PULLMAN, Wash.–The “bugs and drugs” tennis match has no clear winner yet. Almost every time Mother Nature serves up a new bacteria, her serve is returned by a new antibiotic. Antibiotics have done well. But Mother Nature’s not-so-secret weapon – evolution – is providing her with more and more aces.
“I have a lot of concern about resistant bacteria and workable antibiotics,” says Mark Garrison, College of Pharmacy professor at Washington State University at Spokane. Garrison studies bacterial resistance to antibiotics. A story about his research appears in the June issue of WSU Hilltopics, the university’s alumni publication/public relations publication.
A typical bacterial infection involves billions of bacteria. Not all are identical. When treated with an antibiotic, a few are usually resistant to the drug and survive. The resistant ones will be more successful at reproducing, and the next generation will have a larger number of them.
The antibiotics are providing selective pressure for resistance. The more antibiotics bacteria see, the more likely they’ll develop resistance.
History provides many examples, such as Staphlococcus aureus, an easily transmitted bacteria that causes pneumonia, blood and skin infections. Penicillin worked well when it first was used to treat staph infections, but resistance developed quickly. Now more than 95 percent of staph infections are penicillin resistant, and some are also resistant to the other antibiotics that have been developed to treat it. Luckily, vancomycin works, at least for now.
In the laboratory, another species of bacteria has transmitted its vancomycin resistance to staphlococcus. “If it can be done inside a lab, that probably means it can be done outside,” says Garrison. “Mother Nature’s usually a step or two ahead.” And there are many places in nature, even in the human body, where several species of bacteria bump into each other and could trade resistance to antibiotics.
Garrison explores mechanisms of drug resistance in a bacteria you’ve not heard of yet: Stenotrophomonas maltophilia. It causes respiratory and blood infections in hospital patients, especially those with compromised immune systems. “It’s a bug that doesn’t tend to cause a problem for you or me,” says Garrison, “but in patients with weakened defenses it has a stronger opportunity to flourish.”
S. maltophilia is of interest to Garrison primarily because it develops resistance to most any drug thrown at it, and it does so fast. He’d like to learn how.
Garrison studies resistance with a unique method he developed several years ago. It allows him to expose bacteria to amounts of antibiotics more like what they see in real life than is possible with other methods. He’s used it to compare antibiotics, evaluate new antimicrobial agents, optimize treatments, and find the best drug for treating a specific bacteria. He’s pleased that although his research is more basic than clinical, his collaboration with other health care professionals means that it always relates to making people better.
Garrison sees the treatment of bacterial infections changing in the future. Broad spectrum antibiotics should be used with caution and only where they are the best, such as for treating life-threatening disease when the bacterial species is unknown. They should not be routinely prescribed, he says.
When the bacteria is known, says Garrison, it’s better to aim with antibiotics specifically designed to deliver a knock-out punch. “This will help minimize potential for resistance to develop.” And for life-threatening bacteria for which few antibiotics are effective, “prevention will provide the biggest bang for our buck,” he says.