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Arch Ophthalmol. 2003;121:271-273.

Several authors have recently reported successful treatment of diabetic macular edema resistant to conventional laser photocoagulation with the injection of long-acting intravitreal corticosteroids.^1-2 Endophthalmitis after intravitreal injection is unusual. We report a case of Mycobacterium chelonae abscessus endophthalmitis occurring 1 month after the injection of intravitreal triamcinolone acetonide (Kenalog 40; Bristol-Myers Squibb Co, Princeton, NJ) to treat persistent diabetic macular edema.

Report of a Case
A 62-year-old man with a history of non–insulin dependent diabetes mellitus developed clinically significant macular edema. He underwent multiple sessions of focal grid argon laser photocoagulation to the edematous areas of the macula. Despite these sessions of focal grid macular laser photocoagulation, clinical examination showed persistent, widespread macular edema, and fluorescein angiography confirmed continued, diffuse macular leakage. With a visual acuity of 20/60 and no response to laser therapy, he underwent intravitreal injection of 4 mg of triamcinolone acetonide in 0.1 mL, 4 mm posterior to the limbus, using a 27-gauge needle and a 1-mL tuberculin syringe. The patient was reclined in an examining room chair and the eye was prepped using topical povidone-iodine. Four weeks after the treatment, the patient went to his ophthalmologist with a painless decrease in visual acuity to hand motions in the treated eye, a hypopyon, and no view to the fundus. He urgently underwent vitreous tap and injection of intravitreal vancomycin (1 mg/0.1 mL) and ceftriaxone (2 mg/0.1 mL) for presumed endophthalmitis.

When the patient did not improve after the initial intravitreal antibiotics, and acid-fast bacilli were identified growing from the vitreous cultures, he was referred for further evaluation and treatment. With final species identification and susceptibilities still pending, the patient underwent repeated vitreous tap and injection of ceftazidime (2.25 mg/0.1 mL), vancomycin (1 mg/0.1 mL), and amikacin (0.4 mg/0.1 mL). He subsequently underwent pars plana lensectomy and vitrectomy and received an additional injection of vancomycin (1 mg/0.1 mL) and amikacin (0.4 mg/0.1 mL). Vitreous cultures grew M chelonae abscessus sensitive to amikacin and clarithromycin. Susceptibilities were determined by minimum inhibitory concentration (MIC); the MIC for amikacin was 16 µg/mL and the MIC for clarithromycin was 0.5 µg/mL. The patient was treated aggressively with both topical amikacin (8 mg/mL) and oral clarithromycin (500 mg by mouth twice daily). Over the following 3 months, he underwent vitreous cavity tap and injection of vancomycin (1 mg/0.1 mL) and amikacin (0.4 mg/0.1 mL) on 5 separate occasions in addition to the topical and oral treatments. Despite the intensive therapy, the intraocular culture results continued to be positive for organisms, the patient's visual acuity dropped to no light perception, he had persistent pain in the eye, and a hypopyon redeveloped. Three months after the initial examination, the patient underwent enucleation of the involved eye.

Gross examination of the globe showed a 3-mm hypopyon with the remainder of the anterior chamber and vitreous cavity filled with white-tan fibrous tissue (Figure 1). Microscopic examination disclosed the vitreous cavity to be filled with a dense granulomatous infiltrate consisting of lymphocytes, histiocytes, and plasma cells with foci of giant cells. Examination of the infiltrate with a modified Ziehl-Neelson stain disclosed numerous acid-fast bacilli consistent with the Mycobacteria species (Figure 2). Growth of the species M chelonae abscessus was confirmed on Lowenstein-Jensen culture media.

View larger version (72K): [in this window] [in a new window] Figure 1. Gross photograph of the pupil/optic nerve section of the globe with an anterior chamber hypopyon and a white-tan fibrous tissue present in the vitreous cavity.

View larger version (97K): [in this window] [in a new window] Figure 2. Ziehl-Neelson stain displaying numerous acid-fast bacilli consistent with Mycobacteria species (original magnification x40).

Comment
Macular edema is a common cause of visual compromise in patients with diabetes.³ Recently, several small case series and case reports have described encouraging visual and anatomic results with the use of long-acting intravitreal corticosteroids in the treatment of macular edema resistant to conventional laser therapy.^1-2

Mycobacteria species are a rare cause of ocular infections and an even rarer cause of endophthalmitis; the species M chelonae has been described as causing keratitis, most recently in association with laser in situ keratomileusis as well as endophthalmitis.^4-7 These reports detail the deleterious effect corticosteroids can have on mycobacterial infections. In a review of systemic infections due to M chelonae, Wallace and colleagues⁸ described the importance of prior corticosteroid therapy in the development of infections secondary to this organism. Additional reported cases of cutaneous and osseous infections caused by the M chelonae species have identified concurrent long-term corticosteroid therapy as a risk factor for developing such infections.^9-10 In the current case, treatment with a long-acting intravitreal corticosteroid may have increased the susceptibility of this patient to infection with M chelonae abscessus. Inoculation of the organism into the vitreous may have occurred at the time of triamcinolone acetonide injection. Alternatively, the patient may have had a disseminated M chelonae abscessus infection with a distant focus, and an endogenous endophthalmitis may have developed in the setting of local ocular immunosuppression.^{8, 10}

Although encouraging results have been reported with the use of intravitreal triamcinolone acetonide in cases of diabetic macular edema refractory to focal grid laser photocoagulation, caution and close follow-up care is advised in these patients with a locally immunosuppressed intraocular status. In cases of endophthalmitis occurring after intravitreal injection of a long-acting corticosteroid, atypical Mycobacteria species should be considered in the differential diagnosis.

Matthew S. Benz, MD; Timothy G. Murray, MD; Sander R. Dubovy, MD; Randy S. Katz, MD; Charles W. G. Eifrig, MD
Miami, Fla

Corresponding author and reprints: Timothy G. Murray, MD, Bascom Palmer Eye Institute, PO Box 016880, Miami, FL 33101 (e-mail: tmurray{at}med.miami.edu).

REFERENCES
1. Jonas JB, Sofker A. Intraocular injection of crystalline cortisone as adjunctive treatment of diabetic macular edema. Am J Ophthalmol. 2001;132:425-427. FULL TEXT | ISI | PUBMED 2. Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology. 2002;109:920-927. FULL TEXT | ISI | PUBMED 3. Fong DS, Ferris III FL, Davis MD, Chew EY. Causes of severe visual loss in the early treatment diabetic retinopathy study: ETDRS report No. 24. Am J Ophthalmol. 1999;127:137-141. FULL TEXT | ISI | PUBMED 4. Solomon A, Karp CL, Miller D, Dubovy SR, Huang AJ, Culbertson WW. Mycobacterium interface keratitis after laser in situ keratomileusis. Ophthalmology. 2001;108:2201-2208. FULL TEXT | ISI | PUBMED 5. Roussel TJ, Stern WH, Goodman DF, Whitcher JP. Postoperative mycobacterial endophthalmitis. Am J Ophthalmol. 1989;107:403-406. ISI | PUBMED 6. Grenzebach UH, Busse H, Totsch M, Dockhorn-Dworniczak B. Endophthalmitis induced by atypical mycobacterial infection. Ger J Ophthalmol. 1996;5:202-206. PUBMED 7. Ramaswamy AA, Biswas J, Bhaskar V, Gopal L, Rajagopal R, Madhavan HN. Postoperative Mycobacterium chelonae endophthalmitis after extracapsular cataract extraction and posterior chamber intraocular lens implantation. Ophthalmology. 2000;107:1283-1286. FULL TEXT | ISI | PUBMED 8. Wallace RJ Jr, Brown BA, Onyi GO. Skin, soft tissue, and bone infections due to Mycobacterium chelonae chelonae: importance of prior corticosteroid therapy, frequency of disseminated infections, and resistance to oral antimicrobials other than clarithromycin. J Infect Dis. 1992;166:405-412. ISI | PUBMED 9. Safranek TJ, Jarvis WR, Carson LA, et al. Mycobacterium chelonae wound infections after plastic surgery employing contaminated gentian violet skin-marking solution. N Engl J Med. 1987;317:197-201. ABSTRACT 10. Drabick JJ, Duffy PE, Samlaska CP, Scherbenske JM. Disseminated Mycobacterium chelonae subspecies chelonae infection with cutaneous and osseous manifestations. Arch Dermatol. 1990;126:1064-1067. FREE FULL TEXT

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