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

Abstract

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

Disclosure

Supported in Part by NIH Grant K08 EY15713 (DMR), EY10738 (HDC), Infrastructure Grant EY016664, The Pearle Vision Foundation, Dallas, Texas, and an unrestricted grant from Research to Prevent Blindness, Inc., New York, New York. The authors report no conflicts of interest in this work.