Skeletal Tuberculosis

Skeletal tuberculosis
1 de 19
http://www.uptodate.com.wdg.biblio.udg.mx:2048/contents/skeletal-tube...
Official reprint from UpToDate

www.uptodate.com 2015 UpToDate
Authors
Malcolm McDonald, PhD, FRACP,
FRCPA
Daniel J Sexton, MD
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: 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 Potts 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 (Potts 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
03/08/2015 07:16 p.m.
2 de 19
multifocal bony involvement is present.

Spondylitis (Pott's disease) Tuberculous spondylitis (Potts 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 Potts 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) Poncets 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]. Poncets 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].
03/08/2015 07:16 p.m.
3 de 19
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:
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].
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].
03/08/2015 07:16 p.m.
4 de 19
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 Potts 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
03/08/2015 07:16 p.m.
5 de 19
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:
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].
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]:
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 [20,78]. In some circumstances, reconstructive surgery may be
03/08/2015 07:16 p.m.
6 de 19
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.)
03/08/2015 07:16 p.m.
7 de 19
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.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Daniel TM, Bates JH, Downes KA. History of tuberculosis. In: Tuberculosis: Pathogenesis, Protection, and
Control, Bloom BR (Ed), American Society for Microbiology, Washington 1994. p.13.
2. Hershkovitz I, Donoghue HD, Minnikin DE, et al. Detection and molecular characterization of 9,000-year-old
Mycobacterium tuberculosis from a Neolithic settlement in the Eastern Mediterranean. PLoS One 2008;
3:e3426.
3. Arriaza BT, Salo W, Aufderheide AC, Holcomb TA. Pre-Columbian tuberculosis in northern Chile: molecular
and skeletal evidence. Am J Phys Anthropol 1995; 98:37.
4. Donoghue HD, Lee OY, Minnikin DE, et al. Tuberculosis in Dr Granville's mummy: a molecular re-examination
of the earliest known Egyptian mummy to be scientifically examined and given a medical diagnosis. Proc Biol
Sci 2010; 277:51.
5. Watts HG, Lifeso RM. Tuberculosis of bones and joints. J Bone Joint Surg Am 1996; 78:288.
6. Sharma SK, Mohan A. Extrapulmonary tuberculosis. Indian J Med Res 2004; 120:316.
7. Teo HE, Peh WC. Skeletal tuberculosis in children. Pediatr Radiol 2004; 34:853.
8. Fanning A. Tuberculosis: 6. Extrapulmonary disease. CMAJ 1999; 160:1597.
9. Peto HM, Pratt RH, Harrington TA, et al. Epidemiology of extrapulmonary tuberculosis in the United States,
1993-2006. Clin Infect Dis 2009; 49:1350.
10. Pertuiset E, Beaudreuil J, Liot F, et al. Spinal tuberculosis in adults. A study of 103 cases in a developed
country, 1980-1994. Medicine (Baltimore) 1999; 78:309.
11. Fuentes Ferrer M, Gutirrez Torres L, Ayala Ramrez O, et al. Tuberculosis of the spine. A systematic review
of case series. Int Orthop 2012; 36:221.
03/08/2015 07:16 p.m.
8 de 19
12. Trecarichi EM, Di Meco E, Mazzotta V, Fantoni M. Tuberculous spondylodiscitis: epidemiology, clinical
features, treatment, and outcome. Eur Rev Med Pharmacol Sci 2012; 16 Suppl 2:58.
13. Vohra R, Kang HS, Dogra S, et al. Tuberculous osteomyelitis. J Bone Joint Surg Br 1997; 79:562.
14. Kaufmann SH, Cole ST, Mizrahi V, et al. Mycobacterium tuberculosis and the host response. J Exp Med 2005;
201:1693.
15. Ellner JJ. Review: the immune response in human tuberculosis--implications for tuberculosis control. J Infect
Dis 1997; 176:1351.
16. Lifeso R. Atlanto-axial tuberculosis in adults. J Bone Joint Surg Br 1987; 69:183.
17. Nussbaum ES, Rockswold GL, Bergman TA, et al. Spinal tuberculosis: a diagnostic and management
challenge. J Neurosurg 1995; 83:243.
18. Turgut M. Spinal tuberculosis (Pott's disease): its clinical presentation, surgical management, and outcome. A
survey study on 694 patients. Neurosurg Rev 2001; 24:8.
19. Weaver P, Lifeso RM. The radiological diagnosis of tuberculosis of the adult spine. Skeletal Radiol 1984;
12:178.
20. Lifeso RM, Weaver P, Harder EH. Tuberculous spondylitis in adults. J Bone Joint Surg Am 1985; 67:1405.
21. Khoo LT, Mikawa K, Fessler RG. A surgical revisitation of Pott distemper of the spine. Spine J 2003; 3:130.
22. Polley P, Dunn R. Noncontiguous spinal tuberculosis: incidence and management. Eur Spine J 2009; 18:1096.
23. Girdlestone GR, Somerville EW. Tuberculosis of Bone and Joint, 2nd ed, Oxford University Press, London
1952.
