The hypothesis that fowl adenovirus (FAV) and chicken anemia virus (CAV), transmitted vertically and simultaneously, induce the inclusion body hepatitis (IBH)/hydropericardium (HP) syndrome in progeny chickens was tested. Thus, 35-wk-old light brown layer breeders, showing absence of antibodies against FAV and variable titers against CAV, were intramuscularly singly infected with the FAV serotype 4 isolate 341 or dually infected with CAV (isolate 10343) and FAV. All hens (groups A [FAV alone], B [FAV + CAV], and C [noninfected]) were clinically healthy throughout the experimental period. Both infectious viruses FAV and CAV were isolated from progenies obtained as early as 5 days after infection of their breeders. Hematocrit, serum proteins, and aspartate-aminotransferase values showed a few statistical differences between the progeny groups. Most of these differences were detected in the progeny chickens of group B. However, almost all values met reference values for the species. The pathologic findings showed that progeny chickens obtained from both singly and dually infected breeders developed macroscopic and histopathologic changes of IBH/HP. The pathologic findings shown by progeny chickens of group A (FAV) were not expected because neither synergism nor prior immunodepression by CAV was concurrent. Chickens of group B (CAV + FAV) also developed IBH/HP. Although not many differences in the evaluated parameters between groups A and B were statistically significant, most pathologic findings of group B indicated a more severe manifestation of the disease. However, because FAV alone did reproduce the syndrome, the results shown by group B would not allow a definitive confirmation of the hypothesis that the association of FAV and CAV is necessary for the successful induction of the IBH/HP syndrome in chickens when transmitted vertically.
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