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Phillip S. Coburn, Brandt J. Wiskur, Elizabeth Christy, Michelle C. Callegan; The Diabetic Ocular Environment Facilitates the Development of Endogenous Bacterial Endophthalmitis. Invest. Ophthalmol. Vis. Sci. 2012;53(12):7426-7431. doi: 10.1167/iovs.12-10661.
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We tested the hypothesis that changes in the diabetic ocular environment facilitate the development of endogenous bacterial endophthalmitis (EBE).
C57BL/6J mice were rendered diabetic with streptozotocin (STZ) for 1, 3, or 5 months' duration. Diabetic and age-matched nondiabetic mice were tail vein–injected with 108 CFU of Klebsiella pneumoniae , a common cause of EBE in diabetics. After either 2 or 4 days postinfection, the EBE incidence was assessed by electroretinography, histology, bacterial counts, and myeloperoxidase ELISAs. Blood-retinal barrier (BRB) permeability in uninfected diabetic mice also was determined.
No cases of EBE were observed among the 1-month diabetic group. Extending the time from diabetes induction to 3 months resulted in a 23.8% EBE incidence after 2 days, and a 22% incidence after 4 days. The incidence of EBE increased to 27% in the 5-month diabetic group. Infected eyes had an average 8.01 × 102 and 6.19 × 104 CFU/eye for the 3- and 5-month diabetic groups, respectively. There was no significant difference in BRB permeability between control and 1-month uninfected diabetic mice. However, 3- and 5-month diabetic mice had significantly greater BRB permeability than control mice. These results suggested that increasing the time from STZ diabetes induction to 3 and 5 months resulted in an ocular environment more conducive to the development of EBE.
These results demonstrated a correlation between an increase in BRB permeability and an increase in EBE incidence, supporting the hypothesis that diabetic ocular changes contribute to the development of EBE.
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