The stand-alone pathogenicity of fowl adenoviruses (FAdVs) had long been disputed, given the ubiquity of the viruses versus sporadic outbreaks, and variation between experimental studies. However, a globally emerging trend of FAdV-associated diseases has marked the past two decades, with hepatitis-hydropericardium syndrome mainly in Asia besides Arabian and Latin American countries, and geographically more disseminated outbreaks of inclusion body hepatitis. Finally, the appearance of FAdV-induced gizzard erosion (AGE) in Asia and Europe completed the range of diseases. Epidemiological studies confirmed serotype FAdV-4 as agent of hepatitis-hydropericardium syndrome, whereas inclusion body hepatitis is related to FAdV-2, -8a, -8b and -11. Members of the biologically more distant serotype FAdV-1 induce AGE. Urged by increasing problems in the field, numerous pathogenicity studies with FAdVs from outbreaks substantiated the primary aetiologic role of particular strains for distinct clinical conditions. Developments in the poultry industry towards highly specialized genetic breeds and rigorous biosecurity additionally contribute to the growing incidence of FAdV-related diseases. Confirming field observations, recent studies connected a higher susceptibility of broilers with their distinct physiology, implying the choice of bird type as a factor to be considered in infection studies. Furthermore, elevated biosecurity standards have generated immunologically naïve breeding stocks, putting broilers at risk in face of vertical FAdV transmission. Therefore, future prevention strategies should include adequate antibodies in breeders prior to production and - if necessary - vaccination, in order to protect progenies. This review aims to deliver a detailed overview on the current global situation about FAdV-induced diseases, their reproduction in vivo and vaccination strategies.

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The present report documents an outbreak of adenoviral gizzard erosion in 22 broiler flocks in Germany. The clinical picture was characterized by uneven growth of affected broilers that resulted in considerably lower than average weight at slaughtering. Fowl adenovirus serotype 1 (FAdV-1) was isolated from gizzard lesions and histological examinations demonstrated FAdV-1-positive intranuclear inclusion bodies in gizzard epithelial cells of affected broilers by in-situ hybridization. Birds from all affected flocks originated from one broiler breeder farm. During production of affected birds, broiler breeders were between 27 and 32 weeks old. Enzyme-linked immunosorbent assay and specific virus neutralization assay of sera from parent birds demonstrated an acute FAdV-1 infection within the first 5 weeks of the production cycle. Clinically, broiler breeders exhibited a moderate fall in the hatchability of their chicks, while egg production remained normal. No further clinical signs could be observed. Genetically identical FAdV-1 strains were isolated from gizzards of embryos at the lowest point of hatchability and from affected broiler flocks raised on independent farms. For the first time, direct detection of viable FAdV-1 from gizzards of embryos and progenies of one FAdV-1-seropositive broiler breeder farm in the course of an outbreak of adenoviral gizzard erosion could be demonstrated, highlighting the importance of vertical transmission of this disease. Additionally, growth retardation and subsequent reduced average weight at the time of slaughter of broiler chickens underline the economic impact of adenoviral gizzard erosion for poultry production.

In the present study, inclusion body hepatitis (IBH) was experimentally induced by oral inoculation of two groups of specific pathogen-free (SPF) broilers and two groups of SPF layers at day-old with either a fowl aviadenovirus (FAdV)-D or a FAdV-E strain. A substantial variation in the degree of susceptibility was observed with mortalities of 100 and 96% in the FAdV-E and D infected SPF broiler groups, respectively, whereas in the groups of infected SPF layers mortalities of only 20 and 8% were noticed. Significant changes in clinical chemistry analytes of all infected birds together with histopathological lesions indicated impairment of liver and pancreas integrity and functions. Furthermore, significantly lower blood glucose concentrations were recorded at peak of infection in both inoculated SPF broiler groups, in comparison to the control group, corresponding to a hypoglycaemic status. High viral loads were determined in liver and pancreas of SPF broilers already at 4 days post-infection (dpi), in comparison to SPF layers, indicating a somewhat faster viral replication in the target organs. Overall, highest values were noticed in the pancreas of SPF broilers independent of the virus used for infection. The actual study provides new insights into the pathogenesis of IBH, a disease evolving to a metabolic disorder, to which SPF broilers were highly susceptible. Hence, this is the first study to report a significant higher susceptibility of SPF broiler chickens to experimentally induced IBH in direct comparison to SPF layers.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-016-0350-0) contains supplementary material, which is available to authorized users.