Teaching Case

This 19-year-old female patient with no previous medical history presented to A & E with shortness of breath. Under the care of the respiratory physicians, she underwent investigations, including pleural biopsy, with no specific diagnosis ascertained.

She continued to have pyrexia of perceived unknown origin, therefore CT was performed.

Chest X-ray (CXR) on presentation demonstrated a large pleural effusion. No mediastinal lymphadenopathy (Figure 1).

Plain films of the thoracic spine showed very subtle end plate changes at T9-T10 suggestive of a possible disc centred pathology (Figure 2).

Contrast enhanced CT of the chest identified a left sided basal pleural effusion with thickened enhancing pleura (Figure 3). The CT also elucidated bony endplate destruction at T9/T10, prompting the recommendation for an MRI of the spine.

MRI of the whole spine was performed, including sequences following gadolinium.

This showed abnormal signal within the T8, T9, T10 and L4 vertebral bodies, along with high signal within the T9/T10 disc space with adjacent bony endplate destruction (Figure 4).

Following gadolinium the T8, T9, T10 and L4 vertebral bodies avidly enhance, along with a large paravertebral abscess, including in the prevertebral space, stretching the anterior longitudinal ligament (Figure 5).

Mycobacterium tuberculosis infection has increased in prevalence in recent years, typically in Asia and Africa, but also in developed countries, such as the UK. Typically mycobacterium tuberculosis is confined to the respiratory system. However, it is not uncommon for it to involve other sites, including the musculoskeletal system, in which it affects approximately 3% of infected patients [1, 3, 6].

TB spondylodiscitis is a tuberculous infection of the spine, typically the lower thoracic and upper lumbar (Pott's disease) and is the most common site of tuberculous osseous involvement [6]. Haematogenous spread of the bacillus is the cornerstone of pathogenesis. The infection starts as a spondylitis, involving the anterior endplates which contain complexes of end arterioles in which the bacilli become entrapped. It then spreads secondarily to the intervertebral disc, and then potentially beyond to the paravertebral tissues [7].

Typical clinical symptoms at presentation include; progressive back pain, local tenderness, night sweats, weight loss and fever [3, 5]. Physical examination and routine laboratory investigations may be relatively normal, making it more challenging to make an early correct diagnosis.

If not diagnosed early this disease often develops into serious complications, including kyphotic deformity. The most severe complications are; paraplegia, tetraplegia, hemiplegia or monoplegia. This may be caused by mechanical pressure on the spinal cord by an abscess, granulation tissue, tubercular debris and caseous tissue, or by mechanical instability secondary to subluxation or dislocation [4]. However, if diagnosed early, these can be prevented by treatment with anti-tuberculous medications.

The premier imaging modaility is MRI [6]. Plain X-rays are poor at detecting early changes of spinal TB. Typically infection starts at the anterior aspect of the vertebral body, resulting in end-plate oedema seen as reduced signal intensity on T1-weighted and high signal intensity on T2-weighted [6]. An image guided fine needle aspiration or biopsy may be required to aid diagnosis. There are three recognised patterns of vertebral body involvement. The patterns of vertebral body involvement may be (i) para-discal, (ii) anterior or (iii) central. The most common is para-discal [6]. A number of features are more characteristic of TB rather than pyogenic spondylodiscitis, which include; anterior corner destruction, relative sparing of the intervertebral disc, multi-level involvement with skip lesions, a large paraspinal abscess, calcification and thoracic level location [7].

The take home message is - the radiologist plays an important role in making the diagnosis of spinal TB, with MRI features that differentiate it from pyogenic infection.