Abstract

Acinetobacter baumannii is a globally important nosocomial pathogen associated with clinical infections that are difficult to treat due to broad antimicrobial resistance. A. baumannii epidemics are caused by a limited number of strains worldwide, belonging to the initially named European clones, but now regarded to as International clonal lineages (IC) I, II and III and a few additional lineages recently emerged as epidemic clones in some regions, such as the sequence types (ST)10, ST15, ST25, ST78 and ST79 according to Pasteur’s multilocus sequencing typing (MLST) scheme. The spread of extensively drug-resistant (XDR) gram-negative bacteria has boosted colistin use, with a resultant selection of colistin-resistant, often pandrug-resistant strains. In addition to extensively antimicrobial resistance, A. baumannii strains responsible for epidemics show elevated resistance to desiccation, high biofilm-forming capacity on abiotic surfaces and adherence to host epithelial cells, virulence-related features which might have favored the spread and persistence in the hospital environment.As in other microrganisms, the formation of biofilm in A. baumannii is a redundantly organized, multifactorial process involving multiple cellular components.The above data suggest that multiple proteins sharing Ig-like repeats contribute to biofilm formation in Acinetobacter species.

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