Hematogenous dissemination of microorganisms to the eye is an uncommon cause of endophthalmitis. Studies1,2 have reported that it accounts for 2% to 8% of all forms of endophthalmitis. For patients with symptoms of uveitis who have a history of systemic or focal infections or evidence of an immunocompromised state, endogenous endophthalmitis falls readily into the differential diagnosis. However, in an immunocompetent individual without evidence of systemic infection, the diagnosis requires a high index of suspicion.
A 48-year-old woman underwent a routine dental cleaning before development of eye symptoms. She had no history of gingival disease or cavity fillings. At initial examination 10 days later, she had sharp pain and photophobia in the right eye. She had no significant ocular history. Her medical history was remarkable for hypertension, asthma, osteoporosis, and fibromyalgia.
On examination, corrected visual acuity was 20/200 OD and 20/20 OS. Intraocular pressures were 21 and 19 mmHg, respectively. The anterior segment examination was significant for conjunctival hyperemia, fine keratic precipitates, the absence of iris nodules, and nuclear sclerosis in the right eye. The posterior segment was remarkable for vitreous haze secondary to cellular reaction and 3 areas of intraretinal hemorrhages with marked arteriolar sheathing (Figure 1). The left eye examination was unremarkable.
A tentative diagnosis of uveitis and retinal vasculitis was made, and the patient was started on topical corticosteroids and cycloplegics. At 3 days' follow-up examination, her vision had worsened to hand motion, she had developed a hypopyon, and there was no view of the fundus (Figure 2). She was then admitted to the hospital and underwent a vitrectomy with biopsy and injection of vancomycin hydrochloride (1 mg/0.1 mL) and amikacin sulfate (400 µg/0.1 mL). Cultures were positive several days later for α-hemolytic streptococci. A thorough medical workup in search of a nonocular site of infection was negative.
She subsequently developed a macular hole, for which she underwent vitrectomy with gas injection. To date, she is free of infection and maintains a best-corrected vision of counting fingers at 0.9 m.
Ishak and colleagues3 and May and colleagues4 each reported a case of endogenous endophthalmitis in patients with gingival disease that progressed to an abscess. In the latter case, the patient also had undergone a cavity filling 7 days before onset of symptoms.
Our case of endogenous endophthalmitis was in an immunocompetent individual who underwent routine dental cleaning 10 days before seeing an ophthalmologist. She did not undergo any procedures such as cavity filling or tooth extraction on that visit. As noted in previous case reports, 3,4 periodontal disease is well documented as a potential cause of endogenous endophthalmitis. However, as far as we are aware, this is the first reported case indicating that a routine teeth cleaning without evidence of gingival disease or a focal infection, such as a periodontal abscess, can lead to endogenous endophthalmitis. Because α-hemolytic streptococci are known to reside as normal flora in the nasopharynx, we presume that transient bacteremia developed after the dental cleaning, which led to seeding of the organism into intraocular tissues. A lag time of 7 to 10 days before onset of symptoms appears to be consistent with previous reports in the literature.4 In short, a careful history in any patient with symptoms of uveitis should include inquiries regarding routine dental cleaning.
Corresponding author and reprints: Manju L. Subramanian, MD, Ophthalmic Consultants of Boston, 50 Staniford St, Boston, MA 02114.
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