skeletal tuberculosis

Official reprint from UpToDate

www.uptodate.com ©2015 UpToDate

AuthorsMalcolm McDonald, PhD, FRACP,FRCPADaniel J Sexton, MD

Section EditorC Fordham von Reyn, MD

Deputy EditorElinor L Baron, MD, DTMH

Skeletal tuberculosis

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

Literature review current through: Jul 2015. | This topic last updated: Mar 24, 2015.

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 to 9000 BC [1,2], and analysis

of 483 pre-Columbian skeletons in Chile showed lesions consistent with bony tuberculosis 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 tuberculosis (TB) accounts for 10 to 35 percent of cases of extrapulmonary

tuberculosis (10.8 percent of United States extrapulmonary cases in 2013) and, overall, 2.3 percent of all United

States TB cases reported in 2013 [5-9]. Reported rates of extrapulmonary TB are higher among immigrants from

endemic areas to developed countries; this may be due in part to immigration screening procedures for pulmonary

TB. 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 [10]. The proportion of skeletal TB among HIV-infected

individuals is comparable with the proportion of skeletal TB among HIV-uninfected individuals [11,12].

The most common form of skeletal TB is Pott’s 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 in frequency by extraspinal tuberculous osteomyelitis [13].

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 may be contained by the cellular immune

response. CD4 and CD8 lymphocytes play important roles, as does interferon-gamma [14]. Reactivation of infection

with progression to clinically apparent disease may occur when local immune defenses fail, as in the setting of

malnutrition, advancing age, HIV infection, or renal failure [15].

Active tuberculosis (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 most frequently in relatively young patients. Outside endemic areas, musculoskeletal TB is more commonly

associated with late reactivation of infection and occurs mainly in adults.

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 [16].

CLINICAL MANIFESTATIONS — Forms of skeletal tuberculosis (TB) include spondylitis (Pott’s 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 [10,17,18]. The largest report series including nearly 700

cases had the lowest reported rate (2.7 percent) [18]. 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

®

®

Skeletal tuberculosis http://www.uptodate.com.wdg.biblio.udg.mx:2048/contents/skeletal-tube...

1 de 19 03/08/2015 07:16 p.m.

multifocal bony involvement is present.

Spondylitis (Pott's disease) — Tuberculous spondylitis (Pott’s disease) most commonly affects the lower thoracic

and upper lumbar region; disease involving the cervical and upper thoracic region is less common [19,20]. Infection

generally begins with inflammation of the anterior aspect of the 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's 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 [21]. 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 [22].

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 "aldermanic" gait may be observed in which the patient walks with short,

deliberate steps to avoid jarring of the spine [23]. Constitutional symptoms such as fever and weight loss are present

in less than 40 percent of cases [11,17,24-26].

The diagnosis of Pott’s disease is frequently delayed as a result of its subacute course, especially in regions where

the incidence of tuberculosis is relatively low [11,17]. 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 [17,27]. Thus, late diagnosis is a major factor in

determining the outcome of the disease [28].

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 [29]. 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 [24].

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 [30].

Inflammatory (Poncet's disease) — Poncet’s disease is an acute symmetrical 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 [31-33]. Poncet’s disease is relatively rare, and the

pathogenesis is unclear; it is probably immune mediated [33]. HIV coinfection is also a risk factor [34,35]. The

arthritis generally resolves within a few weeks of initiation of antituberculosis therapy, with no residual joint

destruction [32,36].

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 [37].


2 de 19 03/08/2015 07:16 p.m.

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.

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's disease), tuberculous osteomyelitis can

occur in virtually any bone, including the ribs, skull, phalanx, pelvis, and long bones. The onset is often insidious but,

in rare cases, the onset may be acute or subacute [38]. Typically, osteomyelitis occurs at a single site; the location

and presentation can be variable as illustrated by the following case reports:

In some cases, bony infection may spread to contiguous soft tissues or even adjacent joints. Involvement of multiple

bones is rare and may result in an erroneous diagnosis of widespread metastatic malignancy [47-49].

An antecedent history of trauma may lead to diagnostic confusion; tuberculous 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 [13]. Spontaneous drainage may occur.

