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Bone and joint tuberculosis


Author: Jason Stout, MD
Section Editor: John Bernardo, MD
Deputy Editor: Elinor L Baron, MD, DTMH

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2021. | This topic last updated: Nov 30, 2020.

INTRODUCTION

Skeletal tuberculosis (TB) refers to TB involvement of the bones and/or joints. It is an ancient
disease; features of spinal TB have been identified in Egyptian mummies dating back 9000
years [1,2], and analysis of 483 pre-Columbian skeletons in Chile showed lesions consistent
with bony TB in 2 percent of cases [3]. Subsequently, molecular studies have established the
presence of Mycobacterium tuberculosis complex DNA in ancient bony specimens [2,4].

Clinical issues related to skeletal TB will be reviewed here. Other aspects of TB are discussed
separately. (See related topics.)

EPIDEMIOLOGY

Worldwide, skeletal TB accounts for 10 to 35 percent of cases of extrapulmonary TB (9.6


percent of United States extrapulmonary cases [n=185] and 2.0 percent of all United States
TB cases reported in 2017) [5-10]. Reported rates of extrapulmonary TB are higher among
immigrants from highly endemic areas to developed countries; this may be due in part to
immigration screening procedures for pulmonary TB [11]. One retrospective review of
skeletal TB between 1980 and 1994 in France noted 103 cases of spinal TB; 68 percent of
patients were foreign born, the majority from Africa [12]. The proportion of skeletal TB
among HIV-infected individuals is comparable with the proportion of skeletal TB among HIV-
uninfected individuals [13,14].

The most common form of skeletal TB is Pott disease, a disease of the spine; this entity
comprises approximately half of musculoskeletal TB cases. The next most common form of
musculoskeletal TB is tuberculous arthritis, followed by extraspinal tuberculous
osteomyelitis [15].
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PATHOGENESIS

During primary M. tuberculosis infection, bacillemia may lead to seeding of organisms in


bone and/or synovial tissue. In most cases, small foci of infection are confined by local
adaptive immune processes, and infection is subclinical. Following primary infection,
reactivating foci are usually contained by the cellular immune response. CD4 and CD8
lymphocytes play important roles, as does interferon-gamma [16]. The likelihood of
reactivation of infection with progression to clinically apparent disease increases when local
immune defenses fail, as in the setting of malnutrition, advancing age, HIV infection, or
advanced kidney disease [17].

Active TB disease can develop immediately or after decades of latent infection. In highly
endemic regions, musculoskeletal TB usually manifests clinically in the year following
primary lung infection and therefore occurs more frequently in relatively young patients
[18]. Outside highly endemic areas, musculoskeletal TB is more commonly associated with
late reactivation of infection and occurs mainly in adults.

Two types of bone and joint involvement associated with TB infection have been described:
the caseous exudative type and the granular type [19]. The caseous exudative type is
characterized by bone destruction, local swelling, abscess formation, sinus formation, and
constitutional symptoms; it occurs most often in children. The granular type is more
insidious and less destructive than the caseous exudative type, and abscess formation is less
common; it occurs most often in adults. However, host-parasite interactions in TB are
dynamic, often with mixed patterns and transitions along a continuum [20].

Rarely, bones and joints are involved in contiguous spread of TB from another site.
Contiguous spread from an apical pulmonary focus of active TB, for example, can lead to
atlantoaxial TB, involving the joint between the first and second cervical vertebrae [21].

CLINICAL MANIFESTATIONS

Forms of skeletal TB include spondylitis (Pott disease), arthritis, and osteomyelitis. From
published series of spinal TB, there is wide variation in reported rates of active concomitant
pulmonary TB at the time of diagnosis of the spinal TB [12,22,23]. The largest report series
including nearly 700 cases had the lowest reported rate (2.7 percent) [23]. The proportion is
likely to be similarly variable for other TB bone and joint infections, but series are too small
to provide reliable data. Virtually any bone can be infected with M. tuberculosis. The diagnosis
may be delayed when unusual bones such as the hyoid or digits are infected or when
multifocal bony involvement is present.

