New antibiotics are few and far between, and some bacteria seem particularly adept at evolving into stronger forms of themselves, gaining genetic material to protect themselves against even the last-line-of-defense antibiotics, a class of drugs kept carefully out of mainstream consumption.
In the case of a strain of bacteria known as KPC (carbapenem-resistant Klebsiella pneumoniae), roughly half of people with active infections die. It’s a rare infection, but these bacteria evolve quickly and spread elusively. They are resistant to most antibiotics, and have been shown to quickly evolve into resistant forms when introduced to newer antibiotics. KPC is the bacteria of Hollywood, only it’s all-too real.
Genetic sequencing of these bacteria can tell us how they evolve over time, even over the course of a few weeks in a hospital setting. But sequencing has another role: it can help us do the only thing that we can do with antibiotic resistant bacteria: isolate it and kill it.
Genetic sequencing of different bacteria in the same family, like its human counterpart, varies from individual to individual, but has more similarities among closer relatives. When bacteria divide, their resulting “children” will have a small number of mutations. As these newer bacteria divide, more mutations are added to the bunch. These mutations may be beneficial to their survival (or perhaps not) but if they are, then they are likely to be propagated when the bacteria divide again. Over several generations, the bacteria from different “branches” of the family are substantially different from those who descended from a common ancestor more recently.
How could gene sequencing possibly help an outbreak of KPC? As Wired Magazine explains, scientists at a National Institutes of Health hospital were able to track who infected whom in the midst of a deadly outbreak by tracking the mutations of KPC. The results were scary – the infection spread in at first mysterious ways. One patient who had never been in the same room with another infected him via a ventilator that had been sterilized between the two patients – obviously not sufficiently. The missing links among different strains led to the notion that there were more infected patients. This in turn led to a search for bacterial carriers, and a practice of checking for the dormant bacteria through rectal swipes instead of just throat and groin swipes. Sure enough, the bacteria were hiding among these carriers, who unwittingly helped the bacterial survive the quarantine the hospital had placed on people with infections.
A few months of newly vigilant quarantine squashed the hospital’s outbreak. The specific actions need to contain the bacteria were discovered through genetic sequencing – a surprising benefit to those patients without any medicinal intervention at all.
Now if only these tools could be used about the latest strain of antibiotic resistant gonorrhea. In that case, we know how it’s transmitted and there’s essentially no hope of containment. The question is whether gene sequencing and identification of genetic sites related to specific activity can help us develop drugs that target the mechanism by which bacteria evolve their drug resistance.
This article was featured as part of the Genetic Literacy Project’s weekly newsletter GeneTrends: Human.Klebsiella pneumoniae image credit: CDC
After all decimating our internal gut bacteria does us no favors and simply increases the risk of some other bacteria colonizing our environment and causing problems.
Since much of our bacteria becomes resistant, then our bacteria is equally willing to share these genes with any other bacteria that might be present. So, we find that many pathogens acquired antibiotic resistance from our own gut bacteria via horizontal gene transfer. In other words, they don't have to wait for mutations to convey resistance and likely would never be subject to such a constraint.
I think you're absolutely right that gene sequencing will help in identifying a particular pathogen's vulnerabilities, but unfortunately we may find that some of the solutions are much more primitive that many people would like to believe. Of course, I also realize that much of this discussion focuses on the specific and unique problem of hospital infections, but unless we adopt a more stringent approach in our personal lives towards understanding and dealing with pathogens, the problems will simply become more sophisticated. After all, consider that despite all the rhetoric about flu vaccines and exposure, almost no one suggests that staying home is the best approach [i.e. self-quarantine].