Pott's disease
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]
Synonyms and keywords: Pott disease, spinal tuberculosis, skeletal tuberculosis
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pott’s disease or Pott disease is a presentation of extrapulmonary tuberculosis that affects the spine. The lower thoracic and upper lumbar vertebrae are most commonly affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal cord compression.
Historical Perspective
Pott’s disease is named after Percivall Pott (1714–1788), a London surgeon who trained at St Bartholomew’s Hospital, London.
Pathophysiology
Pott’s disease occurs usually due to hematogenous spread of tuberculous infection from a pulmonary or genitounrinary site. Pott’s disease usually involves more than one vertebra and manifests as a combination of osteomyelitis and arthritis. The involvement of the vertebra can be contiguous or non-contiguous based on the mode of spread.
Causes
Pott’s disease is caused by a bacterium called Mycobacterium tuberculosis or Mycobacterium bovis.
Differentiating Pott’s Disease from other Diseases
Pott’s disease presents with chronic back pain, swelling, spine deformity and neurological features in cord compression. All the following conditions present with similar features and must be differentiated from Pott’s disease. The differential include: spinal tumors, spinal cord abscess, Mycobacterium kansasii, nocardiosis, septic arthritis, metastatic cancer, multiple myeloma, miliary tuberculosis
Risk Factors
All the risk factors for developing Pott’s disease are the same as risk factors for developing in pulmonary tuberculosis. They include: HIV, overcrowding, immunosuppression, malnutrition, longterm corticosteriod use.
Natural History, Complications and Prognosis
If left untreated, Pott’s disease can cause severe vertebral deformity and collapse resulting in kyphosis, cord compression and paraplegia. With treatment the prognosis is good with improvement in the spine deformity and neurological deficit.
Diagnosis
History and Symptoms
The history and symptoms of Pott’s disease depends upon the stage of disease, affected site, and presence of complications. Back pain most common symptom of Pott’s disease. Other constitutional symptoms include fever, night sweating, anorexia, and weight loss.
Physical Examination
Physical examination findings suggestive of spinal tuberculosis include local tenderness on the spine, stiffness and spasm of the muscles, cold abscess demonstrates absence of signs of inflammation, limited range of motion, palpable gibbus, spine deformity, kyphosis. Neurologic findings include muscle weakness, quadriplegia, paraplegia, hypotonia, loss of deep tendon reflexes, numbness and paraesthesias.
X-Ray
Plain radiographs of the spine demonstrate changes suggestive of spinal tuberculosis in majority of the patients. The radiographic changes on plain X-Rays are not evident in the early stages of infection, therefore the changes are present in the late stages of the disease. Findings on the plain radiograph include rarefaction of the vertebral end plates, lytic destruction of anterior portion of vertebral body, collapse of the vertebral body, loss of disc height.
CT
CT scan of spine provides extent of involvement of the vertebral bodies, intervertebral disks, sclerosis, and osteoporotic vertebral end plates. It is helpful to detect early lesions and is more effective for defining the shape and calcification of soft-tissue abscesses.
MRI
MRI provides provides the extent of soft tissue involvement and the accurate dimensions of the abscess and its extent.
Other Imaging Findings
Radionuclide bone scanning may be done, but findings are not specific for Pott’s disease.
Treatment
Medical Therapy
Pott’s disease is treated with standard antitubercular therapy for a duration of 6 to 12 months. Compliance to the treatment should be monitored. Response to the treatment is assessed by the improvement of neurological function and reduction of the spinal deformity.
Surgery
Surgery is not the primary treatment option, but it is preferred in patients unresponsive to medical therapy and worsening neurological function. Surgical debridement is performed in such cases.
Primary Prevention
Pott’s disease can be prevented by controlling the spread of tuberculosis infection. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis.
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]
Overview
Pott’s disease is named after Percivall Pott (1714–1788), a London surgeon who trained at St Bartholomew’s Hospital, London.
