No abstract

Fusarium mycotoxins (FUS) occur frequently in poultry diets, and regulatory limits are laid down in several countries. However, the limits were established for exposure to a single mycotoxin, whereas multiple contamination is more realistic, and different studies have demonstrated that it is not possible to predict interactions between mycotoxins. The purpose of this study was thus to compare the toxic effect of deoxynivalenol (DON), fumonisins (FB) and zearalenone (ZON), alone and in combination on broiler chickens, at the maximum tolerated level established by the EU for poultry feed. Experimental corn-soybean diets incorporated ground cultured toxigenic Fusarium strains. One feed was formulated for chickens 0 to 10 days old and another for chickens 11 to 35 days old. The control diets were mycotoxin free, the DON diets contained 5 mg DON/kg, the FB diet contained 20 mg FB1 + FB2/kg, and the ZON diet contained 0.5mg ZON/kg. The DONFBZON diet contained 5, 20, and 0.5 mg/kg of DON, FB1 + FB2, and ZON, respectively. Diets were distributed ad libitum to 70 broilers (male Ross PM3) separated into five groups of 14 chickens each reared in individual cages from one to 35 days of age. On day 35, after a starvation period of 8 h, a blood sample was collected, and all the animals were killed and autopsied. No difference between groups that could be attributed to FUS was observed in performances, the relative weight of organs, biochemistry, histopathology, intestinal morphometry, variables of oxidative damage, and markers of testicle toxicity. A significant increase in sphinganine and in the sphinganine to sphingosine ratio was observed in broilers fed FB. Taken together, these results suggest that the regulatory guidelines established for single contamination of broiler chickens fed with DON, FB, and ZON can also be used in the case of multiple contamination with these toxins.

1. Footpad dermatitis (FPD) is a recognised welfare problem in broiler chickens. Broiler feet (n = 54) were examined macroscopically and microscopically to determine a reliable correspondence between macroscopic and histological features, and to devise a scoring system that was relevant to bird welfare and easy to use at processing plants. 2. Three types of footpad lesion were defined based on their severity. Type I were mild lesions, visually characterised by scale enlargement and erythema, and histologically by hyperplasia and hyperkeratosis of the epidermis, superficial dermal congestion and oedema. Type II were moderate, superficial lesions, visually characterised by hypertrophic and hyperkeratotic scales covered with yellowish to brownish exudate, and histologically by a prominent pustular and crust-forming dermatitis. Type III lesions were the most pronounced, visually characterised by a thick dark adherent crust, and histologically by extensive ulceration. 3. On the basis of the severity and extent of these three types of lesions, a 5-point scale was devised, i.e. no or type I lesion (score 1), type II lesion (<50% or >50% of footpad, scores 2 and 3 respectively) and type III lesion (<50% or >50% of footpad, scores 4 and 5 respectively). 4. The scoring system has the advantage of making sense in terms of welfare compared with previous schemes. Furthermore, it is histologically validated and easy to use for the routine assessment of broiler welfare in processing plants.

Neuropathies are neurodegenerative diseases affecting humans and other mammals. Many genetic causes have been identified so far, including mutations of genes encoding proteins involved in mitochondrial dynamics. Recently, the “Turning calves syndrome”, a novel sensorimotor polyneuropathy was described in the French Rouge-des-Prés cattle breed. In the present study, we determined that this hereditary disease resulted from a single nucleotide substitution in SLC25A46, a gene encoding a protein of the mitochondrial carrier family. This mutation caused an apparent damaging amino-acid substitution. To better understand the function of this protein, we knocked out the Slc25a46 gene in a mouse model. This alteration affected not only the nervous system but also altered general metabolism, resulting in premature mortality. Based on optic microscopy examination, electron microscopy and on biochemical, metabolic and proteomic analyses, we showed that the Slc25a46 disruption caused a fusion/fission imbalance and an abnormal mitochondrial architecture that disturbed mitochondrial metabolism. These data extended the range of phenotypes associated with Slc25a46 dysfunction. Moreover, this Slc25a46 knock-out mouse model should be useful to further elucidate the role of SLC25A46 in mitochondrial dynamics.