A 33-year-old male, apparently healthy manual laborer, presented with history of intermittent fever associated with chills and rigors for 6 days and sudden onset of weakness in both the lower limbs, complete loss of sensations below the level of nipples and urinary retention for 5 days, prior to presentation to our hospital. There was no history of weight loss, loss of appetite, or chronic cough. He was febrile with a temperature of 100 F. The lower limbs were hypotonic with a power of 0/5, and absent deep tendon, superficial reflexes. Bilateral plantars were unelicitable. There was bilateral and complete loss of sensations to all modalities (touch, pin prick, temperature, and vibration) below D4 level. Perianal sensations were absent and anal sphincter was lax. Neck rigidity and Kernig's sign were negative. There was no spinal tenderness or lymphadenopathy. On the basis of sudden onset of flaccid weakness following a brief period of febrile illness, a working diagnosis of acute transverse myelitis (probably viral) was considered and was investigated further.
Complete hemogram, random and fasting blood sugars, total leukocyte count (9700/mm3), erythrocyte sedimentation rate (ESR 4 mm in 1st hour), and X-ray chest were normal. Enzyme-linked immunosorbent assay (ELISA) for human immunodeficiency virus (HIV) was negative. Blood culture and urine cultures were negative. Cerebrospinal fluid (CSF) was positive for antiherpes simplex type I immunoglobulin G (IgG) antibodies, varicella zoster IgG antibodies, antidengue virus IgG and IgM antibodies, which was suggestive of para-infectious acute transverse myelitis. However, CSF microscopic examination showed plenty of polymorphs, reduced sugars, and elevated proteins, which were unusual for viral etiology. No organism was grown on CSF culture. Plain and gadolinium contrast enhanced magnetic resonance imaging (MRI) scans of cervical spine; dorsal spine and screening of lumbar spine was performed. The MRI images showed mild thickening of the spinal cord from C4 to D2 level with hyperintensities in the T2W images, with no enhancement after gadolinium injection [Figure 1a and b]. This radiological picture of central T2 hyperintensity of spinal cord spanning greater than three segments along with the clinical presentation of sudden onset paraplegia with a sensory level and early bladder involvement simulated acute transverse myelitis. But a closer look at the screening MRI of lumbar spine (sagittal sections) revealed a small mass isointense to cord on both T1W and T2W images with no enhancement on contrast attached to conus and filum terminale. Plain and contrast enhanced MRI scans of lumbar spine were performed showing the lesion surrounded by cord matter [Figure 2]. Neutrophil preponderance in CSF and abnormal mass lesion in lumbar region prompted us for surgical exploration with a revised diagnosis of superadded bacterial infection (abscess) in an acute viral transverse myelitis.
Patient was immediately taken up for surgery with a plan to debride the area and obtain tissue for histopathology, culture and sensitivity. D12 to L3 laminectomy was performed and dura was opened. Arachnoid was thin, clear, and transparent. Yellowish, purulent material was seen loosely attached to conus medullaris and filum terminale through the intact arachnoid [Figure 3]. Arachnoid was opened. The CSF was clear. Yellowish, thick, slimy material was seen loose in the subarachnoid plane and on further evacuation was found attached to the conus but was easily separable with a jet of saline. The material was sent for histopathological examination, fungal, tubercular, and bacterial smears and cultures. Histopathological examination was suggestive of nonspecific inflammation with abundant neutrophils and few lymphocytes. KOH mount, gram stain, and smear for acid fast bacilli (AFB) and immunoflorescence staining for tubercular bacilli were negative. Bacterial (aerobic, anaerobic), and fungal cultures were negative. As the CSF was showing plenty of neutrophils and histopathological examination showed abundance of neutrophils, he was started on empirical IV antibiotics (Cefoperazone 2 g TID, amikacin 750 mg OD, and metronidazole 500 mg TID) with a provisional diagnosis of pyogenic abscess. After a week, patient complained of paraesthesias involving both the upper limbs. Repeat MRI scan of spinal cord showed evidence of increase in size of cervico-dorsal lesion, which by now had involved the cord from C4 to D12 (holocord). Patchy enhancement of meninges of dorsal spine (D2-D4) was seen [Figure 4a and b]. Cervico-dorsal laminectomy (C4-D4) was performed and cord was explored with multiple midline myelotomies at C5, C7, and D2 regions. There was yellowish-white cheesy material in the depth of white matter with no clear plane from surrounding neural tissue. Multiple biopsies were taken and were sent for culture and histopathological examination. Grams stain, fungal stains, and AFB smears were again negative. Cultures (as per protocol for aerobic, anaerobic, fungal, and tubercular) failed to grow any organism. Histopathological examination showed features of nonspecific inflammation with neutrophils. No granulomas or signs of demyelination were noted. He was continued on empirical antibiotics, supportive care for bowel, bladder, and back, low molecular heparin, and regular physiotherapy. At 6 weeks, tubercular culture in 12 B medium of BACTEC, 460 TB system showed growth of colonies, having sensitivity to all the first line drugs. Spinal tuberculosis was diagnosed and he was started on anti-tubercular drugs. He was further worked up for his immune status with total proteins, serum albumin, and CD4 counts were within normal limits. His Mantoux was 24 mm (strongly reactive). The patient is under constant follow up, but even at 8 months after starting anti-tubercular drugs, he failed to show neurological improvement.