When antibiotics were first discovered, they revolutionized medicine and were expected to virtually eliminate disease. Over time, widespread use of antibiotics has led to the rise of resistant strains of bacteria. New classes and types of antibiotics have been produced, but over time bacteria are acquiring resistance to these as well. Research into antibiotic resistance has not only focused on the development of new drugs, but also on determining the mechanisms by which resistant stains emerge and how to limit their spread.
In September 2006, Dr. Stuart Levy of Tufts University School of Medicine published a paper describing the identification of a gene in Yersinia pestis, the causative agent of plague, that was similar to an Escherichia coli gene known to cause multiple antibiotic resistance. The Y. pestis gene was studied and found to function in the same way. A non-virulent strain of Y. pestis overexpressing the gene was resistant to several common antibiotics, including those typically used to treat plague infection. Spontaneous antibiotic resistant bacteria were found to frequently have mutations that affect the expression of this gene, suggesting that it is an important and common mechanism by which bacteria acquire resistance.