I’ve written before about CTX-M-15 beta-lactamases which make bacteria resistant to most cephalosporin antibiotics–those antibiotics that begin with cef- (or ceph-) or end with -cillin. I’ve also discussed the role of clonal spread in the rise of antibiotic resistance: most (but obviously not all) resistant infections are not the result of a sensitive strain evolving resistance during the course of infections, but rather due to colonization by a previously resistant strain. A recent article in Emerging Infectious Diseases discusses the role of clonal spread in the dissemination of CTX-M-15 beta-lactamases.
Within E. coli, there are five major groups, given the creative names of A, B1, B2, D, and E. Members of the B2 and D groups cause a disproportionate amount of disease. It turns out that, in a global survey of CTX-M-15 E. coli, many of the strains were from two genetic backgrounds, one in B2 and one in D, which are strongly associated with urinary tract infections. Interestingly, the CTX-M-15 gene was always found on one of three plasmids, all of which appear to be related.
So what does this mean? While the transfer of resistance genes is important, much of the increase in CTX-M-15 is a result of the spread two highly successful and drug resistant urinary tract infection clones. If we want to stop the spread of this gene (and we certainly do), we have to further refine how we are treating UTIs, so as to limit the spread of these particular strains. We also have to determine what the non-disease reservoir habitats of these strains are, and take measures to limit the spread of these strains from those habitats.
Cited article:Coque TM, Novais Â, Carattoli A, Poirel L, Pitout J, Peixe L, et al. Dissemination of clonally related Escherichia coli strains expressing extended-spectrum β-lactamase CTX-M-15. 2008. Emerging Infectious Diseases 14: 195-200.