A 27 year-old African-American male was brought in by his family for altered mental status and possible seizure activity. The family stated that the patient had been complaining of a headache for one to two months. The family noted some mild behavioral and cognitive changes that had progressed over the last month. The week prior to presentation to our facility, the patient had an episode of slurred speech, facial droop, drooling, and seizure-like activity in the left upper extremity. The patient was taken to outlying emergency department (ED) but on arrival to the outside facility his symptoms had resolved. He was evaluated with basic labs and a non-contrasted computed tomography (CT) of the brain. He was discharged from the outside ED with a prescription for naprosyn and doxycycline. Over the next week, he had further behavior changes and became very lethargic. The family brought the patient to our facility for further evaluation at this time. The patient had no known past medical history and no prior surgeries. Current medications included naprosyn and doxycycline that he had received one week prior, no other home medications. Social history was significant for alcohol misuse for 10 years, tobacco use of 1 pack per day for 10 years and occasional marijuana use. The patient had just recently moved back to Tennessee to seek help from his family in quitting alcohol, after living in Texas and working as a bank teller for 7 years. No known travel outside of the country and no known contact with persons with communicable diseases. On physical exam he was well developed, well nourished, profoundly encephalopathic and diaphoretic. Temperature was 103 F, heart rate 87 beats/min, blood pressure 154/84 mmHg, respiratory rate 16 /min, and oxygen saturation 99% RA. His cardiovascular, pulmonary, and abdominal exams where unremarkable, skin was notable for significant diaphoresis without rash. He was unable to follow commands for a full neurologic exam but was confused and combative, moved all extremities spontaneously and with equal strength, and did exhibit significant photophobia or nuchal rigidity.
Initial laboratory data revealed leukocytosis of 11.7 th/mm3 with 92% neutrophils otherwise hemoglobin, hematocrit, and complete metabolic panel where within normal limits. Cerebral spinal fluid evaluation revealed WBC count of 302/mm3 with 98% lymphocytes, glucose 14 mg/dl, protein 144 mg/dl, and was clear in character. Chest x-ray and non-contrast CT of head where without significant pathology. After blood cultures had been obtained and initial CSF studies sent, the patient was place in the neurologic intensive care unit and started on broad spectrum antibiotics with vancomycin and piperacillin/tazobactam. Over the next twelve hours the patient was closely monitored and supportive care was continued as initial results began to return. Gram staining of CSF and blood was negative for bacteria and HIV, RPR, Cryptococcal antigen, HSV PCR where negative. The patient showed minimal mental status improvement within the first 24 hours and an MRI of the brain and Neurologic consult where obtained. MRI with and without contrast revealed right basilar meningeal enhancement with an acute right basil ganglia infarction (Figures 1,2). Given the characteristic finding of the CSF and MRI a PPD was placed and Infectious disease was consulted. PPD was read as negative at 48 hours by nursing staff and re-read as positive at 72 hours by an infectious disease physician. Initial direct smears of two separate samples of CSF where negative for acid fast bacilli, and PCR of the CSF was negative for TB on two different occasions. CT of the chest was obtained to look for possible source of infection and revealed right upper lobe nodules with central cavitations (Figures 3,4). Biopsy of the lung was performed and pathology revealed necrotizing granulomatous inflammation with acid fast bacilli (Figures 5,6). Initial concentrated direct smears for acid fast bacilli from the lung biopsy where negative, but Mycobacterium tuberculosis was isolated and identified by DNA probe with High Performance Liquid Chromatography at 32 days.
Treatment should be initiated on the basis of strong clinical suspicion. As mentioned previously it may take several repeated studies before obtaining positive proof of tuberculous infection and delay in treatment often leads to irreversible deficits or death. Recommended treatment is for 9-12 months and is divided into two phases. The intensive phase is four drug therapy with isoniazid (INH), rifampin (RIF), pyrazinamine (PZA), and either ethambutol (EMB) or streptomycin (STM) for two months followed by a continuation phase of INH and RIF for 7-10 months depending on clinical response and sensitivity of the specimen.
Once empiric TB coverage was started the patient showed significant clinical response with improvement of his mental status, but at the time of discharge still had prominent personality, memory, and functional impairment.
CT guided biopsy right lung nodule reveals acid fast bacilli (arrows).