Tuberculous myositis: a rare but existing clinical entity
J. Y. Wang1,4,
L. N. Lee2,
P. R. Hsueh2,
J. Y. Shih1,,
Y. L. Chang3,
P. C. Yang1 and
K. T. Luh2
1 Departments of Internal Medicine,
2 Laboratory Medicine and
3 Pathology, National Taiwan University Hospital, Taipei and
4 Department of Internal Medicine, Far Eastern Memorial Hospital, Taipei County, Taiwan
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Abstract
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Objectives. To investigate the clinical characteristics of patients with tuberculous myositis.
Methods. From January 1996 to March 2001, patients with positive cultures of Mycobacterium tuberculosis or histology-proven caseous granulomatous inflammation from muscular specimens were identified and their medical records were reviewed.
Results. Thirty-five patients were identified. Infection-related myositis was initially suspected in 20 patients (57.1%). The routes of infection were contiguous spread in 22 patients (62.8%), haematogenous spread in 10 (28.6%) and traumatic inoculation in three (8.6%). Five patients (14.3%), including the three who had received corticosteroids, died of uncontrolled sepsis. The computed tomography or the magnetic resonance imaging of the involved muscles showed findings suggestive of tuberculous myositis in 15 patients (42.9%).
Conclusions. Tuberculosis should be considered as one of the possible aetiologies of myositis, especially among patients with suggestive radiographic findings or in endemic areas of tuberculosis. Patients who develop tuberculous myositis after using corticosteroids have poor prognoses.
KEY WORDS: Mycobacterium tuberculosis, Myositis, Corticosteroids.
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Introduction
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Tuberculosis remains one of the deadliest diseases in the world. The World Health Organization (WHO) estimates that each year more than eight million new cases of tuberculosis occur and approximately three million people die from the disease [1]. In Taiwan, the prevalence of radiographically suspected tuberculosis, including fibrocalcified, cavitary or miliary lesions on chest radiographs, was 650 per 100 000 people in adults over 20 yr of age in 1993 [2]. In 1999, the incidence and mortality of tuberculosis in Taiwan was 61.32 and 6.88 per 100 000 people, respectively [3].
About 3% of patients with tuberculosis have musculoskeletal involvement, mostly spondylitis, osteomyelitis or arthritis [4]. However, tuberculous myositis has rarely been described in the medical literature, and its manifestations may mimic malignant or other inflammatory diseases, leading to misdiagnosis [5]. We describe the incidence of tuberculous myositis and the clinical characteristics of these patients. The radiographic findings of tuberculous myositis are also discussed.
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Patients and methods
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The study was conducted in northern Taiwan at the National Taiwan University Hospital, a tertiary-care referral centre with 2000 beds. We reviewed the records of the mycobacterial laboratory from January 1996 to March 2001 and found all patients with positive cultures of Mycobacterium tuberculosis. We then identified those whose M. tuberculosis was isolated from muscular aspirates or biopsies. We also retrieved cases whose histological examination of the muscular specimen revealed granulomatous inflammation and caseous necrosis even though M. tuberculosis was not isolated from muscle. Myositis was confirmed by computed tomography (CT), magnetic resonance imaging (MRI) or surgical findings. The route of infection was assumed to be one of three causes: traumatic inoculation if there had been a history of local trauma or surgery (i.e. direct inoculation through contaminated instruments was suspected) while the patient did not have pulmonary or other extrapulmonary tuberculosis [6]; contiguous spread if radiographic studies, a gallium scan or thallium scan revealed lesions in adjacent bone or soft tissues [7]; and haematogenous' in all other cases. Pulmonary tuberculosis was suspected if a patient's chest radiographs revealed fibrocalcified or miliary lesions, or if pleural effusion was a lymphocyte-predominant exudate and negative for malignancy, even though M. tuberculosis was not isolated from any respiratory specimens. All muscular aspirates or biopsy specimens were submitted for examination to isolate bacteria, fungi and mycobacteria by conventional methods [8]. The isolates of M. tuberculosis were tested for drug susceptibility using the modified proportion disc elution method on 7H10 agar (BBL, Becton Dickinson, Franklin Lakes, NJ) [9].
