Adenoviruses are widespread throughout all avian species. Studies have demonstrated the presence of antibodies in healthy poultry, and viruses have been isolated from normal birds. Despite their widespread distribution, most adenoviruses cause no or only mild disease; however, some are associated with specific clinical conditions. Avian adenoviruses (AAVs) in chickens are the etiologic agents of two important diseases known as inclusion body hepatitis (IBH) and hydropericardium syndrome (HP). Although in some cases each disease is observed separately, the two conditions have been frequently observed as a single entity; therefore, the name hepatitis hydropericardium has been widely used to describe the pathologic condition. The syndrome is an acute disease of young chickens associated with anemia, hemorrhagic disorders, and hydropericardium. It is a common disease in several countries, where broilers are severely affected, resulting in high mortality rates.
Etiology, Transmission, and Pathogenesis
The AAVs classified in the genus Aviadenovirus (formerly group I), are the etiologic agents of this condition. Although there are 12 different serotypes of AAV, the most common viruses isolated in cases of IBH/HP belong to serotypes 4 and 8. These AAVs are capable of producing the disease without the immunosuppressive effects of associated viruses such as infectious bursal disease (IBDV, see Infectious Bursal Disease) or other immunosuppressive agents. However, the association with immunosuppressive viruses such as IBDV and chicken anemia virus (CAV, see Chicken Anemia Virus Infection) will result in a more severe disease.
Horizontal and vertical transmission play an important role in IBH/HP. Vertical transmission has been described in progeny from breeder flocks infected with AAV serotypes 4 and 8. Horizontal transmission has also been demonstrated; young chicks in contact with infected chicks can die of peracute IBH/HP. Infection with some strains of AAVs may result in minimal hepatic disease; however, if birds have been infected with immunosuppressive viruses (IBDV, CAV, Marek disease), the clinical disease becomes evident.
Clinical Findings, Lesions, and Diagnosis
Sudden mortality usually is seen in chickens <6 wk old and as young as 4 days of age. Mortality normally ranges from 2%–40%, especially when birds are <3 wk old. However, in some outbreaks, mortality has reached 80%. Mortality rates also vary depending on the pathogenicity of the virus and infection with other viral or bacterial agents. Signs associated with diseases caused by other pathogens (eg, bacteria, fungi, or viruses) commonly occur if birds are immunosuppressed.
Flocks of 3- to 5-wk-old broilers with HP may not show specific clinical signs, but abrupt onset of mortality, lethargy, huddling with ruffled feathers, and yellow, mucoid droppings may be seen. The duration of the infection usually ranges from 9–14 days with morbidity of 10%–30% and a daily mortality of 3%–5%. Gross lesions include as much as 10 mL of a straw-colored transudate in the pericardial sac, generalized congestion, and an enlarged, pale, friable liver. Histopathologic lesions include myocardial edema in the heart with degeneration, necrosis, and mild mononuclear cell infiltration. Basophilic intranuclear inclusion bodies may be present in the liver. A tentative diagnosis is based on typical microscopic findings and confirmed by isolating adenoviruses from the liver. Serology, restriction enzyme analysis, and PCR are used to classify adenoviruses isolated from clinical cases. This information is used for epidemiologic studies.
Treatment and Prevention
As with many other viral diseases, there is no treatment. Antibiotics may help prevent secondary bacterial infections. Sulfonamides are contraindicated if evidence of hematologic disease or immunosuppression is seen.
Vaccines against IBH/HP are not commercially available in the USA; however, in other countries both live and inactivated vaccines are used to control the syndrome. The AAV serotypes most frequently used to prepare commercial vaccines are serotypes 4 and 8. Primary breeders with stringent biosecurity practices sometimes use autogenous inactivated vaccines to ensure the transfer of maternal immunity from breeding flocks to their progeny. In Australia, a live vaccine given via drinking water was developed for breeders between 10–14 wk of age. In other countries, including Mexico, Pakistan, and many countries in South America, inactivated vaccines are routinely used to vaccinate breeders and broilers. When breeders are properly vaccinated, antibodies generated by the vaccine are transmitted to the progeny, providing protection against field infections and clinical disease. Broilers are vaccinated at <10 days of age when their parents either do not have serotype-specific adenovirus antibodies or maternal antibody transmission is erratic because of improper vaccination procedures that result in a substantial number of unvaccinated birds.
Last full review/revision October 2013 by Pedro Villegas, DVM, MS, PhD, DACVM, DACPV