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Joint Pain and Swelling: Could It Be Lyme Arthritis?

David H. Wang, MD; Jesse L. Goodman, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 25 - NO. 2 - FEBRUARY 97


In Brief: This report presents two probable cases of Lyme arthritis triggered by athletic activity or trauma. One patient had ankle swelling after he began a jogging program, and a second had knee swelling that followed a twisting injury. The report describes the three stages of the illness and presents diagnostic lab tests and the therapies used. Polymerase chain reaction (PCR) testing of the synovial fluid can be useful in diagnosing active Lyme arthritis, but it may yield a false-negative result when there has been recent remission of the arthritis.

Physicians often evaluate joint swelling in active individuals, and suspicion naturally falls first on the patient's activity as the likely cause. Lyme disease will rarely be the initial diagnosis, particularly in a patient who recalls none of the usual symptoms of the disease. A careful patient history, however, may show that the individual exercised, hiked, or camped in a region where Lyme disease is endemic. In such a case, Lyme arthritis may be the initial presentation, and the physician should proceed with appropriate tests to determine proper diagnosis and treatment. Two illustrative case reports follow.

Case 1

A 38-year-old Russian male presented with a 1-week history of left ankle swelling after having jogged only a couple of times in his new exercise program. The patient denied any history of injury but complained of the insidious onset of pain and swelling, which became so severe it was difficult to walk. On examination the patient demonstrated a noticeable limp and lateral ankle swelling. The ankle was minimally warm, with trace erythema. There was no pain over the medial or lateral ankle ligaments, nor were there signs of instability. The peroneal tendons were nontender, and there was no pain with external rotation of the foot. Ankle radiographs were normal except for lateral soft-tissue swelling.

A laboratory evaluation was obtained because the physical findings were not consistent with a running injury. The patient was given an ankle brace and asked to return in one week; during that time his pain and swelling improved significantly.

The laboratory evaluation demonstrated a normal complete blood count (CBC), erythrocyte sedimentation rate of 12, negative fluorescent antinuclear antibody and a positive titer enzyme-linked immunosorbent assay (ELISA) for antibodies against Borrelia burgdorferi, the causative agent of Lyme disease. The positive titer was confirmed by Western blot analysis.

After review of the lab studies, additional history was obtained. The patient had resided in Minnesota since moving from Russia 5 years earlier. He was an avid hiker who often visited the St Croix River valley (on the Wisconsin border) and the northern shore of Lake Superior. He had had one recognized tick bite 2 years prior. He denied any history of rash, and his neurologic and cardiac exams were normal.

The tests demonstrated exposure to B burgdorferi, but did not prove that the ankle arthritis was due to Lyme disease. It was also possible that the patient was seropositive from a past asymptomatic infection, with unrelated exercise-induced ankle swelling. For this reason, it was decided to aspirate the ankle.

Although minimal swelling was present at the time of aspiration, 3.5 mL of slightly opaque yellow fluid was obtained. Analysis of the joint fluid revealed an RBC count of 603 cells per microliter, glucose 101 mg/dL, protein 2.5 g/dL, and no evidence of crystals. The WBC count was 244 cells per microliter with 4% neutrophils, 33% lymphocytes, and 63% monocytes/macrophages. Polymerase chain reaction (PCR) testing for both plasmid and chromosomal targets showed no evidence of B burgdorferi DNA or RNA. Since the patient had serologic evidence of a B burgdorferi infection, and the arthritis had spontaneously improved prior to the arthrocentesis, it remained possible that Lyme disease was the etiology of the ankle arthritis. Therefore the patient was treated with oral doxycycline for 30 days. After completion of the antibiotics, the patient returned to a vigorous exercise program without recurrence of the ankle swelling, and he has remained asymptomatic to this date.

Case 2

This case was previously reported from our institution in a study (1) that demonstrated, by PCR, the persistence of Lyme disease spirochetes in the synovial fluid in Lyme arthritis. A 21-year-old male presented with swelling of the left knee. Four months earlier, he had twisted the knee while playing basketball and had since experienced intermittent swelling. An MRI showed a possible medial meniscal tear, but arthroscopy did not demonstrate the tear. A synovial biopsy was normal, but the effusion remained. A second evaluation revealed positive serum B burgdorferi antibodies. The patient recalled having had a "flulike" illness with Bell's palsy 2 months earlier, after a trip into the woods of western Wisconsin. He had noted no rash and his symptoms had resolved spontaneously within 1 month. After the second evaluation the patient was treated with 6 weeks of oral doxycycline, which led to resolution of his symptoms.

Two months after the second evaluation he presented to our hospital with left knee swelling after vigorous biking. With rest and anti-inflammatory medication, the swelling improved, but aspiration of the synovial fluid demonstrated 12,810 WBCs (62% neutrophils, 16% lymphocytes, 22% monocytes/macrophages) and PCR testing of the joint fluid was found to be positive for B burgdorferi DNA.

