Major Viral Diseases of Waterfowl and Their Control Prof. Dr
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IV TH KEITH GOODERHAM WATERFOWL LECTURE Major viral diseases of waterfowl and their control By Prof. Dr. Vilmos Palya developed one step or multiplex Director of Scientific Support reverse transcriptase-polymerase and Investigation Laboratory chain reaction (RT-PCR) methods Ceva-Phylaxia Veterinary are capable to detect and distinguish Biologicals Co., Budapest. between the different DHV types including the new variant DHV-1 lthough chickens and turkeys type as well. comprise the majority of Typing of duck hepatitis viruses is Apoultry species seen by the important to identify emerging veterinary practitioner, occasionally serotypes because immunisation is waterfowl such as ducks and geese serotype specific and does not con - are encountered. fer protection against infection with A feature that is unique to water - heterologous serotypes. fowl is that their environment usu - To prevent the disease, keep age ally involves the presence of groups isolated particularly during man-made or natural bodies of the first five weeks of life. Contact water, and this may enhance the co- with wild waterfowl should be mingling of free-living waterfowl avoided. Rats have been reported as species with the domestic flock and a reservoir of the virus, therefore ultimately, promote disease trans - pest control is important. mission. Vaccination of breeder ducks with Additionally, environmental condi - Fig. 1. Dead duckling in a typical ‘arched-backwards’ position from an attenuated live duck virus hepati - tions may also influence disease infection with DHV type 1. tis vaccine, using type 1 virus, pro - manifestation in domestic water - vides maternal immunity that fowl. There are many diseases that induce hepatitis in DHV type 1- lings over four weeks of age. The effectively prevents high losses in can affect waterfowl species. The immune ducklings, they are now onset of the disease is very rapid, it young ducklings. infectious diseases described here classified as member of the spreads quickly through the flock The vaccine is administered by the are the most common viral diseases Astroviridae family. and may cause up to 90% mortality. subcutaneous route in the neck to seen in domestic waterfowl species. Recently, in Taiwan and Korea Sick ducklings develop spasmodic breeder ducks at two or three times It seems likely that viral diseases will new serotypes of duck hepatitis contractions of their legs and die before the birds come into lay and assume greater future importance as virus, belonging to the same virus within an hour in a typical ‘arched- thereafter every 12 weeks during causes of disease in waterfowl. family as DHV-1 have been backward’ position (Fig. 1). The liver the laying period. At least three Greater attention needs to be described, which showed no anti - is enlarged and shows haemorrhagic immunisations are advisable for ade - given to the study of this source of genic relationship with DHV-1 in spots (Fig. 2). quate passive protection of duck - disease. cross-neutralisation test. Ducklings Diagnosis aiming to distinguish lings. Inactivated DHV-1 vaccine for are most susceptible to DHV at between infections caused by DHV- use in breeder ducks that have been younger ages and gradually become 1, DHV-2 and DHV-3 has been previously primed with live vaccine Duck virus hepatitis more resistance as they grow older. regarded difficult by gross and has also been described. The disease is rarely seen in duck - microscopic examination. Recently Modified live DHV-1 vaccine can Duck hepatitis (DH) is a highly fatal, also be used for early vaccination of contagious and rapidly spreading dis - Fig. 2. Enlarged liver with punctuate haemorrhages caused by DHV-1. progeny of non-immune breeders. ease of young ducklings, 1-28 days The vaccine is administered by the of age. So far, three different viruses, subcutaneous route or by foot web duck hepatitis virus (DHV) type 1, 2 stab in a single dose to day old duck - and 3, have been associated with lings. The birds rapidly develop an these disease conditions. active immunity within 3-4 days. DHV-1 has, since the first out - Hyperimmune serum to DHV-1, break in 1949 in Long Island, been prepared from the egg yolk of reported to infect ducklings world - hyperimmunised chickens, applied wide and is of most economic by SC in the neck, at the time of the importance to all duck growing onset of the disease, is an effective farms because of high potential mor - treatment of affected flock. tality when infection is not con - trolled. Molecular characterisation of the DHV-1 genome recently Duck virus enteritis showed that the genome organisa - tion classifies this virus as unassigned Duck virus enteritis (DVE) is an species in the family Picornaviridae. acute, sometimes chronic, conta - DHV type 2 and 3 are recognised as gious virus infection that occurs nat - separate entities because they Continued on page 23 International Poultry Production — Volume 19 Number 4 