Antimicrobial resistance sparks images of superbugs that emerge from the depths of the human body or in a cinematic scene involving antibiotic-induced farm animals; however, the rise of resistance within bacteria is often more subtle.
is a skin bacteria that is so prevalent, the US Centers for Disease Control and Prevention (CDC) classifies it as a common commensal for certain health care-associated infections. Its presence can cause infections, especially in patients with invasive procedures and compromised immune systems; however, the bacteria often fail to get the kind of attention that would make headlines. The results of a new study may soon change the wallflower status of S epidermidis.
Investigators recently reported
the complete genome of an S epidermidis
strain that exhibits near pan-drug resistance, including intermediate resistance to vancomycin. As there is a common lineage of S epidermidis
that tends to plague hospitals, investigators sought to analyze the global strains of all strains found to cause nosocomial (health care-associated) infections. The investigators used multilocus sequence typing [MLST] eBURST analysis of a global strain collection to analyze S epidermidis.
They found that 74% of the isolates from health care-associated infections due to S epidermidis
belong to a specific clonal complex.
Further analysis identified 6 genetic clusters and those responsible for most nosocomial infections; however, what the team discovered next was startling: isolates from 3 lineages were “almost exclusively nosocomial and significantly enriched for antibiotic resistance and biofilm production, suggesting hospital adaptation. [Additionally,] methicillin resistance in S epidermidis
has been reported to be as high as 70% to 92% in some institutions and is frequently associated with co-resistance to other antibiotic classes.”
These 3 linages of S epidermidis
had picked up an rpoB
mutation that allowed them to become resistant to rifampicin.
Investigators also looked at the prevalence of this multidrug-resistant S epidermidis
to determine if its prevalence was increasing. Pulling antibiotic susceptibilities from an 800-bed hospital in Melbourne, Australia, from 2007 through 2013, the investigators found an increase in S epidermidis
teicoplanin resistance from 3.6% in 2007 to 25.3% in 2013. (Teicoplanin resistance is correlated with rifampicin resistance.)
Expanding on this growing prevalence, the investigators tested 32 rifampicin-resistant clinical S epidermidis
isolates from 13 institutions in Australia and 121 global isolates from 61 institutions across Europe and the United States. Isolates from a total of 96 institutions in 24 countries helped to identify the genomic changes that caused 86.6% of the mutations responsible for rifampicin resistance, which encourages resistance to last-line glycopeptide antibiotics such as vancomycin and teicoplanin. The lineage that was dominant in Australia was found in 25 institutions in 4 countries. The other 2 lineages found to have near pan-drug resistance were found in dozens of other institutions across 7 countries.
The results of this study reveal not only the genomic mutations and different lineages that result in resistant S epidermidis,
but also the global spread. Given that resistance to rifampicin encourages resistance to other antibiotics, these findings should be weighed seriously as we consider what bacteria are considered normal and often ignored.