Members of the genus Acinetobacter are oxidase negative, aerobic Gram-negative coccobacilli, which have evolved taxonomically from former strains of the Mima-Herrelia group. Their natural habitat is human skin and mucous membranes, water, soil, vegetation, and sewage. The most common multiresistant nosocomial pathogen among 19 genospecies is the A. calcoaceticus-baumannii complex ( A. baumannii). This species is not a common component of normal human acinetobacter colonization, and its ecological origin remains unknown. Outbreaks of nosocomial acinetobacter infection are due to spread of one or a few clones among patients, personnel, and the inanimate hospital environment. Thus, strict implementation of infection control procedures is the major technique for prevention and suppression of such outbreaks. Surveillance cultures of personnel and the environment; molecular genotyping of isolates; cohorting of colonized or infected patients and staff; and topical application of polymyxin B to colonized wounds have been used to enhance standard infection control procedures. Antimicrobial resistance to beta lactam antibiotics in Acinetobacter is due primarily to a combination of chromosomal beta lactamase production and reduced outer membrane permeability. Carbapenem resistance is an increasing phenomenon and restriction of late-generation cephalosporin and carbapenem utilization should be considered in outbreak control. Effective therapy of multiresistant Acinetobacter infection may require a variety of potentially synergistic antibiotic combinations.