Abstract

Acinetobacter spp. are non-fermentative, strictly aerobic, Gram-negative microorganisms with a confusing taxonomic history. The Acinetobacter baumannii–Acinetobacter calcoaceticus complex is the species most commonly isolated from clinical specimens. It is ubiquitous in nature and has been found as part of the normal skin, throat and rectal flora as well as in food and body lice. It colonises patients in Intensive Care Units and contaminates inanimate hospital surfaces and devices as well as wounds, including war injuries. Although a frequent coloniser, Acinetobacter can be the cause of severe and sometimes lethal infections, mostly of nosocomial origin, predominantly ventilator-associated pneumonia. Bacteraemic infections are rare but may evolve to septic shock. Acinetobacter also emerges as a cause of nosocomial outbreaks and is characterised by increasing antimicrobial multiresistance. Antibiotic use, especially carbapenems and third-generation cephalosporins, is recognised as the most important risk factor for multiresistance. Described resistance mechanisms include hydrolysis by β-lactamases, alterations in outer membrane proteins and penicillin-binding proteins, and increased activity of efflux pumps. Today, Acinetobacter resistant to carbapenems, aminoglycosides and fluoroquinolones presents a challenge to the clinician. However, sulbactam, tigecycline and colistin represent the current therapeutic approaches, which are associated with satisfactory efficacy.

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