title: Bioburden after Staphylococcus aureus inoculation in type 1 diabetic rats undergoing internal fixation.
abstract: Fracture stabilization in the diabetic patient is associated with higher complication rates, particularly infection and impaired wound healing, which can lead to major tissue damage, osteomyelitis, and higher amputation rates. With an increasing prevalence of diabetes and an aging population, the risks of infection of internal fixation devices are expected to grow. Although numerous retrospective clinical studies have identified a relationship between diabetes and infection, currently there are few animal models that have been used to investigate postoperative surgical-site infections associated with internal fixator implantation and diabetes. The authors therefore refined the protocol for inducing hyperglycemia and compared the bacterial burden in controls to pharmacologically induced type 1 diabetic rats after undergoing internal fracture plate fixation and Staphylococcus aureus surgical-site inoculation. Using an initial series of streptozotocin doses, followed by optional additional doses to reach a target blood glucose range of 300 to 600 mg/dl, the authors reliably induced diabetes in 100 percent of the rats (n = 16), in which a narrow hyperglycemic range was maintained 14 days after onset of diabetes (mean ± SEM, 466 ± 16 mg/dl; coefficient of variation, 0.15). With respect to their primary endpoint, the authors quantified a significantly higher infectious burden in inoculated diabetic animals (median, 3.2 × 10 colony-forming units/mg dry tissue) compared with inoculated nondiabetic animals (7.2 × 10 colony-forming units/mg dry tissue). These data support the authors' hypothesis that uncontrolled diabetes adversely affects the immune system's ability to clear Staphylococcus aureus associated with internal hardware.
authors.affiliation: Durham and Chapel Hill, N.C. From Kenan Plastic Surgery Research Laboratories, Duke University Medical Center; the Department of Biomedical Engineering, Duke University; and the Department of Chemistry, University of North Carolina.
authors.forename: Nga L
authors.initials: NL
authors.lastname: Brown
authors.forename: Michael B
authors.initials: MB
authors.lastname: Rose
authors.forename: Gert
authors.initials: G
authors.lastname: Blueschke
authors.forename: Eugenia H
authors.initials: EH
authors.lastname: Cho
authors.forename: Mark H
authors.initials: MH
authors.lastname: Schoenfisch
authors.forename: Detlev
authors.initials: D
authors.lastname: Erdmann
authors.forename: Bruce
authors.initials: B
authors.lastname: Klitzman
mesh_terms: D000818:Animals; D001860:Bone Plates / Q000382:microbiology; D015169:Colony Count, Microbial; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications*; D003922:Diabetes Mellitus, Type 1 / Q000139:chemically induced / Q000150:complications*; D005264:Femoral Fractures / Q000150:complications / Q000601:surgery*; D005593:Fracture Fixation, Internal / Q000295:instrumentation; D008297:Male; D051381:Rats; D013203:Staphylococcal Infections / Q000209:etiology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000254:growth & development* / Q000302:isolation & purification; D013311:Streptozocin; D013530:Surgical Wound Infection / Q000209:etiology* / Q000382:microbiology
chemical_list: D013311:Streptozocin