Acinetobacter baumannii has recently emerged as an important Gram

Acinetobacter baumannii has recently emerged as an important Gram-negative pathogen that is reported to account for up to 10% of hospital-acquired

infections and 8.4% of hospital-acquired pneumonia (Hidron et al., 2008; Kallen et al., 2010). The organism’s success as a pathogen can be, in part, attributed to its ability to tolerate desiccation and disinfectants and form biofilms on abiotic surfaces commonly found in healthcare settings (Getchell-White et al., 1989; Musa et al., 1990; Hirai, 1991; Wendt et al., 1997). Colonization of hospital surfaces is thought to provide a reservoir HM781-36B molecular weight for the transmission and subsequent infection of patients with deficient immune systems. Septicemia and pneumonia, which result in mortality rates of approximately 50% (Seifert et al., 1995; Sunenshine et al., 2007), are the two most severe consequences of A. baumannii infection. Therapeutic intervention of A. baumannii infections has been compromised by an

alarming increase in the organism’s resistance to front-line therapies. Indeed, multidrug resistance in Acinetobacter spp. increased from 6.7% in 1993 to 29.9% in 2004, more than twice that observed in any other Gram-negative bacillus causing nosocomial this website intensive care unit infections (Lockhart et al., 2007). Moreover, strains that are resistant to all currently available antibiotics have been isolated from patients both in the United States and abroad (Siegel, 2008; Doi et al., 2009). Numerous mechanisms

are thought to contribute to the organism’s propensity to circumvent antibacterial agents. Acinetobacter baumannii exhibits an extraordinary ability to acquire antibiotic resistance determinants, which include enzymatic functions such as β-lactamases and aminoglycoside-modifying enzymes (Hujer et al., 2006). Additionally, the organism harbors a repertoire of efflux pumps that have also been hypothesized to Adenosine triphosphate contribute to clinical antibiotic failure (Hujer et al., 2006; Peleg et al.,2007a, b). While progress has been made in characterizing the organism’s antibiotic resistance determinants, little is known about their expression patterns or the mechanism(s) by which they are acquired or controlled. Similarly, little is known about the organism’s virulence factors or their regulation. For instance, while it is well recognized that many bacterial virulence factors are expressed in a cell density-dependent manner, we do not yet have a comprehensive assessment of these properties in A. baumannii cells (van Delden et al., 2001; Thompson et al., 2003). Nevertheless, advances in virulence factor identification are being made; using a proteomics approach, Soares and colleagues recently identified 67 proteins that are differentially expressed as A. baumannii ATCC 17978 cells transition from exponential to stationary phase of growth and hypothesized that a subset of these proteins are virulence factors (Soares et al., 2010).

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