Duck Viral Enteritis

(Duck plague, Anatid herpes, Eendenpest, Entenpest, Peste du canard)

By Alejandro Banda , DVM, MSc, PhD, DACPV, DACVM, Mississippi State University

Last full review/revision Sep 2019 | Content last modified Oct 2019

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.

Etiology and Pathogenesis of Duck Viral Enteritis

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.

Epidemiology and Transmission of Duck Viral Enteritis

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.

MSD MANUAL

Veterinary Manual

The trusted provider of veterinary information since 1955

Clinical Findings of Duck Viral Enteritis

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

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.

Duck viral enteritis, depression

and mild dyspnea

COURTESY OF DR. ALEJANDRO BANDA.

Duck viral enterita

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

Diagnosis of Duck Viral Enteritis

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

Pasteurellosis

Necrotic and hemorrhagic enteritis

Trauma

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 of Duck Viral Enteritis

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.

Key Points

Duck viral enteritis (DVE) is an acute and often severe disease of waterfowl that is caused by Anatid

alphaherpesvirus 1.

Lesions include generalized hemorrhages and necrosis of the GI mucosa and liver.

Prevention includes biosecurity and avoiding contact between captive waterfowl and wild birds.

Immunization of breeders and ducklings with live attenuated vaccines is carried out in countries
wherethese biologics are available.