BackgroundThe so-called “hepatic lipidosis” in turkeys is an acute progressive disease associated with a high mortality rate in a very short time. Dead animals show a massive fatty degeneration of the liver. The cause is still unclear. Previous findings suggest that there may be parallels to human non-alcoholic fatty liver disease. The object of the study was to examine the changes in the fat contents, the fatty acid composition and the iron content in livers of animals, which have died from hepatic lipidosis.MethodsThe conspicuous livers (n = 85) were collected from 20 flocks where the phenomenon of massive increased animal losses accompanied by marked macroscopically visible pathological liver steatosis suddenly occurred. For comparison and as a reference, livers (n = 16) of two healthy flocks were taken. Healthy and diseased flocks were fed identical diets concerning official nutrient recommendations and were operating under standardized, comparable conventional conditions.ResultsCompared to livers of healthy animals, in the livers of turkeys died from hepatic lipidosis there were found massively increased fat levels (130 ± 33.2 vs. 324 ± 101 g/kg dry matter-DM). In all fatty livers, different fatty acids concentrations were present in significantly increased concentrations compared to controls (palmitic acid: 104 g/kg DM, +345%; palmitoleic acid: 18.0 g/kg DM, + 570%; oleic acid: 115 g/kg DM, +437%). Fatty acids concentrations relevant for liver metabolism and inflammation were significantly reduced (arachidonic acid: 2.92 g/kg DM, −66.6%; eicosapentaenoic acid: 0.141 g/kg DM, −78.3%; docosahexaenoic acid: 0.227 g/kg DM, −90.4%). The ratio of certain fatty acids to one another between control and case livers changed analogously to liver diseases in humans (e.g.: C18:0/C16:0 – 0.913 against 0.311; C16:1n7/C16:0 – 0.090 against 0.165; C18:1/C18:0 – 0.938 against 4.03). The iron content in the liver tissue also increased massively (271 ± 51.5 vs 712 ± 214 mg/kg DM).ConclusionThe hepatic lipidosis has a massive impact on the lipid content, the lipid composition and the iron content in the liver. The character of the metabolic disorder includes parallels to the non-alcoholic steatohepatitis in humans.
Background The conventional farrowing crate is criticised due to the limited mobility of sows during farrowing and lactation. The present study aims to investigate the effects of three different farrowing systems on the performance of suckling neonates on the basis of immunocrit (IC; a quantification of immunoglobulins), serum amino acid (AA) concentrations and growth performance. Methods From a total of 149 sows placed in three housing systems (farrowing crate – FC, loose housing – LH, group housing – GH), 18 sows and their respective litters, formed the basis for a two-factorial study design (farrowing system and body weight (BW) of neonates). Therefore, also blood samples of two light (1.0–1.4 kg) and two heavy (≥ 1.4 kg) piglets were taken within 48 h post natum (p.n.) and on the day of weaning (day 26) to determine the immunocrit (IC; a quantification of immunoglobulins) and levels of serum AAs. Results The IC (FC: 0.148 a , LH: 0.153 a , GH: 0.117 b ) as well as serum levels of arginine, leucine, lysine, proline and threonine within 48 h p.n. were significantly lower in GH. Additionally, in general, these piglets showed (except for the first week of life) the lowest average daily weight gain. On the day of weaning, piglets in GH had the lowest levels of arginine (in mg/dL; FC: 3.68 a , LH: 3.40 ab , GH: 2.94 b ) and threonine (in mg/dL; FC: 3.59 a , LH: 3.02 ab , GH: 2.49 b ). The concentrations of leucine, lysine, proline and valine at this time were significantly lower in LH. Conclusion The observed significant lower IC indicates a lower Ig intake of piglets in the tested GH. No significant differences regarding the IC and AA levels within 48 h p.n. of the piglets in FC and LH could be seen. In principle, differences at weaning in AA levels were rather small, although the body weight of GH piglets at weaning was lower. Therefore, further research needs to clarify whether there are medium-term effects on health and performance. Electronic supplementary material The online version of this article (10.1186/s40813-019-0121-1) contains supplementary material, which is available to authorized users.
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.
The hepatic lipidosis (HL) in fattening turkeys is a disease has been known for a long time, but the cause and pathogenesis is still not clarified. A recent study reported unexplained high levels of iron in liver tissue of fattening turkeys suffering from HL.In this study, the iron status, possible infectious or inflammatory influences in form of an acute phase reaction and the analysis of fatty acid pattern in liver tissue of turkeys affected by HL were examined. Three cases of HL on three different fattening turkey farms were investigated during the outbreak of the disease. Clinically affected and non-affected animals were subjected to a pathological examination, where the diagnosis HL or non-affected was made. In total, 70 birds were examined (40 with HL, 30 without HL) and blood and liver samples were taken. Additionally, samples from 15 slaughtered birds were taken as a further control group. In liver tissue, the iron content and the content of long-chain fatty acids were determined; in blood samples, ferritin and transferrin were measured. The iron content in liver tissue was more than three times higher for animals with HL than among non-affected animals and the control group. The transferrin levels were lowest for animals with HL, highest in the control group and in between for non-affected animals. The fatty acid pattern in liver tissue of affected animals indicated a shift from polyunsaturated fatty acids to saturated fatty acids and monounsaturated fatty acids compared to the control group and the non-affected animals. Overall, the non-affected animals of a flock affected by HL were similar to the healthy animals of the abattoir. The low acute phase protein levels for animals with HL together with high iron contents could indicate a previous malnutrition/starvation period and/or severe liver damage for those animals suffering from HL.
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