21 Continued from page 21 from 10-60%, and mortality from 2- urally only in ducks, geese and 20%. Mortality is always higher in swans, all members of the family young flocks (2-3 weeks of age) than Anatidae of the order Anseriformes. if infection occurs at a older age. In duck-producing areas of the The clinical signs in the acute world where the disease has been phase include a general malaise, reported, DEV has produced signifi - accompanied by diarrhoea of sick cant economic losses in domestic birds. and wild waterfowl due to mortality The affected birds are reluctant to and decreased egg production. The move when disturbed. Muscovy aetiological agent, a herpesvirus, is a ducks and goslings that survive the member of the alphaherpesvirinae acute phase of the disease are subfamily of the Herpesviridae fam - markedly stunted in growth and ily. especially geese develop lameness. This disease is most likely to affect The hock and metatarsal or digital mature ducks, but DVE has been joints, as well as the gastrocnemius reported in birds ranging from seven and digital flexor tendons, and days of age to mature breeders. In sometimes the synovial bursae are susceptible flocks the first signs are Fig. 3. Markedly swollen metatarsal joints. Reovirus infection of goose. markedly swollen (Fig. 3). often sudden, high and persistent By post mortem examination, reported to be as efficacious as during the acute phase of the dis - modified live vaccine. This vaccine ease, characteristic lesions can be has been tested only under labora - seen in the liver and spleen: in both tory conditions; it has not been organs multiple disseminated, grey - tested on a large scale and is not ish-white pin-head necrotic foci are licensed. present and they are larger than normal (Fig. 4). Sero-fibrinous epi- and pericardi - Reovirus infection tis, arthritis and tenosynovitis are frequently seen during the acute and Although avian orthoreoviruses have chronic phase of the disease. As a been isolated from different patho - consequence of the rupture of the logical entities of poultry, their tendon and surrounding tissues, pathological role has been con - large haemorrhages in the region of firmed only in a limited number of gastrocnemius flexor tendon are diseases, such as arthritis-tenosyn - observed in the chronic phase of the ovitis of chickens and stunting runt - disease. ing syndrome. By histology, miliary foci of necrotic Fig. 4. Disseminated, greyish- Fig. 5. Granuloma-like foci with A disease of Muscovy ducks hepatocytes or granuloma-like foci white pin-head foci in an necrotic centres and proliferat - caused by reovirus was first with necrotic centres and proliferat - enlarged liver from a reovirus ing macrophages in the liver described in South Africa in 1950, ing macrophages can be found in the infected goose. from a reovirus infected goose. then in France in 1972, where the liver and the spleen (Fig. 5). virus was isolated. Reoviruses have Diagnosis of the disease can be mortality with a significant drop in A live attenuated virus vaccine can been repeatedly isolated from geese based on the characteristic liver and egg production. In chronically be used to control DVE in birds and detection of antibodies to spleen lesions during the acute infected partially immune flocks only over two weeks of age. Fattening or reoviruses has also been reported. phase and on the development of occasional deaths occur. Recovered breeding ducks may be vaccinated However diseases caused by a arthritis/tenosynovitis during the birds may be carriers and may shed subcutaneously or intramuscularly to reovirus in this species was reported subacute-chronic phase. Classical the virus in the faeces over a period produce an active immunity. The only in 2003. The earliest onset of detection methods of the causative of years. vaccine virus is not thought to the disease, both in duck and goose virus involves the isolation of the Clinical signs and gross pathology spread by contact from vaccinated flocks, is between 7 to 10 days of virus in reovirus antibody negative associated with a DVE outbreak to unvaccinated ducks, as the unvac - age and may persist in an affected duck/goose embryo or embryo vary with the species, age and sex of cinated birds remain susceptible to flock until 7-10 weeks of age. liver cell cultures and detection by the affected birds, and the virulence infection. The outbreaks last for 2-4 weeks electron microscopy, all which are of the virus. The range of signs in An inactivated vaccine has been or even longer. Morbidity ranges laborious and time consuming. affected birds includes eye watering Recently however a rapid, sensi - loss of appetite, ataxia, watery diar - Fig. 6. Sero-fibrinous perihepatitis and ascites in subacute form of tive and broad-spectrum RT-PCR rhoea and nasal discharge. Derzsy’s disease. has become available for the detec - In ducklings 2-7 weeks of age, tion and identification of avian losses may be lower than in older reoviruses from cell cultures and birds and the signs associated with clinical samples.