Molecular characterization of fowl aviadenoviruses species D and E associated with inclusion body hepatitis in chickens and falcons indicates possible cross-species transmission
ABSTRACT During the period from 2015 to 2017, frequent outbreaks of inclusion body hepatitis (IBH) were observed in broiler chickens and falcons in Saudi Arabia. Fifty samples were collected from both species. The histopathological examination and polymerase chain reaction confirmed the IBH infection in eight samples (five samples from chickens and three samples from falcons). The genomic sequence and phylogenetic analysis based on nucleotide and amino acid sequences of Saudi strains, reference fowl aviadenoviruses (FAdVs) and field viruses available in Genbank revealed that all investigated FAdVs clustered into FAdV-2 (species D) and FAdV-6 (species E). The host-dependent characterization revealed that falcon origin strains showed low identity (∼35%) with falcon adenoviruses isolated from USA, which clustered into a separate group. The identification of FAdV-D and FAdV-E in diseased falcons and chickens indicates cross-species transmission although falcons and chickens are phylogenetically different. The control of IBH infection in falcons and chickens should be based on the separation of carriers and susceptible chickens as well as falcons to prevent cross-species contact. Vaccination is an important method for prevention of IBH. The characterization of newly emerging FAdV strains provides valuable information for the development of an efficacious control strategy based on the molecular structure of current circulating FAdV strains in different species of birds.
Characterization of a New Species of Adenovirus in Falcons
ABSTRACT In 1996, a disease outbreak occurred at a captive breeding facility in Idaho, causing anorexia, dehydration, and diarrhea or sudden death in 72 of 110 Northern aplomado falcons (Falco femoralis septentrionalis) from 9 to 35 days of age and in 6 of 102 peregrine falcons (Falco peregrinus) from 14 to 25 days of age. Sixty-two Northern aplomado and six peregrine falcons died. Epidemiologic analyses indicated a point source epizootic, horizontal transmission, and increased relative risk associated with cross-species brooding of eggs. Primary lesions in affected birds were inclusion body hepatitis, splenomegaly, and enteritis. The etiology in all mortalities was determined by molecular analyses to be a new species of adenovirus distantly related to the group I avian viruses, serotypes 1 and 4, Aviadenovirus. In situ hybridization and PCR demonstrated that the virus was epitheliotropic and lymphotropic and that infection was systemic in the majority of animals. Adeno-associated virus was also detected by PCR in most affected falcons, but no other infectious agents or predisposing factors were found in any birds. Subsequent to the 1996 epizootic, a similar disease caused by the same adenovirus was found over a 5-year period in orange-breasted falcons (Falco deiroleucus), teita falcons (Falco fasciinucha), a merlin (Falco columbarius), a Vanuatu peregrine falcon (Falco peregrinus nesiotes), and gyrfalcon × peregrine falcon hybrids (Falco rusticolus/peregrinus) that died in Wyoming, Oklahoma, Minnesota, and California. These findings indicate that this newly recognized adenovirus is widespread in western and midwestern North America and can be a primary pathogen in different falcon species.
Demonstration of an avian adenovirus as the causative agent of marble spleen disease.
A purification procedure, using chloroform or fluorocarbon extraction and centrifugation on a cushion of cesium chloride (CsCL), was designed to isolate the causative virus of marble spleen disease. Virus was purified, inoculated into turkeys, and subsequently reisolated by purification from the spleen of inoculated turkeys, thus fulfilling Koch's postulates. Splenic antigen was detected by the agar gel precipitin test, and viral inclusions with viral particles were observed by light and electron microscopy. Results of further studies indicated splenic lymphoreticulum cell hyperplasia was a sensitive indicator of marble spleen disease virus (MSDV) infection. Direct fluorescent antibody staining revealed nuclear fluorescence in virus-infected splenic cells from turkeys inoculated with purified MSDV. With negative stain electron microscopy, MSDV was observed to be 90 nm across with an icosahedral capsid composed of 252 capsomeres. This morphologic feature was consistent with that of an avian adenovirus. Serologic evidence for classification of MSDV as an adenovirus was the cross reaction of MSDV antigen with antiserum to turkey adenovirus serotypes TA-1 and TA-2 in the agar gel precipitin test.