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turkey viral hepatitis

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turkey viral hepatitis

Summary

  • Last modified
  • 25 September 2017
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • turkey viral hepatitis
  • Pathogens
  • turkey viral hepatitis virus
  • Overview
  • Turkey viral hepatitis (TVH) is a highly contagious, but generally subclinical disease of turkeys. The disease occurs primarily in young turkeys of less than 6 weeks of age. It is characterized by multifocal hepatic nec...

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Identity

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Preferred Scientific Name

  • turkey viral hepatitis

International Common Names

  • English: hepatitis and pancreatitis in turkeys; hepatopancreatitis in turkeys; turkey hepatitis; turkey viral hepatitis, tvh; virus hepatitis in turkeys

English acronym

  • TVH

Pathogen/s

Top of page turkey viral hepatitis virus

Overview

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Turkey viral hepatitis (TVH) is a highly contagious, but generally subclinical disease of turkeys. The disease occurs primarily in young turkeys of less than 6 weeks of age. It is characterized by multifocal hepatic necrosis with or without accompanying pancreatic necrosis. The economic significance of TVH is not known.

Turkey viral hepatitis was initially described in 1959. It was described simultaneously by Mongeau et al. (1959) in Canada, and Snoeyenbos et al. (1959) in the USA.

Hosts/Species Affected

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Turkey viral hepatitis has been recognized only in turkeys. Chickens, pheasants, ducks, quails, mice and rabbits have been shown to be refractory to infection (Tzianabos and Snoyenbos, 1965b). Turkey poults are susceptible to infection by intraperitoneal, intravenous and intramuscular routes of exposure. Clinical signs seldom develop in experimentally infected poults, but infection may be demonstrated 5-10 days post-inoculation by necropsy and detection of characteristic lesions (Snoyenbos, 1991).

Systems Affected

Top of page digestive diseases of poultry

Distribution

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Turkey viral hepatitis has been recorded in Canada, the United States, Italy and Great Britian (Mongeau et al., 1959; Snoyenbos et al., 1959; Mandelli et al., 1966; McDonald et al., 1982). The disease is believed to be widely distributed in these countries, but its true incidence and distribution is not known as the disease is commonly subclinical, and serologic diagnostic tests are currently not available.

Distribution Table

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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.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

North America

CanadaPresentMongeau et al., 1959
-OntarioPresentMongeau et al., 1959
USAPresentSnoeyenbos et al., 1959
-CaliforniaPresentKlein et al., 1991
-MassachusettsPresentSnoeyenbos et al., 1959
-North CarolinaPresentWages and Ficken, 1989

Europe

ItalyPresentMandelli et al., 1966
UKPresentMcDonald et al., 1982

Pathology

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Postmortem lesions attributable to TVH are found only in the liver and pancreas. Livers are usually enlarged. Liver lesions consist of focal, grey, sometimes depressed areas up to several millimeters in diameter. Lesion distribution is variable; birds that die usually exhibit very extensive lesions, which often coalesce and may be partially masked by vascular congestion and focal haemorrhage. Pancreatic lesions are less consistently observed than hepatic lesions. Lesions in the pancreas generally are roughly circular, grey-pink, and may extend across a lobe.

Microscopically, vacuolation of hepatocytes is observed early in the course of infection with dense infiltration by mononuclear leukocytes, and proliferation of bile ductules. Lesions progress to overt focal necrosis with pooling of blood around the focus; necrotic cells are scattered among infiltrating lymphocytes. Late in the course of infection lesions are comprised of proliferating reticuloendothelial cells which frequently form giant cells.

Microscopic lesions in the pancreas are similar to those observed in livers. Acinar cell degeneration and necrosis are observed with infiltration of macrophages and lymphocytes.

Diagnosis

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Diagnosis of turkey viral hepatitis may be based on histopathology or virus isolation; serological procedures are not currently available. Histopathology may be utilized to presumptively diagnose turkey viral hepatitis, as the presence of lesions in both the liver and pancreas of turkeys is highly suggestive of the disease. However, similar lesions may be produced in the liver by a variety of bacterial, viral and protozoal agents. These include Salmonella spp., Pasteurella multocida, group I and group II avian adenoviruses (Cho, 1976; Wilcock and Thacker, 1976), reovirus (Van der Heide et al., 1980) and Histomonas meleagridis (Snoyenbos and Basch, 1960).

Virus isolation may be accomplished using a number of tissues including liver, pancreas, spleen, kidney, or faeces; liver is the preferred tissue. Tissues or faeces should be homogenized in an appropriate diluent such as minimal essential medium, and clarified by centrifugation; clarified faecal suspensions should be filtered through a 0.45 µm membrane filter. Homogenates of tissue or faecal suspensions are inoculated into 5 to 7-day-old embryonated chicken eggs by the yolk sac route. In THV-positive cases, embryo mortality generally occurs at 4-11 days post-inoculation (Snoyenbos et al., 1959). Embryo mortality is delayed if low virus titres are present and in some cases a second passage using yolk harvest may be required. Embryos exhibit cutaneous congestion and oedema; dwarfing is observed in those embryos in which mortality is delayed, and less cutaneous congestion is observed in these embryos (Snoyenbos et al., 1959). Liver lesions containing necrotic foci are sometimes observed in embryos that survive to 11 days post-inoculation. Embryonic fluids do not haemagglutinate erythrocytes. Isolates may be further characterized by yolk sac or intraperitoneal inoculation of poults with yolk harvested from infected embryonated eggs; poults are examined for lesions 5-10 days post-inoculation.

