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Duck viral enteritis (DVE) is an acute, highly contagious disease of ducks, geese, and swans of all ages, characterized by sudden death, high mortality (particularly among older ducks), and hemorrhages and necrosis in internal organs. It has been reported in domestic and wild waterfowl in Europe, Asia, North America, and Africa, resulting in limited to serious economic losses on domestic duck farms and sporadic, limited to massive die-offs in wild waterfowl. In the USA, considerable losses due to DVE have been reported in the concentrated duck-producing areas located in Long Island, New York.
Members of the family Anatidae (ducks, geese, and swans) are the natural hosts for the virus. There are differences in susceptibility to the virus, with Muscovy ducks being the most susceptible. However, naturally occurring infections have been reported in a variety of domestic ducks such as Pekin, khaki Campbell, Indian runners, and mixed breeds. The age at infection ranges from 7 days to mature ducks. This disease does not pose a zoonotic risk.
Etiology and Pathogenesis
The causative agent of DVE is an unclassified herpesvirus (Anatid herpesvirus 1). Field strains of this virus display differences in virulence, but all seem to be immunologically identical. The virus is sensitive to lipid solvents and heat (10 minutes at 56°C). Significant titer reduction is observed at pH 5, 6, and 10; rapid inactivation occurs at pH 3 and 11.
The virus induces vascular damage, especially in smaller blood vessels, venules, and capillaries. This results in the development of generalized hemorrhages and progressive degenerative changes of parenchymatous organs. Recently, it has been proposed that apoptosis and necrosis of lymphocytes induced by this virus may result in lymphoid depletion and possibly in the development of immunosuppression. An immunosuppressive state induced by DVE may also explain the presence of secondary infections by Pasteurella multocida, Riemerella anatipestifer, and Escherichia coli, which are frequently seen in natural outbreaks of DVE in ducklings.
Epidemiology, and Transmission
The virus is mainly transmitted by direct contact from infected to susceptible ducks, or by indirect contact with a contaminated environment; water seems to be a natural route of viral transmission. Parenteral, intranasal, or oral administration of infected tissues can establish experimental infection. A carrier condition is suspected in wild birds. Recovered birds become carriers and may shed the virus periodically. DVE virus may undergo latency like other herpesviruses, and the trigeminal ganglion seems to be a latency site for the virus. Recovered birds may have the virus in its latent form, and viral reactivation may be the cause of outbreaks in susceptible wild and domestic ducks.
Clinical Signs
The incubation period is 3–7 days. Sudden high and persistent mortality is often the first sign of the disease. Mortality varies from 5–100% depending on the virulence of the infecting viral strain. Adult ducks usually die in higher proportions than young ones, increasing the economic significance of the disease. Dead males may have prolapse of the penis. Photophobia, inappetence, extreme thirst, droopiness, ataxia, nasal discharge, soiled vents, and watery or bloody diarrhea may be seen. Adult ducks may die in good flesh. In contrast, ducklings frequently show dehydration and weight loss, as well as blue beaks and blood-stained vents. In laying flocks, egg production may drop sharply.
Lesions
Damage of blood vessels throughout the body induces hemorrhages in various tissues or the presence of free blood in body cavities. Petechial and ecchymotic hemorrhages on the heart (“paint brush” appearance), liver, pancreas, mesentery, and other organs are characteristic. Specific mucosal eruptions, found in the oral cavity, esophagus, ceca, rectum, and cloaca, undergo progressive alterations during the course of the disease. Macular hemorrhages initially develop into elevated, yellowish, crusted plaques and organize into green, superficial scabs, which may coalesce into large, patchy, diphtheritic membranes. The mucosal lesions align parallel with the longitudinal folds in the esophagus. Hemorrhagic annular bands can be observed in different portions of the intestines, which correspond to necrosis and hemorrhage of the gut-associated lymphoid tissue. Lumina of the intestines and gizzard are often filled with blood. The liver is enlarged, pale copper in color, and may have pinpoint surface hemorrhages mixed with white necrotic foci. The pancreas may have petechiation and multifocal necrosis.
All lymphoid organs are affected; the spleen may be normal or smaller in size and darkened due to congestion. The thymic lobes may be petechiated, and thymic atrophy has been reported with some strains. The bursa or Fabricius may be severely congested or hemorrhagic. A lesion that can be easily detected on necropsy is a clear, yellow fluid that infiltrates and discolors the subcutaneous tissues from the thoracic inlet to the upper third of the neck. In mature hens, hemorrhages may be observed in deformed and discolored ovarian follicles, and ruptured yolk and free blood may be found in the abdominal cavity.
Microscopically, eosinophilic intranuclear inclusions are observed in the thymus, bursa, spleen, esophagus, cloaca, liver, conjunctiva, and Harderian gland. Occasional intracytoplasmic inclusions are also scattered in the epithelial cells of the conjunctiva, esophagus, bursa of Fabricius, and cloaca.
Diagnosis
Presumptive diagnosis is based on disease history and lesions. Definitive diagnosis may require viral isolation or identification of DVE. Isolation of the virus from liver, spleen, or kidney tissues may be attempted in various cell cultures (preferably primary Muscovy duck embryo fibroblasts or Muscovy duck embryo liver cultures), duck embryos, or ducklings. Inoculating the chorioallantoic membrane of 9- to 14-day-old embryonated Muscovy duck eggs may result in isolation of the virus, but this method is not as sensitive as intramuscular inoculation of day-old ducklings. Muscovy ducklings are more susceptible than White Pekin ducklings. Neutralization with specific antiserum in these systems confirms the identity of the virus. Fluorescent antibody test can demonstrate DVE viral proteins. PCR techniques using DVE virus-specific primers have been developed as a rapid method for the detection of viral DNA in duck tissues or inoculated cell cultures. Serologic tests have little value in the diagnosis of acute infections.
Differential diagnoses include duck viral hepatitis, pasteurellosis, necrotic and hemorrhagic enteritis, trauma, drake damage, and various toxicoses. Newcastle disease, avian influenza, and fowlpox may cause similar lesions but are rarely reported in ducks. Established cases should be reported to the appropriate regulatory agency.
Prevention, Treatment, and Control
There is no treatment. Contact with wild, free-flying waterfowl and direct or indirect contact with contaminated birds or material (free-flowing water) should be avoided. Control is effected by depopulation, removal of birds from the infected environment, sanitation, and disinfection. Prevention is based on maintenance of susceptible birds in a disease-free environment or immunization. A chicken-embryo-adapted, modified live virus vaccine has been approved for use in domestic ducks, in zoological aviaries, and by private aviculturists. A 0.5 mL dose is administered SC or IM to domestic ducklings >2 wk of age. Breeding flocks should be revaccinated annually. The vaccine can be used in the face of an outbreak, because it elicits rapid protection after vaccination. It is not approved for use in wild ducks. An inactivated vaccine, which appears to be as efficacious as the modified live vaccine, has not been tested on a large scale and is not currently licensed.
Last full review/revision March 2012 by Alejandro Banda, DVM, MSc, PhD, DACPV, DACVM
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