Infections of the Spine: A Review of Clinical and Imaging Findings

Vikram K. Sundaram, MD; Amish Doshi, MD


Appl Radiol. 2016;45(8):10-20. 

In This Article

Tuberculous Spondylodiscitis

Clinical Findings

Tuberculous spondylodiscitis can be understood in contrast to pyogenic spondylodiscitis, both in terms of clinical features and regarding typical imaging patterns. Unlike pyogenic spondylodiscitis, which tends to have a more acute time course, tends to affect the lumbar spine, and tends to travel via arterial hematogenous spread or via direct inoculation, tuberculous spondylodiscitis has a more subacute or chronic time course, has a predilection for the thoracic spine, and more often demonstrate venous spread. Clinically, patients eventually diagnosed with tuberculous spondylodiscitis tend to be younger, to have only intermittent fevers, and on laboratory data show at most a mild elevation of CRP and ESR.[10] Due to its indolent spread and lack of clinical symptoms in the early phase, many patients can develop severe architectural damage related to their infection.

Imaging Findings

Plain Radiographs and CT. Early findings on plain radiographs include focal osteoporosis. Later, bony destruction, loss of intervertebral disc height, and soft tissue swelling with or without calcifications may indicate a more chronic process. As the disease advances, one expects reactive sclerotic changes and vertebral body collapse. In tuberculous spondylodiscitis, very progressed cases may demonstrate an extensive loss of vertebral body height with severe kyphotic angulation, known as a gibbus deformity.

The above sequence of findings can be seen with finer bony detail on dedicated CT imaging of the spinal column. Specifically, enhanced details of vertebral endplate destruction, subperiosteal lesions, sclerotic margins, and bony fragmentation can be better visualized with CT compared to plain radiographs. One imaging pattern that can distinguish tuberculous spondylodiscitis from pyogenic is the finding of loss of cortical definition of the vertebral bodies, a finding that is expected in advanced cases of tuberculous infection but is not as common in bacterial infections. The finding of a calcified paraspinal mass with thick, irregular rim enhancement is highly suggestive of tuberculous spondylodiscitis, and is a finding that would prompt percutaneous biopsy and later drainage of the abscess for diagnostic and therapeutic purposes respectively.

MRI. Unless discovered on incidental imaging, tuberculous spondylodiscitis is often imaged when the disease is at a more chronic stage. Like pyogenic spondylodiscitis, the radiologist can expect low T1 and high T2/STIR signal intensity abnormalities as indications of vertebral body edema, and contrast enhancement as an indication of inflammation. What distinguishes tuberculous spondylodiscitis from pyogenic spondylodiscitis on imaging is the pattern of infectious foci. Tuberculous spondylodiscitis tends to affect the anterior regions of the vertebral bodies, and often extends in a subligamentous path to the adjacent vertebral bodies, sparing the disc space (Figures 8). There is also a propensity for developing concomitant paraspinal abscesses. In chronic cases, expected vertebral body changes include bony fragmentation, anterior vertebral osteolysis with wedging, and in very advanced cases an extensive loss of vertebral body height with severe kyphotic angulation, known as the gibbus deformity (Figure 9).

Figure 8.

T1 precontrast (A), T1 postcontrast (B), DWI (C), and T2 FSE (D) sagittal sequences of the thoracic spine of a 72 yr-old man demonstrate disease at T4-T5 (A, B, C, and D, solid arrows), including paraspinal collection, epidural phlegmon, and severe spinal canal narrowing (D, dotted arrow). With no obvious discitis, this pattern can be found with tuberculous of fungal spondylitis.

Figure 9.

T1 postcontrast (A), T2 (B), and DWI (C) sagittal sequences of the thoracic spine of a 55-yr-old woman with history of HIV and previous MRSA osteomyelitis presenting with biopsy-proven tuberculous spondylodiscitis. Findings include T2 hyperintensity centered on collapsed T7 vertebral body, known as the "gibbus" deformity (A and B, solid arrows), classically due to tuberculosis. There is also epidural enhancement (A, dotted arrows).

Much like pyogenic spondylodiscitis, in resolving tuberculous spondylodiscitis the radiologist should expect normalization of low T1 signals and reduction in contrast enhancement, though persistent or even intermittent increase in contrast enhancement does not necessarily indicate deterioration or treatment failure. In these cases, imaging is best interpreted in conjunction with the clinical status of the patient. Some research shows that PET imaging with FDG can be helpful to monitor the progress of treatment regarding active foci of infection. In a 2015 case report, a patient was treated for a tuberculous psoas abscess that had extended from thoracic tuberculous spondylodiscitis. After abscess drainage and treatment with antibiotics for 6 months, PET-CT imaging demonstrated protracted FDG-18 accumulation at the site of vertebral body and psoas infection, suggesting incomplete resolution of tuberculous inflammation.[19] This fact was especially important given the current desire to limit the chance of producing resistant tuberculosis.

Follow-up Imaging

Since tuberculous spondylodiscitis tends to have a more chronic time course, follow-up imaging with CT and MRI tends to focus on documenting patterns of bony destruction, resolution of vertebral infectious foci, and resolution of paraspinal extension. Even after successful use of antibiotics (typically at least from 6 months to 1 year), sequelae of tuberculous spondylodiscitis can persist for years after treatments are completed. With current concerns of resistant strains of tuberculosis, demonstration of at least stability of post-infectious changes is valuable to the treating clinician.