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Multidrug-resistant S. epidermis spreads in hospitals
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Multidrug-resistant lineages of Staphylococcus epidermis are spreading globally in hospitals, turning the common human skin colonizer into a “formidable nosocomial pathogen,” researchers reported in Nature Microbiology.
Analyzing isolates from two dozen countries, Jean Y. H. Lee, BSc(Hons), MBBS, FRACP, a PhD student in the Peter Doherty Institute for Infection & Immunity at the University of Melbourne, and colleagues discovered a dual genetic mutation to be the most common cause of rifampicin resistance in globally disseminated S. epidermis.
As Lee explained to Infectious Disease News, increasing antibiotic resistance has led to the routine use of vancomycin as a first-line treatment of S. epidermidis, and rifampicin — due to its ability to penetrate biofilm — has been used as standard adjunctive therapy for device-related staphylococcal infections.
“Since vancomycin and rifampicin belong to completely different drug classes, there has been a general assumption that the combination of these two particular agents should protect one another against the development of drug resistance to both,” Lee said.
But Lee and colleagues said they collected data that challenge this assumption and that a review of clinical guidelines for the treatment of staphylococci is warranted.
“The combined use of rifampicin and vancomycin for the treatment of staphylococci should no longer be recommended because this combination has likely contributed to the evolution of further drug resistance to both agents,” Lee said.
Using genomics, Lee and colleagues said they identified three multidrug-resistant, hospital-adapted lineages of S. epidermis that have emerged globally over the past several decades. They analyzed isolates from 96 institutions in 24 countries and identified two mutations as the most common case of rifampicin resistance in S. epidermidis, making up 86.6% of mutations.
“By breaching lineage-specific DNA methylation restriction modification barriers and then performing site specific mutagenesis, we show that these rpoB mutations not only confer rifampicin resistance, but also reduce susceptibility to the last-line glycopeptide antibiotics, vancomycin and teicoplanin,” they wrote. “Our study has uncovered the previously unrecognized international spread of a near pan-drug-resistant opportunistic pathogen, indefinable by a rifampicin-resistant phenotype.”
According to Lee, they identified some European isolates that had acquired additional resistance to daptomycin and linezolid, making them potentially untreatable.
Lee said the findings impact treatment decisions made by infectious disease specialists.
“The role of an infectious diseases physician can seem like a balancing act — ensuring the individual patient in front of you has the best possible outcome, but at the same time being mindful that the cumulative decisions you make for each patient will impact how antibiotic resistance in your institution (and the wider community) evolves and contributes to the gradual loss of therapeutic options,” Lee said. “We are recognizing an increasing number of extremely antibiotic-resistant bacteria at a time when the discovery of new agents is few and far between. It is therefore our responsibility to preserve antibiotics as a limited and precious resource to prolong the effectiveness of existing agents.” – by Bruce Thiel
Disclosures: The authors report no relevant financial disclosures.
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