Historical Perspective
- Spinal Tuberculosis is one of the oldest disease and was found in bone samples from five Iron age individuals recovered from a cemetry in Aymyrlyg, South Siberia. The spine lesions demonstrated a positive DNA PCR amplification for mycobacterium bovis, this shows that the infection was present 2000 years ago.[1]
- In 1779, Sir Percival Pott described the classic features of spinal tuberculosis: destruction of the intervertebral discs, body of the vertebra resulting in progressive kyphosis and named the disease Pott’s disease.[2]
References
- ↑ Taylor GM, Murphy E, Hopkins R, Rutland P, Chistov Y (2007). “First report of Mycobacterium bovis DNA in human remains from the Iron Age”. Microbiology. 153 (Pt 4): 1243–9. doi:10.1099/mic.0.2006/002154-0. PMID 17379733.
- ↑ Dobson J (1972). “Percivall Pott”. Ann R Coll Surg Engl. 50 (1): 54–65. PMC 2388056. PMID 4550865.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Aravind Kuchkuntla, M.B.B.S[2]
Overview
Pott’s disease occurs usually due to hematogenous spread of tuberculous infection from an extraspinal source. Pott’s disease usually involves more than one vertebra and manifests as a combination of osteomyelitis and arthritis.
Pathophysiology
Source of infection
- The primary source of infection is either from a pulmonary site or a genitourinary site.[1]
Mode of Spread
- Pott’s disease is a result of hematogenous spread of infection, to the cancellous bone of the vertebral body. The spread can be via the arterial or the venous route.[2]
- Normally, a rich vascular plexus is present in the sub-chondral region of each vertebrae. The blood supply is derived from anterior and posterior spinal arteries. The presence of rich vascular plexus facilitates the hematogenous spread of infection to the spine. The characteristic involvement is multiple contiguous vertebra is due to the blood supply, the segmental arteries from the anterior and posterior spinal arteries divide to form segmental arteries which supply two adjacent vertebra.[3]
- The Batson’s venous plexus is a valve-less venous system and the blood flow through the plexus is bi-directional which is depends on the pressure in the intra-abdominal and intra-thoracic compartments during exertion or activities which such as coughing.[4]
- The spread of infection via the intraosseous venous system causes central vertebral body lesions. Therefore, in patients with non contiguous spinal involvement or involvement of multiple vertebra, it signifies the infection spread is via the venous route.[5]
- The spread of infection below the anterior or posterior longitudinal ligaments affects multiple contiguous vertebrae.
Pathogenesis
- The infection in classic spinal tuberculosis initially affects the anterior aspect of the vertebral body adjacent to the subchondral plate. Then the infection spreads to the adjacent intervertebral discs.[6]
- The common site affected in spinal tuberculosis in children is the intervertebral discs due to the high vascularity. In adults or in old age the vertebral bodies are commonly affected due to age related avascularity.[7][8]
- The common lesions of vertebra in spinal tuberculosis include paradiskal, anterior, and central lesions.
- The most commonly involved sites are the upper lumbar and the lower thoracic vertebrae, the body of the vertebra is typically affected than the arch.[6]
- The infection results in the destruction of the intervertebral disc space and the adjacent vertebral bodies, collapse of the spinal elements, and anterior wedging resulting in a characteristic angulation and gibbus formation. Gibbus is a palpable deformity due to the involvement of multiple vertebra.[6]
- The destruction of the disc space and the wedging results in spinal deformity. Kyphosis is more prominent if the disc and bone destruction occurs in the thoracic spine due to the collapse in the anterior spine. The granuloma or the abscess can cause narrowing of the spinal canal leading to paraplegia secondary to cord compression.[7]
- In patients with anterior spinal tuberculosis, motor fibers are compressed first affecting the motor function. This is because the motor fibres are anteriorly placed in relation to the sensory fibers in spinal cord.
- In patients with posterior spinal tuberculosis, the motor fibers are compressed first again, and this is because the motor fibers are more susceptible to pressure and sensory fibers are susceptible to ischemia.[9]
Genetics
- A study of 109 patients in the china with spinal tuberculosis, showed higher frequencies of FokI polymorphism in the vitamin-D receptor gene of patients with tuberculosis when compared to controls.[10][11]
Microscopic Pathology
- Histologic examination of the biopsy specimen demonstrate epithelioid cell granulomas, lymphocytic infiltration and multinucleated Langhans giant cells.
References
- ↑ Rajasekaran S, Kanna RM, Shetty AP (2014). “Pathophysiology and Treatment of Spinal Tuberculosis”. JBJS Rev. 2 (9). doi:10.2106/JBJS.RVW.M.00130. PMID 27490153.
