Science Biweekly

BETHESDA, MD. A few months ago we explored the topic of antibiotic resistance in some depth. The media has continued to stress our imminent doom that would accompany a post-antibiotic era. However, an additional threat has been on the horizon for some time: antiseptic resistant bacteria.

Antiseptics are different than antibiotics as antiseptics are able to target a wide variety of microorganisms (bacteria, viruses, eukaryotic organisms) and they kill or inhibit the growth of an organism within 30 seconds to 1 minute of topical application. In contrast, antibiotics are narrow spectrum (targeting specific types of bacteria) and have a specific mechanism for killing these organisms. Most people likely use antiseptics on a daily basis unlike antibiotics, which are typically reserved for infections. For example, if you look at your antibacterial kitchen soap you’ll likely find the antiseptic triclosan as the active ingredient.

Triclosan has been used for over 40 years in a wide variety of products and has considerable efficacy when used at correct concentrations. However, when we wash our hands with antibacterial soap and water, triclosan becomes immediately diluted. This dilution permits bacteria to mount a defense against triclosan resulting in antiseptic resistance.

The antibacterial mechanism of triclosan is multifaceted (Petersen, 2016). At high concentrations it disrupts bacterial membranes killing the bacteria. However, at lower concentrations the molecule targets a protein needed for fatty acid synthesis. Scientists have identified bacteria resistant to low concentrations of triclosan. To defend themselves against low concentrations of triclosan, bacteria have developed pumps to extrude triclosan from the cell, or simply accumulated a mutation in their DNA that allows them to make more of the enzyme targeted by triclosan (Yazdankhah, 2006).

Beyond triclosan-resistant bacteria, bacteria that have increased resistance to chlorhexidine have also been identified. Chlorhexidine is used in dentistry and as a pre-surgery scrub in hospitals. Similar to triclosan, the working concentration of chlorhexidine is able to kill bacteria easily; however, if chlorhexidine is diluted with water or applied for a shorter duration than recommended bacterial resistance can occur. My current research focuses on chlorhexidine resistance and resistance mechanism of the efflux pump QacA in Methicillin Resistant Staphylococcus aureus (MRSA). For the sake of space, we will discuss this topic in more detail in another article.

The fact we have bacteria that are able to develop resistance mechanisms to antiseptics is problematic. If antiseptics become less effective, more hospital acquired infections (HAI) will likely occur and these infections may be caused by the difficult to treat superbugs previously discussed. However, antiseptic resistance is a testament to how quickly bacteria can evolve to survive hostile conditions. The FDA recently published a statement recommending normal soap to be used in handwashing instead of soap containing triclosan or its related compound triclocarban. Regardless of your soap of choice, remember in handwashing to lather your hands with soap then scrub for 20-30 seconds with warm water. The time-tested method of handwashing remains a simple and effective way to protect ourselves from getting sick.

Citations:

1. Petersen, R. C. (2016). Triclosan antimicrobial polymers. AIMS molecular science, 3(1).

2. Yazdankhah, S. P., Scheie, A. A., Høiby, E. A., Lunestad, B. T., Heir, E., Fotland, T. Ø., ... & Kruse, H. (2006). Triclosan and antimicrobial resistance in bacteria: an overview. Microbial drug resistance, 12(2), 83-90.