Immunologic aspects of TVH have received little attention. Tzianabos and Snoeyenbos (1965b) were unable to detect neutralizing antibodies in sera from recovered turkeys, or hyperimmunized chickens, turkeys and rabbits. However, immunity to re-infection was observed in previously infected turkeys; re-exposure of recovered birds after an interval of 21 days resulted in less frequent and less extensive lesions than in infected controls (Snoyenbos et al., 1959). Recovery from TVH results in resistance to re-infection but the duration of immunity has not been determined.

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
General Signs / Sudden death, found dead Poultry:Young poultry Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Poultry:Young poultry Sign
Reproductive Signs / Decreased hatchability of eggs Poultry:Embryo Sign
Reproductive Signs / Decreased, dropping, egg production Poultry:Mature female Sign

Disease Course

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The incubation period in poults, as determined by the appearance of lesions, varies between 2-7 days in both intraperitoneally inoculated and in-contact poults (Snoyenbos et al., 1959; Snoyenbos and Basch, 1960).

Turkey viral hepatitis is usually a subclinical infection of turkeys. It is believed that the disease becomes apparent as a result of undefined factors such as concurrent infection and/or environmental stresses. Clinical signs in TVH-affected birds are not well defined. Variable degrees of depression may be observed in affected flocks, but more often, field cases are characterized by sudden death of apparently normal birds. Turkey viral hepatitis virus infection has been suggested as a cause of decreased egg production, decreased fertility, and decreased hatchability in turkey breeder hen flocks but an etiologic role for TVH virus has not been conclusively determined (Snoyenbos, 1991).

Morbidity and mortality vary considerably among affected flocks. Usually morbidity and mortality are very low with mortality occurring during a 7-10 day period (Snoyenbos, 1991). However, morbidity rates of up to 100% have occurred in some flocks, and a 25% mortality was reported in one flock (Snoyenbos, 1991). It is believed that the degree of morbidity and mortality are influenced by other factors such as concurrent infection. Mortality in turkeys over 6 weeks of age has not been reported.

Epidemiology

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Transmission of TVH virus occurs readily by both direct and indirect contact. Faeces from infected turkeys are believed to be the principal source for virus transmission; the virus may be isolated from liver and faeces of experimentally infected birds during the first 28 days post-inoculation (PI), and less frequently from bile, blood and kidney during this period. The virus is not detected in tissues and feces after 28 days PI (Snoyenbos et al., 1959; Tzianabos and Snoyenbos, 1965b). Vertical transmission via the egg has been suggested by field observations and by the isolation of virus from an ovarian follicle of an experimentally infected hen (Snoyenbos and Basch, 1960).

Prevention and Control

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No specific prophylactic measures are available. Prevention of stress and other infections may be helpful in preventing normally subclinical disease from developing into TVH.

References

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Cho BR, 1976. An adenovirus from a turkey pathogenic for both chicks and turkey poults. Avian Diseases, 20:714-723.

Guy JS, 1997. Turkey viral hepatitis. In: Calnek B, Barnes HJ, Beard CW, McDougald LR, Saif YM, eds. Diseases of Poultry, edition 10. Ames, Iowa, USA: Iowa State University Press, 773-777.

King; AMQ; Brown F; Christian P; Hovi T; Hyypia T; Knowles NJ; Lemon SM; Minor PD; Palmenberg AC; Skern T; Stanway G, 2000. Picornaviridae. In: Regenmortel M, Fauquet C, Bishop D, Carstens E, Estes M, Lemon S, Maniloff J, Mayo M, McGeoch D, Pringle C, Wickner R, eds. Virus taxonomy: seventh report of the International Committee on Taxonomy of Viruses. Academic Press, San Diego, USA, 657-678.

Klein PN; Castro AE; Meteyer CU; Reynolds B; Swartzman-Andert JA; Cooper G; Chin RP; Shivaprasad HL, 1991. Experimental transmission of turkey viral hepatitis to day-old poults and identification of associated viral particles resembling picornaviruses. Avian Diseases, 35(1):115-125; 45 ref.

Mandelli GA; Rinaldi A; Cervio G, 1966. Gross and ultramicroscopic lesions in hepatopancreatitis in turkeys. Atti Soc Ital Sci Vet, 20:541-545.

McDonald JWC; Randall CJ; Dagless MD, 1982. Picornaviruslike virus causing hepatitis and pancreatitis in turkeys. Veterinary Record, 111:323.

Mongeau JD; Truscott RB; Ferguson AE; Connell MC, 1959. Virus hepatitis in turkeys. Avian Diseases, 3:388-396.

Snoeyenbos GH, 1991. Turkey viral hepatitis. Diseases of poultry., ed. 9:699-701; 13 ref.

Snoeyenbos GH; Basch HI, 1960. Further studies of virus hepatitis in turkeys. Avian Diseases, 4:477-485.

Snoeyenbos GH; Basch HI; Sevoian M, 1959. An infectious agent producing hepatitis in turkeys. Avian Diseases, 3:377-388.

Tzianabos T; Snoeyenbos GH, 1965a. Some physiochemical properties of turkey hepatitis virus. Avian Diseases, 9:152-156.

Tzianabos T; Snoeyenbos GH, 1965b. Clinical, immunological and serological observations on turkey virus hepatitis. Avian Disease, 9:578-595.

Van der Heide L; Brustolon M; Lawson MG, 1980. Pathogenicity for chickens of a reovirus isolated from turkeys. Avian Disease, 24:989-997.

Wages DP; Ficken MD, 1989. Cryptosporidiosis and turkey viral hepatitis in turkeys. Avian Diseases, 33(1):191-194; 22 ref.

Wilcock BP; Thacker HL, 1976. Focal hepatic necrosis in turkeys with hemorrhagic enteritis. Avian Diseases 20:205-208.

Links to Websites

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WebsiteURLComment
Turkey Health Forumhttp://www.poultry-health.com/fora/turkhelth/index.htm

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