Acinetobacter baumannii is a nosocomial species frequently isolated from the traumatic wounds of injured military personnel and increasingly detected in civilian healthcare facilities. Many clinical isolates of A. baumannii are drug resistant, so new treatments are needed for infections. Recently, the ability of strains of conspecific bacteria to inhibit the growth of other strains has been observed in increasing numbers of species. We previously reported on intraspecific semisolid-phase growth inhibition (antagonism) among 94 clinical isolates of A. baumannii. These antagonistic interactions may be the result of genetically-encoded molecules, so more closely related isolates would be expected to produce similar patterns of interactions caused by identically active gene products. However, the phylogeny of clinical A. baumannii below the species level has not been established for this set of isolates.In this study, we used Phylomark to identify three genetic loci that recapitulated a whole-genome phylogeny of published A. baumannii genomes and we created a parsimony-based phylogeny from the 1.2 kilobase concatenated sequences. One clade appeared to exhibit the highest incidence of antagonistic interactions against all other isolates screened, except for itself and one relatively distant clade. This clade's nearest neighbor was susceptible to the most consistent antagonistic activity by the first clade; both of these clades appear to belong to MLST ST1 with reference strain AYE. Other isolates with high rates of antagonistic activity fall outside of ST1. Future studies aim to elucidate the genetic basis of the antagonism phenotype in clinical Acinetobacter, particularly in the most antagonistic isolates. The next step will be to mine these interactions to identify expressed antimicrobial molecules with potential for drug therapy
