Published online 13 August 1998 | Nature | doi:10.1038/news980813-1


Too much triclosan?

A widely used antibacterial agent that is used in toothpastes, kitchen utensils and toys could cause resistant strains of bacteria to develop, in much the same way that antibiotic-resistant bacterial strains are emerging, according to a report in the 6 August 1998 issue of Nature.

Triclosan is a potent antibacterial and antifungal agent which is being used ever more widely to produce ‘germ-free’ consumer products. It is being used to impregnate products ranging from bedding and socks to bin-liners and soap. A large supermarket chain in the UK recently introduced a range of kitchen utensils and chopping boards impregnated with triclosan.

The indiscriminate or over-use of antibiotics has been widely blamed for the appearance of so-called ‘super-bugs’ - bacteria that have developed resistance to the effects of antibiotic drugs, such as the new strains of tuberculosis. But the widespread use of triclosan has been thought harmless, because it is considered a broad-spectrum ‘antibacterial’ agent or ‘antiseptic’, rather than a true antibiotic. A general biocide such as triclosan is not expected to have any specific target in the bacterial cell, which could gradually evolve resistance.

Laura McMurry and colleagues from Tufts University School of Medicine, Boston, Massachusetts, have now found that triclosan does have a specific action on bacterial cells, meaning that it could be considered an antibiotic. The findings lead the researchers to warn that bacterial resistance to triclosan is a distinct possibility, and that its widespread use may be unwise.

The research team shows that triclosan blocks a specific biochemical pathway that makes lipids, the vital fatty components of cell membranes, in the common bacterium Escherichia coli.

Although the researchers haven’t shown exactly how triclosan works, it seems to involve the gene fabI or the enzyme that this gene produces, known as enoyl reductase. The enzyme is important in making fatty acids - one step in the process of lipid synthesis.

Mutations in fabI that may alter the enzyme in some way, or overactivity of fabI, prevent triclosan from having its usual antibacterial effects. Both are simple ways for an organism to develop resistance. As triclosan kills off normal bacteria, it could make way for the growth of strains with triclosan-insensitive enzymes.

It seems that triclosan acts in a very similar way to the drugs diazaborine and isoniazid. Diazaborine is currently used against Escherichia coli, a common cause of food poisoning. Isoniazid is a front-line anti-tuberculosis drug, but this too is suffering the fate of many drugs before it, in that resistant strains of the tuberculosis bacterium are evolving.

On a positive note, it may be possible to design triclosan derivatives that could be used to treat tuberculosis, food poisoning and other diseases. But this option may not be available to us if we continue to allow triclosan to be used widely in domestic situations, where bacteria can learn to live with it.

And triclosan may not be the only ‘antiseptic’ that has more specific antibiotic activity. The widespread use of all antibacterial agents must be more carefully controlled.

From Nature 11 August 1898.