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Show PHOTO ESSAY Anterior Ischemic Optic Neuropathy Associated With Rickettsia Conorii Infection Moncef Khairallah, MD, Sonia Zaouali, MD, Salim Ben Yahia, MD, Ahmed Ladjimi, MD, Riadh Messaoud, MD, Salah Jenzeri, MD, and Sonia Attia, MD FIG. 1. A. Fundus OD shows optic disc edema, optic disc and retinal hemorrhages, and a small white retinal lesion. B. Early-phase fluorescein angiography OD shows filling defects in the optic disc inferiorly, peripapillary choroid, and choroidal watershed zones. C. Late- phase fluorescein angiography shows optic disc staining and blockage of background fluorescence by hemorrhage. Department of Ophthalmology, Fattouma Bourguiba University Hospital, Monastir, Tunisia. Address correspondence to Moncef Khairallah, MD, Department of Ophthalmology, Fattouma Bourguiba University Hospital, 5019 Monastir, Tunisia; E- mail: moncef. khairallah@ rns. tn 212 J Neuro- Ophthalmol, Vol. 25, No. 3, 2005 Anterior Ischemic Optic Neuropathy J Neuro- Ophthalmol, Vol. 25, No. 3, 2005 Abstract: A 43- year- old man with fever, headache, and skin rash developed unilateral acute anterior ischemic optic neuropathy The indirect immunofluorescence test was positive for Rickettsia conorii. Although retinal lesions have been described in Rickettsia conorii infection, this is the first reported case of ischemic optic neuropathy This infection should be considered in a patient with nonarteritic anterior ischemic optic neuropathy with high fever or skin rash who inhabits or travels from an endemic area. (/ Neuro- Ophthalmol 2005; 25: 212- 214) Apreviously healthy 43- year- old man developed high fever, headache, general malaise, and a maculopapular skin rash without a known history of a tick bite. The patient was diagnosed as having presumed rickettsial disease by an infectious disease specialist. Four days after the onset of fever, he noticed painless acute visual loss in the OD. On examination seven days later, best- corrected visual acuity was counting fingers OD and 20/ 20 OS. A relative afferent pupillary defect was present OD. Slit lamp examination was normal except for trace vitreous cells present bilaterally. Fundus examination OD showed optic disc edema, optic disc and retinal hemorrhages, and small white retinal lesions in the periphery and posterior pole ( Fig. 1 A). A crowded optic disc and a para-papillary hemorrhage temporally were present OS. Fluorescein angiography OD showed filling defects in the inferior optic disc, peripapillary choroid, and choroidal watershed zones, optic disc staining in the late phase, 120 105 90 7i 60 FIG. 2. Goldmann perimetry shows a su and blockage of background fluorescence by hemorrhages ( Fig. IB, C). Optic disc staining was visible OS. Visual field testing revealed a superior altitudinal defect OD and a full field OS ( Fig. 2). Body temperature was 37.5° C and blood pressure was 120/ 70 mm Hg. Cardiovascular, respiratory, gastrointestinal, and neurologic examinations were normal. There were generalized cicatricial skin lesions. The following tests were normal: complete blood count, erythrocyte sedimentation rate, blood sugar, blood lipids, syphilis serology, angiotensin-converting enzyme, antinuclear antibodies, chest x- ray, and magnetic resonance imaging of the brain. The indirect immunofluorescence test was positive for Rickettsia conorii with a titer of 1: 320 ( normal, < 1: 80). The patient was treated with doxycycline 200 mg/ day for 7 days. Four weeks after the initial examination, visual acuity was 20/ 400 OD and 20/ 20 OS. The optic disc edema OD had been replaced by optic disc pallor. The white retinal lesions and hemorrhages OD had completely resolved. Examination of the OS was normal. Six months later, the visual acuity was unchanged. Rickettsia conorii infection, also called Mediterranean spotted fever ( MSF), is commonly associated with asymptomatic or, less frequently, symptomatic retinal involvement ( 1,2). Optic nerve involvement has also been reported, including optic disc edema, optic disc staining on fluorescein angiography, and optic neuritis with reversible visual loss ( 1- 3). We describe the first case of anterior ischemic neuropathy in Rickettsia conorii infection. Rickettsia conorii organisms are known to invade the endothelial cells of blood vessels, causing an obliterative vasculitis ( 4). In our case, such organisms may have invaded altitudinal defect OD and a full field OS. 213 J Neuro- Ophthalmol, Vol. 25, No. 3, 2005 Khairallah et al optic nerve head microvessels, causing endothelial injury and tissue necrosis with subsequent optic disc infarction. Alternatively, the ischemic event might have resulted from an immune- mediated inflammation. Rickettsia conorii infection should be considered in the differential diagnosis of nonarteritic anterior ischemic optic neuropathy in a patient with high fever or skin rash who has lived or traveled in an endemic area. REFERENCES 1. Alio J, Ruiz- Beltran R, Herrero- Herrero JI, et al. Retinal manifestations of Mediterranean spotted fever. Ophthalmologica 1987; 195: 31- 7. 2. Khairallah M, Ladjimi A, Chakroun M, et al. Posterior segment manifestations of Rickettsia conorii infection. Ophthalmology 2004; 111: 529- 34. 3. Castanet J, Costet C, Dubois D, et al. Neuropathie optique au cours d'une fievre boutonneuse mediterraneenne. Presse Med 1988; 17: 439^ 0. 4. Bazin R. Rickettsial diseases. In: Foster CS, Vitale AT, eds. Diagnosis and Treatment of Uveitis. Philadelphia: WB Saunders Co, 2002: 297- 304. 214 © 2005 Lippincott Williams & Wilkins |