Other clinical manifestations — Musculoskeletal tuberculosis 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.

In the setting of tuberculous spondylitis (Pott's 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

[50]. 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 tuberculosis 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 tuberculosis, spinal

tuberculosis without disc involvement was observed in about half of cases; plain radiographs demonstrated

osteolytic lesions and multiple involved sites [10].

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 disc space (image 4) [51,52].

Sternal osteomyelitis due to M. tuberculosis may follow coronary artery bypass surgery [39] as a presentation

of underlying mediastinal tuberculosis [40] or as primary sternal osteomyelitis [41].

●

Bony tuberculosis of the rib may present as a breast mass or chest wall mass [42,43].●

Tuberculosis of the small bones of the hand can occur spontaneously in patients with no clinical signs of

pulmonary tuberculosis [44].

●

Tuberculous mastoiditis can extend into the skull and produce facial nerve palsy [45].●

Lytic bony tubercular lesions in areas as unusual as the symphysis pubis, sacroiliac joint, and elbow can be

misdiagnosed as metastatic malignancy [46].

●


3 de 19 03/08/2015 07:16 p.m.

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 (CT), myelography, and magnetic resonance imaging (MRI) are all useful tools in the

diagnosis of musculoskeletal TB [19,53-57]. 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)

[58].

Chest radiography is not a sensitive test for the diagnosis of skeletal TB since there is no evidence of active chest

disease in more than half of cases [5,13,17,59]. However, chest radiography should always be obtained since it may

inform decisions regarding isolation. The diagnosis of skeletal tuberculosis should be considered in patients with

focal bony or joint abnormalities and a chest radiograph compatible with old or active tuberculosis. (See "Diagnosis

of pulmonary tuberculosis in HIV-uninfected patients", section on 'Chest radiography'.)

DIAGNOSIS

General principles — The greatest challenge in diagnosis of skeletal tuberculosis (TB) is to consider the diagnosis,

especially since there is no evidence of active chest disease in more than half of 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 tuberculosis may be overlooked in patients with HIV infection and

relatively high CD4 counts and no other signs or symptoms of tuberculosis.

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 [60-62]. 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 [63,64].

The diagnosis of tuberculous arthritis can be established by synovial biopsy, although examination of synovial joint

fluid is usually not helpful. The white cell count can be high or low, with preponderance of either neutrophils or

lymphocyte, and no other specific diagnostic features [65].

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 limits

their use in the poorest countries with the highest incidence of tuberculosis [66]. The Xpert MTB/RIF assay is an

automated nucleic acid amplification test that can simultaneously identify M. tuberculosis and rifampin resistance;

issues related to this assay are discussed further separately. (See "Diagnosis of pulmonary tuberculosis in

HIV-uninfected patients", section on 'Xpert MTB/RIF assay'.)

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

tuberculosis in HIV-uninfected patients", section on 'Diagnostic microbiology'.)

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’s disease includes degenerative disc and facet joint disease, spondyloarthropathy,

vertebral body collapse due to osteopenia (due to a variety of causes such as osteoporosis and chronic

corticosteroid therapy), pyogenic spinal infection, and malignancy. Each of these can present with similar clinical


4 de 19 03/08/2015 07:16 p.m.

features; the main challenge for diagnosis of tuberculosis is consideration of the diagnosis. Most of these conditions

can be distinguished with imaging studies where available.

TREATMENT

General approach — Treatment of musculoskeletal tuberculosis 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

tuberculosis is generally the same as that for pulmonary tuberculosis. The drug regimen varies with whether or not

the patient has HIV infection or drug-resistant tuberculosis. These issues are discussed in detail separately. (See

"Treatment of pulmonary tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary tuberculosis in the

HIV-infected patient" and "Diagnosis, treatment, and prevention of drug-resistant tuberculosis".)

The optimal duration of therapy for treatment of musculoskeletal tuberculosis is uncertain. For most patients

receiving first-line agents, six to nine months of therapy is sufficient [67]. 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 [68,69].

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 [70].

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 [71-76].

The efficacy of shorter-course therapy is illustrated by the following:

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 [76].

