Scientists at Lund University have discovered two molecular mechanisms that enhance the antibiotic resistance of Clostridioides difficile (C. diff), a problematic bacterium that can cause serious infections, especially in healthcare settings. C. diff thrives when antibiotic treatments disrupt normal gut flora, leading to increased mortality and extended treatment times. The resistance mechanisms involve a novel protein that interacts with the bacterial ribosome—the target of many antibiotics. This protein ejects antibiotic molecules from the ribosome, while a second mechanism modifies the ribosome, reducing antibiotic binding. Together, these mechanisms confer a “superpower” resistance to C. diff.
Counteracting the threat of antibiotic resistance is crucial, given the estimated 1.27 million deaths linked to resistant infections in 2019. Notably, C. diff infections are known to rise after clindamycin treatment, with this study elucidating the reason behind that increased risk. The findings indicate that even new antibiotics, like iboxamycin, may be ineffective against resistant C. diff strains. Moving forward, researchers aim to design tighter-binding antibiotic molecules and explore ways to prevent the synthesis of resistance factors, potentially leading to more effective treatment strategies. This international collaboration highlights the urgent need for innovative approaches to combat antibiotic resistance.
