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198  |  Kibenge et al.





























          Figure 6.5  Winter mortality in American crow (courtesy of Jordi Segers, University of Prince Edward Island, Canada).



          reassortant orthoreovirus strain was isolated from partridge   1 day old. Those infected orally at 7 days and 3 weeks showed a
          (Perdix perdix) suffering from acute pneumonia and infra-orbital   substantial rise in intestinal IgA. In the subcutaneously infected
          sinusitis (Kugler et al., 2016). Sequencing and phylogenetic   chicks, only those infected at 3 weeks showed an intestinal IgA
          analyses showed that the partridge reovirus strain (D1007/2008)   response. There were very similar reovirus-specific IgG responses
          is composed of a mixture of chicken and turkey orthoreovirus   in the sera of the orally and subcutaneously infected chicks, in
          related genes, suggesting that partridges may serve as natural   all age-groups. Previously, Meanger et al. (1997) had shown that
          reservoirs for orthoreoviruses of domesticated poultry (Kugler   vaccination of breeding hens with avian reovirus resulted in the
          et al., 2016). Most recently in Poland, Styś-Fijoł et al. (2017)   passive transfer of neutralizing antibody to progeny chickens,
          investigated the occurrence of avian reoviruses in 192 dead wild   which completely prevented the development of tenosynovitis
          birds representing 32 species collected between 2014 and 2016.   in 80% of progeny chickens infected with the homologous virus
          Avian reoviruses were detected in 58 (30.2%) wild birds belong-  strain but with only marginal protection against strains of two
          ing to nine orders (Ciconiiformes, Pelecaniformes, Columbiformes,   heterologous serotypes of avian reovirus. The primary mecha-
          Accipitriformes, Anseriformes, Charadariiformes, Strigiformes,   nism for protective immunity against avian reoviruses is via the
          Piciformes,  and  Passeriformes). All collected birds were necrop-  humoral immune response (Kibenge et al., 1987). A suppression
          sied, and often had lesions of swollen liver and spleen with the   of T-cell mediated immunity was shown to contribute to severity
          presence of liver necrosis; lesions characteristic of avian reovirus   of disease (Hill et al., 1989). van Loon et al. (2003) subsequently
          infection (Styś-Fijoł  et  al., 2017). Two avian reovirus isolates   showed that the virus can be controlled in the absence of actively
          from rock pigeon (Columbiformes – Columba livia) and mute swan   produced antibodies, and independent of B lymphocytes, further
          (Anseriformes – Cygnusolor) were antigenically similar to avian   suggesting that cellular immunity is sufficient for protection of
          orthoreovirus S1133, suggesting possible transmission between   broilers with maternal antibodies against reovirus infection fol-
          wild birds and farmed birds (Styś-Fijoł et al., 2017). However,   lowing early age vaccination with live reoviral vaccine.
          there may also be species-specific reovirus strains, some of which
          may be capable of inducing cross-infections among species. Jones
          and Guneratne (1984) showed experimentally that reoviruses   Epizootiology
          isolated from wedge-tailed eagle (Aquila audax) are pathogenic   Maintenance of avian orthoreoviruses in nature is by persistent
          for chickens.                                         infections with continuous transmission to susceptible birds
                                                                (Stott, 1999). Transmission occurs both horizontally and verti-
                                                                cally (Robertson and Wilcox, 1986) with faecal–oral transmission
          Immune responses                                      being considered the most likely route of natural infection (Mac-
          The IgA and IgG responses of chickens to avian reoviruses and   donald et al., 1978). Lateral or horizontal transmission occurring
          the effects of age of chicks (1-day-old, 7-day-old and 3-week-old)   via direct and indirect contact was demonstrated by many stud-
          and route of infection (oral and subcutaneous inoculation) were   ies (Sahu and Olson, 1975; Stott, 1999). Although orthoreovirus
          investigated by Mukiibi-Muka and Jones (1999). Virus titres in   may be excreted from both the intestinal and respiratory tracts
          the gut declined with increasing age of chick at infection. IgA   for at least 10 dpi, the virus generally appears to be shed from
          was not detected in the intestinal contents of chicks infected at   the  intestine  for  longer  periods  of  time  which  suggests  that
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