duck viral enteritis

Identity

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

Pathogen/s

Overview

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.

Host Animals

Hosts/Species Affected

Anatids of the order Anseriformes are the main host species for DVE (Richter and Horzinek, 1993; Sandhu and Leibovitz, 1997). Many species of ducks, geese and swans are susceptible to natural or experimental infection with DVE (Richter and Horzinek, 1993). Some species of waterfowl are more susceptible than others, resulting in a very rapid disease course. Canada geese (Branta canadensis) and blue-winged teal (Anas discors) are particularly susceptible (Wobeser, 1987; Spieker et al., 1996). Conversely, herring gulls (Larus argentatus) and black-headed gulls (L. ridibundus) appear not susceptible to DVE. In the laboratory, DVE can be adapted to chicken cell lines, and in chickens up to 2 weeks of age (Jansen, 1968).

Systems Affected

Distribution

The first reports of duck virus enteritis (DVE)-like disease originate from the Netherlands in 1923. At that time it was concluded that the disease was caused by a duck-adapted strain of fowl plague virus (influenza) (Sandhu and Leibovitz, 1997). In 1967 in the USA the first confirmed outbreak of DVE occurred, where the disease is now considered enzootic. Currently, DVE has also been confirmed in Canada, Europe (Belgium, Denmark, England, Hungary, The Netherlands), Asia (India, Thailand, Vietnam), and is suspected in China (Sandhu and Leibovitz, 1997).

Distribution Table

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Pathology

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).

Diagnosis

The clinical diagnosis can be made upon recognition of the clinical symptoms, such as sudden mortality, listlessness, diarrhoea, drooping wings, assisted by a post-mortem examination. The characteristic haemorrhagic lesions of duck plague are considered pathognomonic.

The laboratory diagnosis is made upon virus isolation. The most sensitive method is intramuscular injection of preferably specific-pathogen-free (SPF) Pekin ducklings of 1-day old with 0.5 ml of blood or tissue suspension. In positive cases, mortality will occur within a few days, and post mortem the pathognomonic lesions will be observed. Alternatively, 8-14-day-old embryonated duck eggs may be used by inoculation of the CAM [chorioallantoic membrane] (Richter and Horzinek, 1993; Sandhu and Leibovitz, 1997). For cell culture, (Muscovy) duck embryo fibroblasts are highly sensitive to DVE. The duck cell line CCL-141 can also be used. Electron microscopy may be helpful in mild cases of DVE. New highly sensitive PCR shows promise to identify DVE more rapidly (Hansen et al., 1999; Hansen et al., 2000).

Serology is used to indicate previous contact with DVE, when a neutralization index of >0.7 is found (Richter and Horzinek, 1993).

Surviving animals have acquired a solid immunity. Although neutralization indices indicative for the level of neutralizing antibodies are being used to indicate the protection level, cellular immunity is also considered important for protection (Glavits et al., 1990; Kulkarni et al., 1998). Superinfection of persistently infected animals may again result in disease (Richter and Horzinek, 1993).

Maternal immunity is not protective in DVE (Toth, 1971; Sandhu and Leibovitz, 1997). Remarkably, protection afforded by vaccination may be induced very quickly. Ducklings vaccinated with a chick-embryo-adapted DVE vaccine were resistant against virulent challenge immediately after vaccination. This phenomenon of interference may be particularly useful because it suggests that vaccination may even be indicated when an outbreak is developing on a farm (Richter and Horzinek, 1993).

List of Symptoms/Signs

Disease Course

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).

Epidemiology

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.

Impact: Economic

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.

Zoonoses and Food Safety

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.

Disease Treatment

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).

Prevention and Control

Disease prevention must be aimed at prevention of exposure to wild waterfowl, or contaminated water. New stock must be free of DVE. Once DVE is introduced, control can be effected by depopulation, removal of birds from the contaminated environments, sanitation and disinfection (Sandhu and Leibovitz, 1997).

Immunization against DVE can successfully be applied (Butterfield and Dardiri, 1969; Toth, 1970; Toth, 1971; Weingarten, 1989). Attenuated vaccines to prevent DVE have been developed, because inactivated vaccines proved not sufficiently immunogenic. Vaccines have been developed by serial passaging of a DVE isolate over embryonated duck eggs, followed by serial passages over chicken embryos. After vaccination the virus is not spread, and the vaccine does not result in immunization of contact animals (Sandhu and Leibovitz, 1997).

