Corneal Infections Predisposing Factors Pathogens and Pathogenesis

When certain pathogens succeed in breaching the corneal defenses through superficial injuries or minor epithelial defects, the bradytrophic corneal tissue will respond to the specific pathogen with characteristic keratitis. Predisposing factors that promote inflammation are:

❖ Infection of the ocular appendages (for example, dacryostenosis accompanied by bacterial infestation of the lacrimal sac).

❖ Changes in the corneal epithelial barrier (bullous keratopathy or dry eyes).

❖ Lagophthalmos.

❖ Neuroparalytic disorders.

❖ Topical and systemic immunosuppressive agents. Pathogens causing corneal infections may include:

❖ Acanthamoeba.

Pathogenesis: Once these pathogens have invaded the bradytrophic tissue through a superficial corneal lesion, a typical chain of events will ensue:

❖ Pathogens invade and colonize the corneal stroma (red eye).

❖ Antibodies will infiltrate the site.

❖ As a result, the cornea will opacify and the point of entry will open further, revealing the corneal infiltrate.

❖ Irritation of the anterior chamber with hypopyon (typically pus will accumulate on the floor of the anterior chamber; see Fig. 5.7).

❖ The pathogens will infest the entire cornea.

❖ As a result the stroma will melt down to Descemet's membrane, which is relatively strong. This is known as a descemetocele; only Descemet's membrane is still intact. Descemet's membrane will be seen to protrude anteriorly when examined under a slit lamp.

❖ As the disorder progresses, perforation of Descemet's membrane occurs and the aqueous humor will be seen to leak. This is referred to as a perforated corneal ulcer and is an indication for immediate surgical intervention (emergency keratoplasty; see p. 152). The patient will notice progressive loss of vision and the eye will be soft.

Bacterial corneal ulcer.

Bacterial corneal ulcer.

Fig. 5.7 a Clinical findings include a central bacterial corneal ulcer with hypopyon.

b Histologic findings include Grampositive rod bacteria in the corneal stroma.

Fig. 5.7 a Clinical findings include a central bacterial corneal ulcer with hypopyon.

b Histologic findings include Grampositive rod bacteria in the corneal stroma.

❖ Prolapse of the iris (the iris will prolapse into the newly created defect) closing the corneal perforation posteriorly. Adhesion of the iris will produce a white corneal scar. This sequence of events can vary in speed and severity. Depending on the voracity of the pathogens and the state of the patient's immune system, an infiltrate can form within a few hours or days and quickly progress to a corneal ulcer, melting of the stroma, and even a descemetocele. This rapidly progressing form of infectious corneal ulcer (usually bacterial) is referred to as a serpiginous corneal ulcer. It penetrates the cornea particularly rapidly and soon leads to intraocular involvement (the pathogens will be active beyond the visible rim of the ulcer). A serpiginous corneal ulcer is one of the most dangerous clinical syndromes as it can rapidly lead to loss of the eye.

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