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Tuberculosis of the Knee Complicating Seronegative Arthritis

To the Editor:

The diagnosis of tubercular arthritis can be challenging, particularly in the presence of confounding factors such as preexisting arthritis. We describe one such case.

A 22-year-old South Asian woman presented to the Orthopaedic Service with an intermittently painful and swollen right knee. The symptoms dated from a fall 7 years previously. On examination in the Orthopaedic Clinic, blood test results and knee radiograph were normal. A synovial fluid aspirate was obtained; standard culture was negative and no acid-fast bacilli (AFB) were isolated from prolonged culture. On her entry to the UK 12 months earlier, a routine Heaf test had shown a grade 3 reaction. At screening in the local tuberculosis (TB) clinic she had denied constitutional symptoms, systemic complaints, and exposure to TB. A series of chest radiographs at 0, 3, and 9 months were normal, leading to discharge from the TB clinic.

Upon referral to the rheumatology clinic 6 months later, examination revealed an effused, painful, restricted right knee with synovitis of the right wrist and metacarpophalangeal joints. Systemic examination was normal. Radiographs of hands and feet and acute-phase indicators were normal. Autoimmune screening tests including rheumatoid factor, antinuclear antibodies, and HLA-B27 genotyping were negative. A diagnosis of seronegative arthritis was made. As pregnancy was planned, disease modifying agents were deferred; intraarticular steroid injection was administered to the right knee followed by physiotherapy, with complete remission.

Within 1 month of a successful full-term pregnancy the right knee and hand joints relapsed. Sulfasalazine was introduced, with complete symptom relief for 18 months. However, the right knee then relapsed, requiring 2 further steroid injections over 12 months. Although magnetic resonance imaging (MRI) showed extensive erosions (Figure 1), the patient chose to discontinue sulfasalazine in preparation for a second pregnancy.

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Figure 1. MRI scan of the right knee. The articular surfaces of both femur and tibia show significant cartilage loss. There is pannus formation, synovial thickening, erosions, and a minor effusion. The patellofemoral joint space is reduced. The medial and lateral menisci are severely damaged.

During the second pregnancy the joint was persistently inflamed and painful, with an extension lag of 45°, rendering her increasingly dependent and requiring repeated hospital admissions. An attempt at aspiration was dry; however, sterile-water lavage fluid revealed AFB on microscopy, a result confirmed on polymerase chain reaction (PCR) testing. The culture grew M. tuberculosis. Early morning urine also grew AFB simultaneously. Chest radiograph was normal. Anti-TB therapy was commenced immediately after a cesarean delivery, initially for 6 months but extended a further 3 months in view of the degree of joint destruction.

After intensive rehabilitation, this patient now walks without aids and has achieved functional independence.

Tubercular arthritis is characteristically monoarticular1 and most commonly affects the spine and weight-bearing joints such as the knee and hip. The mode of transmission is hematogenous from visceral foci such as the lung or kidneys2. Immunosuppressed patients are at greatest risk. Arthritis and/or osteomyelitis may be the first manifestation of tubercular disease. A subclinical or quiescent extraarticular focus must be actively investigated. In our patient, AFB was isolated from urine despite normal renal excretion studies and ultrasound imaging.

Articular disease often starts as a synovitis progressing to arthritis, with demineralization, marginal erosions, and ultimate joint destruction3. While the time period from synovitis to arthritis and erosions may be long, progression to joint destruction can be rapid, particularly in weight-bearing joints. MRI is the investigation of choice to reveal both extent and severity of damage. Tissue necrosis facilitates superadded infection with secondary organisms such as Staphylococcus aureus, resulting in accelerated joint destruction and systemic toxicity4. Conversely, joint sepsis can mask tubercular arthritis.

An underlying arthropathy may predispose to tubercular infection5, as reported in osteonecrotic joints, due to sickle cell disease and chondrocalcinosis6,7. In our case, the knee was damaged over a 4-year period by seronegative arthritis and vulnerable to tubercular infection by hematogenous transfer. Also, our patient had sustained trauma to the joint, a known predisposing factor especially in high-risk groups8.

Submission of synovial or lavage fluid for standard and TB culture is recommended when possible in any at-risk patient, even where previous cultures have been negative. Synovial fluid culture is positive in roughly 80% of cases. PCR analysis is faster9 and more specific, but less sensitive and less widely available. The gold standard for diagnosis is synovial biopsy, with positive results in 90% of cases. Two consecutive pregnancies made arthroscopy impractical in our patient. The case also illustrates the value of early morning urine examination as a screening tool for tubercular disease in all clinical settings.

The cornerstone of treatment is antituberculous quadruple drug therapy for 2 months followed by dual therapy with rifampicin and isoniazid for a further 4 months10 or longer, as in our case, depending on the clinical response, particularly in bone disease1-3. Early antimicrobial therapy can result in near-complete resolution and preservation of function.

The World Health Organization reports the global incidence of TB at around 8.8 million and prevalence at 14 million; of this 1%–3% is skeletal disease2. A low threshold of suspicion even in the developed world, and especially in the context of immunosuppression and preexisting arthritis, is essential for early identification, appropriate treatment, and limitation of joint damage.

SUBHA ARTHANARI, MRCP(UK), Staff Grade Medical Officer; SIRAJ YUSUF, MBBS, Senior House Officer; MOHAMED NISAR, FRCP(UK), Consultant Rheumatologist, Department of Rheumatology, Queen's Hospital, Burton Hospital NHS Trust, Burton on Trent DE130RB, United Kingdom. Address reprint requests to Dr. M. Nisar.

E-mail: mohamed.nisar@burtonh-tr.wmids.nhs.uk

REFERENCES

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1. Sequeira W, Co H, Block JA. Osteoarticular tuberculosis: current diagnosis and treatment. Am J Ther 2000;7:393-8. [MEDLINE]

2. Tuli SM. General principles of osteoarticular tuberculosis. Clin Orthop 2002;398:11-9. [MEDLINE]

3. Furia JP, Box GG, Litner DM. Tubercular arthritis of the knee presenting as a meniscal tear. Am J Orthop 1996;25:138-42. [MEDLINE]

4. Al-Shaikh R, Goodman SB. Delayed onset mycobacterium tuberculosis infection with staphylococcal super-infection after total knee replacement. Am J Orthop 2003;32:302-5. [MEDLINE]

5. Bryan WJ, Doherty JH Jr, Sculco TP. Tuberculosis in a rheumatoid patient, a case report. Clin Orthop 1982;171:206-8. [MEDLINE]

6. Varango G, Bamba I, Kodo M, Dao A, Lambin Y. Osteonecrosis of the hip in sickle cell disease associated with tubercular arthritis. A review of 15 cases. Int Orthop 1998;22:384-9. [MEDLINE]

7. Pointud P, Prudat M, Laluque S, Amaroux J. Tuberculous arthritis and chondrocalcinosis. Report of 2 cases. Rev Rheum Ed Fr 1993;60:617-20.[MEDLINE]

8. Ferris BD, Goldie B, Weir W. An unusual presentation of tuberculosis-injury TB. Injury 1987;18:347-9. [MEDLINE]

9. Verettas D, Kazakos C, Dermon A, Petrov H, Galanis V. Polymerase chain reaction for the detection of Mycobacterium tuberculosis in synovial fluid, tissue samples, bone marrow aspirate and peripheral blood. Acta Orthop Belg 2003;69:396-9. [MEDLINE]

10. Joint Tuberculosis Committee of the British Thoracic Society. Chemotherapy and management of tuberculosis in the United Kingdom: Recommendations 1998. Thorax 1998;53:536-48.[MEDLINE]



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