Acinetobacter baumannii has emerged to become a predominant cause of nosocomial infections in the United States and across the globe. During the past decade, the remarkable increase in the proportion of A. baumannii strains that are carbapenem resistant has ushered in an era of far more lethal infections. In a recent study of 13,796 patients in 1,265 ICUs from 75 countries, A. baumannii was one of only two of 19 organisms studied that were strongly linked to increased hospital mortality by multivariate analysis (1). Patients with bacteremia or ventilator-associated pneumonia due to Carbapenem resistant have more than 50% to 60% mortality rates (2–5). These mortality rates result from the very high frequency with which empiric therapy (e.g., with carbapenems) is inactive against Carbapenem resistant (3–5) and the limited suboptimal definitive therapy (e.g., colistin and tigecycline) available.

Given their very poor outcomes and the lack of new drugs in development to treat these infections, understanding how A. baumannii is transmitted to patients is of critical importance to enable development of new prophylactic strategies. In the last few years, hospital environmental surfaces have been increasingly recognized as important reservoirs for pathogens (6, 7), and A. baumannii is a particularly hardy environmental organism. Indeed, when A. baumannii was inoculated into a plastic bottle with no added nutrients and the liquid was allowed to evaporate, the organism remained viable at detectable culture densities on the dry bottle surface for almost a year (8).

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