Reproduction of inclusion body hepatitis in conventionally raised chickens inoculated with a New Zealand isolate of avian adenovirus

Saifuddin, Md.; Wilks, C. R.

doi:10.1080/00480169.1990.35618

Cited by 22 publications

(19 citation statements)

References 19 publications

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“…Hydropericardium syn- drome caused by FAV serotype 4 is known to occur in uninoculated exposed chickens through direct contact with inoculated chickens [1,3]. Other researchers have reported severe growth depression in uninoculated chickens exposed by direct contact to inclusion body hepatitis-induced FAV serotype 8 [19]. To the best of our knowledge, the present study is the first in which AGE has been spread by horizontal transmission.…”

Section: Discussionmentioning

confidence: 66%

Reproduction of Adenoviral Gizzard Erosion by the Horizontal Transmission of Fowl Adenovirus Serotype 1

Ono

Okuda

Shibata

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. The horizontal transmission ability of fowl adenovirus (FAV) serotype 1 99ZH strain, isolated from chickens exhibiting gizzard erosion, was investigated. Twelve 13-day-old specific pathogen-free chickens were inoculated orally with 10 6 TCID 50 /0.05 ml of the strain. An in-pen contact group (chickens in the same pen with inoculated chickens), hedge contact group (chickens in a pen connected with pens housing inoculated chickens), non-contact group (chickens in a separate pen placed at a distance of 70 cm from the connected pens), human exposure group (chickens in the next room and attended last every day) and negative control group were examined. Each group consisted of 11 or 12 uninoculated chickens. Gizzard lesions were grossly or histologically observed from 10 days after exposure (DAE) in the in-pen contact group, and from 15 DAE in the hedge contact and non-contact groups. The FAV gene was detected by polymerase chain reaction performed on cloacal swabs taken on 5 and 13 DAE from chickens in both contact groups, and on 20 and 26 DAE from those in the non-contact group. Serum neutralizing antibodies against FAV serotype 1 were detected in chickens from 13 and 26 DAE in both contact groups and in the non-contact group, respectively. In the human exposure and negative control groups, no infection was observed. We conclude that FAV-99ZH strain spreads rapidly through direct contact with inoculated chickens, and slowly through non-contact transmission, and that adenoviral gizzard erosion is reproduced by this horizontal transmission.

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Section: Discussionmentioning

confidence: 66%

Reproduction of Adenoviral Gizzard Erosion by the Horizontal Transmission of Fowl Adenovirus Serotype 1

Ono

Okuda

Shibata

et al. 2007

The Journal of Veterinary Medical Science

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“…However, several reports have shown or suggested FAdVs to be capable of causing naturally occurring outbreaks of IBH in the absence of immunosuppressive agents (Reece et al, 1986;Saifuddin & Wilks, 1990;Gomis et al, 2006;Steer et al, 2011). Attempts to experimentally reproduce the disease have had mixed findings (McDougall & Peters, 1974;Fadly et al, 1976;McCracken et al, 1976;Grimes et al, 1978;Erny et al, 1991;Mendelson et al, 1995;Toro et al, 2000;Grgic et al, 2011).…”

Section: Introductionmentioning

confidence: 95%

Chronological analysis of gross and histological lesions induced by field strains of fowl adenovirus serotypes 1, 8b and 11 in one-day-old chickens

et al. 2015

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Fowl adenoviruses (FAdVs) cause diseases in domestic chickens, including inclusion body hepatitis (IBH), with immunosuppression believed to play a role in their pathogenesis. To gain a better understanding of the pathogenesis and chronology of disease caused by FAdVs, the gross pathology, histopathology and dissemination of virus were examined at several different time points, after inoculation of one-day-old specific pathogen-free chickens with FAdV-1, FAdV-8b or FAdV-11 via the ocular route. FAdV-8b had a slightly greater virulence than FAdV-11, but both were primary pathogens. The presence and severity of hepatic lesions were used to define the three stages of the disease: incubation (1-3 days post-inoculation, PI), degeneration (4-7 days PI) and convalescence (14 days PI). Both viruses were detected in the liver, kidney, bursa, thymus and gizzard of most birds during the degenerative stage, and persisted in the gizzard into convalescence. The FAdV-1 isolate was found to be apathogenic, but virus was detected in the bursa and/or gizzard of several birds between 2 and 7 days PI. This is the first study examining the chronology of gross and microscopic lesions of pathogenic and apathogenic FAdVs in association with viral presence in multiple tissues. It was concluded that both FAdV-8b and FAdV-11 are primary pathogens, and that these strains may play a role in immunosuppression.