- ↑ Cooper C, Fellner R, Heubi O, Maixner F, Zink A, Lösch S (2016). “Tuberculosis in early medieval Switzerland–osteological and molecular evidence”. Swiss Med Wkly. 146: w14269. doi:10.4414/smw.2016.14269. PMID 26826871.
- ↑ Batirel A, Erdem H, Sengoz G, Pehlivanoglu F, Ramosaco E, Gülsün S; et al. (2015). “The course of spinal tuberculosis (Pott disease): results of the multinational, multicentre Backbone-2 study”. Clin Microbiol Infect. 21 (11): 1008.e9–1008.e18. doi:10.1016/j.cmi.2015.07.013. PMID 26232534.
- ↑ Formica M, Cavagnaro L, Formica C (2015). “Pott disease”. Spine J. 15 (3): 556–7. doi:10.1016/j.spinee.2014.11.006. PMID 25459741.
- ↑ Kim JH, Kim SH, Choi JI, Lim DJ (2014). “Atypical noncontiguous multiple spinal tuberculosis: a case report”. Korean J Spine. 11 (2): 77–80. doi:10.14245/kjs.2014.11.2.77. PMC 4124923. PMID 25110488.
- ↑ 6.0 6.1 6.2 Ekinci S, Tatar O, Akpancar S, Bilgic S, Ersen O (2015). “Spinal Tuberculosis”. J Exp Neurosci. 9: 89–90. doi:10.4137/JEN.S32842. PMC 4644140. PMID 26609247.
- ↑ 7.0 7.1 Kilborn T, Janse van Rensburg P, Candy S (2015). “Pediatric and adult spinal tuberculosis: imaging and pathophysiology”. Neuroimaging Clin N Am. 25 (2): 209–31. doi:10.1016/j.nic.2015.01.002. PMID 25952174.
- ↑ Tin SS, Wiwanitkit V (2014). “Noncontiguous multiple spinal tuberculosis”. Korean J Spine. 11 (4): 259. doi:10.14245/kjs.2014.11.4.259. PMC 4303286. PMID 25620992.
- ↑ Shim HK, Cho HL, Lee SH (2014). “Spinal tuberculosis at the posterior element of spinal column: case report”. Clin Neurol Neurosurg. 124: 146–50. doi:10.1016/j.clineuro.2014.05.021. PMID 25051165.
- ↑ Zhang HQ, Deng A, Guo CF, Wang YX, Chen LQ, Wang YF; et al. (2010). “Association between FokI polymorphism in vitamin D receptor gene and susceptibility to spinal tuberculosis in Chinese Han population”. Arch Med Res. 41 (1): 46–9. doi:10.1016/j.arcmed.2009.12.004. PMID 20430254.
- ↑ Panwar A, Garg RK, Malhotra HS, Jain A, Singh AK, Prakash S; et al. (2016). “25-Hydroxy Vitamin D, Vitamin D Receptor and Toll-like Receptor 2 Polymorphisms in Spinal Tuberculosis: A Case-Control Study”. Medicine (Baltimore). 95 (17): e3418. doi:10.1097/MD.0000000000003418. PMC 4998689. PMID 27124026.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.
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Overview
Pott’s disease is caused by a bacterium called Mycobacterium tuberculosis. The bacteria usually attack the lungs, but TB bacteria can attack any part of the body such as the spine, kidney, and brain. Pott’s disease is a presentation of extrapulmonary tuberculosis that affects the spine.
References
Differentiating Pott’s Disease from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Aravind Kuchkuntla, M.B.B.S[2]
Overview
Pott’s disease resembles spinal tumors, spinal cord abscess, septic arthritis, metastatic cancer, multiple myeloma, miliary tuberculosis. Therefore it must be differentiated from them.
Differentiating Pott’s Disease from other Diseases
Pott’s disease presents with features of back pain and myelopathy and must be differentiated from the following:
| Disease | Age of Presentation | Common site involved | Risk Factors | Clinical Features | Laboratory Findings | Imaging Findings |
|---|---|---|---|---|---|---|
| Pyogenic abscess of the spine | Any age | Lumbar spine | Diabetes mellitus |
| ||
| Pott’s Disease | Children and adults |
|
Exposure to tuberculous infection |
| ||
| Brucella abscess of the spine | Adults | Lumbar spine | Ingestion of unpasteurized milk |
| ||
| Vertebral Metastasis | Elderly | Thoracic spine | Presence of systemic malignancy |
|
|
Table adopted from Spinal Tuberculosis: A Review[1]
Additional differential diagnosis to be considered include:
- Spinal tumors
- Spinal cord abscess
- Septic arthritis
- Metastatic cancer[2]
- Multiple myeloma
- Miliary tuberculosis
References
- ↑ Garg RK, Somvanshi DS (2011). “Spinal tuberculosis: a review”. J Spinal Cord Med. 34 (5): 440–54. doi:10.1179/2045772311Y.0000000023. PMC 3184481. PMID 22118251.
