Infectious Crystalline Keratopathy Caused by Candida guilliermondii

Infectious Crystalline Keratopathy Caused by Candida guilliermondii

lenses due to a mixed Vahlkampfia and Hartmannella infection. Ophthalmology 1996;103:485– 494. 5. Yagita K, Endo T. Restriction enzyme analysis of mit...

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lenses due to a mixed Vahlkampfia and Hartmannella infection. Ophthalmology 1996;103:485– 494. 5. Yagita K, Endo T. Restriction enzyme analysis of mitochondrial DNA of Acanthamoeba strains in Japan. J Protozool 1990;37:570 –575.

Infectious Crystalline Keratopathy Caused by Candida guilliermondii Darryl J. Ainbinder, MD, Vernon C. Parmley, MD, Thomas H. Mader, MD, and Mark L. Nelson, MD PURPOSE: To describe the manifestations of infectious crystalline keratopathy caused by Candida guilliermondii in a corneal transplant performed for pseudophakic bullous keratopathy. METHOD: Case report. RESULTS: Candida guilliermondii was identified as the causative organism of an indolent infectious crystalline keratopathy. Incisional lamellar biopsy provided diagnostic culture and histopathologic results. Histopathology showed aggregates of yeast elements between corneal stromal lamellae, without inflammation. The infection progressed despite a 6-week course of topical amphotericin B and an additional 6-week course of topical and oral fluconazole. Repeat penetrating keratoplasty resulted in clear graft, with no recurrent infection. CONCLUSIONS: Fungal keratopathy should be included in the differential diagnosis of infectious crystalline keratopathy. Numerous Candida species have been isolated in addition to the most common causative bacterial organism, Streptococcus viridans. Candida guilliermondii is yet one more causative agent of infectious crystalline keratopathy. Candida guilliermondii, a rare human pathogen, was resistant to medical therapy in this case. (Am J Ophthalmol 1998;125:723–725. © 1998 by Elsevier Science Inc. All rights reserved.)

Accepted for publication Dec 5, 1997. Madigan Army Medical Center, Department of Ophthalmology. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or the Department of Defense. Inquiries to Vernon C. Parmley, MD, Madigan Army Medical Center, Department of Ophthalmology, Tacoma, WA 98431; fax: (253) 968-1451.

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75-YEAR-OLD MAN UNDERWENT PENETRATING

keratoplasty with intraocular lens exchange for pseudophakic bullous keratopathy in February 1996. Except for hypertension, he was in good general health. His ocular history was notable for bilateral intracapsular cataract extraction, secondary lens implants (closed-loop anterior chamber intraocular lenses), and chronic open-angle glaucoma. There was no history of diabetes or ocular surface disease. The postoperative course was complicated by chronic open-angle glaucoma and delayed healing of the epithelium. The epithelium over the eventual site of crystalline keratopathy was the last site to heal, at 6 weeks post–penetrating keratoplasty. A minute focus of subepithelial haze persisted in this location. Epithelial debridement of the area followed by gram stain and culture were negative, as were routine donor corneoscleral rim cultures. Eight months after surgery, a 0.4-mm focus of crystalline keratopathy was identified. The epithelium was intact. There was no corneal melting or anterior segment inflammation. Multiple media cultures were obtained, followed by subconjunctival and topical antibiotic therapy. The infectious crystalline keratopathy slowly progressed, despite repeated attempts to debride, culture, and treat with antibiotic therapy (Figure 1, left). Ten months after initial penetrating keratoplasty, a diagnostic and therapeutic lamellar biopsy was performed. Histopathology demonstrated yeast elements dissecting the corneal lamellae, with no inflammatory response (Figure 1, right). Cultures of the corneal tissue grew Candida guilliermondii that was sensitive to amphotericin B, fluconazole, and natamycin. The patient received a 6-week course of topical amphotericin B, followed by a 6-week course of topical and oral fluconazole. Further antifungal therapy was hampered by the development of a notable contact dermatitis to both antifungal agents. The lamellar biopsy site healed well, and the eye remained uninflamed. Thirteen months after initial penetrating keratoplasty, the fungal crystalline keratopathy recurred adjacent to the site of lamellar biopsy (Figure 2). A repeat therapeutic penetrating keratoplasty, with placement of an Ahmed valve, was performed for fungal crystalline keratopathy that was unresponsive to medical therapy and for poorly controlled chronic open-angle glaucoma. Histopathologic evaluation of

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FIGURE 1. (Left) White, branching, crystalline stromal deposits (arrowhead) developed 9 months after penetrating keratoplasty. (Right) Histologic appearance of the lamellar corneal biopsy shows aggregates of yeast elements (Candida guilliermondii) dissecting the corneal stromal lamella (periodic acid–Schiff, 350).

opacities with little evidence of corneal inflammation.1,2 Usually these changes are caused by an accumulation of bacterial colonies, most commonly Streptococcus viridans, that dissect the corneal lamellae.1,2 Several Candida species have also been identified with infectious crystalline keratopathy.3 Although C guilliermondii is rarely isolated in human fungal disease, reports of patients with systemic infection unresponsive to medical therapy have already surfaced.4,5 Fungal crystalline keratopathy should be considered in the differential diagnosis of infectious crystalline keratopathy. This case of indolent infection by C guilliermondii was resistant to medical therapy. Surgery was an effective cure because we were able to remove the localized colonies of C guilliermondii.

FIGURE 2. Recurrence of infectious crystalline keratopathy (arrowhead) after lamellar dissection and antifungal therapy.

