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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Derzsy's disease
International Common Names
- English: Derzsy's disease of geese; goose hepatitis; goose parvovirus infection; goose plague; goose viral enteritis; goose viral hepatitis; goose virus hepatitis; gosling plague; parvoviral enteritis of geese; parvovirus disease of goslings; parvovirus infection of geese; viral disease of goslings; viral enteritis of goslings; virus hepatitis of geese
- French: la maladie de Derzsy; maladie de Derzsy
Pathogen/sTop of page goose parvovirus
Muscovy duck parvovirus
OverviewTop of page
Derzsy's disease is a highly contagious disease of young geese and Muscovy ducks (Cairina moschata) caused by a parvovirus. Depending on the age of affected birds and the pathogenicity of the wild-type virus, the disease may present in acute, sub-acute or chronic forms. The acute form of the disease can result in 100% mortality in goslings and Muscovy ducklings of less than ten days of age. Apart from geese and Muscovy ducks, the disease has not been reported in other avian species or mammals, including humans.
Fang and Wang (1981) reported the first detailed description of a serious disease of goslings, which occurred in China in 1956; the disease was later shown to be caused by a parvovirus. During the 1960s a similar disease was reported from many European countries and the etiological agent was confirmed as a parvovirus by several laboratories (Gough, 1997).
Differences in host range, antigenicity and nucleotide sequences have been reported between isolates of goose and Muscovy duck parvoviruses (Barnes, 1997). Recently, molecular studies have indicated that goose parvovirus is more closely related to the human Dependovirus genus than to other autonomous parvoviruses (Brown et al., 1995).
Host AnimalsTop of page
Hosts/Species AffectedTop of page
Goose parvovirus infection occurs in all breeds of domestic geese and Muscovy ducks. The disease has also been reported in wild geese following accidental infection (Schettler, 1971). Muscovy duck parvovirus infection has been reported to occur in various genetic crosses of Muscovy ducks and several indigenous breeds of waterfowl in the Far East. Geese seem to be less susceptible to Muscovy duck parvovirus than to goose parvovirus. In both geese and Muscovy ducks the disease is strictly age dependant with up to 100% mortality occurring in birds under one-week of age. Progressive resistance to infection occurs so that by the time the birds are 4 to 5-weeks-old negligible losses occur. Following infection, older geese and Muscovy ducks show no clinical signs but respond antigenically. Other breeds of waterfowl and domestic poultry seem to be refractory to infection.
Systems AffectedTop of page blood and circulatory system diseases of poultry
digestive diseases of poultry
multisystemic diseases of poultry
nervous system diseases of poultry
respiratory diseases of poultry
skin and ocular diseases of poultry
DistributionTop of page
Derzsy's disease has been reported from all the major goose and Muscovy duck farming countries of Europe, including the former USSR, and Israel. The disease has also been reported from China, Taiwan, Vietnam and Japan. In countries such as France and Germany, where geese and Muscovy ducks are farmed intensively, the disease has caused serious economic problems.
Distribution TableTop of page
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.
PathologyTop of page
In acute cases with a short clinical course, lesions are commonly found in the heart, which has a pale myocardium characteristically rounded at its apex. The liver, spleen and pancreas may be swollen and congested. A variety of other gross lesions may also be present in cases with a more prolonged clinical course. Typically, a sero-fibrinous perihepatitis and pericarditis is present with large volumes of straw-coloured fluid in the abdominal cavity. Pulmonary oedema, liver dystrophy and catarrhal enteritis may also be present. Less frequently, haemorrhages in the thigh and pectoral muscles may be seen. Diptheritic and ulcerative lesions may be observed in the mouth, pharynx and oesophagus, depending on the presence of secondary infection.
Detailed histopathology studies of goose parvovirus infection by a number of workers have produced similar findings (Gough, 1997). The main lesions reported were pronounced degenerative changes in myocardial cells with associated loss of striation, fatty infiltration and the presence of scattered Cowdrey type A intranuclear inclusions. Similar histological changes were also found in intestinal and smooth muscle cells. In the liver the predominant lesions were degeneration of hepatocytes with vacuolation and fatty infiltration. Small, eosinophilic inclusion-like bodies were sometimes seen in the cytoplasm of the vacuolated hepatocytes. Changes in the pancreas consisted of shrunken, necrotic acinar cells with fatty infiltration. Some lymphoblastic processes were occasionally observed in the spleen, bursa of Fabricius and thymus, together with marked vacuolation of the kidneys.
