known^{11, 34}. 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.  

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.