RESUMEN
Our prior research demonstrated a 20% to 25% reduction in bacterial chondronecrosis with osteomyelitis (BCO) lameness in broilers with organic Zn, Mn, and Cu (Availa® ZMC) supplementation. Expanding on this, we investigated the optimal timing for Availa® ZMC feeding to mitigate BCO lameness and reduce feed additive costs in the poultry industry. In this study, we compared the application of 0.15% Availa® ZMC for 56 days, the first 28 days, and the last 28 days. The experimental design was a randomized block design involving 1560 one-day-old chicks distributed across two wire-floor pens as BCO source infection and four treatment groups with six replicates. The source of BCO infection exhibited a cumulative lameness incidence of 83%, whereas the negative control group showed a 77% cumulative incidence of lameness (p = 0.125). Administering 0.15% of Availa® ZMC during the initial 28 d resulted in a 41.3% reduction in BCO incidence, significantly different from the supplementation during the last 28 d (p < 0.05). However, this reduction did not differ substantially (p > 0.05) from the 56d application period. Hence, administering 0.15% Availa® ZMC during the first four weeks emerges as the optimal timing protocol, providing a defense against lameness comparable to the continuous supplementation throughout the complete production duration. Implementing this feeding approach reduces the cost of feed additive, promotes the health of skeletal bones, and effectively protects against BCO lameness in broilers, offering a valuable consideration for producers seeking optimal outcomes in the poultry industry.
RESUMEN
Bacterial chondronecrosis with osteomyelitis (BCO) lameness is a bone disease characterized by the translocation of bacteria from the gastrointestinal tract, which colonize microfractures in broiler leg bones caused by rapid animal growth rate and weight gain, resulting in lameness. As such, BCO lameness represents a significant challenge for the poultry industry. This study aims to evaluate the effect of spraying broiler chicks on d0 at hatch with an Enterococcus faecium probiotic on the incidence of BCO-induced lameness, utilizing a Staphylococcus aureus challenge model. There were four treatments: (1) negative control (no probiotic + no challenge, NC); (2) positive control (no probiotic + challenge, PC); (3) low dosage (4.0 × 108 CFU/chick + challenge, LOW); and (4) high dosage (2.0 × 109 CFU/chick + challenge, HIGH). On d5, groups two through four were challenged with Staphylococcus aureus through the drinking water at a concentration of 1.0 × 105 CFU/mL. Cumulative lameness incidence was determined through daily evaluations and necropsies conducted on lame birds starting from d22. Data were subjected to a binomial general regression analysis (significant p < 0.05). On d56, the PC group exhibited the highest cumulative lameness incidence (58.0%; p < 0.05), followed by LOW (36.0%), HIGH (28.7%), and NC groups (25.3%), respectively. These results suggest early probiotic application at day-of-hatch successfully reduced the incidence of lameness in challenged birds, thus contributing to understanding of efficient and sustainable broiler production.
RESUMEN
Extensive genomic analyses of Enterococcus cecorum isolates from sepsis outbreaks in broilers suggest a polyphyletic origin, likely arising from core genome mutations rather than gene acquisition. This species is a normal intestinal flora of avian species with particular isolates associated with osteomyelitis. More recently, this species has been associated with sepsis outbreaks affecting broilers during the first 3 weeks post-hatch. Understanding the genetic and management basis of this new phenotype is critical for developing strategies to mitigate this emerging problem. Phylogenomic analyses of 227 genomes suggest that sepsis isolates are polyphyletic and closely related to both commensal and osteomyelitis isolate genomes. Pangenome analyses detect no gene acquisitions that distinguish all the sepsis isolates. Core genome single nucleotide polymorphism analyses have identified a number of mutations, affecting the protein-coding sequences, that are enriched in sepsis isolates. The analysis of the protein substitutions supports the mutational origins of sepsis isolates.