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Spondylitis (Pott disease) — Tuberculous spondylitis (Pott disease) most commonly affects


the lower thoracic and upper lumbar region; involvement of cervical and upper thoracic
region is less common [24,25]. Progression of infection generally begins with inflammation
of the anterior aspect of intervertebral joints; typically, it spreads behind the anterior
ligament to involve the adjacent vertebral body. Once two adjacent vertebrae are involved,
infection enters the adjoining intervertebral disc space. This tends to occur later in Pott
disease than in bacterial vertebral osteomyelitis and may have the radiographic appearance
of relative disc sparing. Eventually, the avascular disc tissue dies; there is vertebral
narrowing and subsequent vertebral collapse. Gibbus deformity, a form of structural
kyphosis, distorts spinal canal anatomy ( image 1). The spinal cord is then at risk of
compression resulting in paraplegia, especially with involvement of the mid-thoracic region
where the spinal canal is relatively "tight" around the cord [26]. Occasionally, late-onset
paraplegia occurs due to osteophytes and other chronic degenerative changes at a site of
prior infection. Formation of a "cold abscess" (soft tissue mass) at the site is common.
Noncontiguous spinal disease (eg, disease at more than one level) is uncommon, although in
one South African series it was described in 16 of 98 cases [27].

The most common symptom is local pain, which increases in severity over weeks to months,
sometimes in association with muscle spasm and rigidity. The muscle spasm can extend
beyond the diseased area. In some cases, a characteristic erect posture and "alderman's"
gait may be observed in which the patient walks with short, deliberate steps to avoid jarring
of the spine [28]. Constitutional symptoms such as fever and weight loss are present in less
than 40 percent of cases [13,22,29-31].

The diagnosis of Pott disease is frequently delayed as a result of its subacute course,
especially in regions where the incidence of TB is relatively low [13,22]. In endemic areas, the
clinical presentation also tends to be relatively late due to limited access to medical care; in
these settings, patients have symptoms and signs of cord compression at the time of
diagnosis in 40 to 70 percent of cases [22,32]. Thus, late diagnosis is a major factor in
determining the outcome of the disease [33].

Arthritis

Infectious — Tuberculous arthritis can occur in virtually any joint, but it tends to occur in
the hip or the knee; usually, it is monoarticular. However, multifocal lesions are reported in
10 to 15 percent of cases in developing countries [34]. Hip involvement is the most common
presentation, the most difficult to diagnose, and the most debilitating [6]. Clinical
manifestations include swelling, pain, and/or loss of joint function that progresses over
weeks to months. The joint is generally "cold" (eg, erythema, warmth, and other signs of
acute infection are usually absent). Constitutional symptoms, fever, and weight loss occur in
only about 30 percent of cases [29].

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Patients who present late in the course of disease often have evidence of joint destruction
including local deformity and restricted range of motion. Some patients with advanced
disease have draining sinuses. Granulomatous changes typically accompany synovial
proliferation in tuberculous arthritis, with joint effusion and erosion of cartilage. The
consequences are slowly progressive destruction, disorganization of joint architecture, and
potential deformity.

Some data suggest that total hip replacement in the setting of active TB is acceptable if
undertaken in association with appropriate debridement and antituberculous therapy [35].

Inflammatory (Poncet disease) — Poncet disease is an acute symmetric polyarthritis


involving large and small joints associated with active extrapulmonary, pulmonary, or miliary
TB. In general, there is inflammation of the involved joints but no objective evidence of
active TB [36-39]. Poncet disease is relatively rare, and the pathogenesis is unclear; it is
probably immune mediated [38]. HIV coinfection is also a risk factor [40,41]. The arthritis
generally resolves within a few weeks of initiation of anti-TB therapy, with no residual joint
destruction [37,42].

Prosthetic joint infection — Rarely, M. tuberculosis can cause infection at the site of a


prosthetic joint. Diagnosis has been described at the time of initial arthroplasty as well as
subsequent to hardware placement [43].

For cases in which TB is identified at the time of initial arthroplasty, the diagnosis is typically
a surprise to the surgeon who sends abnormal-appearing bone for histopathologic
examination or culture at the time of joint replacement. These patients generally have a
favorable outcome after standard antituberculous chemotherapy, even if the joint prosthesis
is not removed [43].

