Illustration by M. Mendez

The triclosan found in toothpaste or soaps is designed to kill or inhibit the growth of a broad spectrum of “undesirable” microbial species. This broad spectrum activity can potentially cause unintended impacts on non-targeted organisms (Wilson et al. 2003). Since triclosan does not discriminate between good or bad bacteria, our model focuses on the beneficial bacteria in the environment. We are examining the impact of triclosan irrigation on which bacteria are affected by the triclosan (specific species or resistant populations), if the bacteria are breaking it down (degradation), and whether or not any of this is affecting plant growth or plant uptake of triclosan.

 TRICLOSAN RESISTANCE 

Mechanisms used by microorganisms to confer triclosan resistance include, but are not limited to, efflux pumps, mutations, and overexpression.

Efflux pumps physically remove constituents, in this case, triclosan, and are found in the intracellular space by pumping them across the membrane and back into the extracellular environment. This is can be the main mechanism to contribute to bacterial antibiotic resistance.

Triclosan has been observed to be a substrate for multiple drug resistant efflux pumps. However, it has been observed that Pseudomonas aeruginosa has triclosan specific efflux pumps. Chuanchuen et al. 2001 determined that P. aeruginosa TCS specific efflux pumps were able to increase minimum inhibitory concentrations by more than six fold.

Mutations, a process by which genetic information of an organism is changed, can confer resistance to triclosan. More specifically, mutations in the fabI gene coding for a fatty acid biosynthesis protein allow for microorganisms to be unaffected by this antimicrobial (Grandgirard et al., 2015). The fabI gene codes for the enoyl-acyl carrier protein (FabI) that is responsible for a reduction in the elongation cycle of fatty acid biosynthesis (Parsons and Rock, 2013). Bacterial fatty acid synthesis is important for the formation of cell membranes (Zhang and Rock, 2008). The importance of this pathway can be stressed by highlighting the multiple antibiotics that target fatty acid biosynthesis. FabI inhibitors, such as triclosan, target a complex formed by the NAD(P) cofactor and the FabI product. Resistance arises from missense mutations in the fabI gene that give rise to altered FabI proteins (Yao and Rock, 2016). In E.coli resistance to triclosan is accomplished via a missense mutation of a glycine to a valine at base pair 93 which creates a mutant strain that renders triclosan 64 times less potent (Heath et al., 1999). This mutation is said to introduce a side chain that causes a clash with the chlorine atom in triclosan which, in turn, decreases the binding affinity of triclosan to the FabI protein (Curiao et al., 2015).