References

Astorga RJ; Cubero MJ; León L; Maldonado A; Arenas A; Tarradas MC; Perea A, 1994. Serological survey of infections in waterfowl in the Guadalquivir Marshes (Spain). Avian Diseases, 38(2):371-375; 24 ref.

Biggs PM, 1982. The epidemiology of avian herpesviruses in veterinary medicine. Dev. Biol. Stand., 52:3-11.

Brand CJ; Docherty DE, 1988. Post-epizootic surveys of waterfowl for duck plague (duck virus enteritis). Avian Diseases, 32(4):722-730; 18 ref.

Burgess EC; Ossa J; Yuill TM, 1979. Duck plague: a carrier state in waterfowl. Avian Dis., 23:940-949.

Butterfield WK; Dardiri AH, 1969. Serologic and immunologic response of wild waterfowl vaccinated with attenuated duck plague virus. Wildl. Dis., 5:99-102.

Converse KA; Kidd GA, 2001. Duck plague epizootics in the United States, 1967-1995. J. Wildl. Dis., 37:347-357.

Glávits R; Rátz F; Sághy E; Meder M; Molnár é; Ivanics é; Szabó E, 1990. Pathological and immunological study of goose embryos experimentally infected with duck plague virus. Acta Veterinaria Hungarica, 38(1/2):33-41; 17 ref.

Goldberg DR; Yuill TM; Burgess EC, 1990. Mortality from duck plague virus in immunosuppressed adult mallard ducks. Journal of Wildlife Diseases, 26(3):299-306; 28 ref.

Hansen WR; Brown SE; Nashold SW; Knudson DL, 1999. Identification of duck plague virus by polymerase chain reaction. Avian Diseases, 43(1):106-115; 27 ref.

Hansen WR; Nashold SW; Docherty DE; Brown SE; Knudson DL, 2000. Diagnosis of duck plague in waterfowl by polymerase chain reaction. Avian Diseases, 44(2):266-274; 20 ref.

Jansen J, 1968. Duck plague. J. Am. Vet. Med. Assoc., 152:1009-1016.

Jansen J, 1971. La peste du canard. In: Les maladies animales a virus. Collection de monographies. l'Expansion Scientific Française, Paris, 107-180.

Kulkarni DD; James PC; Sulochana S, 1998. Assessment of the immune response to duck plague vaccinations. Research in Veterinary Science, 64(3):199-204; 17 ref.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

Proctor SJ, 1975. Pathogenesis of digestive tract lesions in duck plague. Vet. Pathol., 12:349-361.

Proctor SJ, 1976. Pathogenesis of duck plague in the bursa of Fabricius, thymus, and spleen. Am. J. Vet. Res., 37:427-431.

Richter JHM; Horzinek MC, 1993. Duck plague. Virus infections of birds., 77-90; 35 ref.

Sandhu TS; Leibovitz L, 1997. Duck virus enteritis (Duck Plague). In: Calnek BW, Barnes HJ, Beard CW, McDougald LR, Saif YM, eds. Diseases of Poultry, edition 10. Ames, USA: Iowa State University Press, 675-683.

Spieker JO; Yuill TM; Burgess EC, 1996. Virulence of six strains of duck plague virus in eight waterfowl species. Journal of Wildlife Diseases, 32(3):453-460; 26 ref.

Toth TE, 1970. Active immunization of White Pekin ducks against duck virus enteritis (duck plague) with modified-live-virus vaccine: immunization of ducklings. Am. J. Vet. Res., 31:1275-1281.

Toth TE, 1971. Active immunization of White Pekin ducks against Duck virus enteritis (duck plague) with modified-live-virus vaccine: serologic and immunologic response of breeder ducks. Am. J. Vet. Res., 32:75-81.

Weingarten M, 1989. Duck plague : clinical aspects, diagnosis, control. Tierärztliche Praxis, 17(1):53-56; 12 ref.

Wobeser G, 1987. Experimental duck plague in blue-winged teal and Canada geese. Journal of Wildlife Diseases, 23(3):368-375; 21 ref.

Distribution References

CABI, Undated. CABI Compendium: Status as determined by CABI editor. Wallingford, UK: CABI

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.

Sandhu TS, Leibovitz L, 1997. Duck virus enteritis (Duck Plague). In: Diseases of Poultry, [ed. by Calnek BW, Barnes HJ, Beard CW, McDougald LR, Saif YM]. Ames, USA: Iowa State University Press. 675-683.

Distribution Maps