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Avian Adenovirus |   301

          et al., 2012; Totsuka et al., 2015; Matczuk et al., 2017). Interest-  necrotizing hepatitis is seen and inclusion bodies in the hepato-
          ingly, AGE is generally reported from Europe and Asia.  cytes are the hallmark of the disease (Grimes et al., 1977; Itakura
            The characteristic clinical signs of EDS include the production   et al., 1977; Shivaprasad et al., 2001) (Fig. 10.9). These inclu-
          of thin-shelled, soft-shelled and/or shell-less eggs (McFerran et   sion bodies can be eosinophilic or basophilic and usually they
          al., 1978; Yamaguchi et al., 1981; Smyth, 2013). During a typical   are large and round; virus particles can only be recovered from
          4–10-week outbreak the egg production drops about 40%, but   the basophilic inclusions (Itakura et al., 1974, 1977; Ojkic et al.,
          later returns to normal. Some researchers observed changes in the   2008a). Other lesions such as atrophy of the bursa of Fabricius
          quality of the albumen which depends on the age of the birds at   and thymus, aplastic bone marrow and lymphoid depletion in the
          the time of infection (van Eck et al., 1976; Cook and Darbyshire,   spleen have also been reported (Macpherson et al., 1974; Steer et
          1981). There are dissimilar results of the outcomes of experimen-  al., 2015; Matos et al., 2016a). A study by Steer et al. (2015) sug-
          tal infections of chickens with the duck origin EDSV (Villegas et   gests a correlation between the severity of the clinical signs and
          al., 1979; Brugh et al., 1984; Bartha and Mészáros, 1985). The   the extent of lesions in the affected organs. Gross and histopatho-
          results of a recent study suggest that EDSVs of duck origins have   logical lesions of HPS are similar to IBH with a pathognomonic
          varying pathogenicities that may be attributed to key amino acids   feature of hydropericardium, accumulation of fluid in the peri-
          (Kang et al., 2017).                                  cardial sac (Khawaja et al., 1988; Toro et al., 1999; Dahiya et al.,
            Clinical signs of HEV infection are generally seen in turkeys   2002; Kim et al., 2008; Zhao et al., 2015). The macroscopic giz-
          of 6–11 weeks of age after a short incubation period and pro-  zard lesions are described as areas of erosions of keratinoid layer
          gress rapidly (Pierson and Fitzgerald, 2013). The clinical signs   with inflammation and erosion of the underlying mucosa (Abe et
          are depression, bloody droppings and blood around the vent,   al., 2001; Ono et al., 2004; Gjevre et al., 2013; Schade et al., 2013;
          and in about 10–15% mortality in natural cases, while mortality   Matczuk et al., 2017).
          could be a lot higher, up to 80% in experimentally infected birds   The gross lesions in naturally occurring EDS outbreaks are
          (Domermuth and Gross, 1984). The acute phase of the disease is   atrophied oviducts and inactive ovaries. Mild splenomegaly and
          followed by immunosuppression leading to secondary infections   eggs of various stages in the abdominal cavity can also be present.
          (Giovanardi et al., 2014).                            In experimentally infected chickens oedema of the uterine folds
                                                                and exudate in the pouch shell gland are observed (Smyth, 2013).
          Pathology                                             The microscopic lesions are elegantly described by Smyth in the
          At necropsy the characteristic appearance of the liver, swollen, fri-  appropriate chapter of Diseases of Poultry (2013).
          able and pale yellow-white with haemorrhages is suggestive of IBH   In birds that died due to HEV infection, macroscopic disten-
          (Fig. 10.8) (Winterfield et al., 1973; Philippe et al., 2005; Hess,   sion of the small intestine is seen, and the intestinal content is
          2013; Schachner et al., 2018). Haemorrhages can also be seen   mixed with blood. The intestinal mucosa could be congested. The
          on the abdominal walls and muscles and on the swollen kidneys   enlarged spleens are friable and mottled. Petechial haemorrhages
          (Howell et al., 1970). Congestion of the ventriculus and spleen   in different tissues have been described. The liver is enlarged, and
          could be present (Saifuddin and Wilks, 1991). Histologically,   the lungs are occasionally congested (Carlson et al., 1974; Saif,

































          Figure 10.8  Liver from chicken with inclusion body hepatitis (IBH). Courtesy of Dr Marina Brash, Animal Health Laboratory, University of
          Guelph.                   Figure 8. Liver from chicken with inclusion body hepatitis (IBH)
                                    Courtesy of Dr. Marina Brash, Animal Health Laboratory, University of Guelph.
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