A 45 year old Caucasian female with HIV infection, CDC-A3 and HCV, genotype 1b co-infection, Child-Pugh score 5, non-active IV drug habit, on 35 mg day of methadone, smoking habit of 20 cigarettes per day, nutritional disorder that had led recently to a loss of weight >10 kilos and on HIV treatment including tenofovir/emtricitabina and lopinavir/ritonavir was admitted to a local hospital complaining of fever which began a week prior as well as cough over the last 2 days. The patient was taking levofloxacin 500 mg day during the last week. Three months before admission immune-viral assays resulted being: HIV-RNA 71 copies ml, CD4 T 144 mm3. HCV-RNA resulted 780.000 copies ml. On admission, the liver was 5 cm below the costal margin, the erythrocyte sedimentation rate (ERS) was 78 mm 1  hour, hemoglobin 10.8 mg dl, white blood cells 4400 mm3, neutrophils 79.6%, coagulation, liver and renal functional tests were normal. A chest radiograph depicted micro nodular shadowing consistent with miliary TB. This finding was confirmed with a chest computed tomography (CT). A bronchoscopy did not show lesions. Bronco-alveolar lavage (BAL) fluid was negative for acid fast bacilli (AFB) and M. tuberculosis complex strand displacement amplification (SDA) was non-reactive. Culture subsequently identified multi-susceptible Mycobacterium tuberculosis. On the same day, in the absence of neurologic symptoms, cerebrospinal fluid (CSF) was examined leading to the diagnosis of a probable TB meningitis: glucose CSF 25 mg dl (blood glucose 99 mg dl), white cells 150 mm3 and proteins 273 mg dl, Ziehl-Neelsen (ZN), SDA and culture for M. tuberculosis resulted negative. CSF cultures for bacteria and fungi were also negative. Latex agglutination test for Cryptococcus resulted negative both on CSF and blood. Isoniazid 300 mg day, ethambutol 1200 mg day, pyrazinamide 1500 mg day, rifabutin 150 mg day and dexamethasone 4 mg per day were added to anti-retroviral therapy and levofloxacin. Four days later, the patient developed a right side stroke. A brain CT depicted a left frontal parietal cortical sub-cortical post ischemic high density lesion.
On admission to our Infectious Disease Clinic (IDC), 72 hours later, the patient was aphasic with right hemiplegia (Glasgow coma score non-applicable). Tuberculosis skin (TST) and gamma-interferon assay (IGRA) tests resulted negative. The repeated CD4 T cells count showed 72 cells mm3. The rapid plasma reagin treponemal test for syphilis was negative. Ultrasound of carotid arteries, EKG, trans-thoracic heart ultrasound, antinuclear antibodies, anti neutrophil cytoplasm antibodies, lupus anticoagulant factor and factor V Leiden were negative. Protein S, protein C, anti-thrombin III, homocysteine values were in the normal ranges. A repeated brain CT confirmed the fronto-parietal cortical sub-cortical ischemic lesion with minimal hemorrhagic transformation. Magnetic resonance (MRI) and angio-MRI (Figure 1) also depicted recent ischemic cortical sub-cortical lesion with minimal hemorrhagic transformation, absence of flow through the left middle cerebral artery and thickening as well as contrast enhancement on the left Sylvian fissure surrounding the artery. Thus, the patient was diagnosed with TBM complicated with stroke. The patient continued with tenofovir/emtricitabine and lopinavir/ritonavir plus isoniazid 300 mg day, ethambutol 1200 mg day, pyrazinamide 1500 mg day and rifabutin 150 mg day plus meropenem for the first 7 days, whereas corticosteroids and levofloxacin were suspended. Moreover, due to the presence of multiple risk factors for stroke and the absence of an absolute contraindication, aspirin100 mg day was administered. This was done despite the radiological findings evidenced microbleeds in the ischemic lesion. A percutaneus gastrostomy was performed as a nasal gastric tube was not tolerated. General and neurologic conditions improved while on anti-TB, anti-HIV and aspirin treatments. Two weeks later, CFS findings also improved: glucose 41 mg dl (blood glucose 93 mg dl), white cells 32 mm3, all lymphocytes, and proteins 174 mg dl, microscopic and culture for M. tuberculosis, bacteria and fungi were negative. Latex agglutination test for Cryptococcus test resulted once again negative. Real time polymerase reaction (PCR) for Toxoplasma gondii, Human poliomavirus JC-V, Herpes simplex virus type I and type II, Herpes virus type 8, Varicella Zoster virus, Cytomegalovirus resulted negative on CSF. The test for Cytomegalovirus antigen pp65 (Indirect Immunofluorescence, anti-CMV pp-UL83, Argene, Verniolle, France) in blood was also reported being negative.
Five weeks later, the patient was transferred to another hospital where the prescribed treatments and rehabilitation were continued with further improvement.