Surgery — Surgical intervention is warranted for patients in the following circumstances [21,43,77,78]:

Forms of surgical intervention may include decompression, use of hardware for stabilization of spine, abscess

drainage, and/or debridement of infected material [20,78]. In some circumstances, reconstructive surgery may be

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 [71].

●

In three randomized trials of short-course chemotherapy for spinal tuberculosis 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 paraaminosalicylic acid [74].

●

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

paraaminosalicylic acid for nine months, or (4) isoniazid plus ethambutol or paraaminosalicylic 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 paraaminosalicylic acid required

additional treatment [75].

●

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●


5 de 19 03/08/2015 07:16 p.m.

important once antimicrobial therapy has been completed [5]. Hardware is rarely needed for stabilization of debrided

bony lesions [79]. 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 [80].

The role of surgery in treatment of other presentations of musculoskeletal tuberculosis is not always clear [81]. In

one retrospective review of 70 adults with thoracic spinal tuberculosis in India, medical therapy alone was successful

in 69 of 70 patients (mean follow-up of 40 months) [77]. 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 [79,82].

Similar results were noted in a retrospective analysis of 52 children with TB of the knee [83]. 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. 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 [84].

In one study of 43 patients with Pott's paraplegia, the most important prognostic factor that predicted six-month

outcome included muscle power, paraplegia score, sensory-evoked potentials (SEPs), and motor-evoked potentials

(MEPs) [85]. 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".)

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 tuberculosis 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's 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's disease)' above.)

●

The most common symptom of tuberculous spondylitis (Pott's 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 "aldermanic" 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's 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.)

●


6 de 19 03/08/2015 07:16 p.m.

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

Daniel TM, Bates JH, Downes KA. History of tuberculosis. In: Tuberculosis: Pathogenesis, Protection, andControl, Bloom BR (Ed), American Society for Microbiology, Washington 1994. p.13.

1.

Hershkovitz I, Donoghue HD, Minnikin DE, et al. Detection and molecular characterization of 9,000-year-oldMycobacterium tuberculosis from a Neolithic settlement in the Eastern Mediterranean. PLoS One 2008;3:e3426.

2.

Arriaza BT, Salo W, Aufderheide AC, Holcomb TA. Pre-Columbian tuberculosis in northern Chile: molecularand skeletal evidence. Am J Phys Anthropol 1995; 98:37.

3.

Donoghue HD, Lee OY, Minnikin DE, et al. Tuberculosis in Dr Granville's mummy: a molecular re-examinationof the earliest known Egyptian mummy to be scientifically examined and given a medical diagnosis. Proc BiolSci 2010; 277:51.

4.

Watts HG, Lifeso RM. Tuberculosis of bones and joints. J Bone Joint Surg Am 1996; 78:288.5.

Sharma SK, Mohan A. Extrapulmonary tuberculosis. Indian J Med Res 2004; 120:316.6.

Teo HE, Peh WC. Skeletal tuberculosis in children. Pediatr Radiol 2004; 34:853.7.

Fanning A. Tuberculosis: 6. Extrapulmonary disease. CMAJ 1999; 160:1597.8.

Peto HM, Pratt RH, Harrington TA, et al. Epidemiology of extrapulmonary tuberculosis in the United States,

1993-2006. Clin Infect Dis 2009; 49:1350.

9.

Pertuiset E, Beaudreuil J, Lioté F, et al. Spinal tuberculosis in adults. A study of 103 cases in a developedcountry, 1980-1994. Medicine (Baltimore) 1999; 78:309.

10.

Fuentes Ferrer M, Gutiérrez Torres L, Ayala Ramírez O, et al. Tuberculosis of the spine. A systematic reviewof case series. Int Orthop 2012; 36:221.

11.

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 tuberculosis consists of antituberculous therapy. The approach to selection of

therapy for treatment of musculoskeletal tuberculosis is generally the same as that for pulmonary tuberculosis

and is discussed in detail separately. (See "Treatment of pulmonary tuberculosis in HIV-uninfected patients"

and "Treatment of pulmonary tuberculosis in the HIV-infected patient" and "Diagnosis, treatment, and

prevention of drug-resistant tuberculosis".)