24. Hodgson SP, Ormerod LP. Ten-year experience of bone and joint tuberculosis in Blackburn 1978-1987. J R
Coll Surg Edinb 1990; 35:259.
25. Hopewell PC. Overview of clinical tuberculosis. In: Tuberculosis: Pathogenesis, Protection and Control, Bloom
BR (Ed), American Society for Microbiology Press, Washington, DC 1994. p.25.
26. Pigrau-Serrallach C, Rodrguez-Pardo D. Bone and joint tuberculosis. Eur Spine J 2013; 22 Suppl 4:556.
27. 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.
28. Kamara E, Mehta S, Brust JC, Jain AK. Effect of delayed diagnosis on severity of Pott's disease. Int Orthop
2012; 36:245.
29. Kumar K, Saxena MB. Multifocal osteoarticular tuberculosis. Int Orthop 1988; 12:135.
30. Kim SJ, Postigo R, Koo S, Kim JH. Total hip replacement for patients with active tuberculosis of the hip: a
systematic review and pooled analysis. Bone Joint J 2013; 95-B:578.
31. Isaacs AJ, Sturrock RD. Poncet's disease--fact or fiction? A re-appraisal of tuberculous rheumatism. Tubercle
1974; 55:135.
32. Sood R, Wali JP, Handa R. Poncet's disease in a north Indian hospital. Trop Doct 1999; 29:33.
33. Dall L, Long L, Stanford J. Poncet's disease: tuberculous rheumatism. Rev Infect Dis 1989; 11:105.
34. Kawsar M, D'Cruz D, Nathan M, Murphy M. Poncet's disease in a patient with AIDS. Rheumatology (Oxford)
2001; 40:346.
35. Cuende E, Almeida V, Portu J, et al. Poncet's disease and papulonecrotic tuberculid in a patient infected with
the human immunodeficiency virus. Arthritis Rheum 1998; 41:1884.
36. 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.
37. Spinner RJ, Sexton DJ, Goldner RD, Levin LS. Periprosthetic infections due to Mycobacterium tuberculosis in
patients with no prior history of tuberculosis. J Arthroplasty 1996; 11:217.
38. Zahraa J, Johnson D, Lim-Dunham JE, Herold BC. Unusual features of osteoarticular tuberculosis in children.
J Pediatr 1996; 129:597.
39. Rubinstien EM, Lehmann T. Sternal osteomyelitis due to Mycobacterium tuberculosis following coronary artery
bypass surgery. Clin Infect Dis 1996; 23:202.
03/08/2015 07:16 p.m.
9 de 19
40. Gondal GM, Mushtaq S, Masood R, et al. Mediastinal tuberculosis presenting with sternal osteomyelitis and
discharging sinus. J Postgrad Med Inst 2011; 25:379.
41. Platt MA, Ziegler K. Primary sternal osteomyelitis with bacteremia and distal seeding. J Emerg Med 2012;
43:e93.
42. Frouge C, Miquel A, Cochan-Priollet B, et al. Breast mass due to rib tuberculosis. Eur J Radiol 1995; 19:118.
43. Kim YT, Han KN, Kang CH, et al. Complete resection is mandatory for tubercular cold abscess of the chest
wall. Ann Thorac Surg 2008; 85:273.
44. Karanas YL, Yim KK. Mycobacterium tuberculosis infection of the hand: a case report and review of the
literature. Ann Plast Surg 1998; 40:65.
45. Hadfield PJ, Shah BK, Glover GW. Facial palsy due to tuberculosis: the value of CT. J Laryngol Otol 1995;
109:1010.
46. Gothwal S, Varshney P, Mathur S, Songra B. Tuberculosis of the pubic symphysis. BMJ Case Rep 2014; 2014.
47. Ormerod LP, Grundy M, Rahman MA. Multiple tuberculous bone lesions simulating metastatic disease.
Tubercle 1989; 70:305.
48. Muradali D, Gold WL, Vellend H, Becker E. Multifocal osteoarticular tuberculosis: report of four cases and
review of management. Clin Infect Dis 1993; 17:204.
49. Lynn MM, Kukanesen JR, Khan AW. Troublesome Tuberculosis: A Case Report on Multi-focal Tuberculous
Osteomyelitis in An Immunocompetent Patient. J Clin Med Res 2012; 4:73.
50. Yao DC, Sartoris DJ. Musculoskeletal tuberculosis. Radiol Clin North Am 1995; 33:679.
51. Phemister, DB, Hatcher, CH. Correlation of pathological and roentgenological findings in the diagnosis of
tuberculous arthritis. Am J Roentgenol 1933; 29:736.
52. Choi JA, Koh SH, Hong SH, et al. Rheumatoid arthritis and tuberculous arthritis: differentiating MRI features.
AJR Am J Roentgenol 2009; 193:1347.
53. Shanley DJ. Tuberculosis of the spine: imaging features. AJR Am J Roentgenol 1995; 164:659.
54. Jain R, Sawhney S, Berry M. Computed tomography of vertebral tuberculosis: patterns of bone destruction.
Clin Radiol 1993; 47:196.
55. Kim NH, Lee HM, Suh JS. Magnetic resonance imaging for the diagnosis of tuberculous spondylitis. Spine
(Phila Pa 1976) 1994; 19:2451.
56. Desai SS. Early diagnosis of spinal tuberculosis by MRI. J Bone Joint Surg Br 1994; 76:863.
57. Pui MH, Mitha A, Rae WI, Corr P. Diffusion-weighted magnetic resonance imaging of spinal infection and
malignancy. J Neuroimaging 2005; 15:164.
58. Jung NY, Jee WH, Ha KY, et al. Discrimination of tuberculous spondylitis from pyogenic spondylitis on MRI.
AJR Am J Roentgenol 2004; 182:1405.
59. Davidson PT, Horowitz I. Skeletal tuberculosis. A review with patient presentations and discussion. Am J Med
1970; 48:77.
60. Diagnostic Standards and Classification of Tuberculosis in Adults and Children. This official statement of the