- ↑ Mittal S, Khalid M, Sabir AB, Khalid S (2016). “Comparison of Magnetic Resonance Imaging Findings between Pathologically Proven Cases of Atypical Tubercular Spine and Tumour Metastasis: A Retrospective Study in 40 Patients”. Asian Spine J. 10 (4): 734–43. doi:10.4184/asj.2016.10.4.734. PMC 4995258. PMID 27559455.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Aravind Kuchkuntla, M.B.B.S[2]
Overview
Spinal tuberculosis is the most common extrapulmonary tuberculosis affecting the skeletal system affecting 10% of the patients with extra-pulmonary tuberculosis. Pott’s disease affects adults and is more common in males.
Epidemiology and Demographics
Incidence and Prevalence
- Skeletal involvement occurs approximately in 10% of patients with extrapulmonary tuberculosis.[1]
- Spinal tuberculosis is the most commonly affected site in skeletal tuberculosis and accounts for 50% of cases with skeletal tuberculosis.[1]
Age
Pott’s disease occurs primarily in adults in the United States and other developed countries. In developing countries, it occurs primarily in young adults and older children.[2]
Gender
Pott’s disease is more common in males (male-to-female ratio of 1.5-2:1).
Race
Pott’s disease primarily affects African Americans, Hispanic Americans, Asian Americans, and foreign-born individuals.
Developed Countries
In the Netherlands, musculoskeletal tuberculosis accounted for 3.5% of all tuberculosis cases between 1993 and 2001.
Developing Countries
There are nearly 6 million radiologically proven cases of tuberculosis in India. Of all the patients suffering from tuberculosis, nearly 1–2% have involvement of the skeletal system. Pott’s disease is the most common form of skeletal tuberculosis, and constitutes about 50% of all cases of skeletal tuberculosis.
References
- ↑ 1.0 1.1 Gautam MP, Karki P, Rijal S, Singh R (2005). “Pott’s spine and paraplegia”. JNMA J Nepal Med Assoc. 44 (159): 106–15. PMID 16570378.
- ↑ De la Garza Ramos R, Goodwin CR, Abu-Bonsrah N, Bydon A, Witham TF, Wolinsky JP; et al. (2016). “The epidemiology of spinal tuberculosis in the United States: an analysis of 2002-2011 data”. J Neurosurg Spine: 1–6. doi:10.3171/2016.9.SPINE16174. PMID 27982765.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Aravind Kuchkuntla, M.B.B.S[2]
Overview
Risk factors predisposing patients to develop spinal tuberculosis are same as the risk factors which predispose patients to develop pulmonary tuberculosis.
Risk Factors
Risk factors predisposing patients to develop spinal tuberculosis are same as the risk factors which predispose patients to develop pulmonary tuberculosis. The following is a list of risk factors which increase the risk of developing spinal tuberculosis infection:[1]
- Poverty
- Overcrowding
- Illiteracy
- Malnutrition
- Alcoholism
- Drug abuse
- Diabetes mellitus
- Immunosuppressive treatment
- HIV infection
- Older age
- Male gender
- Longterm peritoneal dialysis
- Prison imprisonment
Patients at high risk for developing TB and subsequently Pott’s disease are divided into two categories:
- Patients with recent tuberculosis infection:
- Close contacts of a person with infectious TB disease.
- Persons who have immigrated from areas of the world with high rates of TB.
- Children less than 5 years of age who have a positive TB test.
- Groups with high rates of TB transmission, such as homeless persons, injection drug users, and persons with HIV infection
- Persons who work or reside with people who are at high risk for TB in facilities or institutions such as hospitals, homeless shelters, correctional facilities, nursing homes, and residential homes for those with HIV.
