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Jonathan J. Hunt, Jin-Town Wang, Michelle C. Callegan; Contribution of Mucoviscosity-Associated Gene A (magA) to Virulence in Experimental Klebsiella pneumoniae Endophthalmitis. Invest. Ophthalmol. Vis. Sci. 2011;52(9):6860-6866. doi: 10.1167/iovs.11-7798.
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Endogenous endophthalmitis secondary to Klebsiella pneumoniae liver abscess is a blinding infection that is being reported more frequently in the literature. The K1 capsule and magA contribute to virulence of systemic infection in mice; however, little is known about the role of magA in secondary ocular infections.
To assess the role of K. pneumoniae capsule in endophthalmitis, the authors induced experimental endophthalmitis by direct inoculation of 100 colony-forming unit wild-type, magA-deficient, or magA-complemented K. pneumoniae into the posterior segments of mouse eyes. Eyes were analyzed by quantitation of viable bacteria, retinal function, and inflammatory cell influx as well as by histology.
Wild-type K1 K. pneumoniae caused significant ocular disease. At the end point of 24 hours postinfection, eyes infected with wild-type K. pneumoniae retained significantly less retinal A-wave function than eyes infected with an isogenic magA-mutant strain. B-wave function retention was also greater in eyes infected with the magA mutant than with wild-type K. pneumoniae. Additionally, intraocular growth of the magA-deficient strain was less than it was in the wild-type strain. The amount of myeloperoxidase elicited was also significantly higher for wild-type–infected eyes at 24 hours.
These results indicate that in the eye, the K1 capsule of invasive K. pneumoniae significantly contributes to the ability of the bacteria to disrupt retinal function, to grow to high density, and to persist despite immune cell recruitment.
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