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2019 OMIG Abstract

Characterization of Corneal Endothelial Architecture in Ocular Inflammation Secondary to Rubella Virus

Miel Sundararajan, MD1,2, Nisha R. Acharya, MD, MS1,2, Jeremy Keenan MD, MPH1,2,
John A. Gonzales, MD1,2, Thuy Doan, MD, PhD1,2
1Francis. I Proctor Foundation; University of California, San Francisco, San Francisco, CA;
2Department of Ophthalmology, University of California, San Francisco, San Francisco, CA


Purpose: Rubella virus (RV) is a known cause of the Fuchs heterochromic iridocyclitis phenotype of chronic anterior uveitis. Metagenomic deep sequencing (MDS) has allowed for demonstration of the presence of the RV genome in intraocular fluid samples of multiple patients. This case series seeks to characterize endothelial cell changes associated with this pathogen.

Methods: Six white males were diagnosed with RV-associated uveitis by MDS. Three patients underwent in vivo corneal confocal microscopy for evaluation of the endothelial cell layer and keratic precipitates. Confocal images were further analyzed to quantify endothelial cell density and the area of each of the keratic precipitates.

Results: Multiple features were identified including dendritic keratic precipitates (2 of 6 patients), endothelial infiltrates, spot-like holes, and polymorphism and polymegathism of the endothelial cells as compared to the unaffected fellow eyes. The area of dendritic keratic precipitates ranged from 1217 to 5683 um2. The average endothelial cell density measured 2624 cells/mm2 in unaffected control eyes as compared to 2033 cells/mm2 in affected eyes.

Conclusion: In vivo confocal microscopy reveals characteristic findings in RV-associated ocular inflammation which may be useful in aiding in diagnosis. MDS is unique in that it allows for whole-genome sequencing of pathogens, improving diagnostic yield of aqueous samples. The appearance of dendritic appearing keratic precipitates with angled branches is characteristic of this entity. Additional characteristic changes included endothelial cell infiltration by inflammatory cells, spot-like holes signifying loss of individual endothelial cells, and polymorphism and polymegathism.

Disclosure: S (NRA, JAG, TAD)

 

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