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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.
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====Acute Infections: Non-Preganant Cattle====
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====Acute Infections: Non-Pregnant Cattle====
    
In the naive, non-pregnant, immunocompetent animal, BVD is normally mild: it is estimated that 70 to 90% of BVDV infections cause no clinical signs<sup>30</sup>. If these subclinically affected cattle are observed closely, body temperature may marginally rise and mild leukopenia and agalactia may be seen <sup>31, 32</sup>. 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 15<sup>33</sup>. Although some cattle suffer diarrhoea in BVDV infection, the disease no longer seems to present as herd outbreaks of diarrhoea<sup>34</sup>. Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions<sup>35</sup>, with a rapid respiratory rate resembling pneumonia sometimes apparent<sup>31</sup>. Acutely infected, non-pregnant animals shed low concentrations of virus compared to persistently infected cattle<sup>33</sup>, and antibodies are produced 2-4 weeks post-infection which persist for life<sup>35</sup>.
 
In the naive, non-pregnant, immunocompetent animal, BVD is normally mild: it is estimated that 70 to 90% of BVDV infections cause no clinical signs<sup>30</sup>. If these subclinically affected cattle are observed closely, body temperature may marginally rise and mild leukopenia and agalactia may be seen <sup>31, 32</sup>. 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 15<sup>33</sup>. Although some cattle suffer diarrhoea in BVDV infection, the disease no longer seems to present as herd outbreaks of diarrhoea<sup>34</sup>. Clinical signs more commonly include depression, anorexia, occulo-nasal discharge, decreased milk production and oral lesions<sup>35</sup>, with a rapid respiratory rate resembling pneumonia sometimes apparent<sup>31</sup>. Acutely infected, non-pregnant animals shed low concentrations of virus compared to persistently infected cattle<sup>33</sup>, and antibodies are produced 2-4 weeks post-infection which persist for life<sup>35</sup>.
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