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Clinicians and Pathologists
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Necrotic Hemorrhagic Hetpatitis-Splenomegaly Syndrome in Layer Leghorn Chickens D. H. Read, B. M. Daft, J. T. Barton, P. R. Woolcock, G. Cutler and F. Galey
Over the past 8 years, a necrotic hemorrhagic hepatitis of undetermined etiology caused sporadic episodes of increased mortality in 40- to 60-week-old white leghorn chickens on 2 large commercial properties in southern California. Weekly mortality typically increased over a 2-to 4-week-period from standard levels of 0.1-0.2% to approximately 0.3%, which persisted for periods of several weeks before subsiding. The increased mortality was associated with a 12 to 20% decrease in egg production. On one property, for which information was available, the syndrome occurred during the spring of 1992 and 1993. Different flocks of the same leghorn strain were involved whereas other strains housed separately were apparently unaffected. House-occurrence was sporadic and unrelated to feed. In 1992, the syndrome began in March and for 9 weeks, weekly mortality average 0.29% (range 0.25-0.44%). On week 10 it peaked at 0.98%, 1 week after a forced moult then dropped rapidly over the next 6 weeks to an average level of 0.08% (range 0.22- 0.04%). In 1993, increased mortality began in May, and for 8 weeks, weekly mortality average 0.35% (range 0.30-0.43%). On week 9 it peaked at 1.04%, 1 week after a forced moult then fell rapidly over the next 5 weeks to an average level of 0.11% (range 0.07-0.16%). Affected hens were found dead without premonitory signs. Forty of 49 hens had lesions characteristic of the syndrome. Significant gross lesions were: marked hepatomegaly with diverse combination of pallor, mottling and stippling with red, yellow and/or tan foci, friable or turgid consistency, intralobar and subcapsular hematomas and supra-capsular extensive blood clots; hemoperitoneum; splenomegaly with pallor and friable or turgid consistency; and, regressive ovaries and oviducts. In both years, the pre-moult mortality was associated with a 12-19% decrease in egg production. Feed and water consumption and egg weights remained normal. Post-moult egg production returned to standard levels of about 80%. Characteristic histopathologic lesions of hepatitis and splenitis were observed in 35 hens with typical gross lesions. Four hens had acute lesions whereas the remainder had subacute to chronic-active lesions. Acutely affected livers had generalized nonsuppurative inflammation of portal interstitium, invariably around bile ducks and involving adjacent segment of portal veins by local extension. Subintimal venous inflammation was prominent. Predominant cells were mononuclear leukocytes and lymphocytes. This was sometimes accompanied by acute multifocal vascular lesions, namely, thrombosis of portal veins, deposition of fibrin in sinusoids and parenchymal hemorrhages. Subacute to chronically affected livers had similar inflammatory changes as well as a variety of additional parenchymal lesions, namely; multifocal fibrin deposition; coagulative necrosis and foreign body-type granulomas; diffuse disassociation of hepatocytes caused by edema, dissecting fibrosis and light amyloidosis; and, localized to massive areas of acute dissecting subcapsular and intralobar hemorrhages. Acute and chronic-active splenic lesions were similar in character and consisted of marked lymphoid depletion, deposition of eosinophilic material around arterioles and in sinusoidal areas. The material was weakly positive for collagen and negative for fibrin and it contained small amounts of reticulin and amyloid. No microbiologic agent was consistently demonstrated utilizing aerobic, anaerobic and campylobacter culture techniques, direct EM and histologic stains for bacteria, spirochetes and fungi. By negative staining EM, indistinct 30-40 nm viral-type particles, apparently coated with immunoglobulin, were in the bile of some birds. Attempts to isolate a viral agent in embryonating chicken eggs, primary chicken embryo liver cell cultures and SPF and commercial chickens have not been successful. Toxciologic analyses of liver (n=6) for heavy metals (As, Mo, Zn, Pb, Cd, Fe, Cu), organophosphates, carbamates and organochlorines and of feed (n=1) for aflatoxins (B, B1, G, G1), trichothecenes (T2 and DAS) and methionine were uniformly negative. Analysis of liver from affected (n=6) and non-affected chickens (n=3) for selenium and vitamin E concentrations revealed no significant findings.
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