A 41-year-old female patient was admitted to a local hospital abroad with a 4-week history of lower respiratory tract infection that had been refractory to antibiotic treatment. Several weeks after initial clinical improvement after intravenous antibiotics against pathogens commonly associated with community acquired pneumonia she developed headache, back pain, and fever. Due to an acute onset of spinal cord symptoms with paraparesis accompanied by bladder and bowel dysfunction she was transferred to our neurological department. Spinal magnetic resonance imaging (MRI) showed multiple contrast enhanced nodular masses along the leptomeninges in the cervical, thoracic, and lumbosacral segments of the spinal cord including the cauda equine and a myelopathy in the thoracic segment (Figures 1A1,A2). A lumbar puncture was performed and revealed an elevated cerebrospinal fluid (CSF) cell count (314 cells/mul), highly increased levels of protein (45,300 mg/l), a severe blood-CSF barrier dysfunction (Q-Albumin 694), and increased lactate concentration (7 mmol/l). Initially, neither bacterial (conventional cultural growth, mycobacterial cultures, Borrelia burgdorferi, and Treponema pallidum antibodies test), nor viral (herpes simplex virus, varicella zoster virus, cytomegalovirus, Epstein-Barr virus, enteroviruses, measles virus, rubella virus, tick-borne encephalitis, and JC virus), or fungal (cultural growth and antigen test to Aspergillus and Cryptococcus neoformans) pathogen could be detected in CSF. Laboratory testing for autoimmune causes such as connective tissue diseases (antinuclear antibodies, anti-DNA antibodies, antiphospholipid antibodies, antineutrophil cytoplasmic antibodies, and rheumatoid factor) was unremarkable. Computed tomography (CT) of the chest showed findings suggestive for tuberculosis (Figure 1C) and tuberculostatic therapy with ethambutol, rifampicin, isoniazid, and pyrazinamide was started. Histopathological examination of lung tissue obtained by bronchoscopic transbronchial biopsy revealed granulomas compatible with tuberculosis (Figures 1G,I).
Another spinal MRI after 2 weeks of treatment exhibited a slight progress in the extension of the nodular masses but a regress of myelopathy. CSF examination revealed a decreased cell count (195 cells/mul) accompanied by an unchanged severe blood-CSF barrier dysfunction (Q-Albumin 742).
Further analyses by using the polymerase chain reaction (PCR) technique detected the atypical Mycobacterium genavense in the lung tissue, while this was considered a possible contamination since retesting and cultural growth were negative for this pathogen. Cultural growth of sputum and bronchoalveolar lavage fluid revealed Serratia marcescens and Aspergillus fumigatus. Thereupon, cotrimoxazole, azithromycin, and voriconazole were added to patient's treatment. In addition, the patient was medicated with high-dose methylprednisolone to suppress inflammatory bystander reaction, which is considered responsible for developing granulomas.