Blocking the ‘MIDAS’ touch of Enterococcus faecalis

The treatment and prevention of hospital-acquired infections represents a major challenge to patient care. It is estimated that approximately 1.7 million hospital-acquired infections occur annually in the United States alone, accounting for almost 100,000 deaths and $5-10 billion in associated health care costs (1,2). Catheter-associated urinary tract infections (CAUTI) account for up to 40% of all hospital-acquired infections (3), and thus constitute the greatest burden of acquired disease in the nosocomial environment. The risk of bacteriuria in catheterized patients is estimated to be 5-10% per day (4), and most patients with an indwelling urinary catheter for 30 days or longer develop bacteriuria (5). Multidrug resistance (MDR) is now frequently associated with pathogens that cause CAUTI, leading to increased rates of treatment failure with standard antibiotic therapies and a rise in the use of second and third-line agents. A widerange of Gram-positive and Gram-negative organisms can cause CAUTI, including Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus spp. and Enterococcus spp. (6). Enterococcus spp., in particular Enterococcus faecalis, cause up to 25% of all CAUTIs and are increasingly associated with MDR in the nosocomial setting (7-9). Here we review the exciting new findings reported by Flores-Mireles and coworkers, who have defined the mechanism of growth and biofilm formation by E. faecalis in human urine, and translated this new knowledge into the development of a vaccine that can prevent CAUTI in a mouse infection model (10).