Duck Viral Enteritis

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Also Known As: DEV — DVE — Duck Plague Virus — DPV — Duck Plague

Introduction

Duck with duck plague exhibiting haemorrhagic nasal discharge and typical drooped wing appearance. Source: US Geological Survey via Wikimedia Commons

Duck viral enteritis is caused by a herpesvirus which can also infect geese and swans. The disease is acute and highly infectious, causing high morbidity and mortality.

DVE is not zoonotic.

Distribution

Endemic in Northern America, Europe and Asia.

Transmission is mainly horizontal via the faecal-oral route or contaminated environments and equipment/personnel. Wild waterfowl are often asymptomatic carriers and shedders of DVE.

Vertical transmission also occurs from persistently infected female ducks to their eggs.

Signalment

Although ducks are the primary host, geese, swans and many other waterfowl can be infected with DEV.

Canada geese and blue winged teal appear particularly susceptible and disease course is rapid in these species.

Herring gulls and black headed gulls appear resistant.

Clinical Signs

DVE causes primarily greenish diarrhoea, which can lead to dehydration, anorexia, weakness, a typical drooped wing appearance and neurological signs. Haematochezia is often a feature. Birds often refuse to drink, further exacerbating the dehydration and its sequelae.

Diptheroid plaques commonly form on the eyelids and also internally on the mucosae of the respiratory system and gastrointestinal system.

Opthalmic signs sometimes present in DVE, including lacrimation, watery ocular discharge and photophobia.

Respiratory disease often manifests as a hoarse chirp but is non-specific.

These signs are often accompanied by a drop in egg production and a ruffled, unkempt appearance.

Solid natural immunity develops in recovered birds.

Sudden and persistent increases in flock mortality involving both young and adult birds is often the first observation of DEV. Outbreaks can last for several weeks in natural conditions.

Diagnosis

Diagnosis can usually be made using history of clinical disease and necropsy:

On post-mortem, petechial haemorrhage in the conjunctivae, mucous membranes, trachea, syrinx and intestine are pathognomonic for DEV. This pathology is caused by increased vascular permeability.In advanced disease, the same sites may become covered by yellow-white necrotic plaques, sometimes forming pseudomembranes in the cloaca and oesophagus.

In young birds, these pathological changes are often associated with the gut-associated lymphoid tissue (GALT). Organs often also demonstrate degenerative and necrotic changes and the gizzard and intestines are commonly filled with blood.

Intranuclear inclusion bodies can be detected via electron microscopy. PCR can be used to detect infection.

Serology can indicate previous exposure but is of limited use in active outbreaks.

Treatment

The immediate efficacy of vaccines suggests that they may be indicated for use during developing outbreaks. This rapidity of action is thought to be due to the action of stimulated interferons, known as the "interference phenomenon".

Control

Vaccination is the mainstay of control of DVE. Only attenuated vaccines are efficacious.

Prevention must also focus upon prevention of exposure to wild waterfowl and contaminated water. All new stock should also be screened for DVE. Once DVE is present, depopulation, relocation and intensive disinfection are required to overcome an outbreak which may last for a significant period.

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References

Gough, R.E. (2007) Duck Viral Enteritis. In: Poultry Diseases, 6th Edition (eds. Pattison, M., McMullin, P., Bradbury, J., Alexander, D.) Saunders, Elsevier, pp 258-276

Sandhu, T.S. and Metwally, S.A. (2008) Duck Viral Enteritis (Duck Plague). In: Diseases of Poultry, 12th Edition (eds. Saif, Y.M., Fadly A.M., Glissen J.R., McDougald L.R., Nolan L.K., Swayne D.E.) Wiley-Blackwell, pp 384-393

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project. The datasheet was accessed on 20 June 2011.