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Staph Genes That Turn Commensal to Killer Identified

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Don’t be alarmed, but a bacterium that could turn deadly is on your skin right now. This bacterium, Staphylococcus epidermis, is usually harmless, but it may harbor genes that could help it exploit any opportunity to grow in your bloodstream. Once there, it could shrug off your immune response, resist the antibiotics you receive, and flourish until it kills you.

The question is: Which Staphylococcus epidermis genes spell danger? An answer to that question has been supplied by scientists based at the University of Bath. They have identified 61 genes containing infection-associated genetic elements that correlate with pathogenicity, or in their words, “in vitro variation in known pathogenicity traits” such as biofilm formation, cell toxicity, interleukin-8 production, and methicillin resistance.

Staph Genes

The new findings are significant because they suggest that genetic analyses could tell clinicians which patients are at higher risk of infection when they undergo surgery. For such patients, extra hygiene precautions could be life-saving.

The University of Bath team, led by director of bioinformatics Sam Sheppard, presented their findings in the journal Nature Communications, in an article titled, “Disease-associated genotypes of the commensal skin bacterium Staphylococcus epidermidis.” The article described how skin swab samples were taken from two groups of patients. One group included patients who suffered infections following hip or knee joint replacement and fracture fixation operations. The other group consisted of healthy volunteers.

Swabs in hand, the scientists compared the genetic variation in the whole genomes of bacteria found in samples from diseased and healthy individuals.

“Here we address the underlying evolutionary mechanisms of opportunistic pathogenicity by combining pangenome-wide association studies and laboratory microbiology to compare S. epidermidis from bloodstream and wound infections and asymptomatic carriage,” the article’s authors wrote. From this work, the scientists identified 61 genes in the disease-causing bacteria that weren’t present in most of the healthy samples.

“Horizontal gene transfer spreads these elements, allowing divergent clones to cause infection,” they continued. “Finally, Random Forest model prediction of disease status (carriage vs. infection) identifies pathogenicity elements in 415 S. epidermidis isolates with 80% accuracy, demonstrating the potential for identifying risk genotypes pre-operatively.”

Surprisingly, the scientists found a small number of healthy individuals who were found to be carrying the more deadly form of the bacteria without knowing it.

The disease-causing genes were found to help the bacterium grow in the bloodstream, avoid the host’s immune response, make the cell surface sticky so that the organisms can form biofilms, and make the bug resistant to antibiotics.

Staphylococcus epidermis is a deadly pathogen in plain sight,” emphasized Sheppard. “It’s always been ignored clinically because it’s frequently been assumed that it was a contaminant in lab samples or it was simply accepted as a known risk of surgery.

“Post-surgical infections can be incredibly serious and can be fatal. Infection accounts for almost a third of deaths in the U.K. so I believe we should be doing more to reduce the risk if we possibly can. If we can identify who is most at risk of infection, we can target those patients with extra hygiene precautions before they undergo surgery.”

“Because the bug is so abundant, they can evolve very fast by swapping genes with each other,” he added. “If we do nothing to control this, there’s a risk that these disease-causing genes could spread more widely, meaning post-operative infections that are resistant to antibiotics could become even more common.”

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