Stenotrophomonas maltophilia (steno) is nasty. And it’s everywhere: in rivers, in fresh water and tap water, in the mouths of animals, and — most threateningly — in hospitals and on medical equipment. Among patients with compromised immune systems, steno is associated with a mortality rate of 70 percent.
“Steno is an opportunistic pathogen,” says Joanna Brooke (associate professor, Biology) who’s been studying the bug for 10 years. “Healthy people may have steno, but we aren’t affected by it. But the weak? That’s a different story. Those flowers in a vase, that plastic pitcher of water, that nebulizer or IV line — if they’re harboring the bacteria, they could endanger the patient in the bed.”
With funding from the National Institutes of Health, Brooke and her students (graduate and undergraduate) create genetic variants of steno to observe how it grows and how it might be removed from surfaces in hospitals.
“Recently, scientists have been looking into steno’s genetic makeup,” she says.
“On surfaces, it forms biofilms by clustering with other bacteria — a biofilm is a community of cells, surrounded by lipids, carbohydrates, proteins, and nucleic acids. As its name suggests, a biofilm creates a protective barrier against antibiotics. At the same time, as pathogens in the biofilm swap genes, they also transfer each other’s resistance to specific antibiotics. So, we’re finding many variations of steno, each one resistant in different ways to different antibiotics. It has been suggested that the organism can use antibiotics as food! Isn’t that interesting?”
Brooke says the fight against steno has two fronts: prevention and “cure” — from simple strategies like hand washing and disinfecting surfaces to complex attempts to thwart the bacteria once it’s in the patient.
If hospitals try to remove a biofilm physically, a few cells are always left behind; within hours, a new biofilm is back in place. So, the medical community tries to remove biofilms chemically. Soon enough, the bacteria is multi-drug-resistant.
The new thinking in drug therapy is to combine different antibiotics to target different parts of the bacteria. But steno will continue to adapt. A promising (but not proven) alternative to antibiotics is antimicrobial peptides — short, little proteins that poke holes in a cell’s membranes, causing the pathogen to die.
But can steno be eliminated altogether? “No, I think this problem is forever,” says Brooke. “We’re just trying to stay ahead of what’s going to happen next.”
Last year, Brooke was asked by the prestigious Clinical Microbiology Reviews Journal to write an article covering the steno research done from 1998 to the present, including her own. “When I started working in this area of research in 2002, there were very few papers — now steno is a hot topic!” says Brooke.
“I think there are two reasons for that. One, the organism used to be misidentified; now that it’s been reclassified, awareness and interest have increased. Two, the sophistication and sensitivity of today’s molecular technology make it possible to see steno, to grow it in the lab, and to understand its nature.
“The review article — “Stenotrophomonas maltophilia: an Emerging Global Opportunistic Pathogen” — has generated requests for the paper worldwide and has already been cited in peer-review articles; I’m getting not just questions, but also requests to collaborate. That’s great for my students because, in our labs, we’re sharing the very best thinking about steno in the world today.”
In 2011, Brooke won the Excellence in Teaching Award.