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By Bob Holmes
You’d think that if fighting bacteria one way is good, two ways would be even better. But not always: an antibacterial widely used in soaps and cleaning products actually helps microbes like MRSA beat our most powerful antibiotics.
The antibacterial in question is triclosan. It is not an antibiotic but a different type of compound that, rather than killing bacteria, stops them from growing instead.
Triclosan is so common that it is even found in some cosmetics and toys, prompting concerns that its overuse may encourage bacteria to evolve resistance to it. This could be a problem for some hospitals, which may use antibacterial cleaning products to prevent the spread of infections and superbugs.
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These concerns have helped prompt the US Food and Drug Administration to ban the use of triclosan in consumer hand soaps, and the FDA is considering further restrictions. However, others still argue that triclosan’s use is beneficial.
But now there’s reason to worry that using too much triclosan could have even more serious effects. To see whether antibacterials can help bacteria resist antibiotics, Petra Levin and Corey Westfall, microbiologists at Washington University in St Louis, Missouri, exposed Escherichia coli to common antibiotics and triclosan, and measured their survival over 20 hours.
When streptomycin and ciprofloxacin were the antibiotics used, bacteria exposed to them as well as triclosan were 10,000 times more likely to survive than those that weren’t also given triclosan.
And when the antibiotic was ampicillin, Levin and Westfall found that bacteria were almost completely protected from the drug when triclosan was present.
Alarmingly, further testing found that triclosan protects the MRSA superbug against vancomycin, a crucial antibiotic often used as a last resort for treating MRSA infections.
Speeding up evolution
We don’t know why triclosan has these effects, but one explanation might lie in the different ways that antibiotics and antibacterials work. Most antibiotics kill bacteria by interfering with essential steps in their __life cycle, such as making new cell walls when a bacterium reproduces by dividing. Since triclosan prevents bacteria growing, it makes them less likely to reproduce – and that may make bacteria impervious to antibiotics.
“A dormant cell has not a lot of active targets, so there’s not much to corrupt,” says Kim Lewis at Northeastern University in Boston.
Levin and Westfall have not yet discovered whether triclosan’s apparent ability to help bacteria survive antibiotics could be aiding their survival in the hospital, home, or the bodies of people taking a course of antibiotics. Until we know more, it might be wise for people to reduce their exposure to triclosan while they are on antibiotics. Trouble is, it’s very hard to do that. “Triclosan is all over the place,” says Nathalie Balaban at the Hebrew University of Jerusalem, Israel. “You’re giving a treatment and you’re not even aware it’s there.”
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Triclosan may have another sinister effect. Treatment with antibiotics usually aims to kill all of the bacteria causing an infection – otherwise the survivors could pass on whichever genes helped them resist the drugs. By enabling bacteria to persist in the presence of antibiotics, triclosan may speed up microbes’ ability to evolve drug resistance. If so, that could be a good argument for further restrictions on the use of triclosan, Lewis says.
Levin declined to comment on her work until it is formally published following peer review.
Journal reference: bioRxiv, DOI: 10.1101/090829 (preprint)
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