●

The optimal duration of therapy for treatment of musculoskeletal tuberculosis is uncertain. For patients

receiving treatment with first-line agents in the absence of extensive or advanced disease, we suggest 6

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.)

●


7 de 19 03/08/2015 07:16 p.m.

Trecarichi EM, Di Meco E, Mazzotta V, Fantoni M. Tuberculous spondylodiscitis: epidemiology, clinicalfeatures, treatment, and outcome. Eur Rev Med Pharmacol Sci 2012; 16 Suppl 2:58.

12.

Vohra R, Kang HS, Dogra S, et al. Tuberculous osteomyelitis. J Bone Joint Surg Br 1997; 79:562.13.

Kaufmann SH, Cole ST, Mizrahi V, et al. Mycobacterium tuberculosis and the host response. J Exp Med 2005;

201:1693.

14.

Ellner JJ. Review: the immune response in human tuberculosis--implications for tuberculosis control. J InfectDis 1997; 176:1351.

15.

Lifeso R. Atlanto-axial tuberculosis in adults. J Bone Joint Surg Br 1987; 69:183.16.

Nussbaum ES, Rockswold GL, Bergman TA, et al. Spinal tuberculosis: a diagnostic and managementchallenge. J Neurosurg 1995; 83:243.

17.

Turgut M. Spinal tuberculosis (Pott's disease): its clinical presentation, surgical management, and outcome. Asurvey study on 694 patients. Neurosurg Rev 2001; 24:8.

18.

Weaver P, Lifeso RM. The radiological diagnosis of tuberculosis of the adult spine. Skeletal Radiol 1984;

12:178.

19.

Lifeso RM, Weaver P, Harder EH. Tuberculous spondylitis in adults. J Bone Joint Surg Am 1985; 67:1405.20.

Khoo LT, Mikawa K, Fessler RG. A surgical revisitation of Pott distemper of the spine. Spine J 2003; 3:130.21.

Polley P, Dunn R. Noncontiguous spinal tuberculosis: incidence and management. Eur Spine J 2009; 18:1096.22.

Girdlestone GR, Somerville EW. Tuberculosis of Bone and Joint, 2nd ed, Oxford University Press, London1952.

23.

Hodgson SP, Ormerod LP. Ten-year experience of bone and joint tuberculosis in Blackburn 1978-1987. J RColl Surg Edinb 1990; 35:259.

24.

Hopewell PC. Overview of clinical tuberculosis. In: Tuberculosis: Pathogenesis, Protection and Control, BloomBR (Ed), American Society for Microbiology Press, Washington, DC 1994. p.25.

25.

Pigrau-Serrallach C, Rodríguez-Pardo D. Bone and joint tuberculosis. Eur Spine J 2013; 22 Suppl 4:556.26.

Hsu LC, Leong JC. Tuberculosis of the lower cervical spine (C2 to C7). A report on 40 cases. J Bone Joint

Surg Br 1984; 66:1.

27.

Kamara E, Mehta S, Brust JC, Jain AK. Effect of delayed diagnosis on severity of Pott's disease. Int Orthop2012; 36:245.

28.

Kumar K, Saxena MB. Multifocal osteoarticular tuberculosis. Int Orthop 1988; 12:135.29.

Kim SJ, Postigo R, Koo S, Kim JH. Total hip replacement for patients with active tuberculosis of the hip: asystematic review and pooled analysis. Bone Joint J 2013; 95-B:578.

30.

Isaacs AJ, Sturrock RD. Poncet's disease--fact or fiction? A re-appraisal of tuberculous rheumatism. Tubercle1974; 55:135.

31.

Sood R, Wali JP, Handa R. Poncet's disease in a north Indian hospital. Trop Doct 1999; 29:33.32.

Dall L, Long L, Stanford J. Poncet's disease: tuberculous rheumatism. Rev Infect Dis 1989; 11:105.33.

Kawsar M, D'Cruz D, Nathan M, Murphy M. Poncet's disease in a patient with AIDS. Rheumatology (Oxford)2001; 40:346.

