University of Pittsburgh School of Medicine (UPSOM) scientists say we now know why those suffering uncontrolled diabetes are so vulnerable to the superbug staph infection Staphylococcus aureus.
University of Pittsburgh School of Medicine (UPSOM) scientists say we now know why those suffering with uncontrolled diabetes are so vulnerable to staph infections caused by Staphylococcus aureus.
According to the study published Nov. 13 in Science Advances, uncontrolled diabetes appears to create the perfect living conditions for S. aureus to can gain a foothold, grow and create a variety of deadly infections.
"This explains why a wound or cut in a patient with diabetes really must be treated aggressively,” senior author Anthony Richardson said in a University of Pittsburgh announcement. Richardson is an associate professor in UPSOM's Microbiology & Molecular Genetics Department. “The immune system needs help recognizing and clearing the infection before it’s able to take hold.”
The key risk for staph infections is elevated glucose, according to the study.
"Elevated blood/tissue glucose is a hallmark feature of advanced diabetes, and people with diabetes are prone to more frequent and invasive infections with Staphylococcus aureus," the study abstract said. "Phagocytes [a type of white blood cells that battles bacteria and other harmful things] must markedly increase glucose consumption during infection to generate an oxidative burst and kill invading bacteria."
S. aureus also requires glucose to survive. In non-diabetics, glucose is usually in too short supply for the infection to survive, especially when competing with phagocytes fighting S. aureus-generated infections.
"(T)his limited resource is reminiscent of nutritional immunity," the abstract said.
UPSOM researchers found "that infiltrating phagocytes do not express their high-efficiency glucose transporters in modeled diabetic infections, resulting in a diminished respiratory burst and increased glucose availability for S. aureus."
"We show that excess glucose in these hyperglycemic abscesses significantly enhances S. aureus virulence potential, resulting in worse infection outcomes," the abstract continued. "Last, we show that two glucose transporters recently acquired by S. aureus are essential for excess virulence factor production and the concomitant increase in disease severity in hyperglycemic infections."
Other UPSOM researchers in the study included Research Associate Professor Lance R. Thurlow, and biological sciences researchers Amelia C. Stephens and Kelly E. Hurley.