Molecular characterization of highly virulent fowl adenoviruses associated with outbreaks of inclusion body hepatitis

Abstract

Restriction enzyme analysis of DNA was used to characterize fowl adenoviruses (FAVs) consistently associated with outbreaks of acute inclusion body hepatitis. When low doses of these FAVs were administered via a natural route to chickens they caused IBH. A strong genomic relationship was demonstrated between these virulent FAVs. In contrast, the genomes of serologically related, but non-virulent or mildly virulent FAVs were found to differ substantially from those of the virulent FAVs.

Identification and characterization of an avian adenovirus isolated from a ‘spiking mortality syndrome’ field outbreak in broilers on the Delmarva Peninsula, USA

“…Therefore, the pathogenicity of conventional avian adenoviruses remains a matter of discussion. Nonetheless, this study supports the results of Reece et al (1986), Christensen & Saifuddin (1989), Conrad et al (1991), Erny et al (1991), Lamichhane et al (1991) and Goodwin et al (1993) in which certain highly virulent FAV strains from different serotypes have a primary pathogenic effect in chickens. It should also be considered, that if the first infection of parent flocks with highly virulent FAV strains occurs during the egg laying period, FAV may be vertically transmitted to progeny not sufficiently protected by maternal antibodies.…”

“…In the past few years certain strains of fowl adenoviruses were isolated during epidemics in Pakistan, Australia, New Zealand, the USA and Germany with features such as high mortality, inclusion body hepatitis (JBH), a hydropericardium syndrome and low hatchability. Although the search for a single aetiology for these disease complexes has not yet been successful, there is increasing evidence that suggests a primary involvement of FAV (Christensen & Saifuddin, 1989;Conrad et al, 1991;Erny et al, 1991;Lamichhane et al, 1991;Goodwin et al, 1993;Hess et al, 1993;Monreal & Hess, 1994). One of these disease complexes, so called 'spiking mortality syndrome' (SMS), is observed in 11 to 180-day-old broiler chicks and characterized by a sudden onset of greater than 1% daily mortality lasting 3 to 5 days.…”

Some strains of serotype 4 fowl adenoviruses cause inclusion body hepatitis and hydropericardium syndrome in chickens

“…Imitating a possible natural infection route, we found no mortality with the reference strain KR5, whereas the plaque purified field isolates were highly pathogenic for day-old and 1-week-old chicks. Different patho-genicity within one serotype was also shown for serotype 8 isolates in Australian cases of atypical IBH (Erny et al, 1991).…”

“…Infectious bursal disease virus (IBDV) and chicken anaemia virus (CAV) are known to increase the pathogenicity of FAV infections (Fadly et al, 1976;Biilow et al, 1986). However, in the last few years several cases of IBH occurred without obvious influence of infectious immunosuppression (Reece et al, 1986;Christensen & Saifuddin, 1989;Erny et al, 1991). In Australia and New Zealand FAV8 strains were isolated from atypical IBH cases with mortality up to 30% in chicks less than 3 weeks of age (Erny et al, 1991).…”

Molecular Identification of Fowl Adenovirus Associated with Inclusion Body Hepatitis in Iran

“…Immunosuppression induced by infectious bursal disease virus (IBDV) and chicken anemia virus (CAV) or some mycotoxins, such as aflatoxins appear to assist adenoviruses in producing IBH (3)(4)(5). However, there are many evidences that IBH can be a primary disease in chickens (6)(7)(8)(9)(10) and apparently IBH can possibly occur without the influence of infectious immunosuppression (11). IBH is usually seen in meat-producing birds between three and seven weeks of age.…”