For cases in which infection is identified following hardware placement, a dormant nidus of
infection reactivates, and patients subsequently present with clinical findings of an infected
prosthesis. These patients often have painful, malfunctioning prostheses, and hardware
removal is required for cure. Some patients with late-onset tuberculous prosthetic joint
infections have coexisting bacterial infection that may mask or obscure the underlying
coinfection with M. tuberculosis.

Osteomyelitis — In addition to tuberculous vertebral osteomyelitis (Pott disease),


tuberculous osteomyelitis can occur in virtually any bone, including the ribs, skull, tubular
bones of the hands and feet (dactylitis), wrist, phalanx, pelvis, and long bones. The onset is
often insidious but, in rare cases, the onset may be acute or subacute [44]. Typically,
osteomyelitis occurs at a single site. However, rarely bony involvement can be multifocal.
The location and presentation can be variable as illustrated by the following case reports:

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● Sternal osteomyelitis due to M. tuberculosis may follow coronary artery bypass surgery
[45] as a presentation of underlying mediastinal TB [46] or as primary sternal
osteomyelitis [47].
● Bony TB of the rib may present as a breast mass or chest wall mass [48,49].
● TB of the small bones of the hand can occur spontaneously in patients with no clinical
signs of pulmonary TB [50].
● Tuberculous mastoiditis can extend into the skull and produce facial nerve palsy [51].
● Lytic bony tubercular lesions in areas as unusual as the symphysis pubis, sacroiliac
joint, and elbow can be misdiagnosed as metastatic malignancy [52].

In some cases, bony infection may spread to contiguous soft tissues or even adjacent joints.
Rarely, involvement of multiple bones may be associated with erroneous diagnosis of
metastatic malignancy [53-55].

An antecedent history of trauma may lead to diagnostic confusion; TB can develop in a bone
or joint injured by previous trauma or surgery. Tuberculous osteomyelitis frequently
presents as a "cold abscess" with swelling, modest erythema or pain, and little or no local
warmth [15]. Spontaneous drainage may occur.

Other clinical manifestations — Musculoskeletal TB can occur as an abscess in the


epidural space (creating pressure on the spinal cord), as an extraspinal soft tissue mass
(eroding ribs and adjacent structures), or as a psoas abscess (which can track down to the
groin). (See "Psoas abscess".)

Radiography — Radiographic imaging can be useful to identify and establish the anatomy


of musculoskeletal TB, although there are no pathognomonic radiographic findings [56].

In the setting of tuberculous spondylitis (Pott disease), radiographic abnormalities are


usually first observed in the anterior aspect of a vertebral body, with demineralization of the
end plate and loss of definition of the bony margin [57]. Subsequently, the opposing
vertebra becomes involved and, in some cases, a paravertebral abscess may be seen.
Involvement of contiguous vertebrae is common, although it is not uncommon to see
noncontiguous spinal TB at multiple levels. As infection progresses, the disc space becomes
obliterated with anterior wedging and angulation. Reactive sclerotic changes remain
localized and the remainder of the vertebral structures is often spared ( image 2).

In some patients, spinal TB presents with osteolytic lesions in the absence of disc space
involvement; these lesions may occur at multiple sites. In one study of 103 French patients
with spinal TB, no disc involvement was observed in about half of cases; plain radiographs
demonstrated osteolytic lesions and multiple involved sites [12].

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In the setting of tuberculous arthritis, local soft tissue swelling, osteopenia, and bone
destruction (with relative preservation of cartilage space) are observed. Subsequent findings
include structural collapse, sclerotic changes, and soft tissue calcification ( image 3). In
some cases, Phemister triad may be observed: juxta-articular osteopenia, peripherally
located osseous erosions, and gradual narrowing of the joint space ( image 4) [58,59].

In the setting of tuberculous osteomyelitis in children, cystic changes may be seen in the
metaphyses of long bones and in flat bones, such as the skull. In tuberculous osteomyelitis
involving a hand or foot, phalangeal bone(s) may have a ballooned appearance.

