|Presentation from the 2000 Emerging Infectious Diseases Conference in Atlanta, Georgia|
Antibacterial Household Products: Cause for Concern
Stuart B. Levy
Antibiotics are critical to the treatment of bacterial infections. However, after years of overuse and misuse of these drugs, bacteria have developed antibiotic resistance, which has become a global health crisis (1, 2). The relatively recent increase of surface antibacterial agents or biocides into healthy households may contribute to the resistance problem.
The antibacterial substances added to diverse household cleaning products are similar to antibiotics in many ways. When used correctly, they inhibit bacterial growth. However, their purpose is not to cure disease but to prevent transmission of disease-causing microorganisms to noninfected persons. Like antibiotics, these products can select resistant strains and, therefore, overuse in the home can be expected to propagate resistant microbial variants (3-6). Moreover, these agents, like antibiotics, are not cure-alls but have a designated purpose. Whereas antibiotics are designed to treat bacterial (not viral) infections, antibacterial products protect vulnerable patients from infectious disease-causing organisms. Neither are demonstrably useful in the healthy household.
Proliferation of Antibacterial Products
Seven years ago, only a few dozen products containing antibacterial agents were being marketed for the home. Now more than 700 are available. The public is being bombarded with ads for cleansers, soaps, toothbrushes, dishwashing detergents, and hand lotions, all containing antibacterial agents. Likewise, we hear about "superbugs" and deadly viruses. Germs have become the buzzword for a danger people want to eliminate from their surroundings. In response to these messages, people are buying antibacterial products because they think these products offer health protection for them and their families. Among the newer products in the antibacterial craze are antibacterial window cleaner and antibacterial chopsticks. Antibacterial agents are now in plastic food storage containers in England. In Italy, antibacterial products are touted in public laundries. In the Boston area, you can purchase a mattress completely impregnated with an antibacterial agent. Whole bathrooms and bedrooms can be outfitted with products containing triclosan (a common antibacterial agent), including pillows, sheets, towels, and slippers.
Development of Resistance
Bacteria are not about to succumb to this deluge, however. Through mutation, some of their progeny emerge with resistance to the antibacterial agent aimed at it, and possibly to other antimicrobial agents as well (4). Laboratory-derived mutants of Pseudomonas stutzeri with resistance to the cationic biocide chlorhexidine were also cross-resistant to antibiotics (nalidixic acid, erythromycin, and ampicillin) (7). In a recent study, 7% ofListeria monocytogenes strains isolated from the environment and food products showed resistance to quaternary ammonium compounds (8).
Laura McMurry in my laboratory group conducted experiments to determine whether triclosan had a particular cellular site for its antibacterial activity. She used a classic genetic technique, the isolation of resistant mutants of Escherichia coli, to identify its possible target. Surprisingly, finding the cellular site proved easy. In fact, mutants appeared with low, medium, and high-level resistance (3). They all had a mutation in one gene, the fabI gene (3) (Table 1). This finding indicated that triclosan had a target for the enoyl reductase essential in fatty acid biosynthesis. In the presence of triclosan or a know fabI inhibitor (diazoborine) fatty acid biosynthesis was inhibited, whereas the antibiotics chloramphenicol or ciprofloxacin with other targets had little effect on fatty acid biosynthesis (Table 2). In comparison with the wild-type E. coli, the mutant required up to 100 times more triclosan to show even minimal inhibition of fatty acid biosynthesis (3).
|One might argue that the high concentration of triclosan usually found in soap, e.g. 2,500 µg/ml, is enough to kill even resistant strains. We examined this question by testing triclosan activity in a commercial soap. To achieve a 90% death rate, wild-type E. coli required exposure to 150 µg/mL of triclosan in soap for 2 hours at 37ºC. Two to four times that amount was required by the mutant. By itself, triclosan was more active, killing E. coli at 6 µg/ml, and there was an even greater difference between the amounts required to kill wild-type and mutant E. coli. The soap seemed to decrease triclosan's effectiveness (Table 3). The mutant E. coli strains are truly resistant and would survive in triclosan-treated soaps diluted with as little as 3 parts water. Most importantly, the time, temperature, and amount needed to kill the bacteria greatly exceeded the average 5-second hand washing performed by most people. ... http://www.cdc.gov/ncidod/eid/vol7no3_supp/levy.htm|