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Results
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From January 1996 to March 2001, tuberculosis was diagnosed by positive culture in 1153 patients, 21 (1.8%) of whom had tuberculous myositis. Another 14 patients with tuberculous myositis were identified from those with histologically proven granulomatous disease. The clinical characteristics of the 35 patients and previously reported cases [5, 7, 1031] are listed in Table 1
. The major observed differences between our patients and previously reported cases were the proportion of patients with underlying diseases (29 vs 45%) and the route of infection (contiguous spread: 62 vs 18%; haematogenous spread: 29 vs 82%; traumatic inoculation: 9 vs 0%). Twenty-two patients were examined for anti-HIV antibodies and one was found to have a positive result.
Local inflammatory symptoms and signs were present in 32 (91.4%) of the 35 patients. Systemic symptoms, such as fever, poor appetite, malaise or weight loss occurred in only eight (22.9%) patients. An infective process was initially considered in only 20 (57.1%) patients, among whom four were suspected to be infected by M. tuberculosis. In nine patients, the initial impressions were malignancy with destruction of bone and soft tissue.
The initial leucocyte counts were highly variable, ranging from 3070 to 19 050x1012/l (median 8960x1012/l), with a neutrophil count ranging from 27.6 to 92%. The initial serum levels of C-reactive protein were available in 22 patients and ranged from <0.01 to 28.7 mg/dl (median 1.70 mg/dl). The serum level of creatinine kinase was checked in 12 patients, and was elevated in one patient who had multiple muscle involvement as a result of haematogenous dissemination.
Chest radiographs were abnormal in 18 (51.4%) patients (Table 1
). Of these, eight had M. tuberculosis isolated from sputum or pleural effusions. Tuberculous meningitis was diagnosed in one patient with a positive cerebrospinal fluid (CSF) culture, and was suspected in three patients who had compatible clinical manifestations and CSF findings but negative cultures.
Nine of the 10 patients with contiguous chest wall involvement had abnormal findings on chest radiographs. Eight patients had CT scans of the chest, with six revealing swelling and oedema of the involved muscles, destruction of the ribs, mediastinitis and conglomerated mediastinal lymphadenopathy, which showed low central density suggestive of necrosis.
Of the nine patients with Pott's disease, MRI of the spine was performed in five and revealed paraspinal abscesses with thick enhanced rims, destruction of the vertebrae, relative preservation of the intervertebral disc and epidural involvement (Fig. 1
).

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FIG. 1. Magnetic resonance imaging of the spine in a patient with Pott's disease showing destruction of the vertebral body (arrow), relative preservation of the intervertebral disc (large arrowhead) and epidural involvement (small arrowhead).
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Myositis involving multiple anatomical sites was noted in five of the 10 patients with haematogenous tuberculous myositis. Four of the 10 patients had MRI studies, which consistently revealed that the involved limb muscles had low-signal-intensity centres and very bright peripheral rings on T1-weighted images, suggestive of myositis. But unlike pyogenic myositis, there was neither venous thrombosis nor signs of cellulitis surrounding the infected muscle.
In five patients, the cultures of muscular specimens yielded pathogens other than M. tuberculosis, including one each of Propionibacterium spp., Candida albicans, Morganella morgagnii, Acinetobacter baumannii and Nocardia asteroides. Because pathogens other than acid-fast bacilli were also found in the muscle specimens under microscopy, the possibility of laboratory cross-contamination was not likely.
Thirty-three patients received anti-tuberculous therapy. The median time between the onset of symptoms and anti-tuberculous therapy was 2 months (range: 0.59 months). Surgical debridement and drainage were performed in 29 patients (82.9%), 11 of whom underwent more than one operation. No late post-operative complications, such as delayed wound healing or fistula formation, were noted.
