Gram-Negative Bacteria Holding Together in a Biofilm: The Acinetobacter baumannii Way

Abstract

Bacterial biofilms are a serious public-health problem worldwide. In recent years, the rates of antibiotic-resistant Gram-negative bacteria associated with biofilm-forming activity have increased worrisomely, particularly among healthcare-associated pathogens. Acinetobacter baumannii is a critically opportunistic pathogen, due to the high rates of antibiotic resistant strains causing healthcare-acquired infections (HAIs). The clinical isolates of A. baumannii can form biofilms on both biotic and abiotic surfaces; hospital settings and medical devices are the ideal environments for A. baumannii biofilms, thereby representing the main source of patient infections. However, the paucity of therapeutic options poses major concerns for human health infections caused by A. baumannii strains. The increasing number of multidrug-resistant A. baumannii biofilm-forming isolates in association with the limited number of biofilm-eradicating treatments intensify the need for effective antibiofilm approaches. This review discusses the mechanisms used by this opportunistic pathogen to form biofilms, describes their clinical impact, and summarizes the current and emerging treatment options available, both to prevent their formation and to disrupt preformed A. baumannii biofilms.

Keywords: Acinetobacter baumannii; biofilm; multidrug-resistant; prevention; treatment.

Figure 1

A. baumannii surface structures involved in biofilm formation and maintenance. The picture shows a magnification of A. baumannii forming a biofilm with the bacterial cells embedded in the extracellular polymeric substance. See the text for details. AdeABC, RND efflux pump; Ata, autotransporter; Bap, biofilm-associated protein; BfmRS, two-component system; BlaPER-1, extended-spectrum β-lactamase; CUP, chaperone-usher pili; EPS, extracellular polymeric substance; IM, inner membrane; LPS, lipopolysaccharide; OM, outer membrane; OMPs, outer membrane proteins; OMVs, outer membrane vesicles; PNAG, poly-β-(1-6)-N-acetylglucosamine; T4SS, type IV secretion system; T6SS, type VI secretion system; Tuf, moonlighting protein; Wza-Wzb-Wzc system.