The Impact of Inoculation Parameters on the Pathogenesis of Contact Lens–Related Infectious Keratitis

Abstract

P. aeruginosa induces keratitis in this lens-wearing model after a single inoculation. Delayed disease onset was interesting considering the greater keratitis risk during extended wear. Infection did not require the disruption of corneal barrier function before lens wear and occurred without exposure to lens care solutions. The data suggest that keratitis involves biofilm formation or other bacterial adaptations in vivo.

Role of Defensins in Corneal Epithelial Barrier Function against Pseudomonas aeruginosa Traversal

“…For example, in the cornea, a multilayered epithelium protects the underlying stroma. Indeed, P. aeruginosa corneal infection does not occur in the absence of fullthickness epithelial injury or contact lens wear (32,43,54). For this reason, much of what we understand about host-microbe interactions in vivo has been derived from experimental models that deliberately bypass the epithelial barrier (9,18).…”

The Impact of Cellular Debris on Pseudomonas aeruginosa Adherence to Silicone Hydrogel Contact Lenses and Contact Lens Storage Cases

“…16 In animal models of infection, extended contact lens wear with concurrent bacterial challenge has been shown to result in significant neutrophil accumulation and biofilm formation on posterior lens surfaces. 17,18 Clinically, although biofilms are infrequently found on contact lenses, the presence of lens-associated biofilms have been reported with culture-proven MK during contact lens wear, 19 including lenses worn on an extended wear basis. 20 We recently have reported that PA can exploit the robust neutrophil response that occurs during bacterial challenge in extended wear to enhance biofilm formation on hydrogel contact lenses surfaces.…”

Pseudomonas aeruginosa Infectious Keratitis in a High Oxygen Transmissible Rigid Contact Lens Rabbit Model

“…20 Moreover, low oxygen transmissible lens wear, in the presence of a preexisting epithelial defect, fails to alter the time course of P. aeruginosa infection in the rat eye. 17 Taken together, these studies suggest that either corneal epithelial surface damage alone or that due to hypoxia is not sufficient to produce P. aeruginosa infection of the otherwise healthy corneal epithelium and that the presence of a lens is required. Given the critical role of the lens in the pathogenesis of infection, it is not surprising that current epidemiological evidence indicates that the use of high oxygen transmissible lenses, which eliminate hypoxia-induced corneal surface damage, has failed to alter the overall incidence of microbial infection associated with contact lens wear.…”

“…[11][12][13][14][15][16] In concert with this data, two prior laboratories have used low oxygen transmissible hydrogel lenses inoculated with P. aeruginosa to initiate infection in rodent models. 17,18 While epithelial surface damage resulting from low oxygen transmissible lens wear may promote bacterial adhesion to the corneal surface in vivo, exposure of the human cornea to anoxia using nitrogen goggles alters epithelial desquamation but does not increase P. aeruginosa adherence to exfoliated epithelial cells. 19 Related studies using filter paper injury to mimic epithelial surface damage from lens wear in the mouse eye in the absence of a hypoxic stimulus followed by direct inoculation with P. aeruginosa have also found that the cornea fails to infect from surface damage alone.…”