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  • Results from natural outbreaks have also supported a role for BCoV in BRD pathogenesis. Hick et al. (2012) detected BCoV by reverse transcriptase quantitative PCR (RT-qPCR) in 9-month-old weanlings presenting with BRD in a paddock-based feedlot system; BCoV was identified in nasal samples from 10/30 acutely affected animals and in the lungs of 2/15 with BRD lesions at slaughter. Other viruses were not detected in these animals and bronchointerstitial pneumonia was diagnosed on histopathology. Decaro et al. (2008) reported on four outbreaks involving young calves, both dairy and beef breeds, aged 2–3 months in Italy. BCoV was detected by RT-PCR on a high proportion of nasal swabs from all four outbreaks; no other BRD virus or Mycoplasma spp. was identified in three of the four outbreaks. In two of these outbreaks concurrent respiratory and enteric signs were recorded with nasal and faecal detection of BCoV.
    On balance, epidemiological evidence of BCoV induced BRD is persuasive, however, studies demonstrating BCoV antigen in pneumonic lesions are lacking and would provide more conclusive evidence. Park et al. (2007) demonstrated BCoV antigen in the cytoplasm of degenerated and necrotic epithelial transketolase of the nasal turbinates, trachea and lungs with concurrent interstitial pneumonia using immunohistochemistry (IHC) in calves experimentally infected orally with a winter dysentery strain of BCoV; respiratory clinical signs were not recorded however. Histological changes including multinucleate syncytial epithelial cells identified in the bronchiolar lumina and bronchus associated lymphoid tissue (BALT) hyperplasia have been ascribed to BCoV in a natural outbreak by Hick et al. (2012) based on PCR rather than IHC detection.
    Control of the disease is challenging as respiratory BCoV vaccines have not been developed and while Plummer et al. (2004) reported that intranasal use of modified live BCoV vaccine reduced the risk of treatment for BRD in calves, differences between the strain used in the enteric BCoV vaccine and those strains isolated from BRD cases suggest that the vaccine may not be fully protective against the BCoV isolates in circulation (Fulton et al., 2013). Plummer et al. (2004) assumed that the effect of vaccination was mediated by IgA but further research is required to confirm the factors which confer mucosal protection. Considering the apparent changing tropism of BCoV strains (Kanno et al., 2007) coupled with BCoV transmission by either the nasal or faecal-oral route and considering that experimental oral infection can lead to viral infection of respiratory epithelial cells (Park et al., 2007) it is likely that any effective vaccine will need to confer concurrent enteric and nasal mucosal immunity. Control is further complicated by the potential for re-infection of the same animal and persistence of infection in both the upper respiratory tract (Heckert et al., 1991) and in intestinal tissues and lymph nodes (Oma et al., 2016) of infected animals possibly for weeks after infection.

    Bovine adenovirus 3
    Bovine adenoviruses (BAdV) were first identified by Klein et al. (1959) in the faeces of a healthy cow. Since then, 10 serotypes have been identified in cattle which are distributed between two subgroups – the Mastadenoviruses and the Atadenoviruses (Benko et al., 2000). Although BAdV-10 is unlike other BAdV species, it displays certain characteristics of Mastadenoviruses (Matiz et al., 1998). BAdVs appear to have both respiratory and enteric tropisms (Mattson et al.,1977; Reed et al., 1978) but many serotypes are of uncertain significance as pathogens (Sibley et al., 2011). Shedding of image multiple BAdV genotypes by cattle is prevalent such that, considering the environmental stability of the AdV virion, BAdVs have been suggested as conservative indicators of the presence of viral or faecal contamination in aqueous environments (Sibley et al., 2011).
    Transmission of BAdV-3 is facilitated by enhanced survival in aerosols in conditions of low temperatures and high relative humidity (Elazhary and Derbyshire, 1979) and within infected herds seropositivity to BAdV-3 is often high (Mattson et al., 1988; Sibley et al., 2011). Indeed, the apparent low incidence of clinical disea

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