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Show Bilateral Optic Neuritis due to Malaria Joseph G. Chacko, MD, Sanjeeva Onteddu, MD, Eric R. Rosenbaum, MD, MPH Abstract: Malaria is a mosquito-borne infectious disease caused by protists of the genus Plasmodium. Malaria is widespread in tropical regions around the equator, including much of sub-Saharan Africa, Asia, and the Americas, and uncommonly seen in the developed world. Although a variety of ocular manifestations have been linked to malaria, optic neuritis is rare. We report a patient who developed bilateral optic neuritis after he was treated successfully for acute falciparum malaria. Journal of Neuro-Ophthalmology 2013;33:266-267 doi: 10.1097/WNO.0b013e31829ff911 © 2013 by North American Neuro-Ophthalmology Society A40-year-old African man, who had been living in the United States for 12 years, traveled home to Zimbabwe. Before leaving, he did not take malaria prophylaxis. He returned to the United States after his 2-week trip and became ill with headache, fever, chills, and sweats. A blood smear was positive for malarial parasites, the Centers for Disease Control was contacted, and the patient was started on quinine and transferred to our hospital for further care. On arrival, he appeared well-nourished but was febrile, diaphoretic, and icteric. His vital signs were as follows: temperature 103.7°F, pulse 127 beats per minute, respira-tions 20/min, and blood pressure 146/71 mm Hg. Systemic and neurologic examinations were otherwise normal. His white blood cell count was of 5870 cells/ml (normal, 3000-12,000 cells/ml), hemoglobin 12.2 g/dL (normal, 13.5-17.5 g/dL), and total bilirubin of 6.0 mg/dL (normal, 0.2-1.2 mg/dL). Peripheral blood smear was pos-itive for Plasmodium falciparum (Fig. 1). The patient received 3 days of oral quinine (650 mg every 6 hours) and doxycycline (100 mg twice a day), followed by a 3-day course of artemether/lumefantrine. His repeat blood smear showed no malarial parasites, and he became less icteric and was discharged home. One month later, the patient presented with bilaterally decreased vision. He reported gradually worsening vision in the left eye after discharge, followed 1 week later with involvement of the right eye. He also described pain with eye movement. On examination, visual acuity was count fingers at 1 foot, right eye, and 20/400, left eye. Pupils were 7 mm and sluggishly reactive to light without a relative afferent pupillary defect. Eye movements were full. Slit-lamp examination was significant for FIG. 1. Peripheral blood smear demonstrates classic ring-form trophozoites inside the red blood cells (Wright-Giemsa, ·1000). Department of Ophthalmology (JGC), Jones Eye Institute, and De-partments of Neurology (JGC, SO), and Pathology (ERR), University of Arkansas for Medical Sciences, Little Rock, Arkansas. Supported in part by an unrestricted grant from Research to Prevent Blindness (New York, NY) and the Pat & Willard Walker Eye Research Center, Jones Eye Institute, University of Arkansas for Medical Sciences (Little Rock, AR). The authors report no conflicts of interest. Address correspondence to Joseph G. Chacko, MD, Department of Ophthalmology, Jones Eye Institute, University of Arkansas for Medical Sciences, 4301 W. Markham, 523, Little Rock, AR 72205; E-mail: jchacko@uams.edu 266 Chacko et al: J Neuro-Ophthalmol 2013; 33: 266-267 Photo Essay Section Editor: Timothy J. McCulley, MD Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. 1+ cell in the right anterior chamber and rare cell in the left eye. Goldmann visual field testing revealed bilateral cecocentral scotomas. There was a mild bilateral optic disc edema (Fig. 2), and the retinal examination was normal. Magnetic resonance imaging showed bilateral enhance-ment of the orbital portions of the optic nerves (Fig. 3). Repeat peripheral blood smear did not reveal any malarial parasites, and cerebrospinal fluid analysis was normal. The patient was started on intravenous solumedrol 250 mg every 6 hours for 3 days followed by oral prednisone taper over 4 weeks. Two months later, visual acuity was 20/20 in each eye with resolution of the cecocentral scotomas and optic disc edema. The ocular manifestations of malaria have been described previously, and retinal abnormalities predominate, particu-larly in the setting of anemia (1-4). Optic atrophy may be the result of chronic papilledema, ischemic optic neuropathy, or optic neuritis. Flower et al (1) reported the association with ischemic optic neuropathy in a 56-year-old man with malaria caused by Plasmodium vivax who experienced vision loss in his left eye with a pale, swollen optic disc, peripapillary hemorrhage, and a macular star. Previous reports have documented malaria-associated optic neuritis in the context of active infection, possibly because of tissue hypoxia related to hemolysis, sluggish blood flow, and increased capillary permeability. Wadia (2) reported the first 2 cases of malaria-associated retrobulbar optic neuritis in 1990. Both patients, a 28-year-old man and a 31-year-old woman, developed visual loss concurrently with their systemic malarial symptoms. Both were treated with intravenous quinine and retrobulbar injections of dexa-methasone and each attained full visual recovery. Kale et al (3) reported a 24-year-old woman with P. falciparum who developed bilateral light perception vision with poorly reac-tive pupils and normal fundi 1 day after beginning intrave-nous quinine therapy. She was switched to artemether and given intravenous methylprednisolone for 3 days, followed by oral steroid taper for 6 weeks. Vision improved to 20/60 in each eye over the ensuing 2 months. Our case is unique in that bilateral visual loss occurred approximately 1 month after onset of systemic symptoms. The patient's blood smear after treatment and before dis-charge from the hospital did not show any malarial parasites. The timing of visual loss in our patient, the concomitant mild iritis, and improved vision with steroid therapy supports a postinfection, immune-related mechanism. REFERENCES 1. Flower B, Armstrong-James D, Dance C, Bremner F, Doherty T. Blind, breathless, and paralysed from benign malaria. Lancet. 2011;377:438. 2. Wadia PZ. Retrobulbar neuritis in two patients with falciparum malaria. J Assoc Physicians India. 1990;38:800-801. 3. Kale VP, Bichile LS, Bajpai S. Falciparum malaria induced retrobulbar neuritis. J Postgrad Med. 2004;50:150. 4. Kochar DK, Shubhakaran, Kumawat BL, Thanvi I, Joshi A, Vyas SP. Ophthalmoscopic abnormalities in adults with falciparum malaria. QJM. 1998;91:845-852. FIG. 2. Mild bilateral optic disc edema is present. FIG. 3. Postcontrast axial (A) and coronal (B) magnetic resonance imaging with fat suppression shows bilateral optic nerve enhancement (arrows). Chacko et al: J Neuro-Ophthalmol 2013; 33: 266-267 267 Photo Essay Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
