Survey of bacteria associated with septic arthritis in beef feedlot cattle

Septic arthritis (SA) is a cause of lameness in cattle attributed to bacterial infections. <i>Mycoplasmopsis bovis</i> is the best known and characterized etiological agent of SA; however, cases caused by diverse bacteria have been reported. Accordingly, we surveyed bacteria associated with septic and healthy joints from animals in western Canadian feedlots. Microbial community profiling showed that <i>M. bovis</i> was the most frequently detected pathogen in septic joints, followed by <i>Metamycoplasma alkalescens</i> and <i>Trueperella pyogenes</i>. In most cases, disease was ostensibly caused by a single pathogen, though polymicrobial infections and complex communities were also observed in DNA isolated from septic joints. The application of enhanced metagenomics by target DNA hybridization capture sequencing (CapSeq) provided more robust pathogen detection and characterization. CapSeq revealed resistance determinants that escaped detection using a conventional shotgun metagenomic approach. Notably, a series of nucleotide polymorphisms to <i>M. bovis rrs</i>, <i>rrl</i>, <i>gyrA</i>, and <i>parC</i> gene sequences were observed that confer resistance to macrolides and oxytetracycline-resistant <i>T. pyogenes</i> were also apparent in the CapSeq data. Complementary pathogen isolation, whole-genome sequencing, and phenotyping efforts were focused on the two most prominent pathogens, <i>M. bovis</i> and <i>M. alkalescens</i>, and corroborated metagenomic data sets.IMPORTANCEInformed antimicrobial use for the treatment of septic arthritis (SA) has been limited by overlooking the potential diversity of causative agents and our knowledge of their antimicrobial resistance (AMR) profiles. This survey begins to provide epidemiological insights, offering renewed appreciation of <i>Metamycoplasma alkalescens</i> as an etiological agent of SA and highlighting the prominence of important AMR determinants. Finally, the survey suggests that our knowledge of even the identities of the causative agents of SA is incomplete.