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“…Several researchers have suggested the possibility of maternal antibodies preventing disease in chickens inoculated with FAVs that are associated with IBH. 7,12,33 Maternal antibody also influences the susceptibility of turkeys to infection with the hemorrhagic enteritis virus, which is classified as a group II avian adenovirus. 6 However, maternal antibody does not confer protection against some mucosal viral infections, such as infectious bronchitis (IB) or laryngotracheitis.…”

Section: Discussionmentioning

confidence: 99%

Adenoviral Gizzard Erosion in Commercial Broiler Chickens

et al. 2003

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Abstract. Pathologic and immunohistochemical changes caused by group I of the fowl adenovirus (FAV) serotype-1 99ZH strain, isolated from broiler chickens exhibiting gizzard erosion, were investigated in commercial broiler chickens. One hundred twenty-two chickens were inoculated with the strain by both oral and ocular routes at 1, 3, or 5 weeks of age and euthanatized for necropsy within 4-18 days of inoculation. Focal gizzard erosions were observed in the inoculated chickens of each age group. A histologically degenerative koilin layer, necrotic mucosa, intranuclear inclusion bodies in the glandular epithelial cells, inflammatory cell infiltrations in the lamina propria, submucosa, and a muscle layer were seen in the gizzards. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies. These findings were recognized regardless of their maternal antibody levels for FAV serotype-1. Gizzard lesions appeared later in the lower-dose-inoculated chickens than in the higher-dose-inoculated chickens. Numerous CD3-positive cells and IgY-positive plasma cells were seen in the gizzard lesions. In 5-week-old chickens the heterophil infiltrations in the lesions were milder than in younger chickens. Intranuclear inclusion bodies also were observed in the epithelial cells of the ileum or cecal tonsils of some chickens. Thus, this study shows that FAV-99ZH causes adenoviral gizzard erosion in broiler chickens without hepatic or pancreatic lesions and that cell infiltration is more severe than in dietary gizzard erosions.Key words: Adenovirus; broiler chickens; erosion; gizzard.Fowl adenovirus (FAV) is ubiquitous in chickens, as demonstrated by antibody surveys 11,41 and the high isolation rates of FAV in specimens taken from normal and sick birds. 3,19 FAV is associated with naturally occurring outbreaks of inclusion body hepatitis (IBH), 39 hydropericardium syndrome (HPS), 1 respiratory disease, 5 necrotizing pancreatitis, 32 or gizzard erosion.Gizzard erosions and ulcers in chickens have been associated with diets that are deficient in vitamin B 6 4 or with the ingestion of histamine, 14 gizzerosine, 26 and mycotoxins. 15 Gizzard erosions also have been observed at a high rate in the embryos and chicks of broilers. 36 However, several natural cases of gizzard erosion associated with FAV infection have been reported in layer chickens, broiler chickens, and quails in recent years. 2,10,25,37 Gizzard erosion has been observed in chickens inoculated with group I FAV serotype-8 and affected with hemorrhagic aplastic anemia syndrome. 12 In previous studies, however, the role played by FAV as a pathogen of gizzard erosion was not clearly established, because no viral examinations were conducted and because there were no adenoviral intranuclear inclusion bodies in the gizzard lesions. Some FAVs that had originally been isolated from either the proventriculus or a gastrointestinal pool of the tissues of broiler chickens caused gizzard erosions by experimental infection. 22 In our previous studi...

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Reproduction of inclusion body hepatitis in conventionally raised chickens inoculated with a New Zealand isolate of avian adenovirus

Cited by 22 publications

References 19 publications

Reproduction of Adenoviral Gizzard Erosion by the Horizontal Transmission of Fowl Adenovirus Serotype 1

Reproduction of Adenoviral Gizzard Erosion by the Horizontal Transmission of Fowl Adenovirus Serotype 1

Chronological analysis of gross and histological lesions induced by field strains of fowl adenovirus serotypes 1, 8b and 11 in one-day-old chickens

Adenoviral Gizzard Erosion in Commercial Broiler Chickens

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