American Thoracic Society and the Centers for Disease Control and Prevention was adopted by the ATS
Board of Directors, July 1999. This statement was endorsed by the Council of the Infectious Disease Society
of America, September 1999. Am J Respir Crit Care Med 2000; 161:1376.
61. Colmenero JD, Ruiz-Mesa JD, Sanjuan-Jimenez R, et al. Establishing the diagnosis of tuberculous vertebral
osteomyelitis. Eur Spine J 2013; 22 Suppl 4:579.
62. Merino P, Candel FJ, Gestoso I, et al. Microbiological diagnosis of spinal tuberculosis. Int Orthop 2012; 36:233.
63. Mondal A. Cytological diagnosis of vertebral tuberculosis with fine-needle aspiration biopsy. J Bone Joint Surg
Am 1994; 76:181.
64. Versfeld GA, Solomon A. A diagnostic approach to tuberculosis of bones and joints. J Bone Joint Surg Br
1982; 64:446.
65. Allali F, Mahfoud-Filali S, Hajjaj-Hassouni N. Lymphocytic joint fluid in tuberculous arthritis. A review of 30
cases. Joint Bone Spine 2005; 72:319.
03/08/2015 07:16 p.m.
10 de 19
66. Patwardhan SA, Joshi S. Laboratory diagnosis of spinal tuberculosis: Past and present. ArgoSpine News &
Journal 2011; 23:120.
67. American Thoracic Society, CDC, Infectious Diseases Society of America. Treatment of tuberculosis. MMWR
Recomm Rep 2003; 52:1.
68. Blumberg HM, Leonard MK Jr, Jasmer RM. Update on the treatment of tuberculosis and latent tuberculosis
infection. JAMA 2005; 293:2776.
69. 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 Med
2003; 167:603.
70. Surez-Garca I, Noguerado A. Drug treatment of multidrug-resistant osteoarticular tuberculosis: a systematic
literature review. Int J Infect Dis 2012; 16:e774.
71. A controlled trial of six-month and nine-month regimens of chemotherapy in patients undergoing radical
surgery for tuberculosis of the spine in Hong Kong. Tenth report of the Medical Research Council Working
Party on Tuberculosis of the Spine. Tubercle 1986; 67:243.
72. Upadhyay SS, Saji MJ, Yau AC. Duration of antituberculosis chemotherapy in conjunction with radical surgery
in the management of spinal tuberculosis. Spine (Phila Pa 1976) 1996; 21:1898.
73. A controlled trial of anterior spinal fusion and dbridement in the surgical management of tuberculosis of the
spine in patients on standard chemotherapy: a study in two centres in South Africa. Seventh Report of the
Medical Research Council Working Party on tuberculosis of the spine. Tubercle 1978; 59:79.
74. 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. Fourteenth
report of the Medical Research Council Working Party on Tuberculosis of the Spine. Int Orthop 1999; 23:73.
75. 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 on
Tuberculosis of the Spine. J Bone Joint Surg Br 1993; 75:240.
76. Ramachandran S, Clifton IJ, Collyns TA, et al. The treatment of spinal tuberculosis: a retrospective study. Int J
Tuberc Lung Dis 2005; 9:541.
77. Nene A, Bhojraj S. Results of nonsurgical treatment of thoracic spinal tuberculosis in adults. Spine J 2005;
5:79.
78. Upadhyay SS, Sell P, Saji MJ, et al. Surgical management of spinal tuberculosis in adults. Hong Kong
operation compared with debridement surgery for short and long term outcome of deformity. Clin Orthop Relat
Res 1994; :173.
79. Oguz E, Sehirlioglu A, Altinmakas M, et al. A new classification and guide for surgical treatment of spinal
tuberculosis. Int Orthop 2008; 32:127.
80. Garg N, Vohra R. Minimally invasive surgical approaches in the management of tuberculosis of the thoracic
and lumbar spine. Clin Orthop Relat Res 2014; 472:1855.
81. Jutte PC, Van Loenhout-Rooyackers JH. Routine surgery in addition to chemotherapy for treating spinal
tuberculosis. Cochrane Database Syst Rev 2006; :CD004532.
82. Zhang X, Ji J, Liu B. Management of spinal tuberculosis: a systematic review and meta-analysis. J Int Med
Res 2013; 41:1395.
83. Hoffman EB, Allin J, Campbell JA, Leisegang FM. Tuberculosis of the knee. Clin Orthop Relat Res 2002; :100.
84. Boxer DI, Pratt C, Hine AL, McNicol M. Radiological features during and following treatment of spinal
tuberculosis. Br J Radiol 1992; 65:476.
85. Kalita J, Misra UK, Mandal SK, Srivastava M. Prognosis of conservatively treated patients with Pott's
paraplegia: logistic regression analysis. J Neurol Neurosurg Psychiatry 2005; 76:866.
Topic 7658 Version 15.0
03/08/2015 07:16 p.m.
11 de 19
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
03/08/2015 07:16 p.m.
12 de 19
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.
03/08/2015 07:16 p.m.
13 de 19
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).
03/08/2015 07:16 p.m.
14 de 19
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.
03/08/2015 07:16 p.m.
15 de 19
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.
03/08/2015 07:16 p.m.
16 de 19
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.
03/08/2015 07:16 p.m.
17 de 19
Magnetic resonance imaging (MRI) of 17-year-old fisherman (coronal

