A 9-year-old male patient with a history of backache was referred from a district hospital to the Dr George Mukhari Academic Hospital, Gauteng province, South Africa, due to severe upper back pain and gibbus (kyphosis) deformity that emerged over 8 months prior to admission. He had no history of tuberculosis contact or constitutional symptoms (cough or fever, loss of weight or loss of appetite).
Upon physical examination at admission, the patient was ambulatory but limping, had tenderness at the gibbus area, with pain in the waist. He was cooperative and appeared to have a normal skin condition. There was no Bacillus Calmette-Guerin scar observed. The neurological examination was normal and intact.
X-rays revealed kyphosis at the bottom of the thoracic spine (T12 vertebra) and the first vertebra of the lumbar spine (L1 vertebra). His T12 had vertebral destruction with preserved posterior elements. The L1 upper end plate and T12 lower end plate destruction with a peri-vertebral shadow were indicative of an abscess (Figure 1).
Plain radiography of the chest was unremarkable (Figure 2). Furthermore, the haemoglobin was low (11.5 g/dL), with a normal-range white blood cell count and an elevated C-reactive protein level of 18 mg/L. The erythrocyte sedimentation rate was a bit high at 20 mm/hour; alkaline phosphatase was 211 U/L. The alanine aminotransferase (19 U/L) and aspartate aminotransferase (31 U/L) were within the normal ranges. A serology test for HIV enzyme linked immunosorbent assay was negative. A superficial pus swab microscope analysis was acid-fast bacilli-negative when stained with auramine-O. An MGIT 960 culture was also negative after 42 days.
Magnetic resonance imaging of the entire spine revealed features suggestive of tuberculosis infection (Figure 3). There was kyphotic deformity and pre-vertebral fluid collection at T12/L1 extending to the epidural space. The fluid collection was low on T1, high on T2 and became enhanced post-contrast. There was also an abnormal signal of L1 and T12, as well as associated involvement of the superior end plate of L1. The T12/L1 intervertebral disc was not clearly delineated with the distortion of normal anatomy. Spinal canal stenosis was observed at the level of kyphotic deformity with cord compression, although there was spinal cord edema. Posterior elements were preserved and facet joints were normal (Figure 3).
A second set of the magnetic resonance images of the entire spine, which was done eight months later, revealed progression of the disease (infective process), increased kyphosis, and a paravertebral abscess, as well as complete destruction of lower and upper end plates of T12 and L1 with cord compression (Figure 4).
The patient was admitted and subsequently started on empirical first-line anti-tuberculosis treatment as recommended by the World Health Organization, as well as other supportive treatment, including thoracic lumber spinal orthosis. The patient did not improve clinically after 1 month of administering the empirical treatment.
Non-operative treatment included a thoracic lumber spinal orthosis brace, analgesia and first-line tuberculosis treatment to prevent further collapse and back care. The patient's mother consented to operative management, which included spinal decompression and posterior instrumentation, with rods and screws, as well as a biopsy. The patient was neurologically intact post-surgery (Figure 5). The operation was successful.
The pathological diagnosis of the spine (T12/L1) on the vertebral lesion biopsy revealed the presence of chronic necrotising granulomas with multinucleated Langhans-type giant cells. Ziehl-Neelsen staining, used to confirm acid-fast bacilli, was negative. The patient's first-line anti-tuberculosis treatment, included pyrazinamide, rifampin, isoniazid and ethambutol. The patient's condition deteriorated despite a total of 6 months of first-line anti-tuberculosis treatment, and the surgical wound started to open leaving space between the sides of the incision (gaping).
X-rays showed failed implants; therefore, the pedicular screws were backed off from the distal part of the vertebra (T12/L1) with increased kyphotic deformity of the spine (Figure 6).
When the patient was on rehabilitation, he developed an abscess on the forehead, which was later drained in the ward, and sent to the National Health Laboratory Services - Dr George Mukhari Academic Hospital tertiary laboratory for further mycobacteriological tests. Fluorescent microscopy of the smear stained with auramine-O was negative for fluorescing acid-fast bacilli. The MGIT 960 (Becton Dickinson Diagnostics, Sparks, Maryland, United States) culture was also negative after 42 days.
The patient was sent to surgery for incision and drainage of the abscess on the gibbus area, where from thick pus was drained and sent for tuberculosis microscopy, culture, line-probe assay (MTBDRplus assay, Hain Life Sciences, Nehren, Germany) and phenotypic MGIT 960 drug susceptibility testing. The auramine-O smear results were negative, whereas the MGIT culture was positive after 35 days. The line-probe assay result showed rifampin monoresistance, which was later confirmed by the phenotypic MGIT 960 drug susceptibility testing as rifampin monoresistant, ethambutol resistant and isoniazid sensitive after 9 months of first-line anti-tuberculosis treatment. The second-line MGIT 960 drug susceptibility testing showed that the isolate was susceptible to moxifloxacin and kanamycin. This led to an MDR tuberculosis diagnosis, since tuberculosis caused by rifampin-resistant strains is presumed to be MDR tuberculosis and treated as such (95% of rifampin-resistant strains are MDR). The patient was started on the MDR tuberculosis treatment, including moxifloxacin, ethionamide, amikacin, pyrazinamide, terizidone and pyridoxine; he started improving remarkably on the treatment and rehabilitation. At 15 months, the patient fully recovered and the implants were later removed.