Five patients (14.3%) died of uncontrolled sepsis without bacterial pathogens identified at the terminal stage. Among them, two died before the results of mycobacterial cultures were available and neither received anti-tuberculous therapy. The other three patients had received corticosteroids before the onset of myositis symptoms and had multiple muscle involvement with abscess at different anatomical sites. The routes of infection were all haematogenous. The periods between the onset of symptoms and the administration of anti-tuberculous therapy were 0.5, 1.5 and 2 months. Despite anti-tuberculous therapy, their myositis progressed.
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Discussion
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A total of 1.8% of our patients with culture-proven tuberculosis had tuberculous myositis, which used to be considered as a very rare manifestation of extrapulmonary tuberculosis. Prior to our study, only 38 cases of tuberculous myositis had been reported in the literature published in English [5, 7, 1031]. The cause of this discrepancy is not known, but is probably due to previous underdiagnosis of this unfamiliar disease. Because of non-specific clinical manifestations and laboratory results, the possibility of infection-related muscular disease was often overlooked, especially in patients who presented with bone destruction. Our study showed that half of our patients had abnormal chest radiographs suggestive of pulmonary tuberculosis. A CT or MRI usually demonstrated findings suggestive of tuberculous myositis rather than pyogenic infections or malignancy. These included mediastinal lymphadenopathy with low central density in patients with chest wall tuberculous myositis [23], and the absence of adjacent venous thrombosis or cellulitis (which usually occurs in pyogenic myositis) in patients with tuberculous myositis of the extremities [16].
In addition, because the space of the intervertebral disc is preserved until the later stages of tuberculous spondylitis, image studies may reveal vertebral destruction with relative preservation of intervertebral disc [3234]. In a review of MRI findings of tuberculous spondylitis, Gouliamos et al. [35] concluded that radiologists should be alert to the likely presence of tuberculous spondylitis when they observe relative preservation of the intervertebral disc with disc herniation into the adjacent vertebral body, loss of cortical definition of the affected vertebrae, paraspinal abscesses and epidural involvement. Indeed, the presence of a thick enhanced rim around paraspinal abscesses is nearly pathognomic of tuberculous spondylitis [36].
In contrast to previous reports [5, 7, 1218], most (71.4%) of our patients had no underlying disease (Table 1
) and had tuberculous myositis as a result of contiguous rather than haematogenous spread. These findings probably reflect the prevalence of tuberculosis in Taiwan. Encountering three patients with tuberculous myositis owing to traumatic inoculation might also imply that the environment is highly contaminated and that tuberculosis is endemic in this area.
Haematogenous dissemination plays an important role in tuberculous myositis and is usually limited to one muscle [7, 23]. However, several muscles may be involved [14, 29]. This presentation was noted in half of our patients with haematogenous dissemination. Consistent with the reported cases in the literature [21], the thigh is the most common site involved.
In our study, the mortality rate was 14.3% and was even higher (30%) in patients with haematogenous tuberculous myositis. Our patients who developed tuberculous myositis after using corticosteroids tended to have poorer prognoses, probably related to the high mycobacterium load, evidenced by multiple muscle involvement and huge abscess formation in all three patients.
There were some limitations in our study. First, the incidence of tuberculous myositis may be underestimated because many patients with myositis did not receive mycobacterial cultures or histological examinations. Second, some important laboratory results, such as creatinine kinase, C-reactive protein and anti-HIV antibody were not available in every patient. Third, further investigation is necessary on whether a host genetic susceptibility or a tissue tropism of those M. tuberculosis isolates causes the high incidence of tuberculous myositis in Taiwan.
In conclusion, tuberculous myositis occurred in about 2% of patients with tuberculosis and should be considered as one of the aetiologies of muscular disease, especially in areas where tuberculosis is endemic. The findings of CT scans or MRIs of the involved muscle are very helpful in differential diagnosis. Patients who develop haematogenous tuberculous myositis after corticosteroid use tend to have a poor prognosis.
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Notes
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Correspondence to: J.-Y. Shih, Department of Internal Medicine, National Taiwan University Hospital, No. 7, Chun Shan South Road, Taipei, 100, Taiwan. E-mail: jyshih{at}ha.mc.ntu.edu.tw 
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Submitted 30 May 2002;
Accepted 3 December 2002