Several weeks later, the patient returned with a persistent effusion. Repeat synovial fluid analysis revealed 2,200 WBCs (15% neutrophils, 62% lymphocytes, 25% monocytes/macrophages) and a negative PCR for B burgdorferi. Because of the recurrent arthritis, which did not appear to be mechanical or traumatic, and the previous positive PCR even after doxycycline therapy, the patient was treated with intravenous ceftriaxone for two weeks. His symptoms resolved, and on follow-up more than a year later, he remained asymptomatic.

Lyme Disease

Transmission. Lyme arthritis was first reported in Lyme, Connecticut, in the 1970s, and the causative organism, B burgdorferi, was identified in 1982 (2,3). Since that time, Lyme disease has become the most common vector-borne illness in the United States. The three main endemic areas are the northeastern coastal area from Massachusetts to Maryland, Wisconsin and Minnesota, and northern California and Oregon. Lyme disease is also common in parts of Europe such as Sweden, Germany, Austria, Switzerland, and Russia (4).

B burgdorferi is a spirochete that is transmitted to humans by ixodid ticks (5). In the northeast and central United States, where most cases occur, the deer tick Ixodes scapularis transmits the spirochete, usually during the summer months (4). In the western United States, the tick I pacificus is the vector, while I ricinus carries the disease in Europe and I persulcatus in Asia (4).

During its nymphal stage I scapularis is only the size of a pinhead and bites painlessly, so it is easily overlooked. While the tick feeds, the spirochete is regurgitated into the host (5). The organism may travel rapidly via the blood stream (6) to any area in the body and has an affinity for skin, nerve tissue, synovium, and the conduction system of the heart (7).

Stages. Three general stages of Lyme disease are recognized. (Because the disease varies greatly from person to person, the signs and symptoms of one stage may cross over to another stage.) Stage 1 infections occur 3 to 30 days after the initial exposure. Approximately 75% of patients experience erythema migrans: a rash, usually at the site of the tick bite, that varies in appearance but is classically erythematous with central clearing. This stage is often associated with constitutional symptoms such as fever, myalgias, arthralgias, and headache (8).

Stage 2 occurs weeks to months after the initial infection. In this stage the patient can be quite ill with malaise, myalgias, arthralgias, or neurologic or cardiac involvement (7). Common neurologic manifestations include Bell's palsy, radicular neuronitis, and lymphocytic meningitis. The most common cardiac manifestation is AV nodal block.

Stage 3 occurs months to years later and can involve the synovium, nervous system, and skin, though skin involvement is more common in Europe than in North America. Arthritis occurs in the majority of previously untreated patients; it is usually oligoarticular and intermittent, involves the large joints, particularly the knee, and lasts from weeks to months in any given joint (9). Joint fluid analysis typically shows 500 to 110,000 WBCs per microliter, consisting predominantly of polymorphonuclear neutrophils (10). Late neurologic involvement may include peripheral neuropathy and encephalopathy, manifested by memory, mood, and sleep disturbances. Late skin findings such as acrodermatitis chronica atrophicans (4) and late cardiac involvement are rare in the United States.

Tests. Several laboratory procedures are used to help diagnose Lyme disease. Most common is an ELISA, which determines the presence of antibodies to B burgdorferi. Unfortunately, the quantitative ELISA often does not turn positive until several weeks of illness have elapsed (4), and false-positive results may occur, particularly in patients with connective tissue diseases or syphilis (11,12). The qualitative Western blot is a more specific confirmatory test that identifies the presence of antibodies against individual spirochetal proteins and should be performed to confirm positive or borderline ELISA results (13).

B burgdorferi is very rarely cultured from synovial fluid, but PCR tests reveal spirochetal DNA in most cases of Lyme arthritis. In a retrospective study, 96% of patients with Lyme arthritis who were untreated or only treated with a short course of antibiotics were found to have a positive PCR for B burgdorferi in their joint fluid (14). In a prospective study done at our institution, 86% of individuals with Lyme arthritis had a positive PCR from the joint fluid (1). As yet the PCR test is not routine but when done correctly is highly specific.

Treatments. Recommended treatment for early Lyme disease (stage 1) is a 14- to 28-day course of either oral doxycycline 100 mg twice a day or amoxicillin 500 mg three times a day. Lyme arthritis is also usually first treated with oral therapy as described above for 30 days. If there is no response, then ceftriaxone is administered 2 g IV each day for 14 days.

Lyme arthritis is typically slow to respond to antibiotic therapy. Eleven percent of patients with Lyme arthritis develop chronic arthritis (9), and within this group the presence of spirochetal DNA in synovial fluid varies. Patients who carry the HLA-DR4 or the HLA-DR2 allele may have an ongoing immune response to the spirochete which can lead to a chronic arthritis despite the apparent eradication of the infection (15,16). Despite antimicrobial drug treatment, patients with persistent active arthritis and persistently positive PCR tests may have incomplete microbial eradication, and may be the most likely to benefit from repeated treatment with parenteral antibiotics.

