Sexual attraction in the human world is an enigma epitomized by the fascination with pheromones. These small molecules, usually hormonal in nature have been described as:

While pheromones may have a variety of functions, most of the work in the human world has dealt with their influence on relationships and attracting another person for romantic if not carnal activities.

But pheromones are not limited to humans. Some bacterial species also rely on these chemicals to attract other members of the species for sexual activity. One of the most studied is the bacterium Enterococcus faecalis.

Back in 1979, when the bacterium was known as Streptococcus faecalis, certain chemicals appeared to stimulate cells to get together and start their own version of sexual activity, conjugation. The goal appeared to be the transfer of genetic material to improve the chances for survival in the environment.

While this was interesting from a purely observational perspective, there was a rather sinister consequence associated with these pheromones. Some of the genetic material transferred enabled a cell to become resistant to antibiotics. In light of the growing concern over widespread resistance, this mechanism deserved much study and investigation to figure out ways to prevent this intimate form of sharing.

The study all but revealed a negative consequence of pheromones to human health. They were produced in the body and could contribute to antibiotic resistance in the intestines. One particular promiscuous bacterium happened to be E. faecalis V583. This strain is highly resistant to antibiotics including vancomycin; has been known for over 20 years; and has been a scourge on the healthcare system, particularly in the United States.

This strain is quite different from its normal E. faecalis siblings. It has had so many sexual encounters the amount of genetic material has grown by nearly 25% including several resistance genes. This made the bacterium a priority for study if only to figure out how to stop it from conjugating with other members of the species.

Last week, an American team of researchers put V583 to the test. They wanted to determine how the strain interacted with other non-antibiotic resistant forms. Essentially, they wanted to answer whether V583 was a true sex fiend or could be recognized as a player and avoided. To ensure this had relevance to human health, the interacting strains were those commonly found in our guts, called commensals. When the results came back, the news was uplifting as V583 did not grow well nor did it apparently share any genetic material. Instead, it seemed to die off. This was a surprise that led the group to take a closer look at the mechanism and discover what might be a microbial bombshell.

The first testing process was simple. The group took V583 and mixed it with fecal bacteria. Instead of seeing a higher number of V583 or other strains emerging with antibiotic resistance, the exact opposite occurred. The number of V583 decreased significantly while the other strains prospered. This was rather surprising considering the number of available weapons. There had to be a novel means of killing action. This required a much deeper look at the commensal strains.

The team worked at the genetic level, adding or deleting segments to find the gene responsible for the killing action. Eventually, they found one particular gene segment that fit the bill. Upon closer inspection, the group was surprised to find the cause was not an antimicrobial or some other enzyme. Instead, it was a pheromone called cOB1.

As for the mechanism of killing action, the team wasn’t able to hone in on the specifics although they had a theory. Much like any other pheromone, once cOB1 enters V583, it causes stimulation. But, instead of causing a normal increase in internal activity, this molecule sends the cell into overdrive. The result is an unwanted increase of genes promoting another internal factor to shut the cell down. The end result of this fatal attraction is cell death.

While V583 appeared to show itself as the microbial equivalent of Casanova, for the authors, this revelation offered a more applicable conclusion. The commensal bacteria in the gut are simply not fond of V583 and will use their sexual charms to kill it. In the context of human health, this suggests an increase in commensal flora could potentially slow down or even stop V583 from colonizing the gut and causing problems in patients. Considering the issues with healthcare associated infection and antibiotic resistance, this route of natural intervention may be well worth future exploration and study.