Serological Response of Chickens Exposed to a Type 1 Avian Adenovirus Alone or in Combination with the Adeno-Associated Virus

Yates, Vance J.; Rhee, Young-Ok; Fry, D. E.

doi:10.2307/1589324

Cited by 12 publications

(4 citation statements)

References 3 publications

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“…They are generally considered nonpathogenic, although some serotypes have been associated with reproductive abnormalities in humans and others have been shown to modify cell cycle progression in vitro, either inducing apoptosis or inhibiting it (25,35,43). In birds, latent infections are widespread, and several studies have suggested that AAV can modify humoral immunity and the pathogenicity of adenovirus infections in vivo (39,57). Our data showed no correlation between the severity or distribution of lesions in falcons and the presence of AAV or a particular genotype of AAV.…”

Section: Discussionmentioning

confidence: 99%

Characterization of a New Species of Adenovirus in Falcons

et al. 2005

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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. Adenoassociated 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.

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Section: Discussionmentioning

confidence: 99%

Characterization of a New Species of Adenovirus in Falcons

et al. 2005

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“…4 However, a different study found that it was possible to reinfect chickens with the same strain after 8 weeks. 29 To be able to make appropriate decisions, it is important to determine whether chickens naturally invaded by a primary FAV infection develop resistance to reinfection.…”

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confidence: 99%

Pathogenicity by Parenteral Injection of Fowl Adenovirus Isolated from Gizzard Erosion and Resistance to Reinfection in Adenoviral Gizzard Erosion in Chickens

et al. 2004

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Abstract. The pathogenicity of a serotype-1 fowl adenovirus (FAV-99ZH), which causes adenoviral gizzard erosion by oral inoculation in chickens, was investigated in specific pathogen-free white leghorn chickens. In trial 1, 14 chickens were inoculated intravenously with the virus at 21 days of age and euthanatized for necropsy within 1-14 days of inoculation. Gizzard erosion was grossly observed from day 7 postinoculation (PI), and histologically, FAV-99ZH antigen-positive, basophilic intranuclear inclusion bodies were seen in the gizzard lesions from day 7 to 11 PI. Necrotizing pancreatitis, and cholecystitis and cholangitis associated with the inclusions were observed from day 3 to 14 PI (pancreatitis) and from day 5 to 9 PI (cholecystitis and cholangitis), respectively. The inclusions were also observed in the epithelial cells of the cecal tonsils from day 3 to 5 PI. The virus was recovered from samples of the lesions. It was revealed that FAV-99ZH causes not only gizzard erosion but also pancreatitis, cholecystitis, and cholangitis by intravenous inoculation in chickens. In trial 2, 10 chickens were inoculated orally with the virus twice, at 13 and 36 days of age, and euthanatized for necropsy within 4-17 days after reinfection. Macroscopically, focal gizzard lesions were observed; however, neither necrosis nor inclusions were observed by microscopy. Moreover, FAV was not recovered from the gizzard or rectum of any of the chickens at necropsy. This suggests that the gizzard lesions occurred as a result of the primary infection, and that the chickens were able to resist reinfection.

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“…Thus Burke et al (1959) The DID test has been used for diagnosis and monitoring of specific pathogenfree (SPF) flocks for infection. This observation has been confirmed by others (Grimes et al, 1977a;Yates et al, 1977). McFerran et al (1975) drew attention to the failure of SPF birds experimentally infected by a natural route with one serotype always to develop detectable antibody.…”

Section: Diagnosismentioning

confidence: 53%

Adenoviruses of Vertebrate Animals

McFerran¹

1981

Vertebrate Animal and Related Viruses

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Serological Response of Chickens Exposed to a Type 1 Avian Adenovirus Alone or in Combination with the Adeno-Associated Virus

Cited by 12 publications

References 3 publications

Characterization of a New Species of Adenovirus in Falcons

Characterization of a New Species of Adenovirus in Falcons

Pathogenicity by Parenteral Injection of Fowl Adenovirus Isolated from Gizzard Erosion and Resistance to Reinfection in Adenoviral Gizzard Erosion in Chickens

Adenoviruses of Vertebrate Animals

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