Introduction This experiment investigates the rapidity with which Escherichia Coli can develop complete resistance under strong selection in the lab. Water was chosen as a control, and triclosan, household chlorine/bleach, as well as penicillin were compared amongst each other. Biocides have been incorporated into a wide variety of consumer products because it is thought to protect humans from potentially harmful microbes including bacteria and fungi. If a biocide acts in a general way like an antiseptic, then it is unlikely that any single microbe would evolve to be resistant to that substance; this line of reasoning was initially used to justify widespread use of triclosan as being beneficial without creating the danger of selecting for triclosan-resistance among potentially harmful microbes.
However, some researchers have shown that triclosan acts on bacteria in single specific way - by inhibiting one of the highly conserved enzymes (enoyl-ACP reductase, or FabI) of bacterial fatty-acid biosynthesis.
Further, they have found that, several key pathogenic bacteria do not possess FabI, but rather have a unique triclosan-resistant flavoprotein, FabK, that can also catalyse this reaction in Streptococcus pneumoniae. (Heath + Rock, 2000). Mutations in the FabI gene have been observed in E. coli; utilization of FabK rather than FabI has been observed in Pseudomonas. Some bacteria have also been shown to have developed sensitivity to triclosan in their multiple antibiotic resistance (mar) operon. This activates a pump in the bacterial cell wall that expels a host of unwanted chemicals, including other (possibly still effective) biocides (Clarke, 2001). A final method of triclosan resistance that has been observed is glycosylation of triclosan molecules (Reither, 2002).
The hypothesis is that the E. coli will form a resistance to triclosan and penicillin relatively quickly, and also to chlorine/bleach but over a longer period...