The International Journal of Mycobacteriology

: 2022  |  Volume : 11  |  Issue : 1  |  Page : 113--115

Pott's disease (tuberculous spondylitis)

InÍs Almeida Pintor, FlŠvio Pereira, Susana Cavadas, Pedro Lopes 
 Department of Internal Medicine, Aveiro Hospital Center, Portugal

Correspondence Address:
InÍs Almeida Pintor
Department of Internal Medicine, Aveiro Hospital Center, Avenida Artur Ravara, 3810-164, Aveiro


Pott's disease is a vertebral infection caused by Mycobacterium tuberculosis. Indolent nature and subacute course are associated with late diagnosis. A clinical case is presented whose diagnosis was delayed by atypical presentation with progressive worsening of symptoms. Magnetic resonance imaging (MRI) of the dorsolumbar spine revealed T7–T8 angulation suggestive of secondary injury, with intracanalar extension and spinal cord compression. Gastric aspirate cultures, direct microscopy, and polymerase chain reaction (PCR) were A 79-yearold female came to the emergency department with right back pain, pleuritic, with 12 h of evolution. Anorexia and weight loss,1 month evolution. Computed tomography (CT) of the dorsal spine revealed T7–T8 lytic lesions, suggestive of secondary nature. Objectively:weight loss and pain during thoracic palpation. Annalistically: normocytic/normochromic anemia, hypercalcemia, hepatic cholestasis, C-reactive protein (CRP) 7.12 mg/dL. Chest X-ray and electrocardiogram without alterations. She was admitted in Internal Medicine service. Analytically: hypophosphatemia, parathyroid hormone elevated, CRP 6 mg/dL, Beta-2 microglobulin elevated, dyslipidemia, iron and folicacid deficiency.negative for M. tuberculosis. T8 aspiration CT guided: cultures/direct microscopy negative, PCR positive for M. tuberculosis. Introductionof antitubercular drugs. Worsening of symptomatology, with paraparesia. MRI of the dorsal spine revealed spondylodiscitis and spinal cordcompression in T7–T8. Diagnosis revealed vertebral tuberculosis with spinal cord compression. She was transferred to neurosurgery servicefor surgical treatment. There was clinical and analytical improvement. Draws attention to difficulty in diagnose a treatable disease in a patientwith a rare presentation.

How to cite this article:
Pintor IA, Pereira F, Cavadas S, Lopes P. Pott's disease (tuberculous spondylitis).Int J Mycobacteriol 2022;11:113-115

How to cite this URL:
Pintor IA, Pereira F, Cavadas S, Lopes P. Pott's disease (tuberculous spondylitis). Int J Mycobacteriol [serial online] 2022 [cited 2022 Jul 6 ];11:113-115
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Full Text


Pott's disease (vertebral tuberculosis, tuberculous spondylitis) is an infectious vertebral disease caused by Mycobacterium tuberculosis, first described in 1779 by Percival Pott.[1]

The World Health Organization defines extrapulmonary tuberculosis (20%–25% of tuberculosis cases) as an infection affecting tissues and organs of pulmonary parenchyma, resulting from hematogenic and lymphatic dissemination.[2] Skeletal tuberculosis is responsible for 10%–35% of extrapulmonary cases and its most common form is Pott's disease (50%), followed by arthritis and osteomyelitis.[1],[3],[4]

Clinical presentation is local progressive pain, neurological and constitutional symptoms.[1],[4] It is subacute course is associated with delayed diagnosis and devastating consequences.[1]

We describe a case of Pott's disease with an atypical presentation, with a significant delay in diagnosis, as well as the need of extensive etiologic study.

 Case Report

A 79-year-old female presented to the emergency department with pleuritic back pain, at the right thoracic region, with 12 h evolution, without irradiation or known causing factor. Also referred anorexia and unintentional weight loss (5 kg) over the previous month. She was without fever, dyspnea, cough, sputum, or night sweats.

Medical history

Medical history included depression, osteoarthrosis, and nephrolithiasis. She was taking sertraline 25 mg and hydromorphone 16 mg. She had a family history of breast, gastric, and lung cancer.

Physical examination revealed thin aspect and painful palpation of the thoracic region, without anatomic abnormalities of the spine or movement limitation. Analytically: normocytic/normochromic anemia, hypercalcemia, hepatic cholestasis, and elevated C-reactive protein (CRP) [Table 1].{Table 1}

Computed tomography (CT) of the thoracic spine revealed lytic lesions in T7–T8 vertebrae, suggesting secondary nature. BrainCT, abdominal ultrasonography, colonoscopy, endoscopy, mammography, breast ultrasound, chest radiography, and electrocardiogram without alterations.

She was admitted in Internal Medicine Service for etiological investigation and pain control.

Repeated analytical study [Table 1], with hypophosphatemia, parathyroid hormone elevated, CRP decreasing, Beta-2 microglobulin elevated, and dyslipidemia. Negativetreponemal and serologic testing (hepatitis B and C, humanimmunodeficiency virus).

Thoraco-abdominopelvic CT with micronodularity of upper pulmonary lobes, predominantly at left. Magnetic resonance imaging (MRI) of the dorsolumbar spine revealed T7–T8 lesions suggesting secondary nature, angulation, and intracanalar extension.

Considering the suspicion of tuberculosis, gastric aspirate was collected. It was negative for M. tuberculosis in direct microscopy, culture, and polymerase chain reaction (PCR).

She was submmited to CT-Guided biopsy of the lytic lesionsin T7-T8; the sample was sent to histopathological study that revealed inespecific necrosis. T8 lesion aspiration was guided by fluoro-CT with purulent fluid drainage that was positivefor M. tuberculosis in PCR assay. The diagnosis of vertebral tuberculosis was made, and the patient started antitubercular drugs: rifampicin, ethambutol, pyrazinamide, and isoniazid.

The patient presented new-onset paraparesis (muscle strength Grade 4 in both lower limbs) as well as intense pain. Repeated MRI of the dorsal spine revealed spondylodiscitis involving T6–T7–T8 vertebrae and respective vertebral disc that were collapsed, causing spinal cord compression.

She was transferred to Neurosurgery Service with the diagnosis of tuberculous spondylodiscitis with spinal cord compression. Was submitted to surgical intervention.

Follow-up was conducted on external consultation. Antitubercular drugs and pyridoxine were maintained for 9 months, as well as transdermal fentanyl 100 mcg, pregabalin 50 mg twice daily, and physical therapy, with functional improvement and decreasing pain level.


During primary infection, the hematogenous and lymphatic spread can lead to extrapulmonary seeding of M. tuberculosis. Usually, infection is subclinical, as adaptive and cellular immune processes confine it to foci.[5] Extrapulmonary tuberculosis can occur with foci reactivation after primary infection, frequently in latent tuberculosis.[3]

Pott's disease most commonly affects the lower thoracic region in younger patients and the upper lumbar region in older patients.[1],[3]

Usually, infection begins at the anterior aspect of the vertebral body. Once two vertebrae are involved, the intervertebral disc is also affected with necrosis, vertebral narrowing, collapse, and Gibbus deformity (a form of kyphosis) with risk of spinal cord compression. Infection can spread to adjacent soft tissues, with paravertebral abscesses that can also cause spinal cord compression.[1],[3]

The most common symptom is local pain, increasingly intense over weeks or months, associated with muscle spasm and rigidity. Neurological alterations suggestive of spinal cord compression can also occur, as well as constitutional symptoms (fever and weight loss).[1],[4] Movement limitation and kyphosis may also occur.[4]

The diagnosis of skeletal tuberculosis is particularly difficult, as samples of affected tissue are difficult to obtain. Imaging studies are very important, although they have low specificity.[4]

Radiography may locate lesions and evaluate the extension of the disease, but there are no pathognomonic findings.[3] Suggestive findings (demineralization and loss of definition of bony margin) are usually in the anterior aspect of vertebral body.[6] Commonly two adjacent vertebrae are involved. Progression may cause anterior collapse and Gibbus deformity.[1],[4] Some have lytic lesions without involvement of the vertebral disc.[6]

CT, myelography, and MRI are also useful in establishing a diagnosis, particularly MRI, as it identifies soft-tissue involvement and spinal cord compression.[1],[3]

To diagnose tuberculosis, common specimens are sputum and gastric aspirate. If there is suspicion of vertebral tuberculosis, a CT-guided aspiration of the lesion should be collected.[2],[3],[7],[8] Culture is the preferred method of identification, but it takes up 2–6 weeks. Identification can also be made by PCR, if there is high suspicion. Histological features include necrotizing granuloma or central area of caseous necrosis.[3]

Diagnosis is difficult and usually associated with a significant delay, either for progressive and indolent nature or for capacity to mimic another diseases, such as primary/metastatic neoplasm, traumatic injury, osteoporosis, bacterial/fungal infections, Paget's disease, and others.[4]

Treatment of tuberculous spondylitis consists of antimicrobial therapy or surgical intervention.

Treatment includes the same regimen used for pulmonary tuberculosis but should be prolonged, as there is a risk of recurrence with short cycle therapy.[2],[3],[9],[10] The ideal duration is not known, but usually, 6–9 months of first-line antitubercular drugs are recommended.[2]

Surgical intervention is recommended in cases of therapeutic failure, abscess/fistula, spinal instability, or compression of the spinal cord with neurological deficits,[1],[2],[3] which includes decompression, use of devices for spine stabilization, abscess drainage, or infected material debridement.[1]


This case highlights the difficulty in establishing the diagnosis of vertebral tuberculosis, owing to the need of exclusion of other diseases, such as primary or metastatic neoplasm, traumatic, infections, or others. This is a potentially curable disease, with the resolution of symptoms after effective treatment.

It is important to note the less frequent presentation with lytic lesions in atypical localization. Doctors should be alert to infrequent presentations of diseases in order to reduce delays in diagnosis and treatment and prevent worsening of symptoms.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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