A recent study revealed that diabetes mellitus may contribute to the emergence and proliferation of antibiotic-resistant Staphylococcus aureus in skin and soft tissue infections.
In the study, published in Science Advances, researchers found that antibiotic resistance emerged exclusively in diabetic mice within 5 days of infection, with no resistance observed in nondiabetic mice.
The study involved diabetic and nondiabetic mice infected with methicillin-resistant S aureus (MRSA) and treated with rifampicin. In diabetic mice, rifampicin-resistant mutants rapidly emerged, with counts exceeding 105 colony-forming units (CFUs) per lesion compared with no resistant colonies in nondiabetic controls. Whole-genome sequencing identified rpoB gene mutations as the primary drivers of resistance.
"The diabetic infection environment represents an ideal reservoir for the emergence and proliferation of antibiotic resistance. Controlling the blood sugar of diabetic mice with insulin resulted in significantly decreased incidence of antibiotic-resistant S aureus," said lead study author John C. Shook, of the Department of Microbiology and Immunology at the University of North Carolina at Chapel Hill, and his colleagues.
The study found that hyperglycemia played a dominant role in facilitating resistance by accelerating bacterial proliferation. This rapid growth allowed resistant strains to outcompete sensitive populations under antibiotic pressure. The presence of elevated glucose levels in diabetic mice created conditions conducive to the emergence and survival of resistant bacterial strains.
Additionally, vancomycin-intermediate resistant S aureus strains exhibited increased growth and virulence in diabetic mice. These findings suggested broader risks for the efficacy of frontline antibiotics, raising concerns about the management of such infections in patients with diabetes.
Another significant finding was that insulin treatment in diabetic mice markedly reduced the emergence of resistant bacteria. The outcome highlighted the potential of glycemic control as a strategy to mitigate antibiotic resistance.
The study emphasized the importance of glycemic control in managing diabetic infections and limiting the spread of antibiotic resistance. Its strengths included high-depth genomic sequencing and robust in vivo modeling, which provided reliable insights into the resistance dynamics observed.
Future research should explore the role of other antibiotics and examine long-term resistance dynamics in diabetic infections to develop comprehensive strategies for preventing antibiotic resistance in this vulnerable population.
No conflicts of interest were disclosed by the authors.