How could the differences in colonization with antibiotic-resistant Gram-negative bacteria be explained?
First, a higher therapeutic use of intravenous antibiotics in the control population could indeed have created a higher selective pressure for pre-existent resistant bacteria or may have induced more mutations leading to resistance. Second, SDD may have decreased the total bacterial burden, thereby reducing the colonization pressure and, with equal levels of adherence to infection control measures, reduced the possibilities for clonal spread. This would support the use of SDD to control outbreaks of antibiotic-resistant microorganisms as reported previously [6]. However, it is also possible that there was clonal spread of resistant bacteria in the control ward, whereas tobramycin-resistant bacteria in the non-SDD ward were polyclonal, due to increased selection induced by SDD. If so, the conclusion that SDD prevents emergence of resistance no longer holds true. As adherence to infection control practices was not measured, it is unknown if both units were comparable in this regard. Agai