Computerized tomography, myelography, and magnetic resonance imaging (MRI) are all
useful tools in the diagnosis of musculoskeletal TB [24,60-64]. MRI is particularly valuable in
demonstrating soft tissue extension and encroachment on nearby vital structures, such as
the spinal cord ( image 5 and image 6 and image 7 and image 8) [65,66].

Chest radiography is not a sensitive test for the diagnosis of skeletal TB since there is no
evidence of active chest disease in the majority of cases [5,15,22,67]. However, chest
radiography should be obtained since it may inform decisions regarding isolation, and
collection of sputum specimens for mycobacterial culture should be attempted as the
organism can sometimes be isolated from sputum despite a normal chest radiograph. The
diagnosis of skeletal TB should be considered in patients with focal bony or joint
abnormalities and a chest radiograph compatible with old or active TB. (See "Diagnosis of
pulmonary tuberculosis in adults".)

DIAGNOSIS

General principles — The greatest challenge in diagnosis of skeletal TB is to consider the


diagnosis, especially since there is no evidence of active chest disease in the majority cases.
In addition, delays in diagnosis are common given the indolent nature of tuberculous bone
and joint disease [68]. Clinical clues usually come from the history, which should include
questions about the country of origin and history of prior known or possible TB infection or
contact. In addition, the diagnosis of skeletal TB may be overlooked in patients with HIV
infection and relatively high CD4 counts and no other signs or symptoms of TB.

The diagnosis of musculoskeletal TB is established by microscopy and culture of infected


material. Tissue may be obtained by needle aspiration and/or biopsy; computed tomography
(CT) guidance is useful in regions where available.

Biopsy and culture — The diagnosis of musculoskeletal TB is established by microscopy and


culture of infected material [69-71]. Drug susceptibility testing of isolates is essential. Tissue

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may be obtained by needle aspiration and/or biopsy. CT guidance is useful in regions where
available [72,73].

The diagnosis of tuberculous arthritis can be established by synovial biopsy. Synovial fluid
may be examined [74], but findings are usually nonspecific; the white cell count can be high
or low, with preponderance of either neutrophils or lymphocytes [75].

In the setting of one or more draining sinuses, culture of this material may be useful,
although, in some cases, cultures may demonstrate colonizing bacteria or fungi that are
erroneously assumed to be the causative pathogen.

The high cost and technical demands of rapid automated growth systems and nucleic acid
detection methods often limits their use in the poorest countries with the highest incidence
of TB [76]. The Xpert MTB/RIF assay is an automated nucleic acid amplification test that can
simultaneously identify M. tuberculosis and rifampin resistance; data on use of this assay in
skeletal TB are limited and the test platform is not approved by the Food and Drug
Administration in the United States for use with specimens other than sputum. However, the
available data suggest that Xpert and the more sensitive Xpert Ultra may be useful adjuncts
to diagnosis of skeletal TB, with sensitivity of 79 and 91 percent, respectively [77]. The Xpert
MTB/RIF assay is discussed further separately. (See "Diagnosis of pulmonary tuberculosis in
adults".)

Additional issues related to diagnostic microbiology are discussed further separately. (See
"Diagnosis of pulmonary tuberculosis in adults".)

Differential diagnosis — The differential diagnosis of skeletal TB includes subacute or


chronic infections due to pathogens or diseases such as Staphylococcus aureus osteomyelitis,
brucellosis, melioidosis, actinomycosis, candidiasis, and histoplasmosis, depending upon
epidemiologic factors. Multifocal bone involvement may be confused for metastatic
malignancy.

The differential diagnosis of Pott disease includes degenerative disc and facet joint disease,
spondyloarthropathy, vertebral body collapse due to osteopenia (with a variety of causes
such as osteoporosis and chronic corticosteroid therapy), pyogenic spinal infection, and
malignancy. Each of these can present with similar clinical features; the main challenge for
diagnosis of TB is consideration of the diagnosis. Most of these conditions can be
distinguished with imaging studies where available.

