These elements allow bacteria to capture new genes that are potentially adaptive. There are a few hypotheses as to why antibiotic resistance would be more prevalent in metal-exposed bacteria. The one with the most evidence to date is that you can have a gene that encodes for a metal resistance protein, physically linked to a different gene that codes for antibiotic resistance on the same genetic element like a plasmid, so that when you select for one trait, you indirectly select for the other. Another interesting finding is that we found antibiotic resistance genes in environmental bacteria that are also found in clinical bacteria—suggesting that gene flow is happening between clinical and environmental settings.
Q. What drew you to your current research at the J. Craig Venter Institute? A. Since graduating from UGA, I’ve been involved in a few different research projects on diverse topics in microbiology— ranging from studying groundwater biogeochemistry, to host-pathogen associations in a food-borne pathogen. These experiences helped me realize that I am really interested in understanding the genomic basis for bacterial evolution. The last decade has seen a tremendous change in how microbiologists work, due to advances in genome technology. For example, during my dissertation research, it was a big deal to get one bacteria sequenced. Now, I’m looking at 50 bacterial genomes, and still counting, in my current project at JCVI. With this increase in sequencing capabilities comes a huge demand for increased computational capabilities to make sense of all the data that is generated. Thus, one of the reasons I was drawn to the project at JCVI was for
the opportunity to develop my bioinformatic skills while addressing a very important topic like the spread of antibiotic resistance in A. baumannii.
Q. Can you describe what you do at the J. Craig Venter Institute in layman terms? A. In a nutshell: The organism I am studying now, Acinetobacter baumannii, is a hospital-acquired pathogen, meaning people enter the hospital for other reasons and while they are there, become infected with this organism—through respirators, or catheters, or open wounds, for example. In the last decade or so, this organism has become increasingly antibiotic-resistant due to its exposure to antibiotics in hospital patients. We are studying how this organism evolves by comparing the genomes of closely related strains isolated from the same hospital over the course of a few years.
Q. Have you met (founder) Hamilton Smith? Or other Nobel laureates working there? A. Yes, I run into him in the break room frequently. I once ended up sitting next to him during a training seminar on how to properly fill out timesheets, and it struck me as funny that even Nobel laureates have to sit through mandatory HR training sessions. We recently held a celebration at work for his 83rd birthday. It’s amazing to work with someone who is still so motivated by his research.
Q. If there is little incentive, profit-wise, to develop new antibiotics, what might the future hold? Is there a new-generation drug on the horizon?
Media Reports Contain Some Surprising Sources of Infection Even physicians' neck ties have been banned in some hospitals. A researcher at the New York Hospital Medical Center of Queens proved doctors' natty ties were more septic than sartorial. When he tested the neckties worn by physicians and compared them to those worn by the hospital’s security guards, there was hard proof. Almost half of the neckties worn by doctors at the New York facility harbored dangerous bacteria. The bacteria detected included Staphylococcus aureus, MRSA, Klebsiella pneumoniae and Pseudomonas aeruginosa. These can cause pneumonia and blood infections, and worse. The problem, as the doctor’s necktie illustrates, is the prevention and containment of infection.
26
www.grad.uga.edu