Diagnostic Dilemmas

Approximately 25% of people infected with B burgdorferi never experience erythema migrans, and many infected individuals are also unsure of tick bites. Hence, patients with Lyme disease may present with arthritis as their first complaint (7,17). A previous study of patients with untreated Lyme disease reported that two individuals, after suffering knee trauma, had an exacerbation of knee arthritis because of Lyme disease (9). Thus it appears that activity may promote the initial or subsequent flares of Lyme arthritis in certain individuals.

Both cases presented here followed a similar pattern. Neither patient reported a history of erythema migrans, but in both individuals exacerbation or onset of arthritis occurred with activity. Case 2 demonstrated all the classic findings of Lyme arthritis, including knee involvement and a joint fluid PCR positive for B burgdorferi DNA. This case also demonstrated that oral antibiotic therapy may fail and intravenous therapy may be required. Case 1 involved the ankle (which is the second most common joint to be affected by Lyme arthritis, although it lags far behind the knee (9)), but the PCR testing was negative.

With both patients, PCR tests were useful but problematic. One explanation for the negative PCR test in case 1 may be that the aspiration was performed following immobilization and spontaneous clinical improvement of the arthritis. The natural history of Lyme arthritis can be one of spontaneous remission followed by recurrence. PCR testing of joint fluid is a relatively new diagnostic tool, and it is possible that aspirations performed during spontaneous remissions may not detect B burgdorferi DNA. As demonstrated in case 2, even when there has been no treatment between aspirations, the arthritis may remit, and the PCR analysis may convert from positive to negative. Note also that the negative PCR tests in both cases occurred when the synovial fluid analysis showed a lower WBC count, indicating less inflammation. Nonetheless, synovial fluid PCR testing is a valuable tool in diagnosing Lyme arthritis in cases where serologic results are confusing, other causes of arthritis are possible, or arthritis persists after treatment and there is a question of whether the organism is still present in the synovial tissues.

Consider All Possibilities

These two cases serve to emphasize that not all joint swelling in athletes is secondary to injury or traumatic processes. Primary care physicians should always consider nonathletic causes of joint pain and/or swelling, such as autoimmune, infectious, neoplastic, and other inflammatory processes, particularly when the exam or the history suggests other disease processes.

The authors thank Elizabeth Arendt, MD, for referring one of the patients.

References

  1. Bradley J, et al: The persistence of spirochetal nucleic acids in active Lyme arthritis. Ann Intern Med 1994;120(6):487-489
  2. Steere AC, et al: Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis Rheum 1977;20(1):7-17
  3. Steere AC, et al: The spirochetal etiology of Lyme disease. N Engl J Med 1983;308(13):733-740
  4. Steere AC: Current understanding of Lyme disease. Hosp Prac 1993;28(4):37-44
  5. Burgdorfer W: Discovery of the Lyme disease spirochete and its relation to tick vectors. Yale J Biol Med 1984;39(4):515-520
  6. Goodman J, et al: Blood stream invasion in early
    Lyme disease: results from a prospective, controlled, blinded study using the polymerase chain reaction. Am J Med 1995;99(1):6-12
  7. Steere AC: Lyme disease. N Engl J Med 1989;321(9):
    586-596
  8. Scerpela TA, Engber WD: Chronic Lyme disease arthritis: review of the literature and a report of a case of wrist arthritis. J Hand Surg 1992;17(3):571-575
  9. Steere AC, Schoen RT, Taylor E: The clinical evolution of Lyme arthritis. Ann Intern Med 1987;107(5):725
  10. Steere AC, et al: Erythema chronicum migrans and Lyme arthritis. Ann Intern Med 1977;86(6):685-698
  11. Magnarelli LA, et al: Cross-reactivity in serological tests for Lyme disease and other spirochetal infections. J Infect Dis 1987;156(1):183-188
  12. Fawcett PT, et al: Frequency and specificity of antibodies that crossreact with Borrelia burgdorferi antigens. J Rheumatol 1992;19(4):582-587
  13. Dressler F, et al: Western blotting and the serodiagnosis of Lyme disease. J Infect Dis 1993;167:392-400
  14. Nocton JJ, et al: Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis. N Engl J Med 1994;330(4):229-234
  15. Steere AC, et al: Association of chronic Lyme arthritis with HLA-DR4 and HLA-DR2 alleles. N Engl J Med 1990;323(4):219-223
  16. Kalish RA, et al: Association of treatment-resistant chronic Lyme arthritis with HLA-DR4 and antibody reactivity to OspA and OspB of Borrelia burgdorferi. Infect Immun 1993;61(7):2774-2779
  17. Steere AC, et al: The early clinical manifestations of Lyme disease. Ann Intern Med 1983;99(1):76-82

Dr Wang is director of the general medicine and sports medicine clinics at Boynton Health Service and team physician at the University of Minnesota in Minneapolis. He is also an assistant professor in the Department of Family Practice at the University of Minnesota Medical School and an editorial board member of The Physician and Sportsmedicine. Dr Goodman is associate professor of medicine and infectious diseases at the University of Minnesota Medical School in Minneapolis. Address correspondence to David H. Wang, MD, MS, University of Minnesota, Boynton Health Service, 410 Church St SE, Minneapolis, MN 55455; send e-mail to [email protected]


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