Light is a ubiquitous environmental signal that many organisms sense and respond to by modulating their physiological responses accordingly. While this is an expected response among phototrophic microorganisms, the ability of chemotrophic prokaryotes to sense and react to light has become a puzzling and novel issue in bacterial physiology, particularly among bacterial pathogens. In this work, we show that the opportunistic pathogen Acinetobacter baumannii senses and responds to blue light. Motility and formation of biofilms and pellicles were observed only when bacterial cells were incubated in darkness. In contrast, the killing of Candida albicans filaments was enhanced when they were cocultured with bacteria under light. These bacterial responses depend on the expression of the A. baumannii ATCC 17978 A1S_2225 gene, which codes for an 18.6-kDa protein that contains an N-terminal blue-light-sensing-using flavin (BLUF) domain and lacks a detectable output domain(s). Spectral analyses of the purified recombinant protein showed its ability to sense light by a red shift upon illumination. Therefore, the A1S_2225 gene, which is present in several members of the Acinetobacter genus, was named blue-light-sensing A (blsA). Interestingly, temperature plays a role in the ability of A. baumannii to sense and respond to light via the BlsA photoreceptor protein.

The outer membrane proteins responsible for the influx of carbapenem ␤-lactam antibiotics in the nonfermentative gram-negative pathogen Acinetobacter baumannii are still poorly characterized. Resistance to both imipenem and meropenem in multidrug-resistant clinical strains of A. baumannii is associated with the loss of a heat-modifiable 29-kDa outer membrane protein, designated CarO. The chromosomal locus containing the carO gene was cloned and characterized from different clinical isolates. Only one carO copy, present in a single transcriptional unit, was found in the A. baumannii genome. The carO gene encodes a polypeptide of 247 amino acid residues with a typical N-terminal signal sequence and a predicted transmembrane ␤-barrel topology. Its absence from different carbapenem-resistant clinical isolates of A. baumannii resulted from the disruption of carO by distinct insertion elements. The overall data thus support the notion that CarO participates in the influx of carbapenem antibiotics in A. baumannii. Moreover, database searches identified the presence of carO homologs only in species of the genera Acinetobacter, Moraxella, and Psychrobacter, disclosing the existence of a novel family of outer membrane proteins restricted to the family Moraxellaceae of the class ␥-Proteobacteria.The emergence of antibiotic resistance among both pathogenic and opportunistic microbes resident in hospitals represents a serious and recurrent problem for the treatment of infections (22). It generates a continuous demand for new antimicrobial agents, whose application feeds the undesired vicious circle of selection and dissemination of new patterns of antibiotic resistance. The otherwise bizarre but still elegant mechanisms that underlie some of these patterns of resistance demonstrate that the potential of microbes to challenge eradication attempts remains almost unexhausted (26). Yet, attempts to reduce the dissemination of rapidly evolving antibiotic-resistant pathogens are best based on a detailed knowledge of the causes that promote these patterns of resistance (26).The genus Acinetobacter, recently reassigned to the family Moraxellaceae in the class ␥-Proteobacteria (30), is constituted by gram-negative, pleomorphic aerobic species commonly isolated from many sources in the environment, including drinking and static water, soil, sewage, food, and the skin of humans and animals (5). Certain strains of a particular species of the genus, Acinetobacter baumannii, now account for a large percentage of nosocomial infections, including pneumonia, bacteremia, skin and wound infections, and urinary tract infections. These strains are almost invariably multidrug resistant, having successfully resisted eradication attempts by the use of penicillins, aminoglycosides, cephalosporins, and even fluoroquinolones (5). It is due to this outstanding ability to rapidly respond to the challenge of new antibiotics that the emerging resistance to carbapenems among nosocomial strains of A. baumannii represents a major concern (22).The molecular b...