Acinetobacter baumannii is an opportunistic nosocomial pathogen of substantial concern due to its increasing antibiotic resistance and ability to survive unfavorable conditions in the hospital environment, likely in the form of a biofilm, which potentiates its ability to spread. However, the information about its virulence factors and the regulatory networks that could control their expression is insufficient. This lack of data is compounded by large variations in genotypic and phenotypic traits among clinical isolates as illustrated by the differences in biofilm structures they form on plastic or glass. These biofilm variations did not correlate with properties of abiotic surfaces or other cell properties, such as surface hydrophobicity, pellicle formation, surface-associated motility, or somatic appendages.
It is apparent that environmental signals, such as the concentration of extracellular free iron, could affect the aforementioned interactions, as measured by changes in cell motility on semisolid media and biofilm formation on plastic. These responses are independent of pilT and pilU orthologs, which impact motility and biofilm functions in other pathogens. However, these two genes play a role in the interaction of A. baumannii ATCC 17978 cells with human alveolar epithelial cells which results in the apoptotic death of these epithelial cells.
The A. baumannii responses to multiple environmental cues may be attributable to the sensing and response function of regulators such as that coded by the bfmL locus present in the ATCC 19606T strain. Interestingly, this LysR-type transcriptional regulator (LTTR) is needed for the post-transcriptional expression of the CsuA/BABCDE chaperone-usher pilus assembly system needed for cell attachment and biofilm formation on plastics. Equally interesting is that inactivation of bfmL results in the production of pili different from those produced when the aforementioned assembly system is expressed.
Taken together, these results demonstrate that the interaction of A. baumannii with medically relevant surfaces is affected by a multitude of cellular and environmental factors, most of which remain to be characterized. This missing basic knowledge could be used to develop much needed alternative and more efficient therapies to treat the infections this pathogen causes.