Trends in Contact Lens–Related Corneal Ulcers at a Tertiary Referral Center

Yıldız, Elvin; Airiani, Suzanna; Hammersmith, K.M.; Rapuano, Christopher J.; Laibson, Peter R.; Virdi, Ajoy S.; Hongyok, Teeravee; Cohen, Elisabeth J.

doi:10.1097/ico.0b013e318221cee0

Cited by 60 publications

(39 citation statements)

References 18 publications

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“…117 Compared with bacterial keratitis, fungal keratitis is frequently associated with poorer outcomes 118 and is a recurrent problem in many parts of USA with a recent increase in contact lens wearers. [119][120][121] In developing countries, ocular trauma is a major risk factor. 31,122,123 Fungal spores are able to penetrate compromised epithelium where they germinate, expressing β-glucan and α-mannan molecules on their surface.…”

Section: Onchocerca Volvulus (Onchocerciasis) Onchocerciasis Is Due Tmentioning

confidence: 99%

Pattern recognition receptors in microbial keratitis

Taube

Cendra

Elsahn

et al. 2015

Eye

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Section: Onchocerca Volvulus (Onchocerciasis) Onchocerciasis Is Due Tmentioning

confidence: 99%

Pattern recognition receptors in microbial keratitis

Taube

Cendra

Elsahn

et al. 2015

Eye

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“…It is also the most common cause of corneal infection associated with contact lens wear (5,6). Our research has shown that clinical and laboratory isolates of P. aeruginosa can be divided into invasive or cytotoxic strains based upon how they interact with host cells (7).…”

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confidence: 99%

The Importance of the Pseudomonas aeruginosa Type III Secretion System in Epithelium Traversal Depends upon Conditions of Host Susceptibility

et al. 2015

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Pseudomonas aeruginosa is invasive or cytotoxic to host cells, depending on the type III secretion system (T3SS) effectors encoded. While the T3SS is known to be involved in disease in vivo, how it participates remains to be clarified. Here, mouse models of superficial epithelial injury (tissue paper blotting with EGTA treatment) and immunocompromise (MyD88 deficiency) were used to study the contribution of the T3SS transcriptional activator ExsA to epithelial traversal. Corneas of excised eyeballs were inoculated with green fluorescent protein (GFP)-expressing PAO1 or isogenic exsA mutants for 6 h ex vivo before bacterial traversal and epithelial thickness were quantified by using imaging. In the blotting-EGTA model, exsA mutants were defective in capacity for traversal. Accordingly, an ϳ16-fold variability in exsA expression among PAO1 isolates from three sources correlated with epithelial loss. In contrast, MyD88؊/؊ epithelia remained susceptible to P. aeruginosa traversal despite exsA mutation. Epithelial lysates from MyD88 ؊/؊ mice had reduced antimicrobial activity compared to those from wild-type mice with and without prior antigen challenge, particularly 30-to 100-kDa fractions, for which mass spectrometry revealed multiple differences, including (i) lower baseline levels of histones, tubulin, and lumican and (ii) reduced glutathione S-transferase, annexin, and dermatopontin, after antigen challenge. Thus, the importance of ExsA in epithelial traversal by invasive P. aeruginosa depends on the compromise enabling susceptibility, suggesting that strategies for preventing infection will need to extend beyond targeting the T3SS. The data also highlight the importance of mimicking conditions allowing susceptibility in animal models and the need to monitor variability among bacterial isolates from different sources, even for the same strain. P seudomonas aeruginosa remains a leading cause of respiratory infections, septicemia, and urinary tract and burn wound infections (1-4). It is also the most common cause of corneal infection associated with contact lens wear (5, 6). Our research has shown that clinical and laboratory isolates of P. aeruginosa can be divided into invasive or cytotoxic strains based upon how they interact with host cells (7). Invasive strains can survive and replicate inside epithelial cells dependent on the type III secretion system (T3SS) effector ExoS (8-10), while cytotoxic strains instead encode ExoU, which can induce rapid death of intoxicated host cells (11,12). While details of how invasive and cytotoxic strains impact host cells vary, both types can cause human disease, and they can each be virulent in animal models of infection (13-15).Several in vivo models exist for studying P. aeruginosa pathogenicity. They include Caenorhabditis elegans (16-18) and Drosophila melanogaster (19), in addition to mouse models of pneumonia with sepsis (20-22), burn wound infection with sepsis (23-25), and gastrointestinal colonization and sepsis (26,27) and corneal scarification models (28)(29)(30)...

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“…2,12,15 Nevertheless, it is of note that Pseudomonas aeruginosa is the most frequent isolated agent in contact lens-related ulcers, while gram-positive bacteria were more strongly associated with ocular surface diseases and corneal traumas. 2,16 This might be because Pseudomonas aeruginosa is a water-borne strain that can adhere to and colonize lens materials during wearing. The bacterium usually survives in contact lens storage cases due to both its ability to produce a resistant biofilm on lenses and cases, and its endurance to contact lens disinfectants.…”

Section: Discussionmentioning

confidence: 99%