Granulomatous Amoebic Meningoencephalitis: A Diagnostic Dilemma

An 18-year-old male presented with headache since 30 days, right upper limb weakness and slurring of speech since 20 days and altered sensorium since 5 days. The headache was holocranial, persistent throughout the day, continuous, severe and associated with vomiting. The right-sided hemiparesis was acute in onset and gradually progressive, started with slurring of speech and right upper limb weakness which progressed over 10 days to involve the right leg. He could not recognize his relatives, eat or speak. On general physical examination, he was drowsy (E4 M5 V1), pulse was 64/minute, BP: 114/70 mm Hg and respiratory rate was 24/min. Central nervous system (CNS) examination revealed neck rigidity, right UMN 7th nerve palsy, spasticity in all four limbs (right > left) and plantars were bilateral and equivocal. The hemoglobin was 16 gm%, TLC was 29 × 103 with 90% polymorphs and the platelets were normal. Blood biochemistry revealed a serum creatinine of 2.4 mg%, blood urea of 133 mg%, serum bilirubin of 1.3 mg%, OT: 829, PT: 587, alkaline phosphatase: 123, albumin: 2.5 gm% and globulin: 1.6 gm%. The CSF done outside revealed 27 cells (25 lymphocytes); glucose: 72; protein: 65; ADA: 2.17. The CSF done in PGI revealed 20 cells (all lymphocytes); glucose: 71; protein: 130; cryptococcal Ag negative, culture negative, TB-PCR negative. CT brain done revealed gyri in left parietal lobe to appear bulky and hyperdense forming a focal lesion measuring 3.1 × 2.9 cm with surrounding white matter edema and postcontrast enhancement with central hypodensity. This was effacing the ipsilateral lateral ventricle, causing a midline shift of 3 mm to the right side. A similar lesion was seen in right parafalcine right frontal lobe measuring 1.3 × 0.8 cm. Leptomeningeal enhancement was seen in left frontoparietal temporal region. The impression was focal cerebritis with leptomeningitis in above described regions. MRI brain (Fig. 7) revealed multiple ill-defined heterogeneous intra-axial mass lesions seen in the left cerebellum, bilateral frontoparietal, left temporal and left occipital lobes. These lesions were appearing hypointense with faint hyperintensity within it on T1 and predominantly hyperintense on FLAIR/T2-weighted images. These lesions were showing blooming on SWI suggestive of hemorrhage within the lesions. On postcontrast scans, these lesions showed mild enhancement. Moderate perilesional white matter edema was seen around these lesions with lesion in left frontoparietal lobe producing mass effect seen as partial effacement of the left lateral ventricle with midline shift of about 5 mm. One of the mass is also involving the corpus callosum. A diagnosis of septic emboli/ tubercular meningitis was considered. He was managed with vancomycin and ceftriaxone. He was on antitubercular treatment since 24th Dec 2012, which was continued. He was also given antiedema measures with steroids. However, he did not improve and had further worsening of sensorium and expired on 5th Jan 2013. The unit’s diagnosis was multiple space occupying lesions abscesses with raised intracranial pressure (ICP).