In 2002, 1.7 million nosocomial (hospital-acquired) infections were equal to an average of 4.5 infections reported for every 100 people admitted to the hospital and these infections resulted in 99,000 deaths. The mortality rate resulting from nosocominal infections is staggering, however, the morbidity rate is even greater--as many of the infections acquired in the medical setting result in long-term chronic wounds. Current standards of care for chronic wounds have proven ineffectual, primarily because treatments have been developed for planktonic bacteria with little or no consideration of the biofilm mode of pathogen growth. It has been well demonstrated that the establishment of bacterial biofilm in the wound is the major reason for the failure of acute wound treatment and development of chronic, non-healing wounds. The National Institutes of Health estimates that 80% of microbial inflections in the United States, could be characterized as biofilms.

Treatment of bacterial biofilms in the wound is complicated by the very character of the biofilm mode of growth, including increased resistance of the biofilm to antimicrobial treatments and host immune defense. While previous work has examined the interaction between novel therapeutics and biofilms superficially, there are few in-depth analyses of the metabolic effects of the interactions between chronic wound therapies and contaminating bacterial biofilms. It has been recently speculated that pathogenicity in bacteria is the result of an evolutionary drive to obtain nutritional resources. We propose that comprehensive analysis of the metabolites within a host-pathogen model of the chronic wound may yield important clues to the mechanisms of this interaction and potential targets for therapeutic strategies. In designing novel and effective therapies for wounds, it is necessary to consider, account for, and design accurate models for the unique ability of the biofilm to resist treatment, especially through metabolic changes.