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. 2015 Oct;79(4):261-7.

Association of increased rate of condemnation of broiler carcasses due to hepatic abnormalities with immunosuppressive diseases in the broiler chicken industry in Saskatchewan

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Association of increased rate of condemnation of broiler carcasses due to hepatic abnormalities with immunosuppressive diseases in the broiler chicken industry in Saskatchewan

Keyvan Amini et al. Can J Vet Res. 2015 Oct.

Abstract

The objective of this study was to identify the causative agents of hepatitis observed in broiler chickens at processing. Livers of chickens from 16 broiler farms in Saskatchewan with gross lesions of hepatitis were collected at processing. In addition to routine bacterial isolation and histopathological examination, serologic studies for infectious bursal disease virus (IBDV) and Chicken anaemia virus (CAV), calculation of the ratio of the weight of the bursa of Fabricius (BF) to body weight (BBW), and histopathological examination of the BF were done. Of the 264 livers with gross lesions, 83% had multifocal to coalescing necrotizing hepatitis, 16% had perihepatitis, and 1% had hemorrhages. No definitive causative microorganisms were isolated from the hepatic lesions; however, no significant bacterial isolations were made. Bursal atrophy, low BBW ratio, and high titer of antibody against IBDV each correlated with the rate of total condemnations (P = 0.0188, P = 0.0001, and P = 0.0073, respectively). Nucleotide sequencing of IBDV isolated from the BF identified the variant strains Delaware-E and 586. Condemnation because of hepatic lesions was correlated with titer of antibody against IBDV and BBW (P = 0.016 and P = 0.027). The results of this study demonstrate that hepatic lesions in Saskatchewan chickens are not currently caused by a primary bacterial pathogen but are associated with indicators of immunosuppression that is likely due to variant IBDV.

L’objectif de la présente étude était d’identifier les agents causals de l’hépatite observée chez des poulets à griller au moment de la transformation. Les foies de poulets provenant de 16 fermes de poulets à griller en Saskatchewan avec des lésions macroscopiques d’hépatite furent prélevés. En plus de l’isolement bactérien de routine et de l’examen histopathologique, on effectua des analyses sérologiques pour le virus de la bursite infectieuse aviaire (VBIA) et le virus de l’anémie du poulet (VAP), le calcul du ratio du poids de la bourse de Fabricius (BF) sur le poids corporel (BPC), et l’examen histopathologique de la BF. Sur les 264 foies ayant des lésions macroscopiques, 83 % avaient des lésions multifocales à coalescentes d’hépatite nécrosante, 16 % de la péri-hépatite et 1 % des hémorragies. Aucun agent causal définitif ne fut isolé des lésions hépatiques; toutefois, aucun agent bactérien significatif ne fut isolé. Une atrophie de la bourse, un faible ratio BPC, et un titre élevé d’anticorps dirigé contre VBIA corrélaient tous avec le taux de condamnation totale (P = 0,0188, P = 0,0001, et P = 0,0073, respectivement). Le séquençage nucléotidique des VBIA isolés des BF identifia les souches variantes Delaware-E et 586. La condamnation due aux lésions hépatiques était corrélée avec le titre d’anticorps contre VBIA et le BPC (P = 0,016 et P = 0,027, respectivement). Les résultats de la présente étude démontrent que les lésions hépatiques chez les poulets de la Saskatchewan ne sont pas actuellement causées par un agent bactérien pathogène primaire mais sont associées à des indicateurs d’immunosuppression qui est probablement causée par un variant de VBIA.(Traduit par Docteur Serge Messier).

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Figures

Figure 1
Figure 1
Histopathological appearance of bursa of Fabricius (BF). A — normal follicles. B — mild bursal atrophy: atrophy of some follicles. C — moderate bursal atrophy: small lymphoid follicles and prominent interfollicular architecture. D — severe bursal atrophy: severe, diffuse loss of follicles. E — severe bursal atrophy: widespread depletion of lymphocytes in follicles. F — severe bursal atrophy: prominent follicular epithelium. Hematoxylin and eosin (H&E) staining. A to D — original magnification × 2. E and F — original magnification × 10.
Figure 2
Figure 2
Macroscopic and microscopic appearance of livers condemned at processing. A — mild acute hepatitis, with multifocal yellowish to white necrotic areas 2 to 4 mm in diameter. B — subacute moderate hepatitis, with multifocal to locally extensive spots of the same size. C — severe chronic hepatitis, with locally extensive to diffuse spots of the same size. D — locally extensive moderate to severe chronic perihepatitis. E — multifocal necrotic centers of C; original magnification × 4. F — higher magnification of E; necrotic focus containing cell debris surrounded by macrophages and giant cells, with expansion of extramedullary granulopoiesis (arrow); original magnification × 10. G — higher magnification of an area with expansion of extramedullary granulopoiesis in a liver with hepatitis; original magnification × 40. H — higher magnification of an area with expansion of extramedullary granulopoiesis in a liver with perihepatitis; original magnification × 40. H&E staining.

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