TREATMENT

General approach — Treatment of musculoskeletal TB consists of antimicrobial therapy. In


some cases, surgical intervention is also warranted.
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Antimicrobial therapy — The approach to selection of antituberculous therapy for


treatment of musculoskeletal TB is generally the same as that for pulmonary TB. The drug
regimen may require modification based on concurrent medications (eg, HIV coinfection) or
drug resistance. These issues are discussed in detail separately. (See "Treatment of drug-
susceptible pulmonary tuberculosis in HIV-uninfected adults" and "Treatment of pulmonary
tuberculosis in adults with HIV infection: Initiation of therapy" and "Treatment of drug-
resistant pulmonary tuberculosis in adults".)

The optimal duration of therapy for treatment of musculoskeletal TB is uncertain. For most
patients receiving first-line agents, six to nine months of therapy is sufficient [78]. A longer
duration of therapy (9 to 12 months) is warranted for patients on regimens that do not
include rifampin and/or for patients with extensive or advanced disease, particularly if it is
difficult to assess the response to therapy [78,79].

Data are limited on the optimal drug regimen and duration for treatment of musculoskeletal
infections due to drug-resistant M. tuberculosis. In one small series, 14 of 15 patients were
cured with combined medical/surgical therapy (eight patients) or medical therapy alone
(seven patients). Treatment was continued for 18 to 24 months; follow-up ranged from 5
months to 4.5 years [80].

Previously, longer therapeutic courses (12 to 18 months) have been favored for
musculoskeletal TB because of concerns about poor drug penetration into osseous and
fibrous tissues. However, several studies have shown that six- to nine-month regimens
containing rifampin are at least as effective as longer courses without rifampin [81-86]. The
efficacy of shorter-course therapy is illustrated by the following:

● A large prospective cohort study in Hong Kong demonstrated that 6 months of


antituberculous therapy combined with surgery (radical resection of the lesion and
insertion of autologous bone grafts) was comparable in efficacy with 9 to 18 months of
antituberculous therapy alone [81].

● In three randomized trials of short-course chemotherapy for spinal TB in Hong Kong,


India, and Korea reported after five years of follow-up, six- and nine-month regimens
with isoniazid and rifampin produced comparable results with 18 months of isoniazid
with either ethambutol or para-aminosalicylic acid [84].

● In a randomized trial of 203 Korean patients comparing four different treatment


regimens [(1) isoniazid plus rifampin for six months, (2) isoniazid plus rifampin for nine
months, (3) isoniazid plus ethambutol or para-aminosalicylic acid for nine months, or
(4) isoniazid plus ethambutol or para-aminosalicylic acid for 18 months], a favorable
outcome was achieved in 77 percent of cases after three years from the start of

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therapy; those who received the nine-month regimen with isoniazid plus ethambutol or
para-aminosalicylic acid required additional treatment [85].

One small retrospective study from the United Kingdom did report a high rate of relapse
with a six-month course of therapy (62 percent); no relapse was observed among patients
who received nine months of treatment [86]. In contrast, a Chinese study reported that, in
selected patients and combined with appropriate surgical intervention, ultra-short-course
therapy of 4.5 months was as successful as a 9-month course and associated with fewer side
effects [87].

Surgery — Surgical intervention is warranted for patients in the following circumstances


[26,49,88,89]:

● Patients with spinal disease and advanced neurological deficits


● Patients with spinal disease and worsening neurological deficits progressing while on
appropriate therapy
● Patients with spinal disease and kyphosis >40 degrees at the time of presentation
● Patients with chest wall cold abscess

Forms of surgical intervention may include decompression, use of hardware for stabilization
of spine, abscess drainage, and/or debridement of infected material [25,89]. For the most
part, surgical intervention is safe and sometimes effective in improving neurological deficits;
various approaches have been described, depending on site of infection and related abscess
formation [90-92]. In some circumstances, reconstructive surgery may be important once
antimicrobial therapy has been completed [5]. Hardware is rarely needed for stabilization of
debrided bony lesions [93]. Minimally invasive surgical approaches such as video-assisted
thoracoscopic anterior surgery have been used successfully to manage patients with
neurological symptoms and/or extensive bony destruction involving the thoracic or lumbar
spine [94].

