u REVIEW Tuberculous Brain Abscess in a Patient with HIV Infection: Case Report and Review David J. Farrar, MB, BS, MPH, Timothy P. Flanigan, MD, Norman M. Gordon, MD, Richard L. Gold, MD, Josiah D. Rich, MD, MPH, Providence, Rhode Island S ince 1986, the human immunodeficiency virus (HIV) epidemic in the United States has been as- sociated with a resurgence of tuberculosis, causing substantial mortality in patients with the acquired immunodeficiency syndrome (AIDS). ‘z2 In particular, the increased incidence of extrapulmonary manifes- tations has complicated the diagnosis and early treatment of tuberculosis.3 Much of the resurgence has occurred among HIV-infected drug users in large cities, the diagnosis of tuberculosis often constitut- ing their initial AIDS-defining condition.4a5 HIV infec- tion in intravenous drug users increases the risk of active tuberculosis.‘j This most commonly results from the reactivation of latent tuberculosis infection, but the risk of disease from recent person-to-person transmission is also increased.7-‘0 Tuberculosis, in turn, accelerates the course of HIV disease progres- sion.” Both HIV-infected individuals and injection-drug users are also at increased risk of disease caused by multidrug-resistant strains of Mycobacterium tuber- culosis.‘2 Drug resistance increases the likelihood of treatment failure and relapse, and further spread of tuberculosis, thereby complicating both the treat- ment of infected individuals and the public health measures needed to control tuberculosis.‘3m17 The clinical presentation of tuberculosis in pa- tients with HIV infection varies considerably de- pending on the degree of immunosuppression, with atypical features occurring more frequently at low CD4 T lymphocyte counts.” Where immune function is preserved, classical chest radiograph findings of reactivation tuberculosis such as cavitation and up- per-lobe infiltrates may occur. With HIV-induced im- munosuppression, tuberculosis often involves dif- fuse pulmonary infiltrates, pleural effusions, or hilar lymphadenopathy. Most strikingly, in patients with advanced HIV disease, there is a high frequency of extrapulmonary tuberculosis: extrathoracic lymph- adenopathy, miliary disease, and central nervous Am J Med. 1997; 102:297-301. From the Department of Medicine, The Miriam Hospital, Brown Univer- sity School of Medicine, Providence, Rhode Island. Requests for reprints should be addressed to Josiah D. Rich, MD, The Miriam Hospital, 164 Summit Avenue, Providence, Rhode Island 02906. Manuscript submitted July 19, 1996 and accepted in revised form Oc- tober 23, 1996. 01997 by Excerpta hledica, Inc. ooo2-9343/97/$17.00 297 All rights reserved. PII SOOO2-9343(97)00386-5 system (CNS) tuberculosis, with or without evidence of pulmonary involvement.‘s-21 A variety of CNS complications occur in patients with HIV infection. 22 In patients with tuberculosis, the rate of CNS involvement is five times higher if they have HIV coinfection.23 As the incidence of HIV and tuberculosis coinfection increases, CNS tuber- culosis may be seen more frequently. There is a wide differential diagnosis of focal CNS lesions in HIV-infected patients, including cerebral toxoplasmosis, primary CNS lymphoma, progressive multifocd leukoencephalopathy (PML), focal viral encephalitis (cytomegalovirus,24 varicella-zoster vi- rus, herpes simplex virus), bacterial abscess, and cryptococcoma. 25 We report the case of a tubercu- losis brain abscess in an intravenous drug user with HIV infection and review the literature. CASE REPORT In December 1992, a 43-year-old previously healthy [white] man, with a history of intravenous drug use, came to us after a focal seizure. He de- scribed involuntary movement of the left leg, spreading to the left thigh and left upper extremity, and progressing to more generalized movements with eventual loss of consciousness. Similar move- ments, confined only to the left leg, had occurred during the previous few weeks. Neurological ex- amination on presentation was unremarkable, without any focal abnormality. Brain magnetic res- onance imaging (MRI) showed a ring-enhancing mass with surrounding edema in the right parietal region (Figures 1 and 2). Investigations revealed that he was HIV seropositive with a CD4 T lym- phocyte count of 150/mm3. These findings were considered consistent with cerebral toxoplasmo- sis, and he was treated empirically with pyrime- thamine and sulfadiazine. Lumbar puncture was not performed and toxoplasma serology was un- available during his initial hospital stay. His focal seizures continued, and 3 weeks later, he was hospitalized. He had developed weakness of the left upper and lower extremities and left-sided par- asthesiae. Repeat MRI showed that his brain lesion had doubled in size despite 14 days of antitoxoplas- mosis therapy (Figures 3 and 4). Toxoplasma IgG was undetectable. There was no history of tubercu- losis or known contact with tuberculosis. Chest