Before the era of antibacterial therapy, endogenous endophthalmitis occurred in approximately 5% of meningococcal meningitis cases.1 Since the introduction of antimicrobial therapy, endogenous endophthalmitis is rarely observed as a complication of meningococcal disease.2 In most cases, endophthalmitis occurs by hematogenous spread; direct extension from the optic nerve via inflamed meninges or lymphatics is possible but unlikely.3 Early diagnosis and aggressive treatment are essential to prevent blindness and death. We report a case with the clinical manifestations of meningococcemia with endophthalmitis as the initial presentation.
A 27-year-old white man working as a farmer presented with flu-like symptoms and blurred vision in the right eye shortly after exposure to sheep-dip spray. He had swollen metacarpophalangeal joints and a widespread petechial skin rash (Figure 1). No other signs of systemic disease were present. Neurologic examination was normal except for an afferent pupillary defect in the right eye (1+) and slight lethargy.
On admission, the patient's temperature was 37.5°C; the pulse rate, 120 beats/min; and blood pressure, 90/50 mm Hg. Laboratory tests were performed with the following results: hemoglobin, 14 g/dL; white blood cells, 17 900/cu mm with 60% neutrophils, 30% lymphocytes, and 10% monocytes; platelets, 60 000/cu mm; and Westergren erythrocyte sedimentation rate, 107 mm/hr. The visual acuity in the right eye was counting fingers at 1 m with a cloudy cornea and 2.0 mm hypopyon (Figure 2). The pupil was immobile with a fibrinous exudate (Figure 3). The right eye fundus could not be visualized. The visual acuity in the left eye was 6/12 with a clear cornea and few cells in the anterior chamber and vitreous. The fundus was clouded by vitreous exudates. The intraocular pressure was 30 mm Hg in the right eye and 18 mm Hg in the left eye. Ultrasound scan showed diffuse vitreous involvement in the right eye and mild opacities in the left eye.
Bilateral endogenous endophthalmitis with secondary glaucoma was diagnosed in the right eye. Gram stain of the vitreous specimen and cerebrospinal fluid (CSF) was negative. Culture of the CSF was sterile, but blood cultures and vitreous aspirate grew Neisseria meningitidis serogroup C, which was sensitive to penicillin, vancomycin, and ceftazidime. After the vitreous was aspirated, ceftazidime (2 mg) and vancomycin hydrochloride (1 mg) were injected intravitreally into the right eye. The patient was treated with 2.4 g of intravenous benzyl penicillin every 4 hours and 2.0 g of cefotaxime (Claforan) every 6 hours. Topical therapy consisted of fortified ceftazidime, vancomycin, cyclopentolate 1% (Mydrilate), betaxolol 0.5% (Betoptic), and prednisolone acetate 1% drops. Forty-eight hours after therapy was started, the systemic infection and visual symptoms improved.
Parenteral and topical therapy was continued for 2 weeks, and the topical medications were slowly tapered. The right eye improved steadily. One month after treatment, the visual acuity was 6/18 with scattered areas of iris atrophy and a clearer view of the fundus, revealing a macular scar (Figure 4). The left eye returned to normal with a visual acuity of 6/6 and a normal fundus. The patient made a complete recovery from all signs of meningococcemia and was discharged.
Neisseria meningitidis is a gram-negative intracellular diplococcus with 3 main serogroups: A, B, and C. The meningococcus is carried asymptomatically in the nasopharynx in 2% to 25% of people and is spread from person to person by respiratory droplets.4 Meningococcal ocular infections have been classified as (1) cases occurring without meningitis, as in our patient; (2) secondary cases during or after an attack of meningitis5; and (3) cases in which meningitis follows the ocular infection when the bacteria invade the bloodstream from the nasopharynx and reach the meninges.6
In our patient, the presentation of flu-like symptoms soon after the exposure to sheep-dip spray was suggestive of an allergic reaction but was in fact the presenting symptom of septicemia. Some observers believe that chronic meningococcemia is a hypersensitive state in which many of the clinical manifestations are allergic in nature.7 Our case was unique because bilateral blurring of vision was the initial presentation of meningococcemia. In other reported cases of meningococcal sepsis with endophthalmitis,2,8 septic embolization is the suggested route of infection, with findings compatible with those of an allergy.
Recent advances in the diagnosis and treatment of endophthalmitis emphasize the importance of culturing the aqueous and vitreous to identify the organism.9 A review of 72 cases of metastatic endophthalmitis10 concludes that adequate intravitreal antibiotic therapy is the key to successful treatment of metastatic bacterial endophthalmitis. Misdiagnosis and delayed treatment result in a poor outcome.
No large prospective study of endogenous bacterial endophthalmitis has determined the benefits of intravitreal antibiotics, intravitreal steroids, and vitrectomy.11 An endophthalmitis vitrectomy study12 concludes that routine immediate vitrectomy is not necessary in postoperative endophthalmitis patients whose visual acuity is better than light perception, although it offers theoretical advantages such as removal of the infecting organisms and their toxins, removal of vitreous membranes, clearing of vitreous opacities, collection of abundant sample for culture, and better distribution of intravitreal antibiotics. Although adequate intravenous antibiotics can treat metastatic bacterial endophthalmitis, an argument can be made for early surgical intervention if the initial physical examination or ultrasonography confirms the presence of diffuse vitreous involvement.12
Early, aggressive treatment with topical, intravitreal, and systemic antibiotics was vital in our patient and resulted in visual recovery of 6/18 in the right eye and 6/6 in the left eye. In a case of meningococcal endophthalmitis without meningitis,13 a delay in treatment resulted in poor vision. Our patient was left with a macular scar in the right eye, which may have been the result of retinal necrosis caused by the bacterial invasion or a macular infarction caused by the intravitreal antibiotics. The favorable outcome in our patient was probably from factors such as the patient's young age and good health, the prompt and appropriate administration of antibiotics, and the extreme sensitivity of N meningitidis to the antibiotics.
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