34.

Cuende E, Almeida V, Portu J, et al. Poncet's disease and papulonecrotic tuberculid in a patient infected withthe human immunodeficiency virus. Arthritis Rheum 1998; 41:1884.

35.

Kroot EJ, Hazes JM, Colin EM, Dolhain RJ. Poncet's disease: reactive arthritis accompanying tuberculosis.Two case reports and a review of the literature. Rheumatology (Oxford) 2007; 46:484.

36.

Spinner RJ, Sexton DJ, Goldner RD, Levin LS. Periprosthetic infections due to Mycobacterium tuberculosis inpatients with no prior history of tuberculosis. J Arthroplasty 1996; 11:217.

37.

Zahraa J, Johnson D, Lim-Dunham JE, Herold BC. Unusual features of osteoarticular tuberculosis in children.J Pediatr 1996; 129:597.

38.

Rubinstien EM, Lehmann T. Sternal osteomyelitis due to Mycobacterium tuberculosis following coronary arterybypass surgery. Clin Infect Dis 1996; 23:202.

39.


8 de 19 03/08/2015 07:16 p.m.

Gondal GM, Mushtaq S, Masood R, et al. Mediastinal tuberculosis presenting with sternal osteomyelitis anddischarging sinus. J Postgrad Med Inst 2011; 25:379.

40.

Platt MA, Ziegler K. Primary sternal osteomyelitis with bacteremia and distal seeding. J Emerg Med 2012;43:e93.

41.

Frouge C, Miquel A, Cochan-Priollet B, et al. Breast mass due to rib tuberculosis. Eur J Radiol 1995; 19:118.42.

Kim YT, Han KN, Kang CH, et al. Complete resection is mandatory for tubercular cold abscess of the chestwall. Ann Thorac Surg 2008; 85:273.

43.

Karanas YL, Yim KK. Mycobacterium tuberculosis infection of the hand: a case report and review of theliterature. Ann Plast Surg 1998; 40:65.

44.

Hadfield PJ, Shah BK, Glover GW. Facial palsy due to tuberculosis: the value of CT. J Laryngol Otol 1995;109:1010.

45.

Gothwal S, Varshney P, Mathur S, Songra B. Tuberculosis of the pubic symphysis. BMJ Case Rep 2014; 2014.46.

Ormerod LP, Grundy M, Rahman MA. Multiple tuberculous bone lesions simulating metastatic disease.

Tubercle 1989; 70:305.

47.

Muradali D, Gold WL, Vellend H, Becker E. Multifocal osteoarticular tuberculosis: report of four cases andreview of management. Clin Infect Dis 1993; 17:204.

48.

Lynn MM, Kukanesen JR, Khan AW. Troublesome Tuberculosis: A Case Report on Multi-focal TuberculousOsteomyelitis in An Immunocompetent Patient. J Clin Med Res 2012; 4:73.

49.

Yao DC, Sartoris DJ. Musculoskeletal tuberculosis. Radiol Clin North Am 1995; 33:679.50.

Phemister, DB, Hatcher, CH. Correlation of pathological and roentgenological findings in the diagnosis oftuberculous arthritis. Am J Roentgenol 1933; 29:736.

51.

Choi JA, Koh SH, Hong SH, et al. Rheumatoid arthritis and tuberculous arthritis: differentiating MRI features.

AJR Am J Roentgenol 2009; 193:1347.

52.

Shanley DJ. Tuberculosis of the spine: imaging features. AJR Am J Roentgenol 1995; 164:659.53.

Jain R, Sawhney S, Berry M. Computed tomography of vertebral tuberculosis: patterns of bone destruction.Clin Radiol 1993; 47:196.

54.

Kim NH, Lee HM, Suh JS. Magnetic resonance imaging for the diagnosis of tuberculous spondylitis. Spine(Phila Pa 1976) 1994; 19:2451.

55.

Desai SS. Early diagnosis of spinal tuberculosis by MRI. J Bone Joint Surg Br 1994; 76:863.56.

Pui MH, Mitha A, Rae WI, Corr P. Diffusion-weighted magnetic resonance imaging of spinal infection andmalignancy. J Neuroimaging 2005; 15:164.

