In October, 2008, a 30-year-old man underwent penetrating keratoplasty (PK) for keratoconus. A week later, he presented with ocular pain, ciliary injection, and graft oedema, with keratic precipitates. Despite treatment with antibiotics and steroids there was no improvement, and he underwent a re-grafting procedure in November. Analysis of the excised corneal button showed the presence of acanthamoeba cysts deeply embedded within the stroma (fi gure A). We treated him with topical hexamidine and 0·02% polihexanide. Keratitis recurred and a third PK was done in February, 2009, after the second graft melted. When last seen, in June, 2009, the patient had epithelial defects of the cornea but no signs of acanthamoeba infection; visual acuity was up to counting fi ngers. Also in October, 2008, the fellow cornea from the same donor was transplanted into a 73-year-old woman with post-traumatic corneal leukoma. Con comitant vitrectomy, extracapsular cataract extraction, and intraocular lens insertion were done. Despite treatment with oral and topical antibiotics, a worsening course (fi gure B) led to a second PK in December, 2008. Again, the explanted graft showed stromal acanthamoeba cysts. She was treated with aminoglycoside, 0·02% polihexanide and 0·1% propamidine eyedrops. When last seen, in June, 2009, she showed phthisis bulbi with no light perception. PCR of the 18S ribosomal subunit was done on DNA from both explanted grafts with JDP1 and JDP2 primers. PCR bands of 440 bp were sequenced and BLASTed (Basic Local Alignment Search Tool); they showed 98% homology to Acanthamoeba sp CRIB-20 and Acanthamoeba castellanii 18S sequences. Sequences of PCR bands from the two explanted corneas were identical, suggesting a single source of infection. The transplanted corneas were from a 45-year-old male donor who died after a motorcycle accident in September, 2008. He had never worn contact lenses nor complained of ocular discomfort or redness. He had been wearing his helmet when pronounced dead and his eyes were not exposed to sources of contamination until the corneas were retrieved 26 h later. Slit lamp and light microscopy confi rmed that both corneas were suitable for transplantation. No stromal abnormalities were seen. Routine microbiological tests were negative. We concluded that donor-to-recipient transmission of acanthamoeba from an asymptomatic individual had occurred, with dormant cysts residing in the donor corneas without active infection or morbidity. Acanthamoeba are ubiquitous protozoa in soil, water, and air. Risk factors for infection include use of contact lenses, corneal trauma, and contaminated fl uids. In the USA and the Netherlands, respectively, 1–2 and 3 people per million contact lens wearers are aff ected. Acanthamoeba keratitis can progress to scleritis, and uncontrolled infections require enucleation. Misdiagnosis as herpes or fungal keratitis often delays treatment. It is unlikely that a simultaneous ocular infection occurred in our two patients or that they had been at risk before transplantation (rigid gas-permeable contact lenses were negative for acanthamoeba culture in the fi rst patient; trauma had occurred 40 years earlier in the second patient). Simul taneous contamination of donor tissues in the eye bank was also excluded, because other corneas processed on the same days were transplanted uneventfully. A few cases of painless acanthamoeba keratitis have been reported, also in patients not wearing contact lenses. Since the presence of acanthamoeba in corneas of asymptomatic donors is unlikely, the cost/benefi t ratio of screening for acanth amoeba before transplantation is low. However, because the consequences of donormediated acanth amoeba infec tions are deleterious, eye banks should be aware of these rare events, develop a screening test, and work closely with surgeons to diagnose and treat keratitis rapidly.
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Jan 1, 2020
Jill Bennet Fernandez + 8
Open Access