Occurrence of Duck Virus Enteritis (Duck Plague) in Pennsylvania, 1968-74

Hwang, Jen; Mallinson, E. T.; Yoxheimer, Ronald E.

doi:10.2307/1588997

Cited by 13 publications

(6 citation statements)

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“…Epidemiological investigations suggested the correlation of the incidence of DP in wild birds and farmed poultry as samples from wild birds and poultry were found positive/carrier through various virological and serological investigations (Ziedler & Hlinak 1992). Subsequently, between 1970 and 1995, more than 100 outbreaks have been reported from places such as Maryland, New York, California and Pennsylvania (Hwang et al 1975;Brand & Docherty 1984;Davison et al 1993;Converse & Kidd 2001;Sandhu & Shawky 2003). In addition to outbreaks in the Netherlands and USA, DVE has been reported in China (Jansen & Kunst 1964;Wu et al 2012a), France (Gaudry et al 1970;Gough et al 1987), Belgium (Devos et al 1964), India (Mukerji et al 1963a;Duraiswami et al 1979;Rajan et al 1980), Egypt (ElSamadony et al 2013) England (Hall & Simmons 1972;Gough & Alexander 1990), Canada (Hanson & Willis 1976), Germany (Kaleta et al 2007), Denmark (Prip et al 1983), Poland (Wozniakowski & Samorek-Salamonowicz 2014), Vietnam (Pritchard et al 1999) and Bangladesh (Hoque et al 2011;OIE 2012;Ahamed et al 2015).…”

Section: Epidemiology and Disease Distributionmentioning

confidence: 99%

Duck virus enteritis (duck plague) – a comprehensive update

Dhama

Kumar

Saminathan

et al. 2017

Veterinary Quarterly

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Duck virus enteritis (DVE), also called duck plague, is one of the major contagious and fatal diseases of ducks, geese and swan. It is caused by duck enteritis virus (DEV)/Anatid herpesvirus-1 of the genus Mardivirus, family Herpesviridae, and subfamily Alpha-herpesvirinae. Of note, DVE has worldwide distribution, wherein migratory waterfowl plays a crucial role in its transmission within and between continents. Furthermore, horizontal and/ or vertical transmission plays a significant role in disease spread through oral-fecal discharges. Either of sexes from varying age groups of ducks is vulnerable to DVE. The disease is characterized by sudden death, vascular damage and subsequent internal hemorrhage, lesions in lymphoid organs, digestive mucosal eruptions, severe diarrhea and degenerative lesions in parenchymatous organs. Huge economic losses are connected with acute nature of the disease, increased morbidity and mortality (5%-100%), condemnations of carcasses, decreased egg production and hatchability. Although clinical manifestations and histopathology can provide preliminary diagnosis, the confirmatory diagnosis involves virus isolation and detection using serological and molecular tests. For prophylaxis, both live-attenuated and killed vaccines are being used in broiler and breeder ducks above 2 weeks of age. Since DEV is capable of becoming latent as well as shed intermittently, recombinant subunit and DNA vaccines either alone or in combination (polyvalent) are being targeted for its benign prevention. This review describes DEV, epidemiology, transmission, the disease (DVE), pathogenesis, and advances in diagnosis, vaccination and antiviral agents/therapies along with appropriate prevention and control strategies.

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Section: Epidemiology and Disease Distributionmentioning

confidence: 99%

Duck virus enteritis (duck plague) – a comprehensive update

Dhama

Kumar

Saminathan

et al. 2017

Veterinary Quarterly

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show abstract

“…[2]. Since then, additional and ap parently unrelated outbreaks have occurred on the North American continent [3][4][5][6][7].…”

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confidence: 99%

Improvement in Plaquing Methods for the Enumeration of Anatid Herpesvirus (Duck Plague Virus)

Attanasio¹,

Olson²,

Johnson³

1980

Intervirology

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The Holland strain of anatid herpesvirus (AHV) was 2- to 10-fold more efficiently plaqued under liquid medium or semisolid medium containing methylcellulose than in media containing agar, agarose, or Nobel agar. Virus adsorption was complete in 45 min, with the maximum virus titers obtained under liquid medium at 48 h postinfection. The AHV dose-response curve was linear. Pekin duck embryo cultures were more efficient than CCL-141 in plaque response and gave the maximum virus yield per cell. Virus titers were independent of avian cell passage number (to 6), fetal or newborn calf sera (to 10% v/v), and the presence of polyions during adsorption. The host range included cells from several species of Anseriformes and Galliformes.

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“…Although acid fast intra-nuclear inclusions occur in the epithelial cells of the renal tubules in lead poisoning (Locke et al, 1966) they seldom occur in the liver (Keymer, unpublished) and are quite different from herpesvirus inclusions. It is possible that the infection arose in the swans due to the introduction of some Muscovy ducks about four weeks before the swans became ill, especially as these Downloaded by [University of Massachusetts] at 23:29 27 December 2014 ducks appear to be more susceptible to the infection than many other species (Hwang et al, 1975;Gough, 1984). Indeed, three of these ducks, which were about 2 months old, died before disease was observed in the swans and ulcération was found by the owner affecting the lower oesophagus, proventriculus and the duodenum in each case.…”

Section: Discussionmentioning

confidence: 99%

Duck virus enteritis (anatid herpesvirus infection) in mute swans(Cygnus Olor)

Keymer

Gough

1986

Avian Pathology

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An outbreak of duck virus enteritis (DVE) in mute swans (Cygnus olor) is described. Ninety-nine captive swans in a flock of 440 died within 3 months. The origin was obscure. The infection did not spread to other species on the same premises. Clinical signs included polydypsia, photophobia, inappetance, drooping wings, watery nasal discharge and yellowish diarrhoea. Necropsies were made on eight swans. All showed a diphtheritic oesophagitis especially near the oesophageal-proventricular junction. Whitish, necrotic plaques from 1 mm to 3 cm in extent affected the epithelium of the small intestine. Other lesions were present but less consistent. Histological examination of livers showed typical lesions of DVE associated with intranuclear inclusions. The virus was propagated in duck kidney cell cultures and on second passage caused a cytopathic effect with intranuclear inclusions typical of DVE. Presence of virus was confirmed by electron microscopy. Experimentally the virus infected susceptible, unvaccinated ducklings, but not those vaccinated against DVE.

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Occurrence of Duck Virus Enteritis (Duck Plague) in Pennsylvania, 1968-74

Cited by 13 publications

References 1 publication

Duck virus enteritis (duck plague) – a comprehensive update

Duck virus enteritis (duck plague) – a comprehensive update

Improvement in Plaquing Methods for the Enumeration of Anatid Herpesvirus (Duck Plague Virus)

Duck virus enteritis (anatid herpesvirus infection) in mute swans(Cygnus Olor)

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