57.

Jung NY, Jee WH, Ha KY, et al. Discrimination of tuberculous spondylitis from pyogenic spondylitis on MRI.AJR Am J Roentgenol 2004; 182:1405.

58.

Davidson PT, Horowitz I. Skeletal tuberculosis. A review with patient presentations and discussion. Am J Med1970; 48:77.

59.

Diagnostic Standards and Classification of Tuberculosis in Adults and Children. This official statement of theAmerican Thoracic Society and the Centers for Disease Control and Prevention was adopted by the ATSBoard of Directors, July 1999. This statement was endorsed by the Council of the Infectious Disease Societyof America, September 1999. Am J Respir Crit Care Med 2000; 161:1376.

60.

Colmenero JD, Ruiz-Mesa JD, Sanjuan-Jimenez R, et al. Establishing the diagnosis of tuberculous vertebralosteomyelitis. Eur Spine J 2013; 22 Suppl 4:579.

61.

Merino P, Candel FJ, Gestoso I, et al. Microbiological diagnosis of spinal tuberculosis. Int Orthop 2012; 36:233.62.

Mondal A. Cytological diagnosis of vertebral tuberculosis with fine-needle aspiration biopsy. J Bone Joint Surg

Am 1994; 76:181.

63.

Versfeld GA, Solomon A. A diagnostic approach to tuberculosis of bones and joints. J Bone Joint Surg Br1982; 64:446.

64.

Allali F, Mahfoud-Filali S, Hajjaj-Hassouni N. Lymphocytic joint fluid in tuberculous arthritis. A review of 30cases. Joint Bone Spine 2005; 72:319.

65.


9 de 19 03/08/2015 07:16 p.m.

Patwardhan SA, Joshi S. Laboratory diagnosis of spinal tuberculosis: Past and present. ArgoSpine News &Journal 2011; 23:120.

66.

American Thoracic Society, CDC, Infectious Diseases Society of America. Treatment of tuberculosis. MMWRRecomm Rep 2003; 52:1.

67.

Blumberg HM, Leonard MK Jr, Jasmer RM. Update on the treatment of tuberculosis and latent tuberculosisinfection. JAMA 2005; 293:2776.

68.

Blumberg HM, Burman WJ, Chaisson RE, et al. American Thoracic Society/Centers for Disease Control and

Prevention/Infectious Diseases Society of America: treatment of tuberculosis. Am J Respir Crit Care Med2003; 167:603.

69.

Suárez-García I, Noguerado A. Drug treatment of multidrug-resistant osteoarticular tuberculosis: a systematicliterature review. Int J Infect Dis 2012; 16:e774.

70.

A controlled trial of six-month and nine-month regimens of chemotherapy in patients undergoing radicalsurgery for tuberculosis of the spine in Hong Kong. Tenth report of the Medical Research Council WorkingParty on Tuberculosis of the Spine. Tubercle 1986; 67:243.

71.

Upadhyay SS, Saji MJ, Yau AC. Duration of antituberculosis chemotherapy in conjunction with radical surgeryin the management of spinal tuberculosis. Spine (Phila Pa 1976) 1996; 21:1898.

72.

A controlled trial of anterior spinal fusion and débridement in the surgical management of tuberculosis of thespine in patients on standard chemotherapy: a study in two centres in South Africa. Seventh Report of theMedical Research Council Working Party on tuberculosis of the spine. Tubercle 1978; 59:79.

73.

Five-year assessment of controlled trials of short-course chemotherapy regimens of 6, 9 or 18 months'duration for spinal tuberculosis in patients ambulatory from the start or undergoing radical surgery. Fourteenthreport of the Medical Research Council Working Party on Tuberculosis of the Spine. Int Orthop 1999; 23:73.

74.

Controlled trial of short-course regimens of chemotherapy in the ambulatory treatment of spinal tuberculosis.Results at three years of a study in Korea. Twelfth report of the Medical Research Council Working Party onTuberculosis of the Spine. J Bone Joint Surg Br 1993; 75:240.

75.

