Clinical and Histopathological Observations of Turkey Hepatic Lipidosis in the Ain Touta Area (Algeria): A Preliminary Report

Alloui, N.; Bouhentala, Salaheddine; Lanani, Ismahene; Benoune, Omar; Ayachi, Ammar

doi:10.3923/ajas.2015.167.171

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“…Usually in fattening turkey flocks, the disease occurs suddenly at an age of between 12 and 16 wk, lasting about 7 D with mortality rates of up to 15% (Gazdzinski et al, 1994). The affected animals show clinical characteristics of dyspnea, nonchalance, and prostration (Alloui et al, 2015). Increased beta-hydroxybutyrate levels were measured in the blood of animals with HL, which could suggest enhanced lipolysis due to a fasting period and a negative energy balance (Weier, 2016).…”

Section: Introductionmentioning

confidence: 99%

Amino acid pattern in the liver and blood of fattening turkeys suffering from hepatic lipidosis

Middendorf

Radko²,

Düngelhoef

et al. 2019

Poultry Science

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Hepatic lipidosis (HL) is a well-known disease in fattening and in parent turkey flocks. Among others, dietary effects like (a lack of) essential amino acids (AA) as lipotrophic factors (e.g., methionine) have been considered as potentially predispositing for HL. Several studies have reported abnormal AA profiles in hepatic diseases of humans and other livestock. The ratio of branched-chain amino acids (BCAA) to aromatic amino acids (AAA) in plasma is used to predict hepatic cirrhosis. In this study, the state of supply of AA was investigated by comparing non-affected (NA) animals and those affected by HL. The AA pattern in the liver and blood can provide potential indications of pathogenesis of HL. In cooperation with German poultry veterinarians, 3 cases of HL on 3 different fattening turkey farms were visited (13/14 wk old, “B.U.T. Big 6” and “TP7”). Overall, 73 birds were examined, of which 42 birds suffered from HL and 31 were not affected. Feeding samples of the respective actual feed were taken and analyzed. The selection of animals was carried out (NA randomly) by clinical signs such as apathy and dyspnea and the diagnosis was made at necropsy, which could be confirmed by crude fat content in liver tissue (HL: 309, NA: 155). In liver tissue, the CP and AA contents were lower among animals with HL than among NA ( P < 0.05). In blood samples, the sum of AA, ammonia, and urea was more than 3 times higher among animals with HL (431 mg/dL serum) than among NA (114 mg/dL serum; P < 0.01). The ratio of BCAA to AAA was also significantly different between the groups (HL: 0.85, NA: 1.42; P < 0.05). In the case of HL, entire herds were not affected and the “non-affected” ones were comparable with healthy slaughtered animals. There seems to be a clear change in protein and AA metabolism of HL animals, which could lead to an optimization in feeding practice in repeated cases of HL.

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Section: Introductionmentioning

confidence: 99%