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

Mendelson, C; Nothelfer, H B; Monreal, G

doi:10.1080/03079459508419108

Cited by 44 publications

(22 citation statements)

References 24 publications

(27 reference statements)

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“…Embryo pathogenicity data should be interpreted with some caution because all fowl adenoviruses are more or less pathogenic for chicken embryos. In addition, for some fowl adenoviruses, no relation could be found between embryo and chicken mortality (Mendelson et al, 1995). However, the high mortality rate observed in chicken embryos with the field isolates described here is noteworthy.…”

Section: Discussionmentioning

confidence: 58%

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

et al. 1998

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Fowl adenoviruses were isolated and characterized from severe cases of hydropericardium syndrome in Ecuador and Pakistan. All were neutralized by antibodies against serotypes 4 and 11. Cross-neutralization tests and restriction enzyme analysis strengthen the classification as serotype 4 strains. The restriction endonucleases used allowed the differentiation among field isolates and reference strains. All field isolates tested induced high embryo mortality. One-day-old specific pathogen free (SPF) chicks were infected with 10 5 plaque-forming units by natural routes to reproduce the disease with plaque purified virus. Whereas no mortality was seen with the reference strain, the mortality with the field isolates was 100%. A reduced mortality occurred with a lower infectious dose. Field isolate K1013 from Ecuador was also highly pathogenic for 1-to 3-week-old SPF chicks after intramuscular inoculation. The main pathological signs were swollen livers, severe hydropericardium and nephritis, reflecting the field situation and underlining the role of FAV4 strains in the aetiology of infectious hydropericardium.

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Section: Discussionmentioning

confidence: 58%

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

et al. 1998

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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). The basis of the discrepancy between reports that investigated the role of FAdVs as primary or secondary pathogens may stem from variations in the route of administration, age of chickens and/or strains used for inoculation.…”

Section: Introductionmentioning

confidence: 73%

“…Sequential pathology of recombinant FAdV-1 CELO strains (Le Goff et al, 2005) and a FAdV-8 strain (Reece et al, 1987) has been studied in normal and cyclophosphamide treated chickens, respectively. The pathology of FAdV-11 infection was examined over four time points (Mendelson et al, 1995), and several FAdV-E serotypes were studied with dose rate and mortality as a measure of virulence (Erny et al, 1991). Also kinetics of FAdV-8 has been studied in detail in SPF chickens (Saifuddin & Wilks, 1991).…”

Section: Discussionmentioning

confidence: 99%

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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“…HPS was associated with the same group of viruses, and it devastated the poultry industry of Pakistan (Cowen et al 1978, Asthana et al 2013. The syndrome and its various manifestations have been reported in several countries in North and South America, Europe, Asia and Oceania, causing considerable economic losses (Mendelson et al 1995, Toro et al 1999, Ono et al 2003, Rahul et al 2005, Gomis et al 2006, Manarolla et al 2009, Mase et al 2009, Alemnesh et al 2010, Choi et al 2012. Adenoviruses belong to the family Adenoviridae.…”

Section: Introductionmentioning

confidence: 99%

Fowl adenovirus Group I as a causal agent of inclusion body hepatitis/hydropericardium syndrome (IBH/HPS) outbreak in brazilian broiler flocks

et al. 2014

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Commercial broiler flocks from a farm located in the State of São Paulo, Brazil, presented diarrhea, depression, increased mortality and poor weight gain. Upon post-mortem examination, classical signs of Inclusion Body Hepatitis/Hydropericardium Syndrome (IBH/HPS) were observed, including enlarged pale yellow-colored livers and straw-colored liquid in the pericardial sac. In addition, gross lesions were also observed in the kidneys, pancreas, thymus, intestines and gallbladder. Samples of these organs were analyzed by PCR for the detection of the hexon gene of the Fowl Adenovirus (FAdVs) Group I. The results were positive for both flocks (A and B) assayed by PCR. The macroscopic lesions associated with the detection of FAdV Group I by PCR in several of these affected organs allowed for the identification of IBH/HPS. In fact, this is the first report in Brazil of IBH/HPS in broilers, which identifies FAdVs group I as a causal agent of the disease. These findings may contribute to the worldwide epidemiology of the adenovirus-mediated hepatitis/hydropericardium syndrome.

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

Cited by 44 publications

References 24 publications

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

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

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

Fowl adenovirus Group I as a causal agent of inclusion body hepatitis/hydropericardium syndrome (IBH/HPS) outbreak in brazilian broiler flocks

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