Ramachandran S, Clifton IJ, Collyns TA, et al. The treatment of spinal tuberculosis: a retrospective study. Int JTuberc Lung Dis 2005; 9:541.

76.

Nene A, Bhojraj S. Results of nonsurgical treatment of thoracic spinal tuberculosis in adults. Spine J 2005;5:79.

77.

Upadhyay SS, Sell P, Saji MJ, et al. Surgical management of spinal tuberculosis in adults. Hong Kongoperation compared with debridement surgery for short and long term outcome of deformity. Clin Orthop RelatRes 1994; :173.

78.

Oguz E, Sehirlioglu A, Altinmakas M, et al. A new classification and guide for surgical treatment of spinaltuberculosis. Int Orthop 2008; 32:127.

79.

Garg N, Vohra R. Minimally invasive surgical approaches in the management of tuberculosis of the thoracicand lumbar spine. Clin Orthop Relat Res 2014; 472:1855.

80.

Jutte PC, Van Loenhout-Rooyackers JH. Routine surgery in addition to chemotherapy for treating spinal

tuberculosis. Cochrane Database Syst Rev 2006; :CD004532.

81.

Zhang X, Ji J, Liu B. Management of spinal tuberculosis: a systematic review and meta-analysis. J Int MedRes 2013; 41:1395.

82.

Hoffman EB, Allin J, Campbell JA, Leisegang FM. Tuberculosis of the knee. Clin Orthop Relat Res 2002; :100.83.

Boxer DI, Pratt C, Hine AL, McNicol M. Radiological features during and following treatment of spinaltuberculosis. Br J Radiol 1992; 65:476.

84.

Kalita J, Misra UK, Mandal SK, Srivastava M. Prognosis of conservatively treated patients with Pott'sparaplegia: logistic regression analysis. J Neurol Neurosurg Psychiatry 2005; 76:866.

85.

Topic 7658 Version 15.0


10 de 19 03/08/2015 07:16 p.m.

GRAPHICS

Pott's 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 5.0


11 de 19 03/08/2015 07:16 p.m.

Pott's disease in an adult

Posterioanterior thoracic spine film from a patient with Pott's disease

shows the contours of a tuberculous paraspinal mass (arrows) with

destruction of the T7-8 disc space and adjacent vertebral bodies.




12 de 19 03/08/2015 07:16 p.m.

Tuberculosis arthritis

Tuberculous arthritis of the left wrist with destructive changes in the

carpal bones (black arrow) and radius and prominent soft tissue swelling

(white arrow).




13 de 19 03/08/2015 07:16 p.m.

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.



14 de 19 03/08/2015 07:16 p.m.

Tuberculosis of the spine (Pott's disease)

Magnetic resonance imaging (MRI) 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.



15 de 19 03/08/2015 07:16 p.m.


Magnetic resonance imaging (MRI) 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.



16 de 19 03/08/2015 07:16 p.m.


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

section) showing a large tuberculous paraspinal abscess and pleural

involvement.




17 de 19 03/08/2015 07:16 p.m.

Post-surgical drainage and fixation of spinal

tuberculosis (Pott's disease)

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

spinal fixation.




18 de 19 03/08/2015 07:16 p.m.

Disclosures: Malcolm McDonald, PhD, FRACP, FRCPA Nothing to disclose. Daniel J Sexton, MD Grant/Research/Clinical Trail Support:Cubist [C. difficile infection (Fidaxomycin)]. Consultant/Advisory Boards: Johnson & Johnson [Pelvic mesh-related infection]; Sterilis [Medicalwaste disposal systems]; Magnolia Medical Technologies [Intravenous devices]. Other Financial Interest: National Football League [Infectioncontrol program]. Equity Ownership/Stock Options: Magnolia Medical Technologies [Intravenous devices]. C Fordham von Reyn, MD Nothingto 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 amulti-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content isrequired of all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

Disclosures


19 de 19 03/08/2015 07:16 p.m.

skeletal tuberculosis

Documents

tb involvement

aspects of tb

proportion of skeletal

cases of spinal tb

unitedstates tb cases

active tuberculosis

contiguous spread of

common form of skeletal