full course of amebicidal therapy and a minimum of 3–6 months of treatment and disease-free follow-up. Collagen crosslinking is increasingly described as an adjunctive therapy for Acanthamoeba keratitis; its mechanism of action is unclear, however.
Dart JK, Saw VP, Kilvington S. Acanthamoeba keratitis: diagnosis and treatment update 2009. Am J Ophthalmol. 2009;148(4):487–499.e2.
Tu EY. Acanthamoeba and other parasitic corneal infections. In: Krachmer JH, Mannis MJ, Holland EJ. Cornea. 3rd ed. Vol 1. Philadelphia: Elsevier/Mosby; 2011.
Tu EY, Joslin CE, Sugar J, Shoff ME, Booton GC. Prognostic factors affecting visual outcome in Acanthamoeba keratitis. Ophthalmology. 2008;115(11):1998–2003.
Corneal Stromal Inflammation Associated With Systemic Infections
Nonsuppurative stromal keratitis can be caused by the following:
reactive arthritis
congenital or acquired syphilis Lyme disease
tuberculosis
leprosy (Hansen disease) onchocerciasis
Most of these conditions are discussed in BCSC Section 9, Intraocular Inflammation and Uveitis.
Microsporidiosis
Microsporidia are intracellular protozoa known to cause ocular infection. Initially recognized as an opportunistic pathogen in individuals with AIDS and those with other forms of immunosuppression, this organism is increasingly reported as the cause of infection in immunocompetent persons in Southeast Asia. There are 2 distinct clinical presentations of microsporidial infections, depending on the immune status of the patient. In immunocompetent individuals, a corneal stromal keratitis may develop, and in patients with AIDS, conjunctivitis and an epithelial keratopathy may be seen. The latter group may also have disseminated microsporidiosis involving the sinuses, respiratory tract, or gastrointestinal tract.
Patients present with symptoms that include ocular irritation, photophobia, decreased vision, and bilateral conjunctival injection with little or no associated inflammation. Stromal keratitis is caused by agents of the Nosema genus, whereas the Encephalitozoon and Septata genera have been associated with keratoconjunctivitis. In the keratoconjunctivitis variant, corneal findings include superficial nonstaining opacities described as “mucoid” in appearance, along with dense areas of fine punctate fluorescein staining. The corneal stroma remains clear, with minimal or no iritis.
Light microscopy using the Brown and Hopps stain may identify small gram-positive microsporidial spores in the epithelial cells of the conjunctiva. Transmission electron microscopy, immunofluorescence antibody techniques, or elaborate tissue culture techniques may also be used.
Restoration of immune function can lead to resolution of microsporidial keratitis. Although there is no definitive treatment, topical fumagillin has been used to successfully treat microsporidial keratoconjunctivitis with low toxicity. In severe cases of Vittaforma corneae, granulomatous inflammation may lead to necrotic thinning and perforation. PK may then become the only available treatment for severe stromal thinning. In general, medical regimens require long-term use, and recurrence is common after treatment discontinuation. More recent cases have been reported to be
self-limited or responsive to a wide array of commercially available topical ophthalmic antibiotics.
Joseph J, Sridhar MS, Murthy S, Sharma S. Clinical and microbiological profile of microsporidial keratoconjunctivitis in southern India. Ophthalmology. 2006;113(4):531–537.
Loh RS, Chan CM, Ti SE, Lim L, Chan KS, Tan DT. Emerging prevalence of microsporidial keratitis in Singapore: epidemiology, clinical features, and management. Ophthalmology. 2009;116(12):2348–2353.
Tu EY. Acanthamoeba and other parasitic corneal infections. In: Krachmer JH, Mannis MJ, Holland EJ. Cornea. 3rd ed. Vol 1. Philadelphia: Elsevier/Mosby; 2011.
Loiasis
Loa loa and other filarial nematodes can cause conjunctivitis as well as dermatologic manifestations. After the bite of an infected vector, such parasites can burrow subcutaneously to reach the eye area. The microfilarial stage is transmitted from human to human by the bite of an infected female deer fly (genus Chrysops) indigenous to West and Central Africa. A migrating worm moves under the skin at about 1 cm/min but is most conspicuous when it is seen or felt wriggling under the periocular skin or bulbar conjunctiva. Extraction of the filarial worm cures the conjunctivitis; that is followed by antiparasitic treatment for disseminated infestation. Diethylcarbamazine is generally given 2 mg/kg 3 times a day for 3 weeks and repeated as necessary. Ivermectin 150 mg/kg may also be effective, but significant adverse effects have been reported in patients with prominent intravascular loiasis. Concurrent administration of corticosteroids and/or antihistamines may be necessary to minimize allergic reactions.
Microbial Scleritis
PATHOGENESIS Bacterial and fungal infections of the sclera are very rare. Most cases result from the extension of microbial keratitis involving the peripheral cornea. Trauma and contaminated foreign bodies (including scleral buckles) are possible risk factors. Bacterial scleritis has also occurred in sclera damaged by previous pterygium surgery, especially when beta irradiation or mitomycin has been used (Fig 5-21). Bacteria and fungi can also invade tissue of the eye wall surrounding a scleral surgical wound, but endophthalmitis is more likely in this setting. Scleral inflammation can also be a feature of syphilis, tuberculosis, or leprosy or infection with Acanthamoeba species, Nocardia species, or atypical mycobacteria. Diffuse or nodular scleritis is an occasional complication of varicella-zoster virus eye disease.
Figure 5-21 Bacterial scleritis occurring 2 weeks after pterygium surgery. (Courtesy of Kirk R. Wilhelmus, MD.)
LABORATORY EVALUATION Evaluating suppurative scleritis is similar to evaluating microbial keratitis. Smears and cultures are obtained before antimicrobial therapy is begun. If the overlying epithelium is intact, a scleral or episcleral biopsy should be performed. The workup of nonsuppurative scleritis is guided by the history and results of the physical examination, as described in Chapter 7.
MANAGEMENT Topical antimicrobial therapy is begun just as for microbial keratitis. Because of the difficulty in controlling microbial scleritis, subconjunctival injections and intravenous antibiotics may also be used. Long-term oral therapy shows promise.