Like all genetic disorders, there aren’t many silver linings to having cystic fibrosis.
The best we can say is that life expectancy for people with CF has improved thanks to new treatments and earlier intervention. But CF is a tough opponent that requires continuous attention.
CF causes the buildup of thick mucus in the lungs and digestive track; this mucus is an excellent conductor for bacterial infections, which are the real danger for people living with CF.
For years, maintenance treatments have focused on clearing this mucous out while scientists searched for ways to prevent it from building up in the first place. But a recent study suggests we may have been going about it all wrong.
A group of scientists made a startling discovery about the physical structure of bacterial infections—including those that effect people living with CF.
Typically, most bacterial infections can be found hanging out in something called a “biofilm.” Biofilms are microscopic structures that cling to the infected surface in a thin, slimy layer, which helps the bacteria take root and cause infections. The conventional wisdom was that this biofilm was something produced inside the bacteria and deposited on the surface, kind of like a spider web. That thinking in turn affected how scientists studied the biofilm: as a completely foreign, alien structure.
But in Cell Host & Microbe, study co-author Dr. Paul Bollyky notes that the actual structure is something very different.
Dr. Bollyky compares biofilms to termite mounds: complicated structures that use materials from the world around them (in this case, the body) to create something that can’t be destroyed with traditional antibiotics.
What really shocked Dr. Bollyky and his colleagues was the discovery that bacteria are actually working with viruses to build biofilms.
Why is that so surprising? Because usually viruses try to invade and destroy bacteria, the same way they invade and destroy other lifeforms. But it turns out that these viruses have joined with the bacteria in an unholy alliance, creating something called a “bacteriophage” that collects polymers from the local environment—including your DNA—to build biofilms.
Worse still, these biofilms actually have a crystalline structure, which makes them hardier and more resistant to antibiotics.
That’s the bad news. The good news is that with this knowledge, scientists can begin looking at developing antibiotics that target the crystalline structure of the biofilm… or better yet, the bacteriophages themselves.
And that’s what brings us back to CF.
More targeted antibiotics could knock out bacterial infections in the lungs before they can cause too much damage. That could mean a longer life expectancy—and a better quality of life—for people fighting CF.
There’s still a lot of work to be done, but this could turn out to be one hell of a silver lining!