Purulent disease is the main factor that prevents the population increase of forest musk deer in artificial breeding, and especially the intracorporal suppurative lesions in late-stage with complex bacterial communities normally bring more difficulties for veterinary treatment. Although it is well-recognized that Pseudomonas aeruginosa and Escherichia coli are the two main bacterial pathogens which can be frequently co-isolated from the lung pus of forest musk deer, few studies have explored the interspecific relationship and coexistent mechanism of the two species. In this study, we identified a P. aeruginosa strain MYL-2, which harbored a loss-of-function mutation in the central regulator (LasR) of quorum-sensing (QS) system, from the lung pus of a dying forest musk deer with co-infecting E. coli strain MYL-58. Interestingly, P. aeruginosa MYL-2 could coexist with E. coli MYL-58 compared to the dominant role of lasR-intact P. aeruginosa strain MYL-1 in the competitive experiments. The results of in vitro coevolution assay further revealed that the QS-mediated competitive advantage of P. aeruginosa MYL-1 would be decreased along with the enrichment of lasR mutants in the communities, and P. aeruginosa could finally coexist with E. coli by forming a relatively stable equilibrium. Therefore, these findings provide an evolutionary explanation for the coexistence of P. aeruginosa and E. coli in the suppurative lesions of forest musk deer, and may also contribute to further understanding the pathology of animal purulent disease and the development of novel veterinary therapy.
Keywords: Coexistence; Evolution; Forest musk deer; Mutation; Purulent disease; Quorum-sensing.
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