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2013 OMIG Abstract 5

Torque Teno Virus Associated with Culture Negative Endophthalmitis
Russell N. Van Gelder, MD, PhD1, Aaron Y. Lee, MD, MS2, Lakshmi Akileswaran, PhD1,
Michael D. Tibbetts, MD3, Sunir J. Garg, MD3
1Department of Ophthalmology, University of Washington, Seattle, WA;
2Department of Ophthalmology and Visual Sciences, Washington University, St. Louis, MO;
3Wills Eye Hospital, Thomas Jefferson Medical School, Philadelphia PA

Purpose: To use deep DNA sequencing techniques to identify potential pathogens in culture-negative endopthalmitis.

Methods: Vitreous was collected from 21 consecutive endophthalmitis cases (14 culture-positive and 7 culture-negative) and 7 routine, uninfected vitrectomies. Samples were analyzed by traditional culture, quantitative 16S PCR with sequencing of products, and Biome Representational in Silico Karyotyping (BRiSK), a representational deep DNA sequencing technique.

Results:  None of the control vitreous samples were positive for bacteria by any test. 16S PCR and/or BRiSK recapitulated culture results in the majority of cases. Bacterial loads by qPCR in culture-positive cases were between 104 and 107 genomes/ml. None of the 7 culture-negative samples showed high levels of bacteria by 16S qPCR (all below 104 genomes/ml), and only one showed bacterial DNA with BRiSK. BRiSK tags corresponding to Torque Teno virus were identified in the majority of culture-negative samples as well as two culture-positive samples. qPCR for Torque Teno revealed no viral DNA in any control vitreous sample, but positive results for high level Torque Teno virus in 5/7 culture-negative and 2/14 culture-positive samples.

Conclusions:  There is high degree of agreement between standard culture, 16S qPCR, and BRiSK, particularly for culture-positive endophthalmitis cases. Torque Teno virus has been previously implicated in seasonal hyperacute panuveitis syndrome (SHAPU). The finding of this virus at high levels in culture-negative endophthalmitis raises the possibility that it may contribute to pathogenesis.

Grant funding:  Supported by the Burroughs Wellcome Translational Scientist Award (RVG), NIH R01EY022038-01, CORE grant P30EY001730

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