By Leah Ferentinos
A Harpur College associate professor is close to finding the cure for a deadly strain of drug-resistant bacteria.
Jeffrey Schertzer, a Canadian biochemist and recent hire in the Biological Sciences Department, is researching bacteria communication in order to develop a medication and vaccine that could treat a variety of bacteria that are resistant to antibiotics, such as pseudomonas aeruginosa, the leading cause of death in people with cystic fibrosis. It is also often contracted by patients in hospital settings.
"We used to have this primitive idea about bacteria," says Schertzer, who received his 2007 PhD in biochemistry from McMaster University in Ontario. "We thought they were solitary, and not nearly as complex as large [eukaryotic-celled] organisms like us. But it's now come to light. . . . This is simply not the case."
Scientists have recently discovered that bacteria can function somewhat like our human tissues, where multi-cellular communities (of bacteria) have different properties as a group than their cells have individually. When bacteria clump together, they can attach to a surface and cover themselves in a protective slime coat called a biofilm. That's when they become even more difficult to kill by antibiotics.
"Non-genetically resistant bacteria can become resistant to antibiotics by joining together with medically resistant species of bacteria in these biofilms," Schertzer says.
Certain strains of bacteria, like pseudomonas aeruginosa, secrete a molecule called PQS, which is crucial to bacteria communication in building biofilms. If we can control what they secrete or make them deaf to it (shut off their receptors), Schertzer says, we can stop the bacteria from working together.
"In war, you knock out the enemy's communication so they can't coordinate with each other," he says. "It's the same concept with targeting bacteria cells."
By breaking up the group into individuals, or simply preventing the formation of biofilms entirely, the human immune system has a better chance at fighting infection.
"When one organism enters your body," Schertzer says, "it's unlikely to make you sick because your immune system detects and fights it immediately."
But if a bacterium can enter the body, hide and multiply (using a communication process called Quorum Sensing), the chance of it causing an infection is much greater.
Increased bacterial resistance to antibiotics is just a natural consequence of evolution, but Quorum Sensing is not essential to bacteria survival like the processes our traditional antibiotics target (such as cell wall biosynthesis, protein synthesis, DNA replication). The benefit of developing strategies to reduce disease-targeting communication is that it's a nonessential process; thus bacteria have much less evolutionary pressure to develop resistance. This type of epidemiological strategy is termed "virulence targeting."
"We take the prevalence of antibiotics for granted these days," Schertzer says. "But it wasn't too long ago when a kid could scrape their knee and die from an infection. We don't want to go back to a world like that."
Yet the number of new antibiotics produced is constantly decreasing, while the pharmaceutical industry is less motivated to cure infectious diseases than ever before. Because antibiotics are needed for only a few weeks at a time, pharmaceutical companies are shifting their focus more towards manufacturing drugs for chronic conditions instead.
"It's not financially lucrative to make antibiotics," Schertzer says. "I don't think 'Big Pharma' is evil enough to actually want anyone to be sick, but there's certainly a disincentive to further research and development on their end for this issue."
He says it all comes down to risk.
"It's risky for them to work in these areas. But as they retreat, it opens up opportunities for academia to begin filling the void where industry used to be."
More specifically, it's an opportunity for professors such as Schertzer to move the conversation away from broad-spectrum antibiotics (a single compound that kills many different types of bacteria at once), which is more profitable, but far less effective than medication that individually targets particular species of bacteria.
This is just what Schertzer will be doing this summer: using grant funding that Binghamton University was awarded by the Howard Hughes Medical Institute (HHMI) in order to encourage undergraduate participation in research labs.
"Getting lab exposure is extremely valuable," Schertzer says. "Once I began researching drug development, it really changed my understanding of what I wanted to do. Hopefully exposing undergraduate students to the lab environment early enough will give them that same level of understanding."
The HHMI projects will focus on interdisciplinary research and collaboration between the biological sciences, engineering, and chemistry departments. Schertzer sees this inter-departmental cooperation as a catalyst to approaching previously unanswerable questions with new breadth of knowledge and "big-picture" insight.
"Binghamton University has always had a very strong reputation for education, but it's currently also rapidly increasing its reputation for research," he says.
Schertzer may have earned his position by demonstrating the potential life-saving applications of his research, but he's still rather keen on teaching.
"It's so rewarding to watch somebody understand something," he says. "When you explain complicated material, you can almost see the light bulb go off. At the end of the day, that's what I always look forward to the most."
Last Updated: 9/9/16