DiagnosisTop of page Laboratory Diagnosis
Isolation and Identification of the Causative Agent
A variety of methods have been developed and evaluated for the diagnosis of goose parvovirus infection (Gough, 1997;1998). The virus can be isolated from a variety of suitable postmortem specimens following inoculation of 10 to 15-day-old embryonated goose or Muscovy duck eggs via the allantoic cavity. Embryo mortality occurs 5-10 days post-inoculation with haemorrhages and ochre-coloured livers. The virus can also be isolated in primary cell cultures of goose or Muscovy duck embryos. Isolation of the virus is facilitated by inoculating cultures before they reach confluency. The virus produces a well-defined cytopathic effect (CPE) three to five days post-infection. In haemotoxylin and eosin-stained preparations Cowdrey type A intranuclear inclusions and syncytium formation are often present. Electron microscopic examination of infected cell cultures or neutralization with specific goose parvovirus antiserum can confirm the presence of the virus.
Immunofluorescence has also been used to detect the presence of antigen in both goose embryos and infected cell cultures. Other methods of detecting goose parvovirus have been developed, including the immunoperoxidase technique and reverse indirect haemagglutination test.
An agar gel diffusion technique has been described using hyperimmune rabbit anti-goose parvovirus serum to precipitate parvovirus in allantoic fluid from infected goose embryos. Aggregates of goose parvovirus virions have also been detected by electron microscopic examination of ultra-thin sections of heart and bursa of Fabricius from infected goslings, and in concentrated extracts of faeces from goslings showing clinical signs of goose parvovirus.
A polymerase chain reaction (PCR) has been developed to detect parvoviruses. Primers have been designed from conserved regions of the VP1 and 2 genes that encode for the capsid proteins. These can be used to differentiate strains of goose and Muscovy duck parvovirus following restriction fragment length polymorphism (RFLP) analysis.
Confirmation of goose parvovirus infection can be obtained by serological means. The most commonly used method is the virus neutralization test in embryonated goose or Muscovy duck eggs or primary cell cultures to detect the presence of goose parvovirus neutralizing antibodies. A neutralization test has also been developed for use in Khaki Campbell or Pekin duck eggs using a duck-embryo-adapted goose parvovirus. Though less sensitive than the neutralization test, the agar gel diffusion test is a useful method of rapidly testing large numbers of sera for the presence of goose parvovirus antibodies. Other serological techniques developed include the spermagglutination-inhibition and ELISA tests. Antigen for these tests is readily prepared from allantoic fluid of infected goose eggs by means of polyethylene glycol (PEG) concentration of the virus.
Apart from duck herpesvirus enteritis there are no other known viral infections that cause high mortality in young geese or Muscovy ducklings. However, equivocal results can arise when viruses other than parvovirus are isolated, particularly reoviruses and adenoviruses. In such cases it may be necessary to carry out serological tests in order to confirm the diagnosis.
List of Symptoms/SignsTop of page
|Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces||Poultry:All Stages||Sign|
|Digestive Signs / Abnormal colour of the beak||Poultry:All Stages||Sign|
|Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly||Poultry:All Stages||Sign|
|Digestive Signs / Malformation of the beak||Poultry:All Stages||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Poultry:All Stages||Sign|
|General Signs / Exercise intolerance, tires easily||Poultry:All Stages||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Poultry:All Stages||Sign|
|General Signs / Increased mortality in flocks of birds||Poultry:All Stages||Sign|
|General Signs / Internal abdominal mass, swellings, adhesions abdomen||Poultry:All Stages||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Poultry:All Stages||Diagnosis|
|General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass||Poultry:All Stages||Sign|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Poultry:All Stages||Sign|
|General Signs / Reluctant to move, refusal to move||Poultry:All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Poultry:All Stages||Sign|
|Nervous Signs / Constant or increased vocalization||Poultry:All Stages||Sign|
|Nervous Signs / Head shaking, headshaking||Poultry:All Stages||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Poultry:All Stages||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Poultry:All Stages||Sign|
|Skin / Integumentary Signs / Loss of feathers, loose feathers||Poultry:All Stages||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Poultry:All Stages||Diagnosis|
|Skin / Integumentary Signs / Soiling of the feathers, vent feathers||Poultry:All Stages||Sign|
|Skin / Integumentary Signs / Soiling of the vent in birds||Poultry:All Stages||Sign|
Disease CourseTop of page
The clinical signs, morbidity and mortality in susceptible goslings vary according to the age of the birds. In goslings under one-week-old the course of the disease may be very rapid, with anorexia, prostration and death occurring within 2-5 days. In older birds, or those with variable levels of maternally derived antibody, the disease follows a more protracted course with the appearance of characteristic clinical signs. Initially, affected birds exhibit anorexia, polydipsia and weakness with a reluctance to move. There is a nasal and ocular discharge in many birds with associated head shaking. The uropygial glands and eyelids are often red and swollen, and a profuse white diarrhoea is evident in many of the birds. Examination of the birds at this stage may reveal a fibrinous pseudo-membrane covering the tongue and oral cavity. Goslings that survive the acute-phase may develop a more prolonged disease characterized by profound growth retardation, loss of down around the back and neck, and marked reddening of the exposed skin. There may be an accumulation of ascitic fluid in the abdomen, which causes the goslings to stand in a 'penguin-like' posture.
