A 40-year-old adult male labourer, who was a construction worker mainly engaged in the handling of construction materials, presented with a more than 4-month history of low back pain, pain radiating to the left limb (visual analogue scale score of 9; Oswestry Disability Index score of 70%), and left limb numbness, without symptoms of tuberculosis, such as fever, night sweats, or cough. A physical examination revealed weakness of the left limb of approximately grade IV, sensory disturbance in the left L4 and L5 area, and difficulty in stretching the left hip. The bilateral Achilles tendon and knee jerk reflexes were normal. There was localised tenderness in the lower lumbar spine. The patient had no medical history of tuberculosis, tumour, AIDS, operations, sarcoidosis, treatment with corticosteroids, or organ transplantation. His close relatives had no history of cancer, tuberculosis, Cryptococcus, or other diseases. He denied a past exposure to bird droppings or decaying wood. Therefore, we did not find the source of infection. Lumbar x-ray was performed, which showed that the left pedicle of L4 was unclear and was suspected to be bone destruction. Computed tomography (CT) revealed a lytic lesion at the L4 vertebrae. The entire left half of the vertebral body was involved. The left side of the L4 vertebral body was obviously damaged, and the lesion involved the paravertebral soft tissue. A single photon emission computed tomography (SPECT) scan showed increased uptake in the L4 vertebrae. SPECT did not find any further lesions except the L4 vertebra. Magnetic resonance imaging (MRI) revealed bone destruction in the L4 vertebral body and a portion of the spinal column enclosure. Sagittal T1-weighted MRI of the lumbar spine demonstrated areas of diffuse low signal intensity in L4. Sagittal T2-weighted MRI of the lumbar spine showed a high-intensity zone of oedema around the areas of isointensity in L4. The endplates of the L4 vertebral body were involved, and the upper and lower discs of the L4 vertebra were normal. A transverse MRI scan showed a paraspinal soft tissue lesion that looked like a tumour in L4 (Figure 1). Laboratory investigations revealed that the erythrocyte sedimentation rate (ESR) was 57 mm/h. C-reactive protein (CRP) and procalcitonin were normal. Blood counts, liver and renal function, and other serum chemistries were also normal. The enzyme linked immunosorbent assay (ELISA) test for AIDS was negative. We performed a needle biopsy surgery to identify the nature of the lesion. The pathologist found Cryptococcus in the lesion; thus, the pathological examination suggested cryptococcal infection. After needle biopsy surgery, we drew a sample of the patient's blood for cryptococcal antigen detection, which was positive. At the same time, the patient was examined by chest CT and brain MRI, and no abnormality was found. We suggested surgical treatment for the patient, but he was concerned about the risk of surgery, refused the operation, and required conservative treatment. The patient was referred to the infection department for antifungal therapy. However, in the course of antifungal treatment with oral fluconazole (400 mg/day) for approximately 2 weeks, the lower limb pain symptoms continued to worsen, so the patient returned to our department for surgical treatment. We performed a posterior approach surgery to remove the lesion and relieve spinal nerve compression.
This study was performed according to the guidelines of the Declaration of Helsinki and its amendments. Written informed consent was obtained from the patient for the publication of this study and any accompanying images.
Under general endotracheal anaesthesia, the patient was placed on the operating table in a prone position. At the affected section of the spine, a standard posterior middle approach was made. Through lateral subperiosteal dissection, the resected levels were exposed to the facet joints in the lumbar region. Pedicle screws were inserted one level above and below the lesion by the freehand technique. When inserting pedicle screws into the L4 vertebra, we found that the accessory structure of the left vertebral body had been destroyed so that pedicle screws could not be placed. Therefore, pedicle screws were not placed on the left side of the L4 vertebral body. After all pedicle screws had been inserted into the centre of the pedicles, the laminae, articular processes, and spinous processes at the level of the lesions were resected. The dura and L4 and L5 nerve roots were then carefully exposed. Then, the lesions were debrided by bone curettes and pituitary rongeurs. The lesions looked like jelly (Figure 2). Simultaneously, 360  decompression around the canal and roots was completed. We filled the lesion with a fluconazole-soaked gelatine sponge to provide local antifungal therapy and used longitudinal beams to connect with the pedicle screws to build a complete internal fixture. The resected lesions were histopathologically examined (Figure 3).
Mannitol (125 ml/day) and dexamethasone (10 mg/day) were administered intravenously for 3 days following surgery to relieve nerve root oedema and inflammation. The patient was administered oral fluconazole (400 mg/day) as an antifungal treatment. The patient left the hospital approximately 1 week after surgery. Three months following the spinal surgery, the patient reported relief of his symptoms and had returned to his normal preoperative activities. Physical examination revealed that the left limb strength, sensation in his left L4 and L5 areas, and left hip activity had returned to normal. His erythrocyte sedimentation rate was 41 mm/h, which is higher than normal. Twelve months postoperatively, follow-up MRI images of the lumbar spine showed a significant reduction of the lesion (Figure 4).