REFERENCES

the recipient cornea showed that the fungal infection did not involve the margins of resection. No antifungal agents had been used in the postoperative course, and there has been no evidence of recurrent infection, with 10 months of follow-up evaluation. Infectious crystalline keratopathy is characterized by insidious white, branching, crystalline stromal 724

AMERICAN JOURNAL

1. Meisler DM, Langston RHS, Naab TJ, et al. Infectious crystalline keratopathy. Am J Ophthalmol 1984;97:337–343. 2. Reiss GR, Campbell RJ, Bourne WM. Infectious crystalline keratopathy. Surv Ophthalmol 1986;31:69 –72. 3. Rhem MN, Wilhelmus KR, Font RL. Infectious crystalline keratopathy caused by Candida parapsilosis. Cornea 1996;15: 543–545. OF

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4. Borg-von Zepelin M, Eiffert H, Kann M, et al. Changes in the spectrum of fungal isolates: results from clinical specimens gathered in 1987/88 compared with those in 1991/92 in the University Hospital Gottingen, Germany. Mycoses 1993;36:247–253. 5. Vazquez JA, Lundstrom T, Dembry L, et al. Invasive Candida guilliermondii infection: in vitro susceptibility studies and molecular analysis. Bone Marrow Transplant 1995;16:849 – 853.

Very High Frequency Ultrasound Analysis of a New Phakic Posterior Chamber Intraocular Lens In Situ Daniel Y. Kim, MD, Dan Z. Reinstein, MD, MA(Cantab), Ronald H. Silverman, PhD, David J. Najafi, MD, Sandra C. Belmont, MD, Alexander P. Hatsis, MD, George W. Rozakis, MD, and D. Jackson Coleman, MD PURPOSE: To use very high frequency ultrasound scanning for in situ analysis of a new phakic posterior chamber intraocular lens (No-Touch; International Visions Inc, Cincinnati, Ohio). METHODS: In this pilot study, very high frequency ultrasound (50 MHz) wide-angle (15 mm) full anterior segment scans were obtained in two patients who had undergone phakic posterior chamber intraocular lens implantation into legally blind eyes with normal anterior segment anatomy. RESULTS: Very high frequency ultrasound B-scan images delineated the phakic posterior chamber intraocular lens within the posterior chamber. The relations to the sulci were clearly imaged. Ana-

Accepted for publication Dec 8, 1997. Manhattan Eye, Ear, Nose & Throat Hospital (D.Y.K., S.C.B.); Margaret M. Dyson Vision Research Institute (D.Z.R., R.H.S., D.J.C.), Department of Ophthalmology (D.Y.K., D.J.N., S.C.B., D.J.C.), Cornell University Medical College; Department of Ophthalmology, University of British Columbia, Vancouver, British Columbia, Canada (D.Z.R.); Division of Ophthalmology, Nassau County Medical Center, State University of New York (A.P.H.); and International Visions Inc (G.W.R.). Supported in part by National Institutes of Health grant EY01212; the Dyson Foundation, New York, New York; Research to Prevent Blindness, Inc, New York, New York; and the St Giles Foundation, New York, New York. Dr Rozakis is a paid consultant of International Visions Inc. Inquiries to Dan Z. Reinstein, MD, MA(Cantab), Margaret M. Dyson Vision Research Institute, Department of Ophthalmology, Cornell University Medical College, 1300 York Ave, Rm A-855, New York, NY 10021; fax: (212) 746-8135 e-mail: [email protected]. edu

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tomic relations of the phakic posterior chamber intraocular lens optic and haptics were visualized in both static (light/dark) and kinetic (distance/ accommodative) states. CONCLUSION: Very high frequency ultrasound wide-angle scanning provides a unique tool to noninvasively evaluate the eye preoperatively and the static and kinetic relations of this new refractive device within the posterior chamber. (Am J Ophthalmol 1998;125:725–729. © 1998 by Elsevier Science Inc. All rights reserved.)

T

HE

FIRST

PHAKIC

INTRAOCULAR

LENS

WAS

designed to be implanted in the anterior chamber. Potential corneal endothelial damage1 has led to heightened interest in the development of phakic posterior chamber intraocular lens technology. Phakic posterior chamber intraocular lenses were introduced by Fyodorov in the late 1980s (Fyodorov SN, unpublished data, “IOL implantation and complex treatment of optic nerve atrophies,” presented at the International Symposium on IOL Implantation and Refractive Surgery, Moscow, 1987). Erturk and Ozcetin2 reported initial encouraging results in a small series. Fechner and associates3 described implantation of phakic posterior chamber intraocular lenses in which the development of anterior subcapsular opacities in certain cases was thought to be caused by contact between the phakic posterior chamber intraocular lens and the natural lens. Currently, the monitoring of these lenses in situ is carried out at the slit lamp. This limits the accuracy with which the distances between intraocular lens and anterior capsule can be measured and does not provide information about the relationships of the intraocular lens posterior to the iris. In addition, the dynamic relations (during accommodation and light reflex) are difficult to assess. The advent of digital very high frequency ultrasound scanning enabling high-resolution (30 mm) imaging and high-precision biometry (62 mm)4 in three dimensions5 has revolutionized our ability to examine the cornea and anterior segment anatomy. We studied the potential of very high frequency ultrasound scanning for in situ examination of a new phakic posterior chamber intraocular lens (NoTouch; International Visions Inc, Cincinnati, Ohio). The diameter of the optic is 4 mm, and the

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