duck viral enteritis

Preferred Scientific Name

• duck viral enteritis

International Common Names

• English: duck plague; duck plague enteritis; duck virus enteritis, duck plague, herpesvirus

Local Common Names

• France: peste du canard
• Germany: entenpest
• Netherlands: Eendepest

English acronym

• DPE
• DVE

Duck plague enteritis is an acute, contagious herpesvirus infection of duck, geese and swans causing high morbidity and mortality. The disease has led to massive outbreaks of mortality in farm flocks and in the wild, first documented in the beginning of the twentieth century. Clinical signs include listlessness, drooping wings, diarrhoea and exudate and diphtheroid plaques on eyelids, the respiratory, enteric and cloacal mucosae. Parenchymatous organs show degenerative changes. Post mortem, pathognomonic haemorrhages can be observed in the internal organs such as conjunctivae, the trachea, syrinx and in the intestinal mucosa. The disease is considered endemic in many countries in Northern America, Europe and Asia. After natural infection a solid immunity develops, and for prophylaxis various vaccines have been developed.

Duck plague results in increased vascular permeability, and many petechial bleedings in many internal organs and mucous membranes are apparent (Richter and Horzinek, 1993). Tissues may degenerate and become necrotic. Initially, haemorrhages can be observed in the conjunctivae, the trachea, syrinx (in the male) and in the intestinal mucosa. In a later stage, yellow-white necrotic plaques may cover these sites, which may form pseudomembranes in the cloaca and oesophagus (Richter and Horzinek, 1993; Sandhu and Leibovitz, 1997). Characteristically, in young birds the haemorrhages in the intestines may be circular, predominantly at sites where gut-associated lymphoid tissue (GALT) is situated.

Macroscopically, bleedings may be found in conjunctivae, trachea, syrinx, liver, heart, mesenteric membranes, intestines and ovaries (in laying birds). Diphtheroid plaques may be present in advanced cases, in the oesophagus and cloaca. Lumina of intestines and gizzard are often filled with blood. Microscopically, epithelium of oesophagus, of the crypts of the intestinal mucosa and the cloaca is necrotic (Proctor, 1975). Spleen, thymus and the bursa fabricius may be degenerated (Proctor, 1976). Cells of the liver and pancreas are degenerated and necrotic. DVE antigen may be present in affected organs, and intranuclear inclusion bodies can be detected by electron microscopy (Sandhu and Leibovitz, 1997).

The incubation period ranges from about 4 to 7 days but depends on the age of the bird, the route of infection and the virus strain (Jansen, 1971; Sandhu and Leibovitz, 1997). Environmental contamination may lead to immunosuppression and subsequently aggravate the disease (Goldberg et al., 1990). Sudden high persistent flock mortality, including mature ducks, is often the first observation. As disease progresses, ducks can be seen to be listless, they avoid water, and sit or waddle with drooping wings and ruffled feathers. Ocular secretion occurs, first watery, later more viscous with photophobia. Profuse greenish diarrhoea is frequently seen. In the final stage eyes can no longer be opened due to oedema, and nares are covered by dirty mucous secretions. In addition, the cloaca is dirty and may be covered by a diphtheroid inflammation. The voice is hoarse. The animals are anorectic but drink very much (Richter and Horzinek, 1993; Sandhu and Leibovitz, 1997). The disease in individual animals may last a few days to 2 weeks. An episode of DVE may last for several weeks under natural and farm conditions.

Infected geese show similar symptoms to ducks, with profound excretion and greenish diarrhoea.

Fertility and hatchability are impaired (Richter and Horzinek, 1993).

Horizontal transmission seems the most important transmission route of DVE, either by the faecal-oral route or by a contaminated environment. It was noted that the first outbreaks of DVE occurred near ditches, canals and ponds where waterfowl were present. However, outbreaks also occur in duck breeding and fattening farms. Wild waterfowl are considered healthy carriers of the virus and are implicated in many outbreaks of DVE (Burgess et al., 1979; Brand and Docherty, 1988; Astorga et al., 1994; Converse and Kidd, 2001). New outbreaks may occur when infected waterfowl come into contact with susceptible flocks, or onto water previously free of DVE. The disease can spread very rapidly, but may also take 2 weeks to spread on a farm. DVE is self limiting in waterfowl and duck breeding farms (Richter and Horzinek, 1993). Natural infection is assumed to takes place via the oral route. Experimental infections can be successful after intramuscular, subcutaneous, oral, intravenous, intranasal, intraperitoneal and cloacal administration (Richter and Horzinek, 1993). Recovered ducks and geese may excrete virus for years. Cloacal excretion occurring 4 years after the epizootic has been reported (Burgess et al., 1979).

Vertical transmission occurs, and DVE may be isolated from eggs from persistently infected ducks.

The first outbreak in the USA in 1967 was estimated to cause a loss of $1 million during a 1-year period (Sandhu and Leibovitz, 1997). Natural outbreaks may also result in mass killings of waterfowl, such as the 1973 duck plague outbreak in the South Dakota National Wildlife Refuge, USA, where some 43,000 mallard ducks and geese of a population of 100,000 died (Jansen, 1968; Richter and Horzinek, 1993; Sandhu and Leibovitz, 1997).

DVE has caused significant economic losses in duck-producing areas in market ducklings and layer breeder ducks caused by mortality, condemnations and decreased egg production. In areas where DVE is endemic, presence of DVE in wild waterfowl and the likelihood of transmission of the virus to commercial flocks makes it necessary to vaccinate farm ducks, to prevent disease outbreaks.

Natural DVE infections have not been reported in avian species other than anatids nor in mammals, and the disease does not pose any known risk to humans.

For DVE infections there is no specific treatment available. Interestingly, however, vaccination may be performed at the initial phase of an outbreak, because due to the interference phenomenon, protection is installed immediately after vaccination with a potent attenuated vaccine (Sandhu and Leibovitz, 1997).