The role of surgery in treatment of other presentations of musculoskeletal TB is not always


clear [95]. In one retrospective review of 70 adults with thoracic spinal TB in India, medical
therapy alone was successful in 69 of 70 patients (mean follow-up of 40 months) [88].
Criteria for exclusion included advanced neurologic deficits, worsening neurologic deficits
while on antituberculous therapy, and kyphosis greater than 40 degrees on presentation.
Abscess was observed on presentation in 44 patients (21 of which were epidural), and 7
patients had signs of cord compression at the time of presentation. Routine surgical
intervention is not warranted [93,96].

Similar results were noted in a retrospective analysis of 52 children with TB of the knee [97].
The outcome of medical therapy without synovectomy was excellent in children who
presented with signs and symptoms of synovitis as long as the joint space was normal.

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Monitoring clinical response — The response to therapy may be monitored by clinical


indicators such as pain, constitutional symptoms, mobility, and neurologic findings. Typically,
responses to therapy are relatively slow (several months). The role of inflammatory markers
in monitoring the response to TB therapy is limited. It is not useful to perform serial
radiographs since radiographic findings may appear to progress during appropriate
treatment [98].

In one study of 43 patients with Pott paraplegia, the most important prognostic factor that
predicted six-month outcome included muscle power, paraplegia score, sensory-evoked
potentials, and motor-evoked potentials [99]. Patients with mild weakness and lower
paraplegia scores were more likely to recover completely by six months than patients with
more severe prognostic indicators.

For patients on antituberculous therapy for skeletal TB in the setting of antiretroviral


treatment (ART) for HIV infection, it is important to monitor for immune reconstruction
inflammatory syndrome (IRIS). IRIS typically presents with paradoxical progression of TB
clinical manifestations and constitutional symptoms in the first few weeks following initiation
of ART. In the setting of skeletal TB, new clinical manifestations may appear and/or resolved
manifestations may reappear. IRIS is discussed further separately. (See "Immune
reconstitution inflammatory syndrome".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Diagnosis and
treatment of tuberculosis".)

SUMMARY AND RECOMMENDATIONS

● Skeletal tuberculosis (TB) refers to TB involvement of the bones and/or joints.


Musculoskeletal TB accounts for 10 to 35 percent of cases of extrapulmonary TB and
for almost 2 percent of TB cases overall. The proportion of skeletal TB among HIV-
infected individuals is comparable with the proportion of skeletal TB among HIV-
uninfected individuals. (See 'Epidemiology' above.)

● Tuberculous spondylitis (Pott disease) is the most common form of skeletal TB; it
usually affects the lower thoracic and upper lumbar region. Infection begins with
inflammation of the intervertebral joints and can spread to involve the adjacent
vertebral body. Once two adjacent vertebrae are involved, infection can involve the

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adjoining intervertebral disc space, leading to vertebral collapse. Subsequent kyphosis


can lead to cord compression and paraplegia. (See 'Spondylitis (Pott disease)' above.)

● The most common symptom of tuberculous spondylitis (Pott disease) is local pain,
which increases in severity over weeks to months, sometimes in association with
muscle spasm and rigidity. A characteristic erect posture and "alderman's" gait may be
observed in which the patient walks with short, deliberate steps to avoid jarring of the
spine. Constitutional symptoms such as fever and weight loss are relatively uncommon.
(See 'Spondylitis (Pott disease)' above.)

● Tuberculous arthritis tends to occur in the hip or the knee and is usually monoarticular.
Clinical manifestations include swelling, pain, and/or loss of joint function that
progresses over weeks to months. The joint is generally "cold" (eg, erythema, warmth,
and other signs of acute infection are usually absent). (See 'Arthritis' above.)

● Tuberculous osteomyelitis can occur in virtually any bone, including the ribs, skull,
phalanx, pelvis, and long bones. Typically, osteomyelitis occurs at a single site. The
onset is often insidious but, in rare cases, the onset may be acute or subacute.
Tuberculous osteomyelitis frequently presents as a "cold abscess" with swelling,
modest erythema or pain, and little or no local warmth. (See 'Osteomyelitis' above.)

● The diagnosis of musculoskeletal TB is established by microscopy and culture of


infected material. Tissue may be obtained by needle aspiration and/or biopsy; guidance
with computed tomography or ultrasound to obtain tissue is useful in regions where
available. Radiographic imaging can be useful to identify and establish the anatomy of
musculoskeletal TB, although there are no pathognomonic radiographic findings. (See
'Diagnosis' above.)

● Treatment of musculoskeletal TB consists of antituberculous therapy. The approach to


selection of therapy for treatment of musculoskeletal TB is generally the same as that
for pulmonary TB and is discussed in detail separately. (See "Treatment of drug-
susceptible pulmonary tuberculosis in HIV-uninfected adults" and "Treatment of
pulmonary tuberculosis in adults with HIV infection: Initiation of therapy" and
"Treatment of drug-resistant pulmonary tuberculosis in adults".)

● The optimal duration of therapy for treatment of musculoskeletal TB is uncertain. For


patients receiving treatment with first-line agents in the absence of extensive or
advanced disease, we suggest six months of therapy (rather than 9 or 12 months)
(Grade 2B). A longer duration of therapy (9 to 12 months) is warranted for patients on
regimens that do not include rifampin and/or for patients with extensive or advanced
disease. (See 'Antimicrobial therapy' above.)

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● Surgical intervention is warranted for patients with spinal disease and advanced
neurological deficits or worsening neurological deficits progressing while on
appropriate therapy, as well as for patients with spinal disease and kyphosis >40
degrees at the time of presentation. (See 'Surgery' above.)

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GRAPHICS

Pott disease in a young child

A gibbous deformity has occurred as a consequence of collapse of the 8th, 9th,


and 10th thoracic vertebral bodies with sparing of the posterior vertebral
elements. The paravertebral abscess is extensive projecting laterally and
anteriorly (arrows). Bony debris is present in the abscess.

Courtesy of Charles E Putnam, MD.

Graphic 60628 Version 8.0

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Pott disease in an adult

Posterioanterior thoracic spine film from a patient with Pott disease


shows the contours of a tuberculous paraspinal mass (arrows) with
destruction of the T7-8 disc space and adjacent vertebral bodies.

Courtesy of Charles E Putnam, MD.

Graphic 72424 Version 6.0

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Tuberculous arthritis

Tuberculous arthritis of the left wrist with destructive changes in the


carpal bones (arrow) and radius and prominent soft tissue swelling
(arrowhead).

Courtesy of Charles E Putnam, MD.

Graphic 77123 Version 4.0

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Tuberculosis of the right hip

Plain film of the right hip in a 28-year-old woman with painful joints
and a productive cough demonstrates complete loss of the joint
space and destruction of the cartilage and adjacent joint surfaces
with severe periarticular bony demineralization (arrows).

Courtesy of Jonathan Kruskal, MD.

Graphic 65352 Version 3.0

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Tuberculosis of the spine (Pott disease)

Magnetic resonance imaging with T1-weighted fat-saturated image


showing anterior vertebral body destruction with relative sparing of
adjacent discs and an abscess spreading beneath the anterior
longitudinal ligament.

Courtesy of Denis Spelman, MBBS, FRACP, FRCPA, MPH.

Graphic 86251 Version 5.0

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Tuberculosis of the spine (Pott disease)

Magnetic resonance imaging of 17-year-old fisherman showing


tuberculous infection of adjacent thoracic vertebrae with intervening
disc destruction and an anterior paraspinal abscess.

Courtesy of Malcolm McDonald, PhD, FRACP, FRCPA.

Graphic 86252 Version 5.0

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Tuberculosis of the spine (Pott disease)

Magnetic resonance imaging of 17-year-old fisherman (coronal


section) showing a large tuberculous paraspinal abscess and pleural
involvement.

Courtesy of Malcolm McDonald, PhD, FRACP, FRCPA.

Graphic 86253 Version 5.0

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Postsurgical drainage and fixation of spinal


tuberculosis (Pott disease)

Plain film of 17-year-old fisherman following surgical drainage and


spinal fixation.

Courtesy of Malcolm McDonald, PhD, FRACP, FRCPA.

Graphic 86254 Version 4.0

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Contributor Disclosures
Jason Stout, MD Nothing to disclose John Bernardo, MD Nothing to disclose Elinor L Baron, MD,
DTMH Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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