Mortality sometimes reaches 100% in goslings infected in the hatchery. In 2 to 3-week-old goslings mortality levels may be below 10% although morbidity levels may be high. Complicating factors such as poor management and secondary bacterial, fungal or viral infections may influence the final mortality levels (Kontrimavichus et al., 1980; Kisary 1986). Goslings over 4 weeks of age rarely show clinical signs although a 'late-form' of the disease has been described in goslings of 1-3 months of age (Coudert et al., 1974). Geese of all ages respond immunologically to goose parvovirus infection without necessarily showing clinical signs.
EpidemiologyTop of page
Infected birds excrete large amounts of virus in their faeces resulting in a rapid spread of infection by direct and indirect contact. The most serious outbreaks occur in susceptible birds following vertical transmission of the virus. In older geese and Muscovy ducks that become sub-clinically infected, a latent infection may become established. These birds may then act as carriers of the disease and transmit the virus through their eggs to susceptible goslings or ducklings in the hatchery. Horizontal transmission usually occurs via contaminated drinking water and feed. No biological vectors have been identified. In susceptible goslings and ducklings the incubation period is age-dependent. Experimental infection of day-old goslings results in the appearance of clinical signs 3-5 days later. In 2 to 3-week-old birds the incubation period may vary between 5 and 10 days.
Prevention and ControlTop of page
The subject has been reviewed in detail elsewhere (Gough, 1997). There is no specific treatment for goose parvovirus infection. Antibiotic therapy has been used to reduce losses from secondary bacterial or fungal infections. Because many outbreaks of goose parvovirus are directly attributed to transmission of the disease by congenitally infected goslings during hatching, the practice of incubating and hatching eggs that have originated from different breeding flocks should be discouraged. Only eggs from known parvovirus-free flocks should be incubated together and good hatchery hygiene should be maintained.
On farms where outbreaks of the disease have occurred, the practice of breeding from geese that have survived the disease as goslings should also be discouraged, as these birds are potential carriers of the virus. All contact geese whether goslings or adults, should be serologically tested in order to identify which birds have been infected horizontally. Positive reactors should be removed from the flock, as these birds may also become carriers of the virus.
As the disease is confined to young geese or Muscovy ducklings, control measures have been developed to provide adequate immunity during the first 4-5 weeks of life. Some of the early outbreaks of goose parvovirus occurring in China in 1962 were controlled by the use of hyperimmune serum in newly hatched goslings. Serum therapy was widely used when the disease subsequently appeared in Europe, using serum produced in hyperimmunized geese. However, passive immunization was found to be expensive and time-consuming, particularly as two doses of serum were often required to produce adequate immunity. Active immunization of adult breeding geese and Muscovy ducks with virulent virus has also been reported. The results showed that protection against goose parvovirus was transferred to the progeny via the egg yolk.
One of the first vaccines against the disease was developed in China, and during the period 1962 to 1979 about four million female geese were vaccinated. The virus was attenuated following multiple passage in embryonated goose eggs and a good degree of protection to challenge was recorded in the progeny goslings. Other vaccines have been developed by attenuation of the virus in goose or Muscovy duck embryo cell cultures, for use in breeding geese and goslings. Duck embryo-adapted goose parvovirus vaccines have also been shown to induce a good immune response in goslings and breeder geese.
In flocks of geese where parvovirus has not been diagnosed, inactivated vaccines have been used prophylactically.
