Acanthamoeba Keratitis appears to be on the rise.  If not, it is just my perception, which could be the case as I am caring for patients from a wider referral range (presently active cases from Virginia, Michigan, and Alaska).  Why is this infection not “solved?”  Compare for example P. acnes endophthalmitis first reported a quarter of a century ago by David Meisler MD and subsequently recognized by David J. Apple MD and his group as a localized form of chronic infectious endophthalmitis after cataract surgery.  The most significant change since that time is the almost complete elimination of polypropylene-looped intraocular lenses which appeared to be the culprit facilitating inoculation as well as contributing a microenvironment within the capsular bag supporting replication.   Presumably, this has led to the significant decrease in culture proven cases of P. acnes endophthalmitis – now considered extraordinarily uncommon, also noting that almost every case reported occurred in the setting of a polypropylene looped IOL.  How does this relate to Acanthamoeba Kertatitis?  With respect to Acanthamoeba Keratitis, it appears the wearing the contact lens on an over-night or extended wear basis appears to be the “polypropylene loop” equivalent in facilitating inoculation and subsequent infection.  While making patients aware of the dangers of making their own saline in gallons of (distilled but not sterile) water was a big step toward curbing the problem while the remaining “most significant” risk factor appears to be the contact lens, particularly if they are worn on an over-night or extended wear basis and the person comes into contact with Acanthamoeba from their case, swimming, hot tub, or other.  (Historical perspective: In 1988 I was escorted out of an Eckerd Pharmacy in Durham, North Carolina for photographing the gallon jugs of distilled water that were located in the middle of contact lens supplies).

What makes Acanthamoeba so difficult to treat relates to the creative ability of the organism to transform from and metabolically active and migratory trophozoite into the “hibernating,” more resistant cyst form.  This more resistant form, under-treated, may select further resistance as I have suspected in a few cases that were harder to treat when they developed recurrence.

I attribute our recent success in treating Acanthamoeba Keratitis at the Duke Eye Center to the collaborative work between the Cornea Service and also Dr. John Perfect in the Infectious Disease Department.  Our initial treatment regimen consists of the following:

  1. Discontinue all contact lens wear.  Patients often don’t realize that their other eye is at risk with continued contact lens wear.  Particularly if they are sleeping while wearing their contact lens.
  2. Culturing the case along with their eye often confirms that the contact lens is in fact the source of their infection.
  3. Chlorhexidine gluconate  0.02-0.06% topically 6-12 times per day.   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC180025/pdf/aac00189-0009.pdf
  4. PHMB 0.5% topically 6-12 times per day
  5. Brolene (Dibrompropamidine) 6 times daily]
  6. Neomycin  (Maxitrol) 4-6 times daily
  7. Diflucan (Fluconazole) up to 800 mg daily
  8. Atropine 1% once or twice daily for discomfort
  9. Bromday once daily for pain.
  10. Oral Ibuprofen for pain.