Successful medical treatment of Acanthamoeba keratitis

Purpose: To describe the outcome of a series of Acanthamoeba keratitis treated with a similar regimen. Methods: All cases diagnosed with Acanthamoeba keratitis in a referral centre from June 1994 through June 1997 were included. Diagnosis of Acanthamoeba keratitis was based in clinical presentation and laboratory results. Positive laboratory identification of Acanthamoeba from corneal scraping or contact lens was required, unless the patient had very characteristic symptoms (severe pain) and signs of the infection, including perineural infiltrates. Initial intensive treatment included topical polyhexamethylene biguanide (PHMB) 0.02%, propamidine isothionate 0.1% and broad-spectrum antibiotics. The treatment was gradually tapered. After documented response to anti-acanthamoeba therapy, topical steroids were introduced; they were discontinued before cessation of the antiAcanthamoeba regimen. Results: Six males and four females, with a mean age of 30.0 ± 7.4 years were included in this study. All cases weared contact lenses. On presentation all cases had severe pain, and epitheliopathy was associated with stromal infiltrate in most (seven of ten) cases. Four patients had anterior uveitis. Perineural infiltrates were present in three cases and ring infiltrate in one patient. Anti-amoebic treatment was started 12.7 ± 7.2 days after beginning of symptoms. The clinical response to therapy was very satisfactory in all patients. Within two to three weeks all patients had remarkable lessening of pain and photophobia, and improvement of clinical signs. At two to three months, visual acuity had improved in all patients. Two patients required penetrating keratoplasty for visual rehabilitation. Conclusion: The use of PHMB and propamidine cured all cases of Acanthamoeba keratitis. Cautious introduction of steroids was associated with expedited resolution of inflammation and provided symptomatic relief.

Corneal Allograft Rejection:Risk Factors, Diagnosis, Prevention, and Treatment

Recent advances in corneal graft technology, including donor tissue retrieval, storage and surgical techniques, have greatly improved the clinical outcome of corneal grafts. Despite these advances, immune mediated corneal graft rejection remains the single most important cause of corneal graft failure. Several host factors have been identified as conferring a "high risk" status to the host. These include: more than two quadrant vascularisation, with associated lymphatics, which augment the afferent and efferent arc of the immune response; herpes simplex keratitis; uveitis; silicone oil keratopathy; previous failed (rejected) grafts; "hot eyes"; young recipient age; and multiple surgical procedures at the time of grafting. Large grafts, by virtue of being closer to the host limbus, with its complement of vessels and antigen-presenting Langerhans cells, also are more susceptible to rejection. The diagnosis of graft rejection is entirely clinical and in its early stages the clinical signs could be subtle. Graft rejection is largely mediated by the major histocompatibility antigens, minor antigens and perhaps blood group ABO antigens and some cornea-specific antigens. Just as rejection is mediated by active immune mediated events, the lack of rejection (tolerance) is also sustained by active immune regulatory mechanisms. The anterior chamber associated immune deviation (ACAID) and probably, conjunctiva associated lymphoid tissue (CALT) induced mucosal tolerance, besides others, play an important role. Although graft rejection can lead to graft failure, most rejections can be readily controlled if appropriate management is commenced at the proper time. Topical steroids are the mainstay of graft rejection management. In the high-risk situations however, systemic steroids, and other immunosuppressive drugs such as cyclosporin and tacrolimus (FK506) are of proven benefit, both for treatment and prevention of rejection.