A 42-year-old Chinese man was admitted to the hospital with a generalized seizure, which was witnessed. He recalled feeling twitching of his eyes and mouth prior to a brief period of loss of consciousness. The patient felt well after the episode, with the exception of fatigue. There was no fever, chills, headache, or visual disturbances.
The patient is from China, and has resided in the United States for 8 years. He has used intravenous heroin and alcohol but stopped 10 years previously. He smoked 1 package of cigarettes daily for 20 years.
Past medical history is significant for HIV, hepatitis B and C (HCV), all diagnosed 3 months prior to this admission when he presented with progressive swelling of the lower extremities and elevated blood pressure. A renal biopsy showed membranoproliferative glomerulonephritis. The initial CD4+ cell count was 389/mm3, quantitative HIV RNA 58,254 copies/ml and HCV viral load 202,489 IU/mL.
Treatment with dolutegravir and emtricitabine/tenofovir alafenamide was started 6 weeks previously, followed by sofosbuvir/velpatasvir.
On admission, the oral temperature was 99.30F, pulse 100 beats/minute, respiratory rate 16 breaths/min, blood pressure 155/104 mmHg and oxygen saturation 99% on room air.
Physical examination showed a laceration on the lateral aspect of the tongue and bilateral axillary lymphadenopathy. Neurological assessment revealed an alert and oriented patient with normal speech. No motor deficits were noted, and sensation was intact bilaterally. There was no facial weakness, and the tongue was midline. Cranial nerves were intact, with normal visual fields. Deep tendon reflexes were normal and symmetrical. No gait abnormalities were appreciated, and cerebellar function was intact.
The leukocyte count was 7900/UL, hemoglobin 10.2 g/dL, and platelet count 177,000/UL. Blood urea nitrogen was 16 mg/dL, and creatinine was 1.2 mg/dL. The erythrocyte sedimentation rate was greater than 145 mm/h. Cerebrospinal fluid (CSF) analysis showed 10 leukocytes/mm3, glucose of 45 mg/dL (serum glucose 90 mg/dL) and protein of 48 mg/dL. CSF cryptococcal antigen, VDRL and bacterial cultures were negative. Absolute CD4+ count was 343/mm3 and HIV RNA was undetectable. Hepatitis B viral DNA and hepatitis C RNA were undetectable.
Blood cultures, urine culture, urine toxicology and an echocardiogram were normal. Chest radiograph (CXR) was also normal. Parasitological investigation of stool samples did not reveal pathogens. The initial brain computed tomography (CT) showed numerous areas of white matter edema at the gray-white junction within the bilateral hemispheres, as well as in the left cerebellum (Fig. 1). Gadolinium-enhanced magnetic resonance imaging (MRI) revealed numerous small ring-enhancing masses with targetoid appearance and moderate surrounding vasogenic edema (Fig. 2). Serum cysticercus IgG and toxoplasma IgM and IgG antibodies were negative. Although the CXR was normal, the CT of the chest (Fig. 3) showed extensive lymphadenopathy, with bilateral apical airspace disease with tree-in-bud like appearance. Initial sputum acid-fast smears were negative.
An axillary lymph node biopsy showed granulomatous inflammation with necrosis. Acid fast and fungal stains were negative.
Treatment with isoniazid, rifabutin, ethambutol, and pyrazinamide was started. In addition, dexamethasone 0.3 mg/kg/day was given together with anti-tuberculous medication and gradually tapered over six weeks. The patient was discharged on hospital day 23. Three weeks later, the axillary lymph node and sputum cultures grew Mycobacterium tuberculosis.
Follow-up brain MRI with gadolinium five months later showed that nearly all of the previously demonstrated ring enhancing masses had decreased in size and markedly decreased surrounding vasogenic edema (Fig. 4). In addition, follow-up CT of the chest 2 weeks after initiation of treatment revealed partial resolution of the previously seen bronchial and bronchiolar inspissation in both upper lobes (Fig. 5).
Post-treatment computed tomography of the chest revealing partial resolution of the previously seen bronchial and bronchiolar inspissation in both upper lobes.