Pott's disease
Pott's disease is tuberculosis of the spine, usually due to haematogenous spread from other sites, often the lungs. The lower thoracic and upper lumbar vertebrae areas of the spine are most often affected. It was named for British surgeon Percivall Pott, who first described the symptoms in 1779.
It causes a kind of tuberculous arthritis of the intervertebral joints. The infection can spread 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. In a process called caseous necrosis, the disc tissue dies, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft-tissue mass often forms and superinfection is rare.
Spread of infection from the lumbar vertebrae to the psoas muscle, causing abscesses, is not uncommon.
Diagnosis
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. These symptoms can lead to limited and painful movement in all directions of the spine.The second most common clinical symptom is neurological deficits, which can vary depending on the level of the spine affected. An infection in the neck area can cause nerve problems affecting both the arms and legs, while an infection in the lower back typically affects only the legs and the area around the tailbone.
In the early stages of Pott's Disease, imaging techniques such as computed tomography, magnetic resonance imaging, or traditional radiography are utilized. For a radiolucent lesion to appear on a plain X-ray, there must be a 30% loss of bone mineral, making it difficult to diagnose the early stages of Pott's Disease with a plain radiograph. CT scans are often used as a guide for biopsies. Overall, it is widely documented that MRI is superior to plain radiographs in diagnosing Pott's Disease.
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. The typical lab procedure for clinical specimens involves an AFB stain.
The ESR and CRP are also used as biomarkers for spinal tuberculosis.
Other labs include:
- Blood tests
- * Complete blood count: leukocytosis
- * Elevated erythrocyte sedimentation rate: >100 mm/h
- Tuberculin skin test
- * Tuberculin skin test results are positive in 84–95% of patients with Pott disease who are not infected with HIV.
- Radiographs of the spine
- * Radiographic changes associated with Pott disease present relatively late. These radiographic changes are characteristic of spinal tuberculosis on plain radiography:
- Bone scan
- Computed tomography of the spine
- Bone biopsy
- MRI
Clinical presentation
Non-spinal symptoms include weakness, loss of appetite, weight loss, evening fever, and night sweats. Clinical findings include back pain, paraparesis, kyphosis, sensory disturbances, and bowel and bladder dysfunction. Signs of associated extraskeletal tuberculosis include cough, expectoration, swollen lymp nodes, diarrhea, and abdominal swelling.
The earliest and most common symptom is back pain, which worsens with activity. Muscles relax when asleep which causes pain. As the infection progresses, the pain becomes more severe leading to para-spinal muscle spasms. The spasms cause all spinal movements to be restricted and painful.
The second most common symptom is neurological deficits which depends on the location of the infection. If the cervical spine is affected, upper and lower extremities will show signs of dysfunction. If the infection is in the lumbar, deficits are localized to the lower extremities and sacral area. 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. Deficits progress from the front to the back, thus affecting the front of the spinal tract first. It heightens reflex and upper motor neuron deficit causing it to eventually advance to limb weakness and difficulty walking due to muscle spasms.
Pott's disease presents in children more frequently due to the increased vascularization of their spine. It also presents with back pain, neurological deficits, cold abscesses, and kyphosis deformities. In children, kyphosis is not limited to the disease being active, instead it increases or worsens in periods of growth, which further exacerbates other symptoms.
Certain presentations can cause abscesses to form, which puts the patient at a higher risk of spinal cord damage and possible paraplegia. The lesions responsible for abscesses occur more frequently in younger patients as their spine is highly vascularized compared to adults. Involvement of the front part of the spine or areas not involving the bone initially spares it and the disc of the spinal column. However, abscess formation allows disease to spread over multiple contiguous vertebrae using the front longitudinal ligament. These abscesses are granulomatous and, as they expand, lift the periosteum leading to bone devascularization, necrosis, and eventually deformity. Rear involvement follows a similar process but uses the longitudinal ligament in the back and often affects the neural arch. Paradiscal, central, and non-bone lesions account for 98% of all spinal TB cases, indicating that lesions originating in the back are much more rare.
Cold abscesses develop near lesions, and they are called 'cold' because they lack typical inflammatory signs like warmth and redness. They can grow significantly large which worsens the patient's symptoms. 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.
Pathogenesis
Infection of the lungs by the bacteria Mycobacterium tuberculosis eventually spreads through the host's body. Without treatment and diagnosis, the infection becomes dormant in the lungs or spreads to other parts of the body through hematogenous dissemination.When dissemination occurs, MTB enters the cancellous or spongy bone of the vertebra through the vascular system. It travels specifically from the front and back spinal arteries, and pressures within the torso spreads the infection throughout the vertebral body.
It impacts the front of the vertebral body along the subchondral plate. As it advances, progressive destruction occurs leading to vertebral collapse and kyphosis. The spinal canal may become narrowed due to abscesses, granulation tissue, or direct dural invasion resulting in compression of cord and neurological deficits. Kyphosis is a result of the front of the spine collapsing. Injury to the thoracic spine are more likely to result in kyphosis compared to lumbar spine injuries. A cold abscess can develop if infection spreads to ligaments and soft tissues. In the lower back, there is a chance the abscess can move down along the psoas muscle to the upper thigh and eventually break through the skin.
Transmission
MTB is contracted and spread through aerosol droplets. Respiratory MTB or tuberculosis have been documented in patients that have negative results for specific cultures. The sum of two cases concluded that about 17% of transmission occurs from patients who have negative results. Another study concluded that TB infection outside the lungs increased the transmission rate, which has always been overlooked.Risk factors
Some known risk factors for Pott's Disease include immunodeficiencies, exposure to infected patients, poverty, undernourishment, and lower socioeconomic status.HIV has been identified as one of the primary risk factors for the development of Pott's Disease and this is because HIV compromises the immune system by attacking and destroying crucial immune cells, thereby weakening the body's natural defenses. This impairment significantly reduces the body's ability to combat infections, including tuberculosis, making it more difficult for the body to fight off TB germs effectively. In regions like Sub-Saharan Africa, where the disease is prevalent, HIV often coexists with spinal TB, significantly complicating management and diagnosis. Data collected in New York and Los Angeles shows that this disease primarily affects foreign-born individuals, African Americans, Asian Americans, and Hispanic Americans.
Vitamin D deficiency has also been correlated with an increased risk of Pott's Disease, particularly spinal TB with caseous necrosis, increasing the risk of necrosis compared to individuals with normal vitamin D levels. A deficiency in vitamin D has been associated with the activation of tuberculosis for a long time. TB patients typically have lower serum vitamin D levels compared to healthy individuals. Extended TB treatment also leads to a reduction in serum vitamin D levels. 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.
In developed countries like the United States, Pott's Disease is primarily found in adults. However, in developing countries, data shows that Pott's Disease occurs mainly in young adults and older children. Crowded and poorly ventilated living and working conditions, which are often linked to poverty, significantly increase the risk of tuberculosis transmission. Undernutrition is another crucial factor that raises the likelihood of developing active TB. Additionally, poverty correlates with limited health knowledge and a lack of empowerment to utilize that knowledge, which results in greater exposure to various TB risk factors, including HIV, smoking, and alcohol abuse.