Derzsy's Disease

Also Known As – Goose Hepatitis – Goose Parvovirus – Goose Plague – Goose Viral Enteritis – Goose Viral Hepatitis – Gosling Plague

Caused By – Goose Parvovirus – GPV - Muscovy Duck Parvovirus - MDPV

Introduction

Derzsy’s disease is a highly contagious gastrointestinal disease of young geese and Muscovy ducks, caused by a parvovirus.

There are antigenic and genetic differences between the two viruses but the disease presentation is identical and both viruses can affect both species although susceptibility varies.

This disease is not zoonotic.

Distribution

Derzsy’s is widespread across Asia, Europe, Russia, the UK and also present in California.

Infected birds shed virus faecally in large amounts resulting in rapid direct and indirect transmission. Horizontal transmission also occurs via water and feed contaminated by diseased birds.

Vertical transmission also occurs from infected adults, and this form of disease is often responsible for the most serious outbreaks.

Subclinical infections can produce latent carriers which then transmit the virus to susceptible young birds in the hatchery via their infected eggs.

Signalment

GPV occurs in all breeds of domestic geese and Muscovy ducks.

Geese appear less susceptible to MDPV than GPV but can be infected. MDPV can also affect genetic crosses of the breed.

Disease has not been reported in any other avian or mammalian species, including humans.

Disease is strictly age dependent in both species, with up to 100% mortality occurring in birds under 7-10 days of age. Progressive resistance develops so losses are negligible by 4-5 weeks of age. Adult birds show no clinical signs but respond antigenically.

Clinical Signs

Dependent upon age and pathogenicity, disease can be acute, sub-acute or chronic.

Acute forms can result in 100% mortality in goslings and ducklings under 10 days of age. Anorexia and recumbency are often the only signs preceding death. In goslings 2-3 weeks old mortality may only be 10%.

Birds that are older or have some maternal immunity may develop more characteristic clinical signs. Initially, they are anorexic, polydipsic and weak with a nasal and ocular discharge and associated head shaking. The uropygial glands and eyelids become swollen and red and a white profuse diarrhoea develops. A fibrinous pseudo-membrane can be seen covering the tongue and oral cavity at this stage.

If this acute stage is survived, young birds may develop prolonged growth retardation and erythematous skin. The down may remain lost around the back and neck and ascites may accumulate leading to a “penguin-like” posture.

Goslings over 4 weeks old rarely exhibit any clinical signs.

Diagnosis

Virus isolation van be achieved by innoculation of goose or duck eggs from post-mortem samples. Mortality of the embryos occurs after 5-10 days and the livers become ochre coloured. Embryonic cell cultures can also be used for isolation. Intranuclear inclusions and suncytium formations can be seen on preparations of these primary cell cultures under microscopy.

Immunofluorescence, electron microscopy, virus neutralisation, immunoperoxidase and indirect haemagglutination can then be used to confirm viral identity.

PCR is now available and is very sensitive. This technique can also tell the two viruses apart.

In acute disease, pathological lesions are often found on the heart, which has a pale myocardium and is rounded at the apex. The liver, spleen and pancreas may be swollen and congested.

Where the clinical course has been more prolonged, a sero-fibrinous perihepatitis and pericarditis is common and large volumes of straw coloured ascites often found. Pulmonary oedema, liver lesions and catarrhal enteritis may also be present. Diptheritic lesions and ulcers may be seen in the mouth, pharynx and oesophagus – these are usually due to secondary infection.

Histopathology reveals degenerative muocardial cell changes with loss of striation, fatty infiltration and intranuclear inclusion bodies. Similar changes are seen in intestinal and smooth muscle cells. Hepatocyte vacuolation and fatty infiltration dominate the liver. The hepatocytes also sometimes contain eosinophilic inclusion-like bodies. Pancreatic cells are often necrotic, shrunken and also infiltrated by fat deposits.

Treatment

There is no specific treatment for Derzsy's disease. Antibiotic therapy may help to prevent losses from secondary infections and complications.

Control

Due to transmission from congenitally infected eggs and goslings, incubating and hatching egs from different flocks together should be avoided. Only eggs from known GPV-free flocks should be hatched together and hatchery hygiene should be well maintained.

Any survivors of outbreaks should not be used for breeding as they may be latent carriers. Any incontact geese should be serologically tested and removed from the flock if positive.

Passive immunisation usiny hyperimmune serum is also possible in freshly hatched goslings but is expensive and time consuming, often requiring two doses.

Active immunisation of adults with virulent virus has also been reported and protection is transferred to their progeny via the yolk. There are also attenuated and inactivated vaccines available but the latter should only be used for prophylaxis in flocks where GPV has not been diagnosed.

Derzsy's Disease Learning Resources
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References

Animal Health & Production Compendium, Derzsy’s Disease datasheet, accessed 20/07/2011 @ http://www.cabi.org/ahpc/