Signalment:  

Female adult Muscovy duck (Cairina moschata)The duck was one of 2 birds to die from a total of 75 ducks. Submitted for necropsy. No clinical history was given

Gross Description:  

The bird was in good flesh and tissues were in a good state of postmortem preservation. The liver was uniformly pale and there was generalized congestion of other visceral organs. Matured ovules of the ovary were markedly hemorrhagic. No other lesions were noted grossly.

Histopathologic Description:

Liver: At the subgross level there is multifocal pallor or clear areas interpreted as loss of hepatic architecture. On close examination there is edema around most blood vessels and multifocal necrosis. There is dissociation of hepatocytes and some hepatocytes are swollen, disrupted or ruptured. There is abundance of eosinophilic intranuclear inclusion bodies with thinly marginated chromatin (Fig. 1-1). There are no appreciable inflammatory cell infiltrates.

Morphologic Diagnosis:  

Liver: Multifocal necrosis and degeneration, multifocal, acute, with perivascular edema and abundant eosinophilic intranuclear inclusion bodies.

Lab Results:  

Mixed flora was isolated from the lung, liver, ovule and intestines; duck enteritis virus (DVE) was detected by PCR.

Condition:  

Anatid herpesvirus-1

Contributor Comment:  

DVE is an acute, contagious herpesvirus infection of ducks, geese, and swans, characterized by vascular damage, tissue hemorrhages, digestive mucosal eruptions, lesions of lymphoid organs, and degenerative changes in parenchymatous organs.(6) Although there is no mention of clinical signs in this bird, the disease has an incubation period of 3 to 7 days. Once overt signs appear, death usually follows within 1 to 5 days. Naturally occurring infection has been observed in ages ranging from 7-day-old ducklings to mature breeder ducks.(6) DVE was first diagnosed in the United States in 1967 in a commercial Pekin duck-producing area of Long Island, NY, where it caused serious economic losses.(2,4) Mature ducks die in good flesh. Typically clinical signs consisted of prolapse of the penis in male matured breeders, and a marked drop in egg production in laying flocks. As DVE progresses within a flock more signs are observed: Photophobia, inappetence, thirst, nasal discharges, diarrhea, weakness, tremors of the head and neck. Mortality may range from 5 to 100%.(6) Based on the histopathologic findings the disease is considered non inflammatory and retrograde in nature; and the distribution of the inclusion bodies suggests that the virus is reticulo-endotheliotropic.(6)

In this bird, in addition to the liver lesions, mucosal lesions were noted in the digestive tract (esophagus, proventriculus), characterized by erosions and ulcerations with rare eosinophilic intranuclear inclusion bodies in few remaining epithelial cells.  Typically, lesions of DVE are those of vascular damage, eruptions of specific locations on mucosal surface of the gastrointestinal tract, lesions of lymphoid organs, and degenerative sequelae in parenchymatous organs. When these lesions are collectively present, are diagnostic of DVE.(6) In the present case the diagnosis was confirmed by PCR on tissue pools. 

Differential diagnosis requires consideration of other diseases producing hemorrhagic and necrotic lesions in anseriforms. Such diseases include duck virus hepatitis, pateurellosis, necrotic enteritis, coccidiosis, and specific intoxications.(6)

To prevent this disease from spreading, strict decontamination and depopulation should be carried out whenever possible.(3) A vaccine is also available for prevention of DVE but approval by animal health authorities is required before it can be used.(7)

JPC Diagnosis:  

Liver: Hepatitis, necrotizing, acute, random, moderate with eosinophilic intranuclear inclusion bodies, etiology consistent with herpesvirus

Conference Comment:  

Duck viral enteritis, also known as duck plague, is in the family Herpesviridae, and subfamily Alphaherpesvirinae. Two other extremely important herpes viruses in this subfamily are gallid herpesvirus 1 also known as infectious laryngotracheitis virus, and gallid herpesvirus 2 also known as Mareks disease.(5)

The pathogenicity of this virus depends on the particular species of duck infected. The blue-winged teal (Anas discors) is most susceptible to DVE, while the pintail duck (Anser acuta) is the least susceptible.(2) Muscovy ducks, as seen in this case, are highly susceptible to this particular virus. This virus is a major concern because migratory birds can spread this virus to na+�-�ve populations leading to massive outbreaks with high mortality.(4)

Dr. Raymond briefly integrated some general pathology topics as they relate to this particular case, and he focused on mechanisms by which free radicals cause damage to cells.

Free radicals are molecules with an unpaired electron making them highly reactive. These molecules are generated as by-products of normal cell function via oxidative metabolism or are a by-product of exposure to radiation, toxins, drugs, or other chemicals. Free radicals are also produced by neutrophils and macrophages in inflammation. Free radicals can damage cells by 1) peroxidation of cellular phospholipid membranes; 2) DNA injury; 3) oxidative modification of proteins.(1)

Free radical damage is minimized by several different antioxidants within the body. These antioxidants include enzymatic and nonenzymatic antioxidants. Enzymatic antioxidants include superoxide dismutase, catalase, and glutathione peroxidase. Nonenzymatic antioxidants include transport proteins transferrin, ferritin, lactoferrin, and ceruloplasmin. Vitamins A, C and E, and other dietary compounds such as lycopenes, flavonoids, genistein, and reserpines help to minimize the damage done by free radicals.(1)

References:

1. Abbas, AK: Cellular adaptations, cell injury, cell death. In: Robbins and Cotran Pathologic Basis of Disease, 7th edition, pp. 16-18V. Kumar, A. K. Abbas, N. Fausto (eds). Elsiever, Inc., Philadelphia, PA, 2000
2. Burges, EC, Ossa CJ, Yuill TM: Duck Plague: a carrier state in waterfowl. Avian Dis 23:940-949. 1979
3. Davidson S, Converse KA, Hamir NA, Eckroade RJ: Duck viral enteritis in domestic muscovy ducks in Pennsylvania. Avian Dis 37:1142-1146, 1993
4. Leibovitz L, Hwang J: Duck plague on the American continent. Avian Dis 12:361-378, 1967
5. Murphy FA, Gibbs EPJ, Horzinek MC, Studdert MJ: Herpesviridae. In: Veterinary Virology, eds. Murphy FA, Gibbs EPJ, Horzinek MC, Studdert MJ, 3rd ed., pp. 301-325. Academic Press, San Diego, California, 1999
6. Sandhu, TS, and Leibovitz L: Duck virus enteritis (duck plague). In: Disease of Poultry, eds., Calneck BW, Barnes HJ, Beard CW, McDougald LR, Saif YM, 10th ed., pp. 675-682. Iowa State University Press, Ames, IA, 1997
7. Whiteman CE, Bickford AA: Avian disease manual. 3rd ed. American Association of Avian Pathologists, Kennett Square, PA, 1988
8. Kumar V, Abbas AK, Fausto N: Robbins and Cotran, Pathologic Basis of Disease, 7th ed., pp. 16-18. Elsevier Saunders, Philadelphia, PA, 2005

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1-1. Liver, duck

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