treatment plan
Acanthamoeba: Not Gone, but Forgotten?
BY BRUCE E. ONOFREY, RPH, OD
July 1999
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This devastatingly destructive, difficult-to-treat organism still lurks in the shadows waiting to strike. Correct diagnosis is critical, yet difficult in this great mimicker. Acanthamoeba keratitis is a result of the colonization of the cornea by the free-living, ubiquitous protozoan acanthamoeba. The infection results in significant inflammation, which is intensified by the release of proteolytic enzymes and the stimulation of the immune system. To make matters worse, the organism lives in two forms: a free-living trophozoite, which is mobile, and a cyst form, which is dormant. Treatment of corneal disease may force the organism into the cystic form, which is impervious to most treatments, and may result in continuing infection. Bacteria on dirty contact lenses provide food for the organism. A break in the epithelium provides access for infection of the cornea.
Warning Signs
The organism attacks the corneal nerves and there is therefore marked pain even in the early phases of this disease. Keratitis may begin as an epithelial haze associated with epithelial breakdown, but can be quite variable. Generally, there is no discharge. The development of pseudodentrites is of great significance. The infection is easily mistaken for Herpes simplex keratitis due to dendriform raised lesions, which may be gray or white and linear or branching. One particularly helpful finding is cuffing of the stromal nerves with inflammatory cells. This radial keratoneuritis occurs less than 50 percent of the time and appears as midstromal infiltration, which usually begins paracentrally and extends peripherally to the limbus, following the course of the corneal nerves. The tendency of the disease to affect neural tissue explains the variable symptomatology, ranging from relative hypoesthesia to excruciating pain. It is not unusual to find iritis, scleritis, hypopyon, increased IOP, preauricular lymphadenopathy and conjunctival follicles.
Acanthamoeba is most common among young adults who are immunocompetent. Contact lens users account for approximately 85 percent of cases. Using homemade saline, tap water rinsing and placing lenses in the mouth also increase the risk of infection.
Laboratory Tests
Corneal biopsy is often necessary for definitive diagnosis. Samples are plated on nonnutrient agar overlaid with E-coli bacteria. Acanthamoeba consumes the bacteria and leaves tracks on the plates. Trophozoites usually appear within 3 days. Staining visualizes both cysts and trophozoites and is best done with calcofluor white dye. Lenses and solutions should also be cultured.
Treatment
Initial loading dose of Polyhexamthyline biguanide 0.02% (PHMB) (Baquacil), propamadine isethionate 0.1% (Broline) and Neomycin every hour for 1-3 days. Intensive treatment every 2 hours daily and every 4 hours at night for 4-7 days. Maintenance every 4 hours for 7-21 days. After 3 weeks, taper off Neomycin and other drugs that produce toxicity. Continue PHMB and propamadine daily for 6-12 mos. Use ocular lubricants frequently. Corticosteroids are not advised. If a secondary infection arises, use an antibiotic. Neomycin may be restarted for its double antibacterial/antiamebic activity. Avoid PKP until the infection is eradicated. Some specialists also use antifungal agents. Miconazole and clotrima topically and ketoconazole 200-400mg/D orally.
Most primary care ODs and MDs would not be equipped to perform these specialized testing and treatment regimens. Consider consulting a corneal specialist for evaluation of the patient.
Dr. Onofrey, editor and author of ophthalmic texts, practices in Albuquerque, New Mexico.