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The clinical and cellular basis of contact lens-related corneal infections

Authors :
Danielle M Robertson
H Dwight Cavanagh
Source :
Clinical Ophthalmology, Vol 2008, Iss Issue 4, Pp 907-917 (2008)
Publication Year :
2008
Publisher :
Dove Medical Press, 2008.

Abstract

Danielle M Robertson, H Dwight CavanaghDepartment of Ophthalmology, The University of Texas Southwestern Medical Center, Dallas, TX, USAAbstract: Microbial keratitis (MK) is the most visually devastating complication associated with contact lens wear. Pseudomonas aeruginosa (PA) is highly invasive in the corneal epithelium and is responsible for more than half of the reported cases of contact lens-related MK. To protect against Pseudomonas-mediated MK, the corneal epithelium has evolved overlapping defense mechanisms that function to protect the ocular surface from microbial invasion. Research has shown that contact lens wear disrupts these protective mechanisms through breakdown of normal homeostatic surface renewal as well as damaging the corneal surface, exposing underlying cell membrane receptors that bind and internalize PA through the formation of lipid rafts. Human clinical trials have shown that initial adherence of PA with resulting increased risk for microbial infection is mediated in part by contact lens oxygen transmissibility. Recently, chemical preserved multipurpose solutions (MPS) have been implicated in increasing PA adherence to corneal epithelial cells, in addition to inducing significant levels of toxic staining when used in conjunction with specific silicone hydrogel lenses. This review summarizes what is currently known about the relationship between contact lenses, the corneal epithelium, MPS, and infection.Keywords: cornea, epithelium, contact lens, microbial keratitis

Subjects

Subjects :
Ophthalmology
RE1-994

Details

Language :
English
ISSN :
11775467 and 11775483
Volume :
2008
Issue :
Issue 4
Database :
Directory of Open Access Journals
Journal :
Clinical Ophthalmology
Publication Type :
Academic Journal
Accession number :
edsdoj.653682a513bd49e4a0ed36fbaf67ed7e
Document Type :
article