The brown plaque trap: Pigmented fungal keratitis mimicking iris tissue after ocular trauma

Fungal keratitis is a major cause of corneal morbidity in tropical and subtropical regions, particularly following ocular trauma. Filamentous fungi such as Fusarium and Aspergillus are most frequently implicated, while dematiaceous (pigmented) fungi account for a smaller proportion of cases.[1–4] The presence of melanin within the fungal cell wall imparts a characteristic brown or black coloration to clinical lesions, which may appear as pigmented infiltrates or plaques.[5,6] Aureobasidium pullulans is a ubiquitous saprophytic dematiaceous fungus found in soil, decaying vegetation, and humid environments. It is an uncommon cause of keratitis, with the literature largely limited to isolated case reports and small case series.[7–9] Reports from India are sparse and sporadic, with very few documented cases from North India. We report a rare case of A. pullulans keratitis presenting as a dense pigmented corneal plaque following ocular trauma. Case Report A 35-year-old man presented with pain, redness, watering, and progressive diminution of vision in the right eye for 15 days following accidental trauma while working in a paddy field likely by a paddy leaf. There was no history of contact lens use, prior ocular surgery, topical steroid use, or systemic immunosuppression. On examination, the unaided visual acuity in the right eye was hand movements close to face, while the left eye had normal visual acuity. Slit-lamp biomicroscopy revealed a central brown-colored, elongated, plaque-like lesion adherent to the corneal surface, measuring approximately 5 × 2 mm [Fig. 1a]. A surrounding 1-mm zone of stromal infiltrates was noted, along with a 3-mm hypopyon. Corneal sensation was reduced in the affected eye. The left eye examination was unremarkable. The dense brown, tissue-like plaque was mistaken for prolapsed iris tissue covered by pseudocornea, and the patient was started empirically on broad-spectrum fortified topical antibiotic cover. On subsequent review by a corneal specialist, the lesion was recognized to represent pigmented fungal plaque rather than iris tissue, and antibacterial agents were discontinued. Although there was symptomatic improvement with a reduction in hypopyon height, the central pigmented plaque persisted. Given its dense and adherent nature, corneal debridement was performed to reduce fungal load and improve antifungal penetration.Figure 1: (a). Slit-lamp photograph showing a dense brown, plaque-like lesion adherent to the central corneal surface with surrounding stromal infiltrates and hypopyon. (b). Sabouraud dextrose agar culture (early growth) showing moist, yeast-like colonies after 6-7 days of incubation at 25°C. (c). Mature culture demonstrating brown-black pigmented, leathery colonies with dark reverse. (d). Lactophenol cotton blue mount showing hyaline hyphae with thick-walled dematiaceous arthroconidia (labeled with blue arrow), consistent with Aureobasidium pullulans.(40x). (e). Post-treatment slit-lamp photograph showing healed keratitis with residual central macular corneal opacityThe debrided corneal tissue was submitted for microbiological evaluation. Potassium hydroxide (10%) preparation demonstrated thin, septate fungal hyphae, suggestive of filamentous fungal infection. The specimen was inoculated onto Sabouraud dextrose agar and incubated at 25°C. After 6–7 days, the culture revealed moist, yeast-like colonies, which progressively developed brown to black pigmentation on further incubation [Fig. 1b and c]. Lactophenol cotton blue (LPCB) mount prepared from the culture demonstrated hyaline hyphae along with thick-walled dematiaceous arthroconidia, characteristic of a dematiaceous yeast-like fungus [Fig. 1d]. Based on colony morphology and microscopic features, the isolate was identified as Aureobasidium pullulans. The organism was reported to be sensitive to natamycin and azole antifungals. Antifungal therapy was continued accordingly. Over subsequent follow-up, the hypopyon resolved completely, and there were no signs of active infection. Visual acuity improved from perceiving hand movements to an unaided distance visual acuity of 6/24. A central macular corneal opacity persisted [Fig. 1e]. The patient was advised a rigid contact lens trial, with deep anterior lamellar keratoplasty (DALK) planned if visual rehabilitation remains inadequate. Discussion Dematiaceous fungal keratitis represents a distinct subset of mycotic keratitis characterized by pigmented corneal lesions due to melanin-containing fungi.[5,6] While pigmented infiltrates and plaques are recognized features, Aureobasidium pullulans remains a rare etiologic agent. The largest published clinical series by Panda et al.[7] demonstrated that A. pullulans accounted for a small proportion of fungal keratitis cases and emphasized its rarity in world literature. Most reports consist of isolated cases or small series, underscoring its low prevalence. Indian reports are limited and sporadic, with very few cases originating from North India. Clinically, A. pullulans keratitis has been described as presenting with central corneal involvement, hypopyon, and occasional pigmentation.[7] In the present case, the dense, adherent brown plaque created diagnostic ambiguity regarding the nature of the lesion. Corneal debridement played a dual role by reducing fungal load and enabling definitive microbiological diagnosis. Microbiologically, A. pullulans is a dematiaceous, yeast-like fungus capable of producing both hyaline hyphae and pigmented thick-walled cells, accounting for its characteristic colony morphology.[7] Previous reports suggest variable response to natamycin, with improved outcomes using azole antifungals, often aided by debridement to enhance drug penetration.[7–9] The favorable clinical response and visual recovery in our patient are consistent with these observations. Conclusion Aureobasidium pullulans keratitis is rare and may present as a dense pigmented corneal plaque following ocular trauma. Corneal debridement with microbiological confirmation and targeted antifungal therapy can result in favorable anatomical and visual outcomes. Authors’ contributions Dr Parul Jain: Conceptualization, clinical diagnosis, surgical decision-making, supervision, manuscript drafting and critical revision. Dr Rishita Rao: Data collection, literature review, manuscript drafting. Dr Jyoti Choudhary: Microbiological evaluation, data interpretation, manuscript inputs. Dr Oves Siddiqui: Microbiological analysis, image documentation, manuscript review. Dr Sonal Saxena: Data acquisition, literature support, manuscript editing. All authors have read and approved the final manuscript. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest.