Case report reveals longitudinal myelitis linked to nontuberculous mycobacterial infection in an immunocompetent male, indicating diagnostic challenges.
Introduction Central nervous system involvement of disseminated nontuberculous mycobacterial (NTM) infections in patients with HIV are usually rare and diagnostically challenging; patients usually present with pulmonary or other systematic manifestations. We present a case of a 41-year-old immunocompromised male who developed disseminated Mycolicibacter arupensis infection with associated longitudinal myelitis. Description 41-year-old male, never smoker, originally from Haiti, without known medical problems presented with acute metabolic encephalopathy associated with diarrhea, weight loss, fever and productive cough. The physical exam revealed flaccid paralysis of the lower extremities, urinary, and fecal incontinence. CT of the chest without contrast showed a right upper lobe consolidation. MRI of the brain and spine showed multifocal subcentimeter areas of parenchymal enhancement at the level of T12, L2, L3, L4, L5. Cerebrospinal fluid demonstrated a lymphocytic pleocytosis (257 WBC/µL), markedly elevated protein (600 mg/dL), and low glucose (29 mg/dL). CD4 count of 269 cells/µL. QuantiFERON was positive, however CSF and serum MTB PCR, serum HIV 1/2, HSV ½, HTLV I/II were negative. Initial interleukin-6 (25.51 pg/ml), CRP (4.1 mg/dl) and ESR (39 mm/hr) were elevated. At that time, disseminated Mycobacterium tuberculosis infection was suspected, and the patient completed two months of therapy with ethambutol, rifabutin, levofloxacin and clarithromycin. Despite extensive testing and therapy, the patient was not improving clinically. Finally, a bone biopsy which demonstrated non-necrotizing granulomas was sent for broad-range 16S rRNA sequencing and detected Mycolicibacter arupensis. Patient continued to receive supportive care and underwent a slow taper of dexamethasone, with a starting dose of 3mg/daily with improvement of neurological symptoms. Discussion This case underscores the difficulty of diagnosing NTM CNS infection, especially given the rarity of M. arupensis causing longitudinal myelitis. Molecular testing, including 16S rRNA sequencing, was pivotal for diagnosis. In our patient, disseminated M. arupensis infection was the unexpected cause of longitudinal myelitis. Although a positive Quantiferon initially suggested tuberculosis, repeated MTB cultures and PCR were negative, highlighting the diagnostic overlap between MTB and NTM infections. The diagnosis was confirmed only through molecular sequencing, underscoring the value of advanced diagnostics in culture-negative granulomatous disease. Disseminated M. arupensis should be included in the differential diagnosis of longitudinal myelitis patients, particularly when standard cultures and initial diagnostic studies are unrevealing.
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