ReferencesTop of page
Alexandrov MT; Ivanov IG; Simeonov KB; Lasarova SL; Alexandrova RI; Doumanova LI; Gurov BI; Chenchev II, 1995. Isolation of goose parvovirus in Bulgaria. Bulgarian Journal of Agricultural Science, 1(3):279-283; 14 ref.
Barnes JH, 1997. Muscovy Duck Parvovirus. In: Calnek BW, ed. Diseases of Poultry. Iowa, USA: Iowa State University Press, 1032-1033.
Coudert MM; Fedida M; Dannacher G; Peillon M, 1974. Parvovirus disease of goslings. Late form. Recueil de Medicine Veterinaire, 150:899-906.
Dannacher D; Coudert M; Fedida M; Peillon M; Fouillet X, 1972. Etiology of the virus disease of geese. Recueil de Medecine Veterinaire, 148:1333-1349.
Derzsy D; Dren C; Szedo M; Surjan J; Toth B; Iro E, 1970. A viral disease of goslings. III. Isolation, properties and antigenic patterns of the virus strains. Acta Veterinaria Academiae Scientiarum Hungaricae, 20:419-428.
Devos A, 1982. Report on clinical and postmortem findings in poultry, other birds and rabbits during 1982. Vlaams Diergeneeskundig Tijdschrift, 52(4):291-297.
Dvorakova D; Smid B; Valicek L, 1982. Laboratory diagnosis of Derzsy's disease. Sbornik Vedeckych Praci Ustredniho Statniho Veterinarniho Ustavu, 12:38-45.
Fang DY; Wang YK, 1981. Studies on the etiology and specific control of goose parvovirus infection. Scientia Agricultura Sinica, 4:1-8.
Gough RE, 1998. Goose Parvovirus (Derzsy's disease). In: Swayne D, ed. Isolation and Identification of Avian Pathogens. Pennsylvania, USA: American Association of Avian Pathologists, 219-222.
Gough RE; Spackman D; Collins MS, 1981. Isolation and characterisation of a parvovirus from goslings. Veterinary Record, 108:399-400.
Hanh NV, 1994. A disease of goslings in Vietnam. Magyar Allatorvosok Lapja, 29:262-265.
Hansen HC, 1980. Derzsy's disease (Parvovirus infection) in geese. Dansk Veterinaertidsskrift, 63(5):191-194.
Jestin V, 1991. Actualité sur la maladie de Derzsy. Semaine Veterinaire, 606:28.
Kisary J, 1986. Diagnosis and control of parvovirus infection of geese (Derzsy's disease). Acute virus infections of poultry, 239-242; [Current Topics in Veterinary Medicine and Animal Science volume 37]; 13 ref.
Kontrimavichus LM; Makogon VF; Navrotskii VV, 1980. Epidemiological, clinical and pathological features of goose viral enteritis. Veterinariya Moscow, 7:34-35.
Mandelli G, 1984. Goose plague (Derzsy's disease). Rivista di Zootecnia e Veterinaria, 12(2):2pp.
Samberg Y; Bock R; Perlstein Z, 1972. A new infectious disease of goslings in Israel. Refu Veterinaria, 29:29-33.
Schettler CH, 1971. Goose virus hepatitis in the Canada goose and Snow goose. Journal of Wildlife Diseases, 7:147-148.
Schettler CH, 1973. Virus hepatitis of geese. III. Properties of the causal agent. Avian Pathology, 2:179-193.
Tantaswasdi U; Sirivan P; Chaisingha A; Trongwongsa L; Mahantachaisakul C, 1994. Goose parvovirus infection in Thailand. Journal of Thai Veterinary Medicine Association, 45:47-57.
van Cleef SAM; Miltenburg JT, 1966. A serious virus disease with an acute course and high mortality in goslings. Tijdschrift Diergeneesk, 91:372-382.
Wachnik Z, 1974. Viral diseases of geese. Medycyna Weterynaryjna, 30(3):134-137.
Woolcock PR; Jestin V; Shivaprasad HL; Zwingelstein F; Arnauld C; McFarland MD; Pedersen JC; Senne DA, 2000. Evidence of muscovy duck parvovirus in Muscovy ducklings in California. Veterinary Record, 146(3):68-72; 20 ref.
Zarzara M, 1980. Derzsy's disease (viral disease of goslings). Revista de Cresterea Animalelor, 30(9):67-70.
Distribution MapsTop of page
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