section) showing a large tuberculous paraspinal abscess and pleural
involvement.
03/08/2015 07:16 p.m.
18 de 19
Post-surgical drainage and fixation of spinal

tuberculosis (Pott's disease)
Plain film of 17-year-old fisherman following surgical drainage and

spinal fixation.
03/08/2015 07:16 p.m.
19 de 19
Disclosures
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 [Medical
waste disposal systems]; Magnolia Medical Technologies [Intravenous devices]. Other Financial Interest: National Football League [Infection
control program]. Equity Ownership/Stock Options: Magnolia Medical Technologies [Intravenous devices]. C Fordham von Reyn, 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
03/08/2015 07:16 p.m.

Skeletal Tuberculosis

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Skeletal Tuberculosis

Uploaded by

Copyright:

Available Formats

Skeletal tuberculosis

Official reprint from UpToDate

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

multifocal bony involvement is present.

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

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

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

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

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

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

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

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

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

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

Pott's disease in an adult

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

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

Tuberculous arthritis of the left wrist with destructive changes in the

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

Tuberculosis of the right hip

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

Tuberculosis of the spine (Pott's disease)

Magnetic resonance imaging (MRI) with T1-weighted fat-saturated image

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

Tuberculosis of the spine (Pott's disease)

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

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

Tuberculosis of the spine (Pott's disease)

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

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

Post-surgical drainage and fixation of spinal

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

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

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

You might also like