Anyone who has needed strong antibiotics knows the trade-off: the drug that kills the infection also wipes out much of the helpful flora in the gut. Researchers in Germany now report a compound that seems to avoid that collateral damage, at least in mice.
The substance is argyrin B, a molecule made by myxobacteria, predatory microbes that live in soil and use such chemicals to kill and digest other bacteria. Scientists at HIPS in Saarbrücken, the Saarland university clinic and the medical school in Hannover pitted it against Clostridioides difficile, a germ behind a large share of the diarrhoea cases that follow antibiotic courses. The findings are now out in a Nature-family journal, npj Antimicrobials and Resistance.
Plenty of healthy people carry this microbe without noticing. Trouble starts when broad-spectrum drugs clear away its competitors: the bacterium multiplies, releases toxins and can trigger severe, sometimes life-threatening inflammation that often returns. Patients with repeated relapses may end up needing a stool transplant.
In the lab, argyrin B stopped the pathogen at very low doses, and in infected mice it cut the bacterial load about as well as vancomycin, a standard treatment. The difference showed up afterwards. Common gut microbes were largely unaffected, and the animals’ microbial communities bounced back toward normal, something the authors did not see with vancomycin. The compound blocks a protein the bacteria need to build new proteins, the same target already known from the hospital germ Pseudomonas aeruginosa.
Another useful trait: when swallowed, argyrin B hardly reaches the bloodstream and stays mostly in the large intestine, right where the infection sits. That could mean fewer side effects elsewhere. HIPS researcher Jennifer Herrmann hopes this would let a patient’s intestinal flora recover faster. Next, the team wants to work out the right dose and test the molecule against recurring infections. Human trials are still some way off.
