Duck viral hepatitis (DVH) is an acute, highly contagious, viral disease typically affecting ducklings less than six weeks of age. DVH is characterized by a short incubation period, sudden onset, high mortality, and characteristic liver lesions. The viruses that cause DVH in ducklings should not be confused with duck hepatitis B virus, a hepadnavirus infection of older ducks.
The originally described, most widespread, and most virulent subtype of duck viral hepatitis, traditionally referred to as DVH Type I, has been renamed duck hepatitis A virus type 1 (DHAV-1) and is now classified in the genus Avihepatovirus in the Picornaviridae family. Two antigenically distinct genotypes have been identified in Taiwan (DHAV-2) and identified in China and South Korea (DHAV-3). DHAV is readily propagated in chicken and duck embryos, and they do not produce hemagglutinins. Field experience with DHAV-1 indicates that egg transmission does not occur. The disease can be transmitted experimentally by parenteral or oral administration of infected tissues.
Viruses that differ from DHAV have been recognized as causes of DVH in ducklings. DVH Type II, now classified as duck astrovirus type 1 (DAstV-1), is difficult to propagate under laboratory conditions; DVH Type III is also now classified as an astrovirus (DAstV-2) and can be propagated in duck (but not chicken) embryos.
The incubation period for DHAV-1 is 18–48 hours. Affected ducklings become lethargic, lose balance, paddle spasmodically, and die within minutes, typically with opisthotonos. Although adults may become infected, clinical signs have not been seen in ducks >7 weeks old. Mortality may be as high as 95% in fully susceptible ducklings. Practically all deaths occur within 1 week after onset of signs.
The clinical course of DAstV-1 infection is similar to that of DHAV-1 and can be seen in ducklings immune to DHAV-1 infection. DAstV-2 infections are seen in ducklings despite immunity to DHAV-1. The clinical course of DAstV-2 infection is less severe, and mortality is rarely >30%.
The lesions caused by all three types of DVH are similar. The liver is enlarged and covered with hemorrhagic foci up to 1 cm in diameter. The spleen may be enlarged and mottled. Kidneys may be swollen, and renal blood vessels congested.
Presumptive diagnosis is based on history and lesions
Confirmation of diagnosis requires virus isolation or PCR
A presumptive diagnosis of duck viral hepatitis can be based on the history and lesions. Sudden onset, rapid spread, and short course, together with characteristic liver lesions, are highly suggestive of duck viral hepatitis. Confirmatory diagnosis of DVH requires detection of the viral etiological agent, usually from liver homogenate. Immunologic antibody detection tests have little value in the diagnosis of acute infection.
DHAV-1 may be isolated in duck embryos and duck-embryo liver cell cultures, or less easily in chicken embryos. The virus can also be identified by virus neutralization with specific antisera or by inoculation into both susceptible and immune day-old ducklings. DAstV-1 and DAstV-2 are not neutralized by classic DHAV-1 antiserum.
DHAV, DAstV-1, and DAstV-2 can be identified by reverse transcriptase (RT) PCR. Several multiplex RT-PCR tests have been developed for differentiation of the DHAV genotypes.
Prevention and Treatment
There is no specific treatment
Control is based on vaccination and biosecurity
There is no specific treatment.
Control is based on vaccination and biosecurity.
There is no specific treatment for duck viral hepatitis infection. Prevention and control is based on strict biosecurity and implementation of vaccination protocols. Strict isolation, particularly during the first 5 weeks of age, is recommended. Contact with wild waterfowl should be avoided. Rats have been reported as a reservoir host of the virus; therefore, pest control is indicated.
Immunization of breeder ducks with modified-live virus vaccines, using DHAV, DAstV-1, and DAstV-2 , provides parenteral immunity that effectively prevents high losses in young ducklings. The DHAV-1 vaccine is administered SC in the neck to breeder ducks at 16, 20, and 24 weeks of age and every 12 weeks thereafter throughout the laying period. Three immunizations are advisable for passive protection of ducklings.
An inactivated DHAV-1 vaccine for use in breeder ducks that have been previously primed with live DHAV-1 has been described. A single dose of the inactivated vaccine, given IM before the birds come into lay, provides passive immunity for a complete laying cycle to progeny ducklings.
The chick-embryo origin, modified-live DHAV-1 vaccine also can be used for early vaccination of ducklings susceptible to DHAV-1 (progeny of nonimmune breeders). This vaccine is administered SC or by foot web stab in a single dose to day-old ducklings. Vaccinated ducklings rapidly develop an active immunity within 3–4 days.
Antibody against DHAV-1, prepared from the eggs of hyperimmunized chickens and administered SC in the neck at the time of initial loss, is an effective flock treatment.
The clinical and pathologic presentation of duck viral hepatitis in susceptible ducklings is attributed to several viral etiologic agents.
DVH pathology can be induced by at least three genotypes of DHAV as well as DAstV-1 and DAstV-2.
Antigen detection is typically the focus of diagnosis, whereas serologic tests can be used for serologic and epidemiologic surveillance.
Management is based on biosecurity as well as implementation of appropriate vaccination protocols.