A 37-year-old woman with a history of migraine headaches 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 culture yielded no growth, while acid-fast stain and cryptococcal antigen were negative. Antinuclear antibody, Lyme antibodies, angiotensin-converting enzyme, anti-neutrophil cytoplasmic antibody, complement factors, blood cultures, and Toxoplasmosis 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 μg/dL (normal, 6–23 µg/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 without 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.
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 neuroretinitis who later developed a full-thickness macular hole. Donnio et al (2) reported a case of treated B. henselae neuroretinitis 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, intraocular 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 traction on the macula by inflammatory contraction of the premacular 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 positive 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.
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