Lactobacillus rhamnosus JYLR-005 Prevents Thiram-Induced Tibial Dyschondroplasia by Enhancing Bone-Related Growth Performance in Chickens.

Tibial dyschondroplasia (TD) is a leg disorder caused by the abnormal development of the tibia in fast-growing poultry. Lactobacillus rhamnosus (L. rhamnosus) strains have been reported to have effects on increasing bone growth and improving osteoporosis in animals. However, whether L. rhamnosus JYLR-005 can improve bone growth in TD chickens remains unclear. In this study, we noted that L. rhamnosus JYLR-005 could not reduce the suppression of the production performance of TD broilers (p > 0.05) but had a slight protective effect on the broiler survival rate (χ2 = 5.571, p = 0.062). However, for thiram-induced TD broiler chickens, L. rhamnosus JYLR-005 could promote tibia growth by increasing tibia-related parameters, including the tibia weight (day 11, p = 0.040), tibia length (day 15, p = 0.013), and tibia mean diameter (day 15, p = 0.035). Moreover, L. rhamnosus JYLR-005 supplementation improved the normal growth and development of the tibial growth plate by maintaining the morphological structure of the chondrocytes and restored the balance of calcium and phosphorus. Taken together, these findings provide a proof of principle that L. rhamnosus JYLR-005 may represent a therapeutic strategy to treat leg disease in chickens.

The fungicide thiram perturbs gut microbiota community and causes lipid metabolism disorder in chickens.

Fungicide thiram, a representative dithiocarbamate pesticide can cause potential health hazards to humans and animal health due to the residues in various agricultural products. However, the effects of thiram on lipid metabolism by perturbing gut microbiota of chickens are not clear. Our study was aimed to explore the protective of polysaccharide extracted from Morinda officinalis (MOP) on acute thiram-exposed chickens, and to analyze the association between alteration of gut microbiota and lipid metabolism. Three hundred chicks are fed with a normal diet, thiram-treated diet (100 mg/kg), and a thiram-treated diet supplemented with 250, 500, or 1000 mg/kg MOP was used in this study, respectively. The results showed that thiram exposure prominently elevated liver index, changed liver function by histopathological examination and serum biochemistry diagnoses, and increased blood lipid parameters. Meanwhile, the expression level of some key genes in hepatic lipid metabolism dysregulated significantly in the thiram-exposed chickens. Furthermore, 16S rRNA gene sequencing indicated that thiram exposure can significantly alter the richness, diversity, and composition of the broiler fecal microbiota, and the relative abundance of Firmicutes and Proteobacteria was also affected at the phylum level. In addition, some microbial populations including Lactobacillus, Ruminococcus, Oscillospira, Blautia, and Butyricicoccus significantly decreased at the genus level, whereas the Klebsiella was opposite. Correlation analysis further revealed a significant association between microorganisms and lipid metabolism-related parameters. Optimistically, 500 mg/kg MOP can alleviate the damage of thiram in the gut and liver. Together, these data suggest that thiram exposure causes the imbalance of the gut microbiota and hepatic lipid metabolism disorder in chickens.

The role of blood vessels in broiler chickens with tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is an intractable tibiotarsal bone disorder of rapid growing avian species, which leads to huge economic losses and compromised poultry welfare. However, the exact pathogenesis and treatment of TD remain largely unknown. Based on continuous research findings, we propose the TD pathogenesis hypothesis: during skeletal development of TD chickens, due to the absence of vasculature of proximal tibial growth plates (TGP), hypertrophic chondrocytes of the TGP are unable to complete calcification in normal bone development and less dead chondrocytes in the corresponding area can be timely transported through the blood vessels. Moreover, recent studies demonstrate that the TD formation mechanism gradually tends to a large number of dead chondrocytes in the TGP region or apoptosis occur due to various factors (such as, reduction of vascular invasion and blood cells, and increased weight or mechanical force of the tibia), while the reduction of blood vessels is insufficient to remove these chondrocytes and eventually leads to the TD formation. Recognizing the possible role of the blood vessels in the incidence of TD and can propose that the improvement in vasculature might be a novel therapeutic approach for ending TD in chickens.