- Patients with medical conditions associated with weakening of the immune system:
- Babies and young children often have weak immune systems.
- HIV infection (the virus that causes AIDS)
- Substance abuse
- Silicosis
- Diabetes mellitus
- Severe kidney disease
- Low body weight
- Organ transplants
- Head and neck cancer
- Medical treatments such as corticosteroids or organ transplant
- Specialized treatment for rheumatoid arthritis or Crohn’s disease
References
- ↑ McLain RF, Isada C (2004). “Spinal tuberculosis deserves a place on the radar screen”. Cleve Clin J Med. 71 (7): 537–9, 543–9. PMID 15320363.
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Aravind Kuchkuntla, M.B.B.S[2]
Overview
Pott’s disease may be complicated by severe vertebral deformity and collapse resulting in kyphosis, cord compression, and paraplegia. It responds well to treatment with improvement of the neurological function and spinal deformity.
Natural History
Spinal tuberculosis is one of the common extra-pulmonary manifestation involving the skeletal system. The common affected sites include the upper lumbar and lower thoracic spine. The infection affects the body of the vertebra or the the intervertebral discs. The progression of the disease is slow with a wide variation in the time of infection to manifest the clinical symptoms of the disease . The average disease duration ranges from 4 to 11 months. Patients take medical help when they develop severe pain, marked deformity or neurological symptoms.[1][2]
Complications
The destruction of the intervertebral disc, body of the vertebra and spread of the infection can result the following complications:[1][3][4]
- Vertebral collapse resulting in kyphosis
- Spinal cord compression
- Paraplegia (so called Pott’s paraplegia) or tetraplegia can result from spinal cord compression.
- Formation of a cold abscess when the infection spreads to the adjacent ligaments. [5]
- Cold abscess in the cervical spine, can cause the spread of infection to form a retropharyngeal abscess.
- The infection can spread to the mediastinum or trachea when the abscess develops in the thoracic spine.
- Infection can spread down the sheath of the psoas muscle to the femoral trigone to form a sinus .
Prognosis
Pott’s disease responds well to treatment with antitubercular treatment. Improvement in pain and neurological deficits are indicators for response to treatment. Prognosis is good in all patients, if a lack of improvement persists other differential must be considered. If other differentials are ruled out and medical therapy is not successful surgery is considered and it has good prognosis.[6]
References
- ↑ 1.0 1.1 Kumar K (2016). “Spinal tuberculosis, natural history of disease, classifications and principles of management with historical perspective”. Eur J Orthop Surg Traumatol. 26 (6): 551–8. doi:10.1007/s00590-016-1811-x. PMID 27435619.
- ↑ Ratnappuli A, Collinson S, Gaspar-García E, Richardson L, Bernard J, Macallan D (2015). “Pott’s disease in twenty-first century London: spinal tuberculosis as a continuing cause of morbidity and mortality”. Int J Tuberc Lung Dis. 19 (9): 1125, i–ii. doi:10.5588/ijtld.15.0091. PMID 26260836.
- ↑ Liu C, Lin L, Wang W, Lv G, Deng Y (2016). “Long-term outcomes of vertebral column resection for kyphosis in patients with cured spinal tuberculosis: average 8-year follow-up”. J Neurosurg Spine. 24 (5): 777–85. doi:10.3171/2015.8.SPINE15534. PMID 26745350.
- ↑ Batirel A, Erdem H, Sengoz G, Pehlivanoglu F, Ramosaco E, Gülsün S; et al. (2015). “The course of spinal tuberculosis (Pott disease): results of the multinational, multicentre Backbone-2 study”. Clin Microbiol Infect. 21 (11): 1008.e9–1008.e18. doi:10.1016/j.cmi.2015.07.013. PMID 26232534.
- ↑ de Araújo GC, Ferreira Junior Dde S, Escarso Junior Lda R, Gameiro VS (2014). “Spinal tuberculosis presenting with hip abscesses: a diagnostic challenge”. BMJ Case Rep. 2014. doi:10.1136/bcr-2014-205569. PMC 4173196. PMID 25253485.
- ↑ Patankar AP (2016). “Tuberculosis of spine: An experience of 30 cases over two years”. Asian J Neurosurg. 11 (3): 226–31. doi:10.4103/1793-5482.145085. PMC 4849291. PMID 27366249.
Diagnosis
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