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Microspaeropsis olivacea keratitis and consecutive endophthalmitis
Serial ultrasonography showed clearing of the vitreous and mild choroidal thickening. The corneal infiltrate decreased in size, but progressive thinning led to perforation, which was sealed with cyanoacrylate tissue adhesive. The patient refused penetrating keratoplasty. Four months later, the visual acuity was light perception, with an adherant leucoma. The anterior chamber aspirate was cultured on Sabouraud’s dextrose agar slants with antibiotics and incubated at 24° C and 37° C. Black, expanding hairy colonies appeared after 7 days of incubation. Slide culture mount showed dark brown septate hyphae with erect, unbranched conidiophores (Figure 2). Conidia (20 to 30 ⫻ 8 to 11 ) were ellipsoid, often curved with 3 true septae. The same organism was grown from the vitreous tap. Dematiaceous fungal endophthalmitis has a very poor prognosis.3–5 This case highlights the value of anterior chamber aspiration for diagnosis, although the risk of subsequent development of a corneal infiltrate should be kept in mind. Intravitreal amphotericin B was employed once there was increasing inflammation within the vitreous cavity on ultrsonography. The endophthalmitis resolved, but the indolent keratitis was less responsive. Vitrectomy may possibly be beneficial, although the corneal status precluded this management option in our patient.
PURPOSE:
To report a case of fungal keratitis with consecutive endophthalmitis caused by Microsphaeropsis olivacea. METHODS: Case report. RESULTS: A 51-year-old man developed fungal keratitis and consecutive endophthalmitis after sustaining a penetrating injury to the right eye. Cultures of the aqueous humor yielded M. olivacea. Infection resolved after intraocular fungal debridement, intravitreous amphotericin B, and aggressive topical natamycin and oral fluconazole. Persistent, low-grade smoldering corneal and intraocular inflammation required topical corticosteroid therapy. CONCLUSION: M. olivacea is an exceedingly rare ocular pathogen. The intraocular portion of the infection responded quickly to intravitreal antifungal treatment; however, the course was prolonged by smoldering corneal inflammation. Prompt recognition of intraocular spread and aggressive treatment may be beneficial in fungal infections caused by unusual organisms with uncertain virulence. (Am J Ophthalmol 2001;131:142–143. © 2001 by Elsevier Science Inc. All rights reserved.)
A
REFERENCES
1. Forster EK, Rebell G, Wilson LA. Dematiaceous fungal keratitis. Clinical isolates and management. Br J Ophthalmol 1975;59:76. 2. Luque AG, Nanni R, De Braaclenti BJC. Mycotic keratitis caused by Curvularia lunata varaeria. Mycopathologica 1985; 93:9 –12. 3. Rummelt V, Ruprecht KW, Boltze HJ, et al. Chronic Alternaria alternata endophthalmitis following intraocular lens implantation. Arch Ophthalmol 1991;109:178. 4. Holting-Lima AL, Freitas D, Fischman O. Exophialia jeansemei causing late endophthalmitis after cataract surgery. Am J Ophthalmol 1999;128:512–514. 5. Borderie VM, Bourcier TM, Poirot J-LP. Endophthalmitis after Lasiodiplodia theobomae corneal abscess. Graefe’s Arch Clin Exp Ophthalmol 1997;235:259 –269.
