"Anti-antibiotic" aims to slow rise of drug-resistant bacteria

"Anti-antibiotic" aims to slow...
A new combination therapy may be able to help reduce antibiotic resistance
A new combination therapy may be able to help reduce antibiotic resistance
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A diagram demonstrating the process for the new "anti-antibiotic"
A diagram demonstrating the process for the new "anti-antibiotic"
A new combination therapy may be able to help reduce antibiotic resistance
A new combination therapy may be able to help reduce antibiotic resistance

Antibiotics are one of the most important medical breakthroughs of the last century, but decades of overuse means bacteria are quickly developing resistance to them. Now, a team of scientists has found that a drug already approved by the FDA can act as an "anti-antibiotic,” reducing the development of drug resistance when taken alongside an antibiotic.

Antibiotic resistance is an example of evolution at work. When a drug wipes out a population of bacteria, a few out of millions will inevitably survive, often thanks to random genetic mutations that might have given them an edge. And because these “superbugs” were the only ones to survive, those genes are more likely to be passed onto future generations.

Over time, drugs can become ineffective against entire species, so scientists and doctors move onto new drugs – until they also begin to fail. Now here we are decades later, with the drugs forming our last line of defense now becoming ineffective, threatening to throw us into a new “dark age of medicine” where the most basic of infections can become life threatening.

New antibiotics can’t come soon enough, so other interventions are needed. And that’s where the new study, from scientists at Pennsylvania State University and the University of Michigan, comes in.

“We have created a therapy that may help in the fight against antimicrobial resistance, an ‘anti-antibiotic’ that allows antibiotic treatment without driving the evolution and onward transmission of resistance,” says Andrew Read, lead author of the study.

The team focused on Enterococcus faecium, a bacterium commonly found in the gut. While it’s harmless there, it can spread to other parts of the body and cause more serious infections such as UTIs, and if it gets in the bloodstream, even sepsis.

A diagram demonstrating the process for the new "anti-antibiotic"
A diagram demonstrating the process for the new "anti-antibiotic"

Worse still, there’s a dangerous superbug strain known as vancomycin-resistant Enterococcus faecium (VRE). A drug called daptomycin is commonly used to kill VRE in the bloodstream, but it’s now becoming resistant to that as well. That’s often because when the drug is injected intravenously, a small percentage of it makes its way into the intestines and drives evolution of resistance in the local population.

So, the researchers set out to find a way to protect the gastrointestinal population from the wandering antibiotic. An existing drug called cholestyramine had previously been found to bind to daptomycin, so the team hypothesized that taking that at the same time as the antibiotic would render it inert in the gut.

The researchers injected daptomycin into the bloodstream of mice, and gave some of them cholestyramine orally at the same time. They found that the two drugs together reduced the amount of VRE in their feces by about 80 times compared to mice that hadn’t received the second drug.

“We have shown that cholestyramine binds the antibiotic daptomycin and can function as an ‘anti-antibiotic’ to prevent systemically administered daptomycin from reaching the gut,” says Read.

The hope is that the new method could be added to our arsenal of tools to help slow the rise of antibiotic resistance, while scientists come up with new drugs and other methods to kill superbugs. Helpfully, cholestyramine is already approved by the US FDA to help control cholesterol levels, so it should be relatively simple to roll out.

The research was published in the journal eLife.

Source: Penn State University

Great synopsis Mr. Irving, but I find the hype both premature and simplistic. Yes we can reduce the gut depletion of susceptible bacteria with the off-chance (actually, most likely chance) of resistant bacteria thriving to colonize the gut and be shed in feces. And yes, cholestyramine is well tolerated in most patients when take for the cholesterol lowering effects. But the contraindications - reduced vitamin absorption, risk with liver disease, CAD, DM, and other conditions means it has a narrow efficacy (binding daptomycin when prescribed) and limited 'anti-antibiotic' potential. We have hundreds of antibiotic formulations and so far this study proves cholestyramine useful as a daptomycin adjunct. Whoopee. Won't change my practice nor make my patients less susceptible to antibiotic resistant infections.

We keep nibbling at the edges of the problem, not meeting it head on. I do not look forward to a completely antibiotic resistant world, but we are headed there faster and faster. Oh the 1950s - 1980's were a great time to prescribe antibiotics....almost anything worked. Now with all your knowledge and skill, some bacterial infections are serious illnesses - again! But we do keep nibbling at the edges, don't we.
Whoever came up with the term “anti-antibiotic” needs some remedial vocabulary training STAT.

The “anti-“ prefix means “against” (as in “opposed to”). For obvious example, an antibiotic is something that works against “biotics” (loosely, “life forms”).

So, an “anti-antibiotic” could only be something that works against antibiotics, which is EXACTLY THE OPPOSITE of what this new therapy does.

Call it an antibiotic enhancer or an antibiotic fortifier or an antibiotic shield; even simpler, call it a new therapy that prevents bacteria from developing resistance to antibiotics.

Just don’t call it the exact opposite of what it is. That makes everyone talking about it sound like they have, at best, a rudimentary command of the English language.