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Acinetobacter baumannii is an important opportunistic pathogen that causes several healthcare-associated infections that have high rates of morbidity and mortality in hospital settings, particularly in intensive care units [1]. Treatment of infections caused by A. baumannii has become increasingly limited due to the emergence of multidrug-resistant isolates, including resistance to carbapenems, leaving polymyxins as the last therapeutic resource. Although the standard antimicrobial scheme against A. baumannii infections has not been fully established, evidence supports the fact that combination therapies including polymyxin B are more effective than polymyxin B monotherapies. Moreover, polymyxin B combined with a second antimicrobial agent was able to reduce hospital mortality rates, and has been widely recommended due to resistance emerging in some A. baumannii strains during treatments [2–4]. Nevertheless, antimicrobial therapy failure has been reported, especially in recalcitrance of chronic infections, which may be due to the tolerance mediated by persister cells [5, 6] – a microbial subpopulation able to survive to normally lethal concentrations of bactericidal antimicrobials [7], as has been previously described in Acinetobacter spp. exposed to polymyxin B [8]. This tolerance appears to be a transient phenotype that may be understood as arising from a combination of epigenetic inheritance and cellular noise [9], whose regulation involves a multiplicity of pathways [10]. Thus, eradication of persister cells is unusually challenging, and, to the best of our knowledge, the influence of combined therapy has not been investigated in A. baumannii persister cells. In this context, we evaluated the effect of polymyxin B and meropenem in combination to eradicate the persister cells produced by clinical A. baumannii strains.

Combination of polymyxin B and meropenem eradicates persister cells from Acinetobacter baumannii strains in exponential growth