Microspaeropsis olivacea Keratitis and Consecutive Endophthalmitis Chirag V. Shah, MD, Dan B. Jones, MD, and Eric R. Holz, MD
Accepted for publication Jul 24, 2000. From the Baylor College of Medicine, Cullen Eye Institute, Houston, Texas. Inquiries to Eric R. Holz, MD, 6565 Fannin NC-205, Houston, TX 77030; fax: (713) 798-8763; e-mail: [email protected]
142
AMERICAN JOURNAL
51-YEAR-OLD MAN SUSTAINED CORNEAL LACERATION
and traumatic cataract of the right eye after a penetrating injury from a tree branch. His past general and ocular health were normal except for diabetes mellitus of 5 years duration. Emergent corneal laceration repair and anterior chamber reformation were performed at another facility. Postoperative treatment included tobramycin/ dexamethasone twice daily, homatropine 5% twice daily, ketorolac twice daily, and dichlorphenamide three times daily. Four days after the initial surgery, the patient underwent an extracapsular cataract extraction with implantation of a posterior chamber intraocular lens. During the next 5 weeks, the patient developed worsening visual acuity, a white endothelial plaque, and significant anterior chamber cell and flare, prompting referral to the Cullen Eye Institute, Houston, Texas. Examination of the right eye 6 weeks after the original injury revealed an uncorrected visual acuity of 20/200 (pinhole 20/30-2), no afferent pupillary defect, and intraocular pressure of 17.5 mmHg. The left eye was normal with visual acuity of 20/25⫹. The right eye presented hyperemic bulbar conjunctiva, corneal endothelial opacity with deep stromal infiltrate near the full-thickness laceration site, and anterior chamber extension of fine white fibrous processes. Mild (⫹1) anterior chamber cells and trace flare (Figures 1 and 2) existed. The intraocular lens was well centered in a capsular bag that was clear of inflammatory plaque and debris. The vitreous was clear of cells and the retina was normal. Post-traumatic fungal keratitis and endophthalmitis were suspected. On the right eye, the patient underwent an anterior chamber tap, aspiration of intraocular fungal elements
OF
OPHTHALMOLOGY
JANUARY 2001
FIGURE 1. Right eye 6 weeks after the injury with corneal laceration suture in place, deep stromal infiltrate, and extension of fibrous processes into the anterior chamber (noted by arrow).
apy yielded no organisms to smear or culture. Low-grade smoldering corneal inflammation continued, and topical corticosteroid drugs (prednisolone acetate 1%) were initiated 34 days after the laboratory procedure. Two months of treatment resulted in a stable corneal scar without evidence of corneal or intraocular inflammation. Topical corticosteroids were discontinued 8 weeks later. Best-corrected visual acuity, 10 months after the initial injury, was 20/100, attributable to focal corneal opacification and irregular astigmatism. We are unaware of previous reports of this ocular infection caused by M. olivacea and could find no reference to it in a computer search using Medline. The only report of this organism as a human pathogen involves dermatitis with clinical appearance similar to “ringworm.”1 The fungus was isolated from a rapidly progressing superficial, maculopapular lesion of the left shoulder in an otherwise healthy patient. The species M. olivacea belongs to the order Sphaeropsidales, which are distinguished by the presence of pycnidial conidiomata, and the class Coelomycetes, which are parasitic to higher plants, lichen, and other fungi. Our case required long-term topical and oral antifungal therapy and subsequent topical corticosteroid therapy after initial aggressive treatment. The mechanism of prolonged corneal and intraocular inflammation remains uncertain. REFERENCE
1. Guarro J, Mayayo E, Tapiol J, Aguilar C, Cano J. Microsphaeropsis olivacea as an etiological agent of human skin infection. Med Mycol 1999;37:133–7. FIGURE 2. Right eye 6 weeks after the injury. Higher magnification of deep corneal stromal infiltrate and extension of fine fibrous processes into the anterior chamber.
using the vitrectomy probe, subtotal pars plana vitrectomy, and intravitreal injection of amphotericin B (7.5 g/0.15 ml). Postoperative therapy included natamycin 5% drops 6 times daily, atropine 1% drops twice daily, and oral fluconazole 200 mg twice daily. Endothelial plaque and anterior chamber suppuration resolved within 48 hours. Culture from the aqueous humor showed dematiaceous mold in blood and chocolate agars and thioglycollate broth after 19 days, subsequently identified as Microsphaeropsis olivacea at the Fungus Testing Laboratory, University of Texas Health Science Center at San Antonio. Topical natamycin and oral fluconazole were continued for 2 months. Subsequent examinations showed slowly progressive improvement characterized by reduction in the area and density of deep stromal opacity. Curettage of a suspicious granular area near a corneal laceration suture 117 days after initial antifungal therVOL. 131, NO. 1
Leber Hereditary Optic Neuropathy Associated with Antiretroviral Therapy for Human Immunodeficiency Virus Infection Saad Shaikh, MD, Christopher Ta, MD, Arthur A. Basham, MD, and Sam Mansour, MD PURPOSE:
Antiretroviral therapy has reduced the morbidity and mortality associated with human immunodeficiency virus (HIV) infection. However, side effects are increasingly recognized, including a commonly reported toxic mitochondrial myopathy. We report such a case of Leber hereditary optic neuropathy in a patient with antiretroviral therapy for HIV infection and speculate on Accepted for publication Jul 17, 2000. From the Department of Ophthalmology, Stanford University School of Medicine, Stanford, California (S.S., C.T., S.M.), and Los Gatos, California (A.A.B.). Inquiries to Saad Shaikh, MD, Department of Ophthalmology, Stanford University School of Medicine, Stanford, CA 94305; fax: (650) 723-7918; e-mail: [email protected]
BRIEF REPORTS
143
PURPOSE:
To report a case of fungal keratitis with consecutive endophthalmitis caused by Microsphaeropsis olivacea. METHODS: Case report. RESULTS: A 51-year-old man developed fungal keratitis and consecutive endophthalmitis after sustaining a penetrating injury to the right eye. Cultures of the aqueous humor yielded M. olivacea. Infection resolved after intraocular fungal debridement, intravitreous amphotericin B, and aggressive topical natamycin and oral fluconazole. Persistent, low-grade smoldering corneal and intraocular inflammation required topical corticosteroid therapy. CONCLUSION: M. olivacea is an exceedingly rare ocular pathogen. The intraocular portion of the infection responded quickly to intravitreal antifungal treatment; however, the course was prolonged by smoldering corneal inflammation. Prompt recognition of intraocular spread and aggressive treatment may be beneficial in fungal infections caused by unusual organisms with uncertain virulence. (Am J Ophthalmol 2001;131:142–143. © 2001 by Elsevier Science Inc. All rights reserved.)
A
REFERENCES
1. Forster EK, Rebell G, Wilson LA. Dematiaceous fungal keratitis. Clinical isolates and management. Br J Ophthalmol 1975;59:76. 2. Luque AG, Nanni R, De Braaclenti BJC. Mycotic keratitis caused by Curvularia lunata varaeria. Mycopathologica 1985; 93:9 –12. 3. Rummelt V, Ruprecht KW, Boltze HJ, et al. Chronic Alternaria alternata endophthalmitis following intraocular lens implantation. Arch Ophthalmol 1991;109:178. 4. Holting-Lima AL, Freitas D, Fischman O. Exophialia jeansemei causing late endophthalmitis after cataract surgery. Am J Ophthalmol 1999;128:512–514. 5. Borderie VM, Bourcier TM, Poirot J-LP. Endophthalmitis after Lasiodiplodia theobomae corneal abscess. Graefe’s Arch Clin Exp Ophthalmol 1997;235:259 –269.
Microspaeropsis olivacea Keratitis and Consecutive Endophthalmitis Chirag V. Shah, MD, Dan B. Jones, MD, and Eric R. Holz, MD
Accepted for publication Jul 24, 2000. From the Baylor College of Medicine, Cullen Eye Institute, Houston, Texas. Inquiries to Eric R. Holz, MD, 6565 Fannin NC-205, Houston, TX 77030; fax: (713) 798-8763; e-mail: [email protected]
142
AMERICAN JOURNAL
51-YEAR-OLD MAN SUSTAINED CORNEAL LACERATION
and traumatic cataract of the right eye after a penetrating injury from a tree branch. His past general and ocular health were normal except for diabetes mellitus of 5 years duration. Emergent corneal laceration repair and anterior chamber reformation were performed at another facility. Postoperative treatment included tobramycin/ dexamethasone twice daily, homatropine 5% twice daily, ketorolac twice daily, and dichlorphenamide three times daily. Four days after the initial surgery, the patient underwent an extracapsular cataract extraction with implantation of a posterior chamber intraocular lens. During the next 5 weeks, the patient developed worsening visual acuity, a white endothelial plaque, and significant anterior chamber cell and flare, prompting referral to the Cullen Eye Institute, Houston, Texas. Examination of the right eye 6 weeks after the original injury revealed an uncorrected visual acuity of 20/200 (pinhole 20/30-2), no afferent pupillary defect, and intraocular pressure of 17.5 mmHg. The left eye was normal with visual acuity of 20/25⫹. The right eye presented hyperemic bulbar conjunctiva, corneal endothelial opacity with deep stromal infiltrate near the full-thickness laceration site, and anterior chamber extension of fine white fibrous processes. Mild (⫹1) anterior chamber cells and trace flare (Figures 1 and 2) existed. The intraocular lens was well centered in a capsular bag that was clear of inflammatory plaque and debris. The vitreous was clear of cells and the retina was normal. Post-traumatic fungal keratitis and endophthalmitis were suspected. On the right eye, the patient underwent an anterior chamber tap, aspiration of intraocular fungal elements
OF
OPHTHALMOLOGY
JANUARY 2001
FIGURE 1. Right eye 6 weeks after the injury with corneal laceration suture in place, deep stromal infiltrate, and extension of fibrous processes into the anterior chamber (noted by arrow).
apy yielded no organisms to smear or culture. Low-grade smoldering corneal inflammation continued, and topical corticosteroid drugs (prednisolone acetate 1%) were initiated 34 days after the laboratory procedure. Two months of treatment resulted in a stable corneal scar without evidence of corneal or intraocular inflammation. Topical corticosteroids were discontinued 8 weeks later. Best-corrected visual acuity, 10 months after the initial injury, was 20/100, attributable to focal corneal opacification and irregular astigmatism. We are unaware of previous reports of this ocular infection caused by M. olivacea and could find no reference to it in a computer search using Medline. The only report of this organism as a human pathogen involves dermatitis with clinical appearance similar to “ringworm.”1 The fungus was isolated from a rapidly progressing superficial, maculopapular lesion of the left shoulder in an otherwise healthy patient. The species M. olivacea belongs to the order Sphaeropsidales, which are distinguished by the presence of pycnidial conidiomata, and the class Coelomycetes, which are parasitic to higher plants, lichen, and other fungi. Our case required long-term topical and oral antifungal therapy and subsequent topical corticosteroid therapy after initial aggressive treatment. The mechanism of prolonged corneal and intraocular inflammation remains uncertain. REFERENCE
1. Guarro J, Mayayo E, Tapiol J, Aguilar C, Cano J. Microsphaeropsis olivacea as an etiological agent of human skin infection. Med Mycol 1999;37:133–7. FIGURE 2. Right eye 6 weeks after the injury. Higher magnification of deep corneal stromal infiltrate and extension of fine fibrous processes into the anterior chamber.
using the vitrectomy probe, subtotal pars plana vitrectomy, and intravitreal injection of amphotericin B (7.5 g/0.15 ml). Postoperative therapy included natamycin 5% drops 6 times daily, atropine 1% drops twice daily, and oral fluconazole 200 mg twice daily. Endothelial plaque and anterior chamber suppuration resolved within 48 hours. Culture from the aqueous humor showed dematiaceous mold in blood and chocolate agars and thioglycollate broth after 19 days, subsequently identified as Microsphaeropsis olivacea at the Fungus Testing Laboratory, University of Texas Health Science Center at San Antonio. Topical natamycin and oral fluconazole were continued for 2 months. Subsequent examinations showed slowly progressive improvement characterized by reduction in the area and density of deep stromal opacity. Curettage of a suspicious granular area near a corneal laceration suture 117 days after initial antifungal therVOL. 131, NO. 1
Leber Hereditary Optic Neuropathy Associated with Antiretroviral Therapy for Human Immunodeficiency Virus Infection Saad Shaikh, MD, Christopher Ta, MD, Arthur A. Basham, MD, and Sam Mansour, MD PURPOSE:
Antiretroviral therapy has reduced the morbidity and mortality associated with human immunodeficiency virus (HIV) infection. However, side effects are increasingly recognized, including a commonly reported toxic mitochondrial myopathy. We report such a case of Leber hereditary optic neuropathy in a patient with antiretroviral therapy for HIV infection and speculate on Accepted for publication Jul 17, 2000. From the Department of Ophthalmology, Stanford University School of Medicine, Stanford, California (S.S., C.T., S.M.), and Los Gatos, California (A.A.B.). Inquiries to Saad Shaikh, MD, Department of Ophthalmology, Stanford University School of Medicine, Stanford, CA 94305; fax: (650) 723-7918; e-mail: [email protected]
BRIEF REPORTS
143