Contact lens wearer presents with 2 weeks of worsening vision
Examination found a feathery-white anterior stromal corneal infiltrate with no epithelial defect.
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A 34-year-old man presented to the New England Eye Center with 2 weeks of worsening vision, tearing and photophobia in his left eye.
The patient had eye pain early in the course of his symptoms, but the pain had since resolved. An outside ophthalmologist diagnosed a corneal ulcer and started Vigamox (moxifloxacin, Alcon) every other hour and oral acyclovir. Cultures obtained 4 days before presentation showed no growth of organisms. Because the ulcer continued to progress, the patient was referred to the cornea service for further evaluation.
The patient wore soft contact lenses. He admitted to sleeping in the lenses, wearing the same pair for several months and cleaning the lenses in tap water. Medical history and review of systems were unremarkable.
Examination
Distance visual acuity with correction was 20/30 in the right eye and 20/40 in the left eye, improving with pinhole to 20/25 in the right eye and 20/30 in the left eye. IOPs by applanation were 14 mm Hg in the right eye and 13 mm Hg in the left eye. Pupils were equal and reactive to light bilaterally, and there was no afferent pupillary defect. Extraocular movements and confrontational visual fields were within normal limits.
Anterior segment photos of the left eye
showing a feathery-white anterior stromal infiltrate with satellite colonies
and no epithelial defect.
Images: Carmody JN, Raizman
MB |
Slit lamp exam of the anterior segment of the left eye revealed mild swelling and erythema of the upper lid, trace conjunctival injection and a 1 mm × 1.3 mm feathery-white anterior stromal corneal infiltrate without an epithelial defect (Figures). There was no anterior chamber inflammation. The remainder of the anterior segment exam and the dilated fundus exam of the left eye were within normal limits. Examination of the right eye was normal.
What is your diagnosis?
Feathery-white corneal infiltrate
This patient presented with a slowly progressive corneal infiltrate unresponsive to antibacterial or antiviral medication. The feathery-white appearance of the infiltrate as well as the lack of an epithelial defect led to a high clinical suspicion for fungal keratitis. Bacterial keratitis not covered by the current treatment regimen also remained a concern. Although Acanthamoeba should be strongly suspected in a contact lens wearer with poor lens hygiene who is refractory to treatment, the lack of involvement of the corneal epithelium, absence of pain and absence of uveitis lessened this possibility. Inflammation of corneal nerves or a ring infiltrate is often seen with Acanthamoeba keratitis.
Repeat corneal scraping and culture from our patient grew filamentous fungi, at which point treatment with natamycin was initiated. Amphotericin B was also started prophylactically, as there was concern for co-infection with yeast. The species was later identified as Paecilomyces.
Discussion
There are approximately 1,500 cases per year of fungal keratitis in the United States, accounting for 5% to 10% of all corneal infections. The most common organisms isolated are Fusarium, Aspergillus and Candida. Risk factors for fungal keratitis include corneal trauma, contamination with plant material, immunosuppression, contact lens-related trauma, corneal surgery and chronic keratitis. Patients present with a slowly progressive corneal infiltrate unresponsive to treatment. The infiltrate is characteristically gray-white with feathery edges, may be elevated and has a rough, gritty texture. Satellite lesions can be observed. There is often no epithelial defect and minimal conjunctival injection and anterior chamber inflammation.
Diagnosis of fungal keratitis is made by culture on blood agar, on Sabouraud agar or in brain-heart infusion broth. The organisms may also be identified by Gram, Giemsa or Gomori methenamine silver stains. When there is high clinical suspicion for fungus but no organism has been identified, confocal microscopy or corneal biopsy may be necessary to identify infection deep in the stroma. Corneal biopsy leads to isolation of the organism in 82% of cases.
Antifungal therapy of a corneal ulcer is usually not used until a definitive diagnosis is made. If fungal keratitis is suspected but no organism has been isolated, repeated corneal scraping or biopsy is obtained. Once identified, filamentous fungi are initially treated with hourly natamycin 5% drops, and yeast fungi are treated with hourly amphotericin B (0.15% to 0.3%). Oral antifungals, such as ketoconazole or fluconazole, can also be started. Alternative antifungals are used if the infection is unresponsive to traditional treatment. Mechanical debridement of the ulcer surface can help increase corneal penetration of the medication. Topical steroids are not recommended as they enhance microbial viability. The standard treatment course is 12 weeks.
The medical failure rate of fungal keratitis is 20%, in which case penetrating or lamellar keratoplasty is indicated. Cyclosporine or fluorometholone drops should be used postoperatively in place of prednisolone, unless there is significant inflammation. The infection recurs in 5% to 14% of cases after keratoplasty. The risk of recurrence is increased with steroid use before surgery, corneal perforation, hypopyon, or limbal or deep stromal involvement.
The organism identified in this case was Paecilomyces, a saprophytic fungus. This fungus is abundant in soil and decomposing plants. Half of all reported Paecilomyces infections affect the eye, but the organism has also been found to cause infection in the heart, sinus, kidney, lung, peritoneum and skin. Paecilomyces endophthalmitis outbreaks associated with lens implants and contaminated irrigation solutions have been reported. This organism is often resistant to natamycin and amphotericin, and recent studies suggest topical voriconazole to be first-line treatment. Paecilomyces keratitis has a poor visual outcome, with 69% of eyes requiring keratoplasty.
Summary
A 34-year-old man with poor contact lens hygiene presented with a nonhealing corneal ulcer of the left eye. Clinical suspicion was high for fungal keratitis. Culture from repeated corneal scrapings isolated a filamentous fungus, and he was started on natamycin as a well as prophylactic amphotericin B. The patient responded well to the medications, and he was continued on this regimen even after identification of Paecilomyces. Visual acuity after resolution of the infection was 20/50.
References:
- Alexandrakis G, Haimovici R, Miller D, Alfonso EC. Corneal biopsy in the management of progressive microbial keratitis. Am J Ophthalmol. 2000;129(5):571-576.
- Anderson KL, Mitra S, Salouti R, Pham TA, Taylor HR. Fungal keratitis caused by Paecilomyces lilacinus associated with retained intracorneal hair. Cornea. 2004;23(5):516-521.
- Gokhale NS. Medical management approach to infectious keratitis. Indian J Ophthalmol. 2008;56(3):215-220.
- Shi W, Wang T, Xie L, et al. Risk factors, clinical features, and outcomes of recurrent fungal keratitis after corneal transplantation [published online ahead of print Jan. 15, 2010]. Ophthalmology. doi:10.1016/j.ophtha.2009.10.004.
- Sponsel W, Chen N, Dang D, et al. Topical voriconazole as a novel treatment for fungal keratitis. Antimicrob Agents Chemother. 2006;50(1):262-268.
- Xiaoyong Y, Wilhelmus KR, Matoba AY, Alexandrakis G, Miller D, Huang AJW. Pathogenesis and outcome of Paecilomyces keratitis. Am J Ophthalmol. 2009;147(4):691-696.
- Xie L, Dong X, Shi W. Treatment of fungal keratitis by penetrating keratoplasty. Br J Ophthalmol. 2001;85(9):1070-1074.
- Jill N. Carmody, MD, and Michael B. Raizman, MD, can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; website: www.neec.com.
- Edited by Mark E. Patron, MD, and Andre J. Witkin, MD. Drs. Patron and Witkin can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; website: www.neec.com.