The biofilms where bacteria congregate are like little apartment buildings

Biofilm Under Construction Bacteria first glue themselves together on whatever surface they can find purchase, then encase themselves in a protein shell, creating a firmly entrenched biofilm that can be thousands of times more resistant to antibiotics as the individual bacteria comprising it. via U.C. Berkeley Media Relations

In an effort to outfox antibiotic resistance, a team of researchers based out of U.C. Berkeley--and including none other than Nobel laureate Steven Chu--want to build a wrecking ball that tears down bacterial cities. It’s not quite there yet, but in a paper released today the research group announced that via a new imaging technique it has for the first time revealed the structure of these biofilms -- and where they are vulnerable to attack.

Biofilms organize themselves into complex structures when they colonize, and bacteria generally spend most of their lives as part of one of these biofilms. And while these very bacteria, taken individually, might be susceptible to certain drugs or antibiotics, they can be several orders of magnitude more resistant when they are fortified inside the protein shell of a biofilm. Biofilms are often the cause of chronic illnesses and wounds, because they are so difficult to uproot once they’ve taken root. Some can only be dealt with surgically.

But if bacteria find strength in numbers, the Berkeley team reasoned that the glue that binds them together is a serious weakness, and one that could be exploited to clinical effect. Veysel Berk, a post-doctoral in the physics department at the California Institute of Quantitative Biosciences at UC Berkeley first built a super-resolution telescope so he could physically observe the way biofilms developed, then devised a novel method of staining called continuous immunostaining to track individual target molecules throughout the process of biofilm construction.

His findings: Using a strain of cholera bacteria, Berk noticed that within roughly six hours of settling on a surface the bacterium laid down a kind of glue to attach itself in place before dividing into daughter cells. It cemented each daughter to itself before completely splitting in two, growing quickly into a cluster of firmly glued bacteria. The colony then began secreting a protein that encased the entire group--a kind of outer cement wall for the cluster that insulates them from the outside. These clusters further group themselves into biofilms, with tiny channels running between clusters to allow waste to pass outward and nutrients inward.

It’s a clever biological mechanism, but now that we can see what’s happening, we can target parts of this structure--either the initial glue binding the bacteria together or the protein cement encasing the larger cluster (or both). Collapse the outer wall, and it becomes vastly easier for antibiotics to get inside and dismantle the rest of the structure.

This imaging technique is not just a potential healthcare breakthrough. Biofilms exist everywhere--in plumbing and sewage pipes, on the hulls of oceangoing vessels, as the plaque on our teeth--so finding a means of breaking them down could have potential applications across industry and in environmental protection and remediation.

2 Comments

I've said it many times: the solution is phage therapy. Phages are naturally ocurring bacterial viruses against which the bacteria cannot develop resistance. The bacteria just die. Phages are harmless for humans. Phages cannot be patented, copyrighted or "owned" and financially exploited. Of course Big Pharma doesn't want you to know about this, want to keep you ignorant and continue holding you hostage to their unsavoury commercial practices working together with your physician and pharmacist. Just type "phage therapy" into your Google video search.

Peter10,
While bacteriophages work initially, they are just a temporary fix because there are some phenotypes that might be resistant towards the phage. Those phenotypes that do escape the phage treatment will just divide into cells resistant to the phage.You have to keep up with the ever changing strains of bacteria. In order to kill off a strain of bacteria, you have to have the corresponding bacteriophage to kill it or else it can not bind to the bacterial surface receptors needed to initiate entry/infection. I would strongly suggest reading a microbiology textbook before going off on some tangent about some "Big Pharma conspiracy."



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