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Skeletal tuberculosis

Authors: Daniel J Sexton, MD, Malcolm McDonald, PhD, FRACP, FRCPA

Section Editor: C Fordham von Reyn, 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: Aug 2018. | This topic last updated: Jul 24, 2018.

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 — Skeletal TB accounts for 10 to 35 percent of cases of extrapulmonary TB (9.7 percent of

United States extrapulmonary cases in 2016) [5] and, overall, 2.3 percent of all United States TB cases
reported in 2013 [6-10]. 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].

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.

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].
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 [7]. 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].

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:

● 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 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].

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 [6,15,22,67]. However, chest radiography should be obtained since it
may inform decisions regarding isolation. 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. Clinical clues usually
come from the history, which should include questions about the country of origin and history of prior known
or possible TB 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 [68-70]. Drug susceptibility testing of isolates is essential. Tissue may be obtained by
needle aspiration and/or biopsy. CT guidance is useful in regions where available [71,72].

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

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 [75]. 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. 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.

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 HIV-infected adults: 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 [76]. 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 [76,77].

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 [78].

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 [79-84]. 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 [79].
 ● 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 [82].

● 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
therapy; those who received the nine-month regimen with isoniazid plus ethambutol or para-
aminosalicylic acid required additional treatment [83].

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 [84]. 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 [85].

Surgery — Surgical intervention is warranted for patients in the following circumstances [26,49,86,87]:

● 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 [25,87]. 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 [88-90]. In some circumstances, reconstructive
surgery may be important once antimicrobial therapy has been completed [6]. Hardware is rarely needed for
stabilization of debrided bony lesions [91]. 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 [92].

The role of surgery in treatment of other presentations of musculoskeletal TB is not always clear [93]. 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) [86]. 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 [91,94].

Similar results were noted in a retrospective analysis of 52 children with TB of the knee [95]. 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.

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 [96].
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 [97]. 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 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 HIV-infected adults: 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.)

● 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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Topic 7658 Version 29.0

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

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

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

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

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

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

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

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