New Products Containing Triclosan Feared 

Breeding Tougher Germs 

Joseph B Verrengia / AP 07aug98

An anti-bacterial agent widely used in soaps, lotions and other consumer products triggers a genetic change in bacteria that could widen the scope of life-threatening drug resistance a new study shows.

Now germ hunters from Tufts University Medical School in Boston are hoping to capture some of the drug-resistant bacteria they suspect may lurk in households where heavily advertised products containing the compound triclosan are being used every day.

The researchers, whose study appears in Thursday's issue of Nature, described the use of anti-bacterials outside of hospitals as a "fad that has crept up on us over the past three or four years to the point where it is overwhelming when you go to the supermarket." (See Summary Below)

"People think they are sterilizing the world by using these products and, in fact, they are potentially changing it," said Dr. Stuart Levy, director of the Tufts research group. "They really are over-the-counter antibiotics."

Companies that use triclosan in their products said the agent has been used safely for more than 30 years.

"There is no real-world evidence of a link between resistant bacteria and triclosan," said Glenn Cueman, president of North Carolina-based Microban Inc., which adds the agent to inhibit germ growth on plastics (which can go into the making of high-chair trays).

The Tufts study was started because of infection experts' concern that they are running out of medicines that they know will kill dangerous bacteria.

Germs can genetically mutate into tougher super-strains if they are repeatedly exposed to, but not killed by, antibiotic drugs and anti-bacterial agents. Federal figures show the top six bacteria found in hospitals are resistant to at least one drug.

Public health officials have blamed the indiscriminate prescription of antibiotics by doctors for the spread of drug-resistant bacteria.

The Tufts study suggests the recent widespread use of anti-bacterial agents in everyday products might have similar results.

• See triclosan in your toothpaste

Summary of the Nature article:

Perinuclear localization of chromatin facilitates transcriptional silencing Transcriptional silencing in Saccharomyces cerevisiae at the HM mating-type loci and telomeres occurs through the formation of a heterochromatin-like structure. HM silencing is regulated by cis-acting elements, termed silencers, and by trans-acting factors that bind to the silencers. These factors attract the four SIR (silent information regulator) proteins, three of which (SIR2–4) spread from the silencers to alter chromatin, hence silencing nearby genes. The authors show here that an HMR locus with a defective silencer can be silenced by anchoring the locus to the nuclear periphery. This was accomplished by fusing integral membrane proteins to the GAL4 DNA-binding domain and overproducing the hybrid proteins, causing them to accumulate in the endoplasmic reticulum and the nuclear membrane. The authors expressed the hybrid proteins in a strain carrying an HMR silencer with GAL4-binding sites (UASG) replacing silencer elements, causing the silencer to become anchored to the nuclear periphery and leading to silencing of a nearby reporter gene. This silencing required the hybrids of the GAL4 DNA-binding domain with membrane proteins, the UASG sites and the SIR proteins. These results indicate that perinuclear localization helps to establish transcriptionally silent chromatin. E D Andrulis, A M Neiman, D C Zappulla & R Sternglanz Perinuclear localization of chromatin facilitates transcriptional silencing (Letter to Nature) Nature 394, 592 (1998)

Dr. Stuart Levy  Email: stuart.levy@tufts.edu Microbiology-Basic Sci/Medical, Levy Lab, Medical & Vet-136, Harrison Ave., Boston, MA Tel: 617- 636-6764 Fax: 617- 636-0458 http://www.healthsci.tufts.edu/labs/sblevy/home.html