Cultivation of Borrelia burgdorferi from Joint Fluid Three Months After Treatment of Facial Palsy Due to Lyme Borreliosis

COLLEAGUES Lyme arthritis is a common manifestation of Lyme disease in the United States and in Europe [1,2]. Thus far, Borrelia burgdorferi has been demonstrated in synovial biopsy specimens [3] and in joint fluid [4], but attempts to isolate and subculture the organism have failed. We report the case of a girl with Lyme disease, from whom we were able to isolate and propagate B. burgdorferi from joint fluid and to then perform serological tests on this isolate. Casereport. In October 1986, a 15.5-y-old girl was bitten by a tick in Austria. There was no local skin manifestation, such as erythema chronicum migrans, and she also never perceived any generalized symptoms such as malaise, fatigue, headache, musculoskeletal pain, or fever. Her history was free of any relevant disease. At the end of January 1987, she was diagnosed with peripheral paralysis of the left facial nerve. Physical examination was otherwise normal, and she was afebrile; the patients' body weight was 58 kg. A complete blood count; her erythrocyte sedimentation rate; and radiographs of paranasal sinuses, mastoid processes, and petrous pyramids revealed normal findings. Repeated serological studies (table 1) confirmed the assumed B. burgdorferi etiology of facial palsy and excluded a viral etiology (i,e., herpes simplex virus, cytomegalovirus, Epstein-Barr virus, mumps virus, or coxsackievirus). Oral treatment with amoxicillin-clavulanate (625 mg, four times per day) was discontinued after 12d because the patient developed a maculopapular rash. A two-week course of an oral corticosteroid (1 mg of betamethasone, two times per day) was prescribed. A lumbar puncture, performed because of only partial resolution of facial palsy, showed no pathological findings. Staining and culture attempts for B. burgdorferi in CSF were negative; the specific antibody titers are listed in table 1. During treatment with oral doxycycline (100 mg, two times per day) for two weeks, residual paralysis of the left facial nerve completely resolved, and the patient remained free of neurological symptoms. 'IWo months later, the patient developed isolated arthritis of the right knee without any preceding trauma. A laboratory examination showed the following: a peripheral leukocyte count of 7000 cells/rum", with a normal differential; erythrocyte sedimentation rate, 27 mm/h; normal levelsof creatinine and liver enzymes in serum; negative rheumatoid factors and antinuclear antibodies; and normal values for circulating immune complexes and complement analysis (CH50 and APH50). Using arthrocentesis, we collected 60 mL of cloudy joint fluid; microscopic analysis showed two to 11granulocytes per visual field, a test for rheumatoid factor was negative, and a culture for B. burgdorferi was positive. The antibody titers against B. burgdorferi in serum and joint fluid are included in table 1. Ceftriaxone was administered intravenously in high doses (4 g per day), in the clinic, over a three-