[4] The most common and earliest clinical symptom of Pott's Disease is back pain, often associated with local tenderness, worsening muscle spasms along the spine, and focal edema.

Initial suspicion of Pott’s Disease is usually based on clinical symptoms and imaging findings, but a definitive diagnosis requires isolating the organism by culture, identifying it, and determining its drug susceptibility.

[6] These neurological symptoms are caused by direct pressure on nerves, invasion of neural tissue, tuberculous meningitis, dislocation or subluxation of vertebrae, or reduced blood flow to the spinal cord.

[6] It heightens reflex and upper motor neuron deficit causing it to eventually advance to limb weakness and difficulty walking due to muscle spasms.

[6] For example, if the primary lesion is located in the cervical spine, a cold abscess could form in the area behind the pharynx causing symptoms such as difficulty swallowing, breathing issues, or a hoarse voice.

The spinal canal may become narrowed due to abscesses, granulation tissue, or direct dural invasion resulting in compression of cord and neurological deficits.

[7] Some known risk factors for Pott's Disease include immunodeficiencies (such as those caused by alcohol and drug abuse or HIV), exposure to infected patients, poverty, undernourishment, and lower socioeconomic status.

[8] In regions like Sub-Saharan Africa, where the disease is prevalent, HIV often coexists with spinal TB, significantly complicating management and diagnosis.

Research has indicated that vitamin D plays a crucial role in modulating innate immune responses, acting as a cofactor in the induction of antimycobacterial activity.

[10] Crowded and poorly ventilated living and working conditions, which are often linked to poverty, significantly increase the risk of tuberculosis transmission.

Known risk factors like lower socioeconomic status, overcrowding, immunodeficiency, and interactions with people with tuberculosis can influence the rate of diagnosis.

[14] Underdeveloped countries have a higher incidence rate of Pott's disease as it is associated with less ventilated rooms, crowded spaces, poorer hygiene, and less access to healthcare facilities.

Increasing food security, reducing poverty, and improving living and working conditions will help to prevent infection and generally enhance the care of those sick.

[citation needed] Individuals who have use immunosuppressants or have compromised immune systems, chronic diseases like diabetes, or use tobacco have a significantly increased risk of becoming ill with tuberculosis infections.

[17] Guidelines from the WHO, CDC, and American Thoracic Society all present chemotherapy to be the first line when it comes to treatment of Pott's disease with surgical interventions being administered as needed for patients who are indicated for it.

Rehabilitation for patients who have just undergone surgery or are recovering from Pott's disease often consist of analgesics for pain management, immobilization of the affected spinal region, and physical therapy for pain-relieving modalities.

[17][22] The regimen usually consists of an initial 2-month intensive phase of Isoniazid (INH), Rifampin (RIF), Pyrazinamide (PZA), and Ethambutol (EMB).

[22] Surgical intervention is required for patients with Pott's disease in the event that there is a need for tissue sampling to clarify diagnoses, resistance to chemotherapy (often found in patients with HIV), neurologic deficits (including but not limited to abnormal reflexes, problems with speech, decreased sensation, loss of balance, decreased mental function, vision/hearing problems, and paraplegia), paravertebral abscesses formed from bacterial induced immune response, and kyphotic deformities leading to instability of the spine.

[23] However, surgery is up to shared clinical decision making and not an intervention that is defaulted to, as guidelines tend to lead towards less invasive procedures such as chemotherapy and anti-tuberculosis medications.

[24] Typical surgical techniques used are as follows: In posterior decompression and fusion with bone autografts, the goal is to relieve pressure on the spinal cord and nerves in the lower back and prevent the progression of kyphosis in active disease.

[26][27] In this procedure, the lumbar (lower back) vertebrae (L1-L5) are exposed and the intervertebral discs and vertebral material impinging on the spinal cord and/or nerves are removed.

[26] The vertebrae (typically L4-L5 due to their load bearing nature and vulnerability to degradation) are then fused together with grafts or instrumentation to help provide more support to the back and spine of the patient.

[28] In anterior debridement and decompression, tissue damaged by the onset of disease is removed along with vertebral elements and intervertebral discs that are impinging on the spinal cord and/or nerves in the spine.

[23][29] Due to the proportions of their bodies (larger head), limited muscular development, and increased flexibility, gravity can lead to greater deformation and presentation of kyphosis.

[29] Evidence of tubercular lesions of the vertebral column have been found from the fourth millennium BC in the form of Mesolithic remains in Liguria, Italy.

[35] Important milestones in the development, understanding, and management of tuberculosis spondylitis include the Bacilli Calmette Guerin (BCG) vaccination in 1945, radiological exams, and accessibility of necessary anti tubular medications in the mid 1900's.