Endogenous endophthalmitis is a potentially devastating infection resulting from hematogenous spread of infection to the eye. Common predisposing factors for endogenous endophthalmitis include a malignant neoplasm and immunosuppressed states. Streptococci are a common cause of endogenous endophthalmitis, although Streptococcus agalactiae (or group B Streptococcus [GBS]) endophthalmitis in adults is rare.1 We report a case of endogenous GBS endophthalmitis occurring as a presenting sign of precursor T-cell acute lymphoblastic leukemia. To our knowledge, this is the first reported case of acute lymphoblastic leukemia manifesting as GBS endophthalmitis.
A 56-year-old man was in good health until developing a febrile illness 6 days prior to his first visit, followed 3 days later by the onset of redness and photophobia in the right eye. He was evaluated for presumed uveitis and treated hourly with topical steroid eyedrops, but he was referred to the uveitis clinic owing to progressive worsening and posterior segment extension. On examination, his visual acuity was light perception OD and 20/40 OS. Examination of the right eye revealed eyelid edema, conjunctival congestion, and a 1-mm hypopyon with fibrinous exudates in the anterior chamber, with no view of the ocular fundus. Results from examination of the left eye were unremarkable. Intraocular pressure was 10 mm Hg OU. He underwent urgent pars plana vitrectomy with injection of intravitreous vancomycin hydrochloride and amikacin sulfate and also received intravenous vancomycin, clindamycin phosphate, and cefotaxime sodium. Vitreous, anterior chamber, and blood cultures grew GBS. A complete blood cell count showed pancytopenia with toxic granulation. Diagnostic inpatient workup including echocardiography revealed no focus of infection. Bone marrow biopsy revealed the diagnosis of precursor T-cell acute lymphoblastic leukemia (Figure). The patient continued to receive parenteral cefotaxime for bacteremia and had systemic chemotherapy initiated by the oncology service, with repeat intravitreous tap and injection of vancomycin 3 days later. Results from the repeat cultures were negative. His visual acuity remained light perception OD 10 days after surgery.
Endogenous endophthalmitis is a potentially devastating condition characterized by intraocular infection by organisms that access the eye through the bloodstream. Endogenous endophthalmitis accounts for 2% to 6% of all cases of endophthalmitis.2 In a recent review of cases of endogenous endophthalmitis, GBS was the causative agent in about 5% of cases.3 Group B Streptococcus most commonly causes infection in neonates and pregnant women, although in the last 2 decades there has been a 2- to 4-fold increase in the incidence of invasive GBS in nonpregnant adults.4 Most patients with GBS infection have a predisposing condition such as being older than 65 years and having diabetes mellitus, a malignant neoplasm, and compromised immunity. Bacteremia with no evident source of infection is the manifestation of invasive GBS in about 15% of nonpregnant adults.4 The most common identifiable sources of GBS are skin or soft-tissue infections, urinary tract infections, pneumonia, bone and joint infections, and endocarditis. In a review of cases of GBS endogenous endophthalmitis, most had ocular involvement within 5 days of onset of sepsis, and ocular infection was not the initial manifestation of sepsis in any patient.1 The visual prognosis in GBS endophthalmitis is poor, with 76% of cases resulting in visual acuity of light perception or worse.1
Our case is unusual because GBS endophthalmitis was the presenting factor leading to the diagnosis of precursor T-cell lymphoblastic leukemia. This case exemplifies the importance of having a high index of suspicion for endogenous endophthalmitis in uveitis cases with a rapidly progressive course that do not respond to standard therapy with corticosteroids. It also shows the important role an ophthalmologist can play in diagnosing serious underlying medical conditions.
Correspondence: Dr Suhler, Casey Eye Institute, 3375 SW Terwilliger Blvd, Portland, OR 97239 (suhlere@ohsu.edu).
Financial Disclosure: None reported.
Funding/Support: This work was supported by an unrestricted grant from Research to Prevent Blindness to the Casey Eye Institute and by the Department of Veterans Affairs (Dr Suhler).
1.Lee
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