Lameness disease attributed to bacterial chondronecrosis with osteomyelitis in broilers affects production, animal welfare, and food safety in the poultry industry. The disease is characterized by necrotic degeneration of the rapidly growing femora and tibiae due to bacterial translocation from the respiratory or gastrointestinal tracts into the blood circulation, eventually colonizing the growth plate of the long bones. To investigate the etiology, pathogenesis, and intervention measures for BCO, developing an experimental model that reliably induces BCO lameness is of the utmost importance. In the past, we have employed a wire-flooring model and a litter-flooring model administered with a bacterial challenge to investigate strategies for mitigating BCO. However, multiple issues on labor-intensive barn setup and cleanout efforts for the wire-flooring system and concern of direct pathogenic exposure to the broilers for the litter-flooring models rendered these research models less effective. Thus, we investigated a new approach to induce experimental BCO lameness using an aerosol transmission model employing a group of birds reared on wire-flooring pens as a BCO infection source, and the disease is further disseminated through the airborne transmission to other birds reared on litter flooring in the same housing environment. The effectiveness of the aerosol transmission model in inducing BCO lameness was concluded from 4 independent experiments. The cumulative lameness generated from the BCO source group on the wire floors versus negative control treatments on the litter floors from Experiments 1, 2, 3, and 4 were 84% vs. 69.33%, P = 0.09; 54.55% vs. 60%, P = 0.56; 78% vs. 73.50%, P = 0.64; 81% vs. 74.50%, P = 0.11. Overall, the cumulative lameness generated from the wire floors was successfully transmitted to the birds on litter floors without significant statistical differences (P > 0.05). The effectiveness of the aerosol transmission model for experimentally triggering BCO lameness provides a reliable system for evaluating practical intervention strategies for BCO lameness in broilers.

DNA extraction for downstream molecular diagnostic applications can be an expensive, time-consuming process. We devised a method to quickly extract total bacterial DNA from environmental samples based on the sodium hydroxide lysis of cells with or without capture by magnetic beads for subsequent PCR or quantitative PCR. The final DNA extraction method using NaOH is extremely low-cost and can be completed in as little as 10 min at room temperature with dilution, or the DNA can be further purified using silica-coated paramagnetic beads. NaOH extraction was effective for Gram-negative and Gram-positive bacteria in samples from air, soil, sewage, food, laboratory surfaces, and chicken cloacal swabs. The NaOH extraction method was comparable to commercial kits for extraction of DNA from pig fecal samples for 16S amplicon sequencing analyses. We demonstrated that an impinger and portable pump can efficiently capture bacteria from the air in poultry facilities for rapid NaOH extraction to quantify total bacteria and for detection of specific species using qPCR. The air sampling and NaOH extraction procedures are well suited for routine, high-throughput screening and for metagenomic analyses for specific pathogens, even in resource-limited situations.

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.

Bacterial chondronecrosis with osteomyelitis (BCO) lameness is the most critical animal health and welfare issue facing the broiler industry worldwide. It is estimated that 1 to 2% of bird condemnation at marketing age is caused by BCO lameness, resulting in tens of millions of dollars in annual losses. Fast-growing broilers are prone to mechanical stress that triggers bacterial translocation across epithelial barriers into the bloodstream, followed by bacterial colonization in the growth plate of long bones, and eventually, bone necrosis and lameness. Mycotoxins (MTX) are secondary metabolites produced naturally by microfungi, of which deoxynivalenol (DON), fumonisin (FUM), and zearalenone are the most prevalent in corn and soybean-meal-based diets. The presence of these mycotoxins in feed has been proven to reduce the barrier strength of the intestinal tracts and trigger immunosuppressive effects. In this study, we investigated the effects of the DON and FUM-contaminated feeds on the incidence of BCO lameness in broilers reared in both wire- and litter-floors. 720 one-day-old broiler chicks were assigned to the 2 × 2 factorial design: 2 MTX diets containing DON and FUM on wire flooring (MTX-W) and litter flooring (MTX-L), and 2 diets without MTX contamination on control wire flooring (CW) and control litter flooring (CL). Throughout the trial, the cumulative incidence of lameness per treatment was assessed by necropsying the lame birds. Birds in the MTX-W group had a higher incidence of lameness compared to those in CW (73.3% vs. 62.0%) (P < 0.05), and birds in the MTX-L group had a higher incidence of lameness compared to birds in CL (54.0% vs. 34.0%) (P < 0.05). MTX elicited net increases in BCO to a greater degree on litter (+20%) than on wire flooring (+12%). The increased incidence of BCO lameness in the MTX-W coincided with increased intestinal permeability supporting a correlation between intestinal barrier integrity and BCO lameness. To conclude, DON and FUM are predisposing factors for increasing BCO. However, no significant interaction exists between the diet and floor types in inducing lameness in broilers.

The exponential increase in global population continues to present an ongoing challenge for livestock producers worldwide to consistently provide a safe, high-quality, and affordable source of protein for consumers. In the last 50 years, the poultry industry has spearheaded this effort thanks to focused genetic and genomic selection for feed-efficient, high-yielding broilers. However, such intense selection for productive traits, along with conventional industry farming practices, has also presented the industry with a myriad of serious issues that negatively impacted animal health, welfare, and productivity–such as woody breast and virulent diseases commonly associated with poultry farming. Bacterial chondronecrosis with osteomyelitis (BCO) lameness is one such issue, having rapidly become a key issue affecting the poultry industry with serious impacts on broiler welfare, meat quality, production, food safety, and economic losses since its discovery in 1972. This review focuses on hallmark clinical symptoms, diagnosis, etiology, and impact of BCO lameness on key issues facing the poultry industry.

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.