Diabetes can drive antibiotic resistance to staph, study finds
NEW YORK, Feb. 12 (UPI) -- People with diabetes are more prone to developing Staphylococcus aureus, a leading cause of infections and death associated with resistance to antibiotics, a new study has found.
The findings were published Wednesday in Science Advances.
An interaction between bacteria and diabetes could be a major force fueling the swift evolution and spread of antibiotic resistance, the researchers said.
Staph is the most widespread bacterial infection among individuals with type 2 diabetes, a chronic condition that impairs blood sugar control and decreases the body's ability to combat communicable diseases.
"Diabetes and antibiotic resistance are two major and growing problems worldwide," study senior co-author Brian Conlon, an expert on antibiotic treatment failure, told UPI.
"Antibiotic resistance evolves rapidly in diabetics," said Conlon, an associate professor in the Department of Microbiology and Immunology at the University of North Carolina-Chapel Hill.
"This further emphasizes the importance of controlling insulin in diabetics during infection. It may be useful to take a personalized medicine approach to prescribe antibiotics differently -- more than one antibiotic, for example -- in diabetics," he added.
Diabetes affects control of a sugar called glucose, often causing an excess amount to accumulate in the bloodstream. Staph thrives on high sugar levels, enabling it to multiply more quickly.
As the numbers of bacteria proliferate in a diabetic infection, the chance of resistance increases. Random alterations occur and some build up resistance to external stressors, such as antibiotics. Once a resistant mutant appears in a diabetic infection, it speedily takes over the population, recruiting the excess glucose to power speedy growth.
Senior co-author Lance Thurlow, an expert on Staph's disease-causing mechanism in diabetes, said they undertook this research because they were "both aware that there was a high incidence of antibiotic treatment failure associated with infections in individuals with diabetes."
"We started to question if the diabetic infection environment was contributing to antibiotic treatment failure," said Thurlow, an assistant professor in the Department of Biomedical Sciences at the University of North Carolina-Chapel Hill's Adams School of Dentistry.
"The increase in antibiotic resistance is a major global health concern," he said. "Diabetes is expected to afflict nearly a billion people by 2050."
Conlon and Thurlow had expressed a longstanding interest in comparing the effectiveness of antibiotics in a model with and without diabetes. The researchers brought their labs together to conduct a study with antibiotics in a diabetic mouse model of the Staph infection.
First, they prepared a mouse model with bacterial infection in the skin and soft tissue. Then they divided the mouse models into two groups: One half received a compound that selectively kills cells in the pancreas, rendering them diabetic, while the other half did not get the compound.
Researchers then infected both diabetic and non-diabetic models with Staph and treated them with rifampicin, an antibiotic with a high rate of causing resistance.
After five days of infection, they observed the antibiotic had practically no effect in diabetic models. In investigating samples, they were stunned that the bacteria had evolved to become resistant to the antibiotic -- and even more surprised this had transpired in only four days. Meanwhile, there were no antibiotic-resistant bacteria in the non-diabetic models.
The researchers said the evolution of antibiotic resistance in people with diabetes could spell trouble for the population at large. Antibiotic-resistant strains of bacteria spread from person to person in the same ways as other bacteria and viruses do -- in the air, on doorknobs and through food. This means preventing these types of infections should be a major priority.
Their findings also suggest that controlling blood sugar with insulin could be significant in averting antibiotic resistance.
Other experts commended the researchers for undertaking a study revealing that the interplay between bacteria and diabetes could be a key driver in the rapid evolution and spread of antibiotic resistance globally.
"It becomes harder and harder to treat Staphylococcus aureus infections. There is likely to come a time when we will not have antibiotics to treat these infections," said Patrick Schlievert, emeritus professor of microbiology and immunology and internal medicine at the University of Iowa Carver College of Medicine in Iowa City.
"Diabetic patients develop serious foot ulcers and other infections that may lead to amputation and death. The development of further antibiotic resistance is a serious problem," said Schlievert, who has published studies showing that this bacterium is a cause of type 2 diabetes.
People with less-than-optimal control of their diabetes are more vulnerable to infections, and they also may have more antibiotic resistance. "The mechanism for this is not fully clear," said Dr. Marilyn Tan, chief of the Endocrine Clinic at Stanford Health Care in Palo Alto, Calif.
Controlling blood sugar "is critical to reducing infection risk and promoting wound healing," Tan said.
Dr. Shira Doron, chief Infection control officer at Tufts Medicine in Boston, said this research "underscores the importance of controlling diabetes in the fight against antibiotic resistance. It will be important to study what other chronic conditions might also predispose people to higher risk for resistance."
