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USGS · 1003916

Characterization of a herpes virus isolated from domestic geese in Australia

Abstract

A herpesvirus (GHV 552/89) associated with high mortality in a flock of domestic geese in Australia was compared with duck virus enteritis (DVE) herpesvirus by cross-protection studies in domestic geese, Muscovy ducks and commercial Pekin ducks. In DVE-vaccinated geese, Muscovy ducks and Pekin ducks, mortality levels of 100, 50 and 0%, respectively, were recorded following challenge with GHV 552/89. Conversely, in geese, Muscovy ducks and Pekin ducks immunized with inactivated GHV 552/89, 100% mortality was observed in the geese and Muscovy ducks, and 80% in the Pekin ducks following challenge with DVE virus. The isolate was also compared with six other avian herpesviruses using cross-neutralization tests in cell cultures. No detectable cross-neutralization occurred with any of the avian herpesviruses tested. Further characterization of GHV 552/89 was undertaken by comparing its genome with strains of DVE herpesvirus using restriction endonuclease analysis of the viral DNA and a polymerase chain reaction (PCR) test. Following digestion with HindIII, the DNA fragment pattern of GHV 552/89 was found to be completely different from the DVE viruses. Similarities were found between the digestion patterns of a UK and a US DVE isolate, but both were distinguishable from a UK vaccine strain. The results of the PCR analysis and comparison using two DVE-specific primer sets did not produce specific amplification products of expected molecular weights (603 and 446 base pairs) from the GHV 552/89 genome. The PCR products derived from the DVE strains were similar to those derived from the DVE control DNA. From the results of this study, it is concluded that the goose herpesvirus GHV 552/89 is antigenically and genomically distinct from DVE herpesvirus.

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90° N90° S · 180° W ← longitude → 180° E
Source-reported bounding extent: -43.6346° to -10.66819° latitude; 113.33895° to 153.56947° longitude. This indicates report coverage, not an exact sampling location. View area on OpenStreetMap.

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BibTeXRIS

R. E. Gough, W. R. Hansen. 2010-06-17. Characterization of a herpes virus isolated from domestic geese in Australia. https://doi.org/10.1080/030794500750047162

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Apparent discrepancies in the review “Avian host range of Chlamydophila spp. based on isolation, antigen detection and serology” by Kaleta, E.F. & Taday, E.M.A. (2003), Avian Pathology, 32, 435–462

Citing published reports and their own diagnostic data, Kaleta and Taday ( Citation 2003 ) ( https://doi.org/10.1080/03079450310001593613 ) reported that 469 domestic and free-living bird species were determined to be chlamydia-positive, based on isolation of the organism and antigen detection or on serological detection of circulating antibodies. However, I was unable to reconcile the designation of chlamydia-positive in some of the species listed by Kaleta and Taday ( Citation 2003 ) with the information provided in the corresponding references cited. For example, Eddie et al . ( Citation 1966 ) tested sera from 24 species of birds in Alaska (see their Table 1 ) by “direct and indirect complement fixation techniques in the presence of the standard psittacosis antigen.” Eddie et al . ( Citation 1966 ) reported that serum samples from only two species reacted, and the authors considered those titres too low to be of diagnostic significance. However, Kaleta and Taday ( Citation 2003 ) listed 20 bird species from Eddie et al . ( Citation 1966 ) as being positive for chlamydia. Additional apparent discrepancies are listed in Table 1 of the current article.

Avian Pathology↗

The pathogenesis of a 2022 North American highly pathogenic clade 2.3.4.4b H5N1 avian influenza virus in mallards (Anas platyrhynchos)

Highly pathogenic (HP) avian influenza viruses (AIVs) of the clade 2.3.4.4 goose/Guangdong/1996 H5 lineage continue to be a problem in poultry and wild birds in much of the world. The recent incursion of a H5N1 clade 2.3.4.4b HP AIV from this lineage into North America has resulted in widespread outbreaks in poultry and consistent detections of the virus across diverse families of birds and occasionally mammals. To characterize the pathobiology of this virus in mallards ( Anas platyrhynchos ), which are a primary reservoir of AIV, a challenge study was conducted with 2 week-old birds. The 50% bird infectious dose was determined to be <2 log 10 50% egg infectious doses (EID 50 ) and all exposed ducks, including ducks co-housed with inoculated ducks, were infected. Infection appeared to be subclinical for 58.8% (20/34) of the ducks, 1 duck was lethargic, about 20% developed neurological signs and were euthanized, and 18% developed corneal opacity. The mallards shed virus by both the oral and cloacal routes within 24-48hr post-infection. Oral shedding substantially decreased by 6-7 days post-infection, but 65% of the ducks continued to shed virus cloacally through 14 days post-exposure (DPE) for the direct inoculate and 13DPE for contact exposed ducks. Based on the high transmissibility, high virus shed titers, and mild-to-moderate disease, mallards could serve as efficient reservoirs to amplify and disseminate recent North American clade 2.3.4.4b viruses.

Avian Pathology↗

Pancreatitis in wild zinc-poisoned waterfowl

Four waterfowl were collected in the TriState Mining District (Oklahoma, Kansas and Missouri, USA), an area known to be contaminated with lead, cadmium and zinc (Zn). They were part of a larger group of 20 waterfowl collected to determine the exposure of birds to metal contamination at the site. The four waterfowl (three Branta canadensis, one Anas platyrhynchos) had mild to severe degenerative abnormalities of the exocrine pancreas, as well as tissue (pancreas, liver) concentrations of Zn that were considered toxic. The mildest condition was characterized by generalized atrophy of exocrine cells that exhibited cytoplasmic vacuoles and a relative lack of zymogen. The most severe condition was characterized by acini with distended lumens and hyperplastic exocrine tissue that completely lacked zymogen; these acini were widely separated by immature fibrous tissue. Because the lesions were nearly identical to the lesions reported in chickens and captive waterfowl that had been poisoned with ingested Zn, and because the concentrations of Zn in the pancreas and liver of the four birds were consistent with the concentrations measured in Zn-poisoned birds, we concluded that these waterfowl were poisoned by Zn. This may be the first reported case of zinc poisoning in free-ranging wild birds poisoned by environmental Zn.

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