Visual acuity without correction was 20/25 OU. Ocular motility was normal. The left eye and adnexa were normal. The right lower eyelid showed minimal edema and mild redness, which was worse nasally (Figure, A). There was +3 large vessel bulbar conjunctival injection that was greater nasally. The inferior palpebral conjunctiva was intensely inflamed and had 2 areas of ulceration down to the tarsus (Figure, B). A narrow tract of deep tissue necrosis with a blind end originated inferior to the caruncle; it probed inferonasally to a depth of approximately 7 mm. The anterior segment was otherwise normal. An orbital computed tomographic scan showed preseptal and postseptal edema with inflammatory changes in the nasal extraconal fat, without discrete abscess. Culture of the drainage grew MRSA susceptible to vancomycin hydrochloride, rifampin, and clindamycin phosphate but resistant to penicillin and cefazolin sodium. The patient was treated for 7 days with intravenous vancomycin and tobramycin sulfate as well as oral rifampin and then for 7 days with oral trimethoprim sulfa double strength with clinical resolution. Nasal cultures for MRSA were negative.

View larger version (200K): [in this window] [in a new window] [as a PowerPoint slide]   Figure. External photographs showing marked inflammation of the caruncle with mild nasal upper and lower eyelid edema (A) and tarsal conjunctival ulceration (short arrow) and the opening of a necrotic tract under the caruncle (long arrow) (B).

Comment
We report an unusual case of a healthy young patient who developed necrotizing community-acquired MRSA conjunctivitis that caused palpebral conjunctival ulceration and destruction of postseptal soft tissue with invasion of extraconal fat. Despite the depth of infection, external signs of eyelid inflammation were modest. There is 1 reported case of MRSA dacryocystitis with fistula formation,² but fistulas can occur with any severe bacterial dacryocystitis. Our patient had a true invasive infection that arose from the ocular surface. He had no apparent risk factors for MRSA colonization. In the setting of diffuse palpebral conjunctival inflammation, the deeper tissue destruction might have been overlooked; an important historical clue was the repeated accumulation of pus over the caruncle but not elsewhere. Dacryocystitis was unlikely owing to the lack of epiphora.

Community-acquired MRSA can produce large abscesses or carbuncles, possibly through production of a specific skin necrotic cytotoxin.³ Culture with sensitivity is critical as these MRSA strains are resistant to all β-lactam antibiotics and may be resistant to clindamycin.⁴ The proportion of staphylococcal ocular surface infections showing methicillin resistance has increased from 4% in 1999 to 17% in 2006.⁵ Approximately 96% of MRSA ocular isolates are resistant to ciprofloxacin hydrochloride and 82% are resistant to levofloxacin.⁶ A typical empirical treatment for moderately severe conjunctivitis with preseptal inflammation is an oral cephalosporin combined with a topical fourth-generation quinolone; this is ineffective for MRSA.

Physicians should consider MRSA in patients with atypical conjunctivitis showing patchy necrosis of conjunctiva and should investigate any dimpled or eroded areas for evidence of deeper invasion. If invasion is found, the patient should be presumptively treated for MRSA with systemic vancomycin⁵ while awaiting the results of bacterial culture. An orbital MRSA abscess within fat is relatively sequestered from antibiotic penetration, may require surgical débridement, and could lead to extensive necrotic damage to orbital structures such as extraocular muscles and the lacrimal sac.

AUTHOR INFORMATION
Correspondence: Dr Brown, Cabarrus Eye Center, 201 LePhillip Ct NE, Concord, NC 28025 (sbrownmd{at}cabarruseye.com).

Financial Disclosure: None reported.