Various Acanthamoeba species can cause chronic and progressively destructive keratitis in normal hosts. The main risk factor (85% of cases) is contact lens use, particularly if lenses are worn while swimming or if unsterile lens cleaning solution is used. Some infections follow corneal abrasion.
Acanthamoeba are present worldwide in water, soil, and dust. The life cycle of Acanthamoeba involves only 2 stages: cysts and trophozoites (the infective form). The trophozoites form double-walled cysts, which resist eradication. Both forms can enter the body through various means (eg, eyes, nasal mucous membranes, broken skin). When Acanthamoeba enter the eye, they can cause severe keratitis. In infected patients, cysts and trophozoites may be found in tissues.
Lesions in patients with amebic keratitis are typically very painful and produce a foreign body sensation. Initially, lesions have a dendriform appearance resembling herpes simplex keratitis. Later, there are patchy stromal infiltrates and sometimes a characteristic ring-shaped lesion. Anterior uveitis is usually also present. Vision is diminished.
Consultation with an ophthalmologist is important for diagnosis and treatment of amebic keratitis.
Diagnosis of amebic keratitis is confirmed by examination of Giemsa- or trichrome-stained corneal scrapings and by culture on special media. Viral culture is done if herpes is considered.
Early, superficial amebic keratitis responds better to treatment. The encysted stage of the life cycle appears to cause most problems.
Epithelial lesions are debrided, and intensive drug therapy is applied. The initial choice is
For the first 3 days, drugs are given every 1 to 2 hours. Other topical drugs used as adjunct therapy include propamidine (0.1%) and hexamidine (0.1%).
Systemic treatment with itraconazole has been used in conjunction with topical therapy, particularly in patients with anterior uveitis or involvement of the sclera.
Early recognition and treatment have eliminated the need for therapeutic keratoplasty in most instances, but keratoplasty remains an option when pharmacologic therapy fails. Intensive treatment is required for the first month; it is tapered per clinical response but often continued for 6 to 12 months. Recurrence is common if treatment is stopped prematurely.
Various Acanthamoeba species can cause chronic and progressively destructive keratitis in otherwise healthy hosts, mainly in contact lens users.
Consult with an ophthalmologist about management.
Diagnose by examining Giemsa- or trichrome-stained corneal scrapings and by culturing the sample using special media.
Herpes simplex keratitis can cause similar lesions; if it seems a possible diagnosis, do viral culture.
Debride corneal lesions, and treat with topical chlorhexidine, polyhexamethylene biguanide, or both.
For severe infections, consider treatment with systemic itraconazole.