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Pott Disease

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Pott Disease
Author: Jose A Hidalgo, MD; Chief Editor: Burke A Cunha, MD more... Updated: Jul 13, 2012

Background
Pott disease, also known as tuberculous spondylitis, is one of the oldest demonstrated diseases of humankind, having been documented in spinal remains from the Iron Age and in ancient mummies from Egypt and the Pacific coast of South America.[1] In 1779, Percivall Pott, for whom the disease is named, presented the classic description of spinal tuberculosis. (See the image below.)[2]

MRI of a 31-year-old man w ith tuberculosis of the spine. Images show the thoracic spine before and after an infusion of intravenous gadolinium contrast. The abscess and subsequent destruction of the T11-T12 disc interspace is marked w ith arrow heads. Vertebral body alignment is normal. Courtesy of Mark C. Diamond, MD, and J. Antonio Bouffard, MD, Detroit, Mich.

Since the advent of antituberculous drugs and improved public health measures, spinal tuberculosis has become rare in industrialized countries, although it is still a significant cause of disease in developing nations. Tuberculous involvement of the spine has the potential to cause serious morbidity, including permanent neurologic deficits and severe deformities. Medical treatment or combined medical and surgical strategies can control the disease in most patients.

Patient education
Patients with Pott disease should be instructed on the importance of therapy compliance. For patient education information, see the Infections Center, as well as Tuberculosis.

Pathophysiology
Pott disease is usually secondary to an extraspinal source of infection. Pott disease manifests as a combination of osteomyelitis and arthritis that usually involves more than 1 vertebra. The anterior aspect of the vertebral body adjacent to the subchondral plate is usually affected. Tuberculosis may spread from that area to adjacent intervertebral disks. In adults, disk disease is secondary to the spread of infection from the vertebral body. In children, the disk, because it is vascularized, can be the primary site.[3]
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Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canal can be narrowed by abscesses, granulation tissue, or direct dural invasion, leading to spinal cord compression and neurologic deficits. The kyphotic deformity is caused by collapse in the anterior spine. Lesions in the thoracic spine are more likely to lead to kyphosis than those in the lumbar spine. A cold abscess can occur if the infection extends to adjacent ligaments and soft tissues. Abscesses in the lumbar region may descend down the sheath of the psoas to the femoral trigone region and eventually erode into the skin.

Epidemiology
Occurrence in the United States
Although the incidence of tuberculosis increased in the late 1980s to early 1990s, the total number of cases has decreased in recent years. The frequency of extrapulmonary tuberculosis has remained stable. Bone and soft-tissue tuberculosis accounts for approximately 10% of extrapulmonary tuberculosis cases and between 1% and 2% of total cases. Tuberculous spondylitis is the most common manifestation of musculoskeletal tuberculosis, accounting for approximately 40-50% of cases.[4]

International occurrence
Approximately 1-2% of total tuberculosis cases are attributable to Pott disease. In the Netherlands, between 1993 and 2001, tuberculosis of the bone and joints accounted for 3.5% of all tuberculosis cases (0.2-1.1% in patients of European origin, and 2.3-6.3% in patients of non-European origin).[5]

Race-, sex-, and age-related demographics

Data from Los Angeles and New York show that musculoskeletal tuberculosis affects primarily African Americans, Hispanic Americans, Asian Americans, and foreign-born individuals. As with other forms of tuberculosis, the frequency of Pott Disease is related to socioeconomic factors and historical exposure to the infection. Although some series have found that Pott disease does not have a sexual predilection, the disease is more common in males (male-to-female ratio of 1.5-2:1). In the United States and other developed countries, Pott disease occurs primarily in adults. In countries with higher rates of Pott disease, involvement in young adults and older children predominates.[6, 7]

Prognosis
Current treatment modalities are highly effective against Pott disease if the disorder is not complicated by severe deformity or established neurologic deficit. Deformity and motor deficit are the most serious consequences of Pott disease and continue to be a serious problem when diagnosis is delayed or presentation of the patient is in advanced stages of the disease.[8] Therapy compliance and drug resistance are additional factors that significantly affect individual outcomes. Paraplegia resulting from cord compression caused by the active disease usually responds well to chemotherapy. However, paraplegia can manifest or persist during healing because of permanent spinal cord damage. Operative decompression can greatly increase the recovery rate, offering a means of treatment when medical therapy does not bring rapid improvement. Careful long-term follow up is also recommended, since late-onset complications can still occur (disease reactivation, late instability or deformity).[9]
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Morbidity
Pott disease is the most dangerous form of musculoskeletal tuberculosis because it can cause bone destruction, deformity, and paraplegia. Pott disease most commonly involves the thoracic and lumbosacral spine. However, published series have shown some variation.[10, 11, 12, 13] The lower thoracic vertebrae make up the most common area of involvement (40-50%), followed closely by the lumbar spine (35-45%). In other series, proportions are similar but favor lumbar spine involvement.[14] Approximately 10% of Pott disease cases involve the cervical spine.

Contributor Information and Disclosures

Author Jose A Hidalgo, MD Assistant Professor, Universidad Nacional Mayor de San Marcos; Attending Physician, Department of Internal Medicine, Division of Infectious Diseases, Guillermo Almenara Hospital, Peru Jose A Hidalgo, MD is a member of the following medical societies: HIV Medicine Association of America and Infectious Diseases Society of America Disclosure: Nothing to disclose. Coauthor(s) George Alangaden, MD Professor, Department of Internal Medicine, Division of Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine George Alangaden, MD is a member of the following medical societies: American College of Physicians Disclosure: Nothing to disclose. Chief Editor Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America Disclosure: Nothing to disclose. Additional Contributors Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, and Infectious Diseases Society of Ohio Disclosure: Nothing to disclose. Joseph F John Jr, MD, FACP, FIDSA, FSHEA Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment

References
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