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Show Macular Hole: A Rare Complication of Ocular Bartonellosis Michael Adam Alterman, DO, Blair Katherine Young, DO, Eric Robert Eggenberger, DO, David Irwin Kaufman, DO Abstract: A 37-year-old woman presented with an anterior optic neuropathy related to Bartonella henselae. Twenty-nine days after symptom onset, a partial thickness macular hole developed in the involved eye. Fundus photography and optical coherence tomography confirmed the conversion to a full-thickness macular hole in 2 months. Macular hole as a complication of cat scratch disease is a rare entity, with 2 prior reported cases in children. The development of a mac-ular hole following cat scratch disease can appear without the clinical picture of multiple white chorioretinal lesions, macular star, or vitritis. Journal of Neuro-Ophthalmology 2013;33:153-154 doi: 10.1097/WNO.0b013e3182899375 © 2013 by North American Neuro-Ophthalmology Society CASE REPORT A37-year-old woman with a history of migraine head-aches and hypothyroidism developed fever and noticed a scotoma in the right upper quadrant of the right eye, which progressed over 3-4 days. Visual acuity was 20/40 in the right eye and 20/25 in the left eye. There was a right relative afferent pupillary defect and mild edema of the right optic disc, with a corresponding enlarged blind spot on automated perimetry. The patient developed pain with eye movement, headache, dizziness, and fever of 103.5°F prompting hospital admission. Magnetic resonance imaging of the brain and orbits was normal. Cerebrospinal fluid opening pressure was 17.5 cm of water with 35 mg/dL of protein (normal, 15-45 mg/dL), 59 mg/dL of glucose (normal, 48-95 mg/dL), 4 red blood cells (RBCs), 1 white blood cell (WBC), and no malignant cells or oligoclonal bands. Bacterial and fungal cul-ture yielded no growth, while acid-fast stain and cryptococcal antigen were negative. Antinuclear antibody, Lyme antibodies, angiotensin-converting enzyme, anti-neutrophil cytoplasmic FIG. 1. A. Appearance of right fundus 13 days after symptom onset showing a diffusely swollen disc with peripapillary hemorrhages. A white chorioretinal lesion is seen inferior and nasal to the disc. B. Twenty-nine days after the symptom onset, there is decreased optic disc swelling with resolution of the peripapillary hemorrhages and the chorioretinal lesion. However, a macular hole has developed. C. Optical coherence tomography of the right eye confirming a full-thickness macular hole 2 months after the initial examination. Department of Neurology and Ophthalmology (MAA, BKY), Michi-gan State University College of Osteopathic Medicine (ERE, DIK), East Lansing, Michigan; and Osteopathic Division (MAA, BKY), St. John Providence Health System, Warren, Michigan. The authors report no conflicts of interest. Address correspondence to Michael Adam Alterman, DO, 501 South Crooks Road, Clawson, MI 48017; E-mail: altermanm@yahoo.com Alterman et al: J Neuro-Ophthalmol 2013; 33: 153-154 153 Photo Essay Section Editor: Timothy J. McCulley, MD Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. antibody, complement factors, blood cultures, and Toxoplas-mosis gondii polymerase chain reaction were negative. Initial Bartonella henselae IgM titer was ,1:20 with IgG titer ,1:128. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were elevated at 99 mm/hour and 10 mg/dL (normal, 0.0-1.0 mg/dL), respectively. A urine specimen showed positive nitrites, moderate leukocyte esterase, 15-20 WBCs, 5-10 RBCs, and many bacteria. She was discharged on oral fluoroquinolone. The patient was reevaluated 13 days later because of persistent fever, headache, chills, diplopia, eye pain, nausea, vomiting, abdominal pain, and difficulty with memory. On further questioning, she reported living with 1 cat and 1 dog, but she did not recall a scratch or bite. Visual acuity was 20/80 in the right eye and 20/20 in the left eye, with decreased color vision in the right eye and a right relative afferent pupillary defect. Fundus examination revealed severe disc edema in the right eye with surrounding peripapillary hemorrhages and a solitary white chorioretinal lesion without macular star (Fig. 1A). The left optic disc had a splinter hemorrhage at 12-o'clock without edema. Repeat ESR and CRP were 99 mm/hour and 5.5 mg/dL, respectively. Cortisol was 28.3 mg/dL (normal, 6-23 mg/dL), and fibrinogen was 976 mg/dL (normal, 200-400 mg/dL). Repeat B. henselae IgG and IgM titers were both elevated at $1:1,024 and $1:20, respectively. The patient was started on 500 mg of ciprofloxacin twice a day for 3 weeks for suspected B. henselae infection. One month later, she reported that her headache and vision were improving and had been afebrile for 1 week. Visual acuity was 20/50 in the right eye with normal color vision and diminished optic disc edema. A macular hole had developed in the right eye (Fig. 1B), and this was confirmed on optical coherence tomography (Fig. 1C). Fluorescein angiography showed optic disc edema in the right eye with-out macular edema, and B-scan ultrasound revealed normal scleral thickness. Laboratory testing showed CRP ,1.0 mg/dL, fibrinogen 391 mg/dL, ESR 41 mm/hour, negative rapid plasma reagin and Lyme antibodies, and elevated B. henselae IgG (.1:1,024) and IgM (.1:20) titers. DISCUSSION Macular hole formation following infection with B. henselae has been reported in 2 previous cases, both of which were children. Albini et al (1) noted vitritis, anterior uveitis, keratic precipitates, serous retinal detachment, and deep white patchy chorioretinal lesions in a 10-year-old girl with Bartonella neu-roretinitis who later developed a full-thickness macular hole. Donnio et al (2) reported a case of treated B. henselae neuro-retinitis in an 11-year-old boy with the formation of a macular hole 7 months after the infection. Other reported inflammatory causes of macular holes include idiopathic posterior uveitis, presumed ocular histoplasmosis, fungal endophthalmitis, intra-ocular nasal T/NK lymphoma, immune recovery uveitis, and juvenile rheumatoid arthritis after cataract extraction (1). It has been proposed that inflammation could result in vitreous trac-tion on the macula by inflammatory contraction of the pre-macular cortical vitreous, but the pathogenesis of inflammatory causes of macular holes remains poorly understood (1,3). Before serologic testing, the diagnosis of B. henselae was made via clinical criteria, a lymph node biopsy, and a posi-tive skin test (4). Initial antibody titers to Bartonella often are negative and become positive weeks later. Therefore, high clinical suspicion warrants repeat blood work (5, 6), as demonstrated in our report. REFERENCES 1. Albini T, Lakhanpal RR, Foroozan R, Holz ER. Macular hole in cat scratch disease. Am J Ophthalmol. 2005;140:149-151. 2. Donnio A, Jean-Charles A, Merle H. Macular hole following Bartonella henselae neuroretinitis. Eur J Ophthalmol. 2008;18:456-458. 3. Nussenblatt RB. Macular alterations secondary to intraocular inflammatory disease. Ophthalmology. 1986;93:984-988. 4. Rost MS. Neuroretinitis: a clinical syndrome of cat-scratch disease. Clin Eye Vis Care. 2000;12:155-159. 5. Solley WA, Martin DF, Newman NJ, King R, Callanan DG, Zacchei T, Wallace RT, Parks DJ, Bridges W, Sternberg P Jr. Cat scratch disease: posterior segment manifestations. Ophthalmology. 1999;106:1546-1553. 6. Buzzacco DM, Lubow M, Davidorf FH, Cebulla CM. Atypical cat scratch disease with vitritis, serous macular detachment, neuroretinitis, and retrobulbar optic neuritis. Graefes Arch Clin Exp Ophthalmol. 2013;251:1001-1002. 154 Alterman et al: J Neuro-Ophthalmol 2013; 33: 153-154 Photo Essay Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
