SEMINARS IN NEUROLOGYVOLUME 20, NO.

3 2000

Brain Abscess
David P. Calfee, M.D. and Brian Wispelwey, M.D.

ABSTRACT
The epidemiology of brain abscess has changed with the increasing incidence of this infection in immunocompromised patients, particularly solid organ and bone marrow transplant recipients, and the decreasing incidence of brain abscess related to sinusitis and otitis. A number of new neuroimaging modalities, including single photon emission computed tomography, positron emission tomography, perfusion magnetic resonance imaging, and magnetic resonance spectroscopy, provide an initial noninvasive approach to diagnosis. The recommendations for the management of intracranial mass lesions in human immunodeficiency virusinfected individuals has changed as the incidence of toxoplasmic encephalitis has decreased with the use of trimethoprim-sulfamethoxazole prophylaxis. The epidemiology, pathogenesis, microbiology, clinical presentation, diagnosis, treatment and prognosis of brain abscess in the beginning of the 21st century are provided in this review. Keywords: Central nervous system, abscess, immunosuppression

A brain abscess is a focal suppurative infection within the brain parenchyma. Although rare, it is one of the most common intracranial suppurative processes. Although some controversy exists regarding optimal management of the patient with a brain abscess, modern scientific advances in diagnostic and treatment modalities have greatly improved the prognosis of this once universally fatal disease.

EPIDEMIOLOGY Approximately 1500 to 2500 cases of brain abscess are diagnosed in the United States each year.1 Population studies spanning five decades determined an incidence rate of 1.3 per 100,000 person-years.2 This study found that the incidence of brain abscess has decreased during this century from 2.7 (1935 to 1944) to 0.9 (1965 to

Objectives On completion of this article the reader will be able to outline the current concepts of the epidemiology, diagnosis, and management of brain abscess. Accreditation The Indiana University School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Credit The Indiana University School of Medicine designates this educational activity for a maximum of 1.0 hours in category one credit toward the AMA Physicians Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the educational activity.

Disclosure Statements have been obtained regarding the authors relationships with financial supporters of this activity. There is no apparent conflict of interest related to the context of participation of the author of this article.

Department of Medicine, University of Virginia School of Medicine, Charlottesville, Virginia. Reprint requests: Dr. Wispelwey, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA 22908. Copyright 2000 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. +1(212) 584-4662. 0271-8235,p;2000,20,03,353,360,ftx,en;sin00085x.

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SEMINARS IN NEUROLOGY VOLUME 20, NUMBER 3 2000

MICROBIOLOGY The vast majority of brain abscesses that occur in patients with intact immune systems are bacterial (Table 1) and are frequently (approximately 60%) polymicrobic with an average of 1.5 organisms per patient.1,3,4,13 There is a slight predominance of aerobic bacteria, although 33 to 49% of isolates in some series have been anaerobes.3,13 Streptococcal species, making up approximately one third of the aerobic organisms isolated from brain abscesses, are found in nearly 70% of all brain abscesses. Members of the Streptococcus milleri group are the most commonly identified species. Staphylococcus aureus is found in 10 to 31% of bacterial brain abscesses and is most commonly found in the settings of penetrating head injury and neurosurgical infections.1,4,13 Enteric gram-negative rods are found in 10 to 20% of cases. Bacteroides and Fusobacterium species are the most commonly isolated anaerobic organisms. Peptostreptococci, clostridia, and propionibacteria are found less frequently. The rates of sterile cultures, often the result of antibiotic administration prior to the abscess drainage procedure, have ranged from 3.2 to 48.6%.1,4,25 The microbiology of brain abscesses in immunocompromised individuals is dependent upon the type of immune deficit (Table 2). In general, patients with neutropenia or other neutrophil defects are at higher risk for CNS infections with enteric gram-negative rods (such as Enterobacteriaceae and Pseudomonas aeruginosa) and certain fungi including Aspergillus species, Candida species, and Mucoraceae. T-cell dysfunction predisposes to infection with Listeria monocytogenes, Nocardia asteroides, mycobacteria, Cryptococcus neoformans, and T. gondii. In the bone marrow transplant setting, a single fungal pathogen has been identified in 92% of brain abscesses.7 Aspergillus was the most frequently isolated fungus (58%), followed by Candida (33%) and sporadic cases of other fungi, such as Rhizopus, Absidia, Scopulariopsis, and Pseudoallescheria species. Eighty-five percent of cases of aspergillus brain abscess were associated with concomitant pulmonary disease. Candida abscess was associated with fungemia and neutropenia.

PATHOGENESIS Although the primary source of infection in most cases of brain abscess can be identified, anywhere from 10 to 63% of brain abscesses in case series have had no identified predisposing condition.13,13,14 Contiguous spread of infection from adjacent sites has been reported in nearly half of all brain abscess cases.1517 The most common primary infections have historically been sinusitis and otitis, but dental abscesses (particularly those involving molar teeth) are reported in up to 10% of cases.15,18 However, with improved diagnostic and treatment strategies for these primary infections, the development of a brain abscess in association with these conditions has decreased in frequency. Development of a brain abscess secondary to bacterial meningitis is unusual, but when it occurs it is most frequently associated with gram-negative meningitis in neonates. Hematogenous spread from distant sites of infection has been implicated in approximately 25% of brain abscess cases.1517,19 Endocarditis and pulmonary infections are among the most commonly reported distant foci of infection leading to brain abscess, but other sites of infection (intraabdominal, pelvic, and bone) should also be considered. Brain abscesses of hematogenous origin are frequently (up to 50%) multifocal20 and commonly involve the middle cerebral artery distribution. Certain chronic conditions, such as congenital cyanotic heart disease and pulmonary arteriovenous malformations, increase the risk of hematogenous spread of infection to the brain. Penetrating head injury, especially if associated with a gunshot wound or retained bone fragments, is a clearly established risk factor.21,22 Invasive neurosurgical procedures place a patient at a small risk (0.06 to 0.17%) of developing a brain abscess.21 A number of additional risk factors have been identified among the population of individuals with compro-

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1991) per 100,000 person-years. In the general population, brain abscess is a disease of young males. Case series have reported male to female ratios of 2 to 3:1.24 Although brain abscesses can occur at any stage of life, the majority of cases occur during the third and fourth decades. Immunosuppressed individuals, including those with the acquired immunodeficiency syndrome (AIDS), bone marrow and solid organ transplants, and neutropenia, are at greater risk for developing a brain abscess than immunocompetent individuals. In AIDS, toxoplasmic encephalitis alone has been reported to occur in up to 50% of patients not receiving prophylaxis.5,6 Brain abscess was found to occur in 1 of every 49 bone marrow transplant recipients at one large center.7 Central nervous system (CNS) infections occur in approximately 2.7 to 12% of all solid organ transplant recipients,811 and the CNS is one of the most common sites of infection in these patients.12 In one series of solid organ transplantations, the overall rate of brain abscess was 0.61% with the highest