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PubMed1976

An outbreak of duck virus enteritis (duck plague) in Alberta.

Duck plague (Duck virus enteritis) was disgnosed in a resident population of Muscovy ducks (Cairina moschata) on a small game farm in Alberta. This disease has not been reported previously in Canada. Clinical signs consisted of cyanosis, depression and acute death. Necropsy of two Muscovy ducks revealed lesions typical of the disease. There were ulcerations with pseudomembranes in the small intestine, ulcerations with caseous plaques in the esophagus and eosinophilic intranuclear inclusion bodies in the spleen. Clinical disease with mortality was reproduced in young ducklings injected with tissue homogenates from field cases. All surviving inoculated ducklings seroconverted to highly significant titres of neutralizing antibodies to duck virus enteritis (DVE) virus. All attempts to isolate the agent in embryonating duck eggs or primary tissues cultures of duck and chicken kidney were negative. Identification of the DVE virus was accomplished by serum neutralization with ducklings as the host system.

Alberta↗
PubMedDate not supplied

Occurrence of duck virus enteritis (duck plague) in Pennsylvania, 1968-74.

During the 7-year period 1968-74 cases of duck virus enteritis (duck plague) were diagnosed in waterfowl in Pennsylvania. Muscovy ducks were affected in 8 cases, geese in 3 cases, and mallard ducks in 1 case. In 5 of these cases either domestic or wild ducks were closely associated with infected waterfowl but were unaffected.

Animals↗
PubMed2026

Research note: Development of a recombinant duck enteritis virus vector expressing DHAV-3 VP1 and DTMUV prM/TE genes.

Duck enteritis virus (DEV) is a promising viral vector for vaccine development. In a previous study, an HDR-CRISPR/Cas9-based strategy was used to generate a recombinant virus, rDEV-DHAV-VP1, by inserting the VP1 gene of duck hepatitis A virus type 3 (DHAV-3) into the UL27/UL26 intergenic region of DEV vaccine strain, resulting in good genetic stability and immunogenicity. In the present study, the same strategy was applied to insert the EGFP gene into the US7/US8 and LORF11/UL55 intergenic regions of a DEV vaccine strain. Among the evaluated insertion sites, the highest level of EGFP expression was observed at the US7/US8 locus, followed by the UL27/UL26 locus. Based on rDEV-DHAV-VP1, the pre-membrane (prM) and truncated envelope (TE) genes of duck Tembusu virus (DTMUV) were further inserted into the US7/US8 locus, resulting in a bivalent recombinant virus, rDEV-VP1-prM/TE. The recombinant virus exhibited growth kinetics comparable to those of the parental virus, while maintaining efficient expression and high genetic stability of the inserted genes. These findings indicate that the HDR-CRISPR/Cas9 system is an efficient strategy for generating stable DEV-based recombinant vectors and provides a promising platform for the development of multivalent vaccines against major duck viral diseases.

CRISPR/Cas9 genome editing↗
PubMedDate not supplied

Duck viral enteritis: a comparison of replication by CCL-141 and primary cultures of duck embryo fibroblasts.

Cultures of primary cells and a line of fibroblast-like cells from the Pekin duck were both compared for their replication of the herpesvirus of duck viral enteritis. The two kinds of cells were equally accurate for quantifying virus upon isolation. Also, one-step growth curves showed that in both kinds of cultures new virus appeared by the 18th hour and that infectivity peaked at about 36 hours. Primary cultures yielded about 5.6 times as much virus as did the cell line, though plaques were more easily discerned in the latter. Because of availability, uniformity, and their known health history, CCL-141 cells offer some advantages for work with the agent of duck viral enteritis.

Animals↗
PubMed1975

Duck viral enteritis (duck plague) characteristics and immune response of the host.

Duck viral enteritis (DVE) is caused by a herpesvirus whose biologic and physical characteristics are similar to those described for the group of herpesviruses. Only one immunologic and serologic type is known. A low level of neutralizing antibodies is developed in waterfowl vaccinated with the chicken embryo attenuated DVE virus. A marked anamnestic serologic response resulted from challenge with virulent virus. Waterfowl resisting exposure with virulent virus were solidly immune. However, waterfowl which possessed moderate level of neutralizing antibodies succumbed when their immunity was challenged with virulent virus when secondary or latent microbial invaders were present. This may partially explain the lack of correlation between the levels of neutralizing antibodies and mortality from infection with DVE virulent virus.

Animals↗
PubMed1976

An epornitic of duck viral enteritis in a zoological park.

An epornitic of duck viral enteritis occurred at the National Zoological Park in the spring of 1975. The disease affected 8 different species of ducks; geese and swan were spared. Diagnosis was based on characteristic pathologic changes, with herpetic inclusion bodies in the epithelium of the digestive tract and liver, and by viral isolation from 4 ducks. An experimental attenuated live-virus vaccine and sanitizing procedures were used to control the epornitic.

Animals↗
PubMed1975

Pathogenesis of digestive tract lesions in duck plague.

White Pekin ducklings were inoculated orally with duck plague virus. Tissues from the digestive tract were collected daily after inoculation and examined by light, electron and fluorescent microscopy. There were necrosis and degeneration of stratified squamous epithelium of the esophagus and cloaca, epithelium of intestinal crypt and esophageal submucosal glands, macrophages in the lamina propria, and submucosal fibrocytes and lymphocytes. Submucosal hemorrhages occurred after degeneration and necrosis of lymphocytes, macrophages, fibrocytes and epithelial cells. Viral antigens were detected in all these cells by use of fluorescein-labeled antibodies. With the electron microscope, nucleocapsids were seen in the nuclei, budding through the inner nuclear membrane; enveloped virions were present in cytoplasmic vacuoles of macrophages, epithelial cells and fibrocytes. In lymphocytes, nucleocapsids were also in the nuclei, but karyorrhexis and cytolysis occurred before viral maturation was completed.

Animals↗