Duck Viral Enteritis - Poultry - Merck Veterinary Manual (2022)

Duck viral enteritis (DVE) is an acute and often severe disease of both wild and domestic waterfowl induced by Anatid alphaherpesvirus 1.Lesions include generalized hemorrhages and necrosis of the GI mucosa and liver. Prevention includes biosecurity and avoiding contact with captive waterfowl with wild birds. Some producers in the USA, Canada, and Europe use attenuated-virus vaccines to immunize breeders and ducklings.

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. DVE 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 on 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 maturity. The infection has not been reported in other avian species, mammals, or people and does not pose a zoonotic risk.

The causative agent of duck viral enteritis (species Anatid herpesvirus 1) is a member of the family Herpesviridae, subfamily Alphaherpesvirinae, and genus Mardivirus. 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 [132.8°F]). 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. It has been proposed that apoptosis and necrosis of lymphocytes induced by this virus may result in lymphoid depletion and possibly 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.

The virus causing duck viral enteritis 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. Outbreaks are frequent in duck flocks with access to bodies of water cohabited with free-living waterfowl. Parenteral, intranasal, or oral administration of infected tissues can establish experimental infection. A carrier condition is suspected in wild birds. Recovered birds become latently infected 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 carry the virus in its latent form, and viral reactivation may be the cause of outbreaks in susceptible wild and domestic ducks. One study demonstrated that captive-reared and released Mallard ducks can be infected with the virus, and those latently affected may potentially transmit the virus to native waterfowl when they are released.

The incubation period is 3–7 days. Sudden high and persistent mortality is often the first sign of the disease. The mortality rate varies and can be 5%–100%, depending on virulence of the infecting viral strain. Adult ducks usually die in higher proportions than young ones, increasing the economic significance of the disease. Sick birds are unable to stand, and they show indication of weakness and depression. 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. Dead males may have prolapse of the penis. In laying flocks, egg production may drop sharply.

Lesions from duck viral enteritis are indicative of DIC and necrosis of the mucosa and submucosa of the GI tract and lymphoid tissues. 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.

Mucosal eruptions, found in the oral cavity, esophagus, ceca, rectum, and cloaca, undergo progressive alteration 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. Diphtheritic esophagitis may be commonly seen in swans. 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.

The lymphoid organs are severely 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 of Fabricius may be severely congested or hemorrhagic. In ducklings, the lesions of the lymphoid tissues are more evident than the lesions in other visceral organs. Hemorrhagic annular bands can be seen in different portions of the intestines, which correspond to necrosis and hemorrhage of the gut-associated lymphoid tissue. In geese, intestinal lymphoid disks are analogous to the annular bands in ducks, and “button-like" ulcers may be seen.

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 maybe seen in deformed and discolored ovarian follicles, and ruptured yolk and free blood may be found in the abdominal cavity.

Microscopically, eosinophilic intranuclear inclusions may be seen in the epithelial cells of the GI tract and 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.

(Video) Characteristic clinical sign of infectious laryngotracheitis disease of poultry
  • Clinical examination and necropsy

  • Viral isolation and viral detection by molecular techniques

  • Serology may have little diagnostic value

Presumptive diagnosis of duck viral enteritis is based on disease history and lesions. Definitive diagnosis may require viral isolation or identification of DVE. Different diagnostic protocols based on PCR are available, either by conventional or quantitative real-time PCR. These molecular techniques provide much more rapid and efficient diagnosis of this disease than other methods. The tissues to collect are liver, spleen, esophagus, and portions of small intestine that show suggestive lesions.

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 IM 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 testing can demonstrate DVE viral proteins.

Serologic tests have little value in the diagnosis of acute infections. Serum neutralization tests have been used to monitor exposure to the virus in wildfowl.

Differential diagnoses should include:

  • Duck viral hepatitis Duck Viral Hepatitis

  • Pasteurellosis

  • Necrotic and hemorrhagic enteritis

  • Trauma

  • Various toxicoses

Newcastle disease Newcastle Disease and Other Paramyxovirus Infections , avian influenza Avian Influenza , and fowlpox Fowlpox may cause similar lesions but are rarely reported in ducks. Established cases should be reported to the appropriate regulatory agency.

  • There is no treatment

  • Contact between susceptible captive waterfowl with wild, free-flying waterfowl should be avoided

  • Live attenuated vaccines are used in countries where available

There is no treatment for duck viral enteritis. 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 in the USA to immunize domestic ducks in zoologic aviaries and by private aviculturists. A 0.5-mL dose is administered SC or IM to domestic ducklings >2 weeks old. Breeding flocks should be revaccinated annually. The vaccine can be used in 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.

Avian astroviruses are common in several species of poultry and typically cause enteritis and growth retardation in young birds.. There are no treatments or commercial vaccines available, so prevention relies on good biosecurity and husbandry.. Older birds are generally less susceptible to the viruses, and many strains are of low or no pathogenicity and so are frequently detected in healthy birds.. Astrovirus infections are typically harmful to very young birds , whereas older birds appear more resistant.. There are no confirmatory tests... read more of chickens and poult enteritis complex in turkeys, and they often cause diarrhea, enteritis, and growth restriction in young birds.. Avian astroviruses are highly prevalent viruses, globally infecting diverse avian species, including many wild birds.. Avian nephritis and chicken astrovirus infections are highly common in broilers, and broiler breeders often present as coinfections and with other enteric viruses such as fowl adenovirus and avian orthoreovirus.. Infections are rapid, and signs are variable, ranging from subclinical to mortality approaching 50% in young birds, depending on the age of the flock and pathogenicity of the strain.. Although mainly enteric infections, all astroviruses can be detected in other organs.. Typically, commercial vaccines do not exist for avian astroviruses, although autogenous vaccines have been reportedly used successfully.. Astroviruses are associated with enteritis, diarrhea, growth retardation, and production diseases in young birds, including hatchery diseases.

The hemorrhagic enteritis virus belongs to the family Adenoviridae , genus Siadenovirus , species turkey adenovirus 3 (TAdV3), and it is serologically indistinct from the marble spleen disease virus.. Marble spleen disease (MSD) is an acute respiratory disease of pheasants characterized by depression, enlarged mottled spleens, pulmonary congestion, and death.. Concomitant or prior exposure to necrotic enteritis Necrotic Enteritis , coccidiosis Coccidiosis , Newcastle disease virus Newcastle Disease in Poultry Newcastle disease is an infection of domestic poultry and other bird species with virulent Newcastle disease virus (NDV).. In pheasants with acute respiratory disease, differential diagnoses include Newcastle disease Newcastle Disease in Poultry Newcastle disease is an infection of domestic poultry and other bird species with virulent Newcastle disease virus (NDV).. Prevention of hemorrhagic enteritis or marble spleen disease normally relies on the use of live vaccines administered in the drinking water at ~4–5 weeks of age, when maternally derived antibodies are below the breakthrough level of the vaccine.

Prices: Omega Seamaster Diver 300M How much does a Diver 300M cost?. )Diameter, material(s), caliber 210.93.42.20.01.00182,600 USD42 mm, platinum, 8807210.62.44.51.01.00123,800 USD44 mm, Sedna gold, 9901210.62.42.20.03.00118,500 USD42 mm, Sedna gold, 8801210.20.44.51.01.00111,200 USD44 mm, stainless steel and Sedna gold, 9900210.90.42.20.01.00110,000 USD42 mm, titanium, 8806210.22.42.20.01.0048,400 USD42 mm, titanium, 8800210.32.44.51.01.0016,400 USD44 mm, stainless steel, 9900212.32.41.20.04.0015,600 USD41 mm, stainless steel, 2507212.30.41.20.01.0055,300 USD41 mm, stainless steel, 2507210.30.42.20.01.0014,600 USD42 mm, stainless steel, 88002534.50.002,800 USD41 mm, stainless steel, 11282551.80.002,300 USD36.25 mm, stainless steel, 1120. Prices for an Omega Seamaster Diver 300M range from 1,700 USD for a pre-owned quartz watch to over 82,600 USD for the James Bond Numbered Edition in platinum.. You can purchase this watch on a stainless steel bracelet for about 4,600 USD new and 4,100 USD pre-owned on Chrono24.. While its official list price sits at 27,300 USD, you can find this watch on Chrono24 for approximately 18,500 USD.. (Video) The Omega Seamaster Diver 300m Review - New Ceramic Master Chronometer. Omega lists this watch for 8,500 USD.. The version in 18-karat Sedna gold costs around 23,800 USD in mint condition and 21,000 USD pre-owned on Chrono24.. It uses Omega's Co-Axial caliber 2628 – a modified version of Omega's first movement with a Co-Axial escapement, the caliber 2500.. This model looks more like a diving watch than a GMT watch due to its helium escape valve at 10 o'clock and 60-minute bezel.. Other Omega James Bond watches include the Seamaster Diver 300M Casino Royale and the Diver 300M James Bond 50th Anniversary Edition.. (Video) Omega Seamaster Diver 300M: The Ultimate High-Low Watch?. Omega Seamaster Diver 300M - Unboxing - ( I have bought My Dream Watch ). New OMEGA SEAMASTER 300 Watch Review (2022 Novelties). Rolex Submariner vs Omega Seamaster Diver 300M: Luxury Dive Watch Comparison and Contrast

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