Abstract
Purpose
To report a case of chronic endophthalmitis caused by Aquamicrobium lusatiense following phacoemulsification surgery.
Observations
A 71 year-old woman was referred for chronic ocular inflammation after cataract surgery. Serologic testing was negative for common infectious etiologies. Her condition deteriorated on immune-modulating therapy prompting vitreous biopsy, which confirmed infection with A. lusatiense. She was managed successfully with intravitreal antibiotic pharmacotherapy and intraocular lens explantation.
Conclusion and Importance
This is the first reported case of A. lusatiense causing endophthalmitis, or disease in a human, in the literature.
1
Introduction
Chronic postoperative endophthalmitis is a vision-threatening complication of ophthalmic surgery that can be caused by a range of organisms, from Propionibacterium acnes , to Staphylococcus epidermidis , to other atypical bacteria and select fungal species. , These cases often pose a diagnostic challenge, typically presenting with smoldering inflammation, which can respond initially to corticosteroid therapy. Herein we describe the first case of Aquamicrobium lusatiense causing endophthalmitis, or indeed, disease in a human, in the English language literature.
2
Case report
A 71 year-old immunocompetent Caucasian woman underwent uncomplicated phacoemulsification surgery with an outside provider. Immediately following surgery, Snellen visual acuity was measured at 20/20. At the one-month post-operative visit, anterior chamber cell was noted, and she was treated with topical 0.1% preservative-free dexamethasone due to a self-reported allergy to 1% prednisolone acetate. After completing a taper, she presented with rebound inflammation and was treated with twice daily 0.05% difluprednate for three days before transitioning back to 0.1% dexamethasone, remaining on twice daily dosing for maintenance. At her six-month follow-up visit she underwent yttrium-aluminum-garnet (YAG) laser posterior capsulotomy without complication. Sixteen months after cataract surgery, she transferred care to a new provider who tapered her off dexamethasone drops. She returned one month later with acute-onset unilateral hypopyon uveitis with a visual acuity of 20/400 and was initiated on topical 0.05% difluprednate every 2 hours and referred for evaluation to the retina service at Vanderbilt Eye Institute.
Initial examination showed mild corneal edema with diffuse, pigmented keratic precipitates and 3+ anterior chamber cell in the right eye. The vitreous was clear and there was no macular edema on optical coherence tomography (OCT). Serologic testing for treponemal IgG, herpes simplex virus (HSV) type 1 and 2 IgM, quantiferon gold, and Lyme ELISA were negative. Chest radiography was normal. Due to the corneal edema and pigmented keratic precipitates, herpetic etiology remained high on the differential. Therefore, empiric oral valacyclovir was started and difluprednate slowly tapered. One month later she returned with 20/60 visual acuity. The anterior chamber was quiet, and she transitioned to 0.1% fluorometholone taper. She returned two months later with stable exam findings but reported that she had flared twice and resumed difluprednate after consultation with an outside provider. Oral prednisone and 15 mg weekly methotrexate were started. Her disease quieted and vision improved to 20/50, but two months after initiation of methotrexate visual acuity deteriorated to 20/150, and examination showed 1+ anterior chamber cell and 2+ vitreous cell. Methotrexate was increased to 25 mg weekly. One month later, her vision improved to 20/70, but she remained active, with 2+ anterior chamber and vitreous cell, and was started on adalimumab 40mg every other week.
Following initiation of adalimumab, her visual acuity deteriorated to count fingers. Slit lamp examination showed increase in keratic precipitates ( Fig. 1 A) with a hazy view of the anterior and posterior chambers. B-scan ultrasonography demonstrated hyperechoic vitreous opacities concerning for vitritis ( Fig. 1 B). Her inflammation continued to worsen despite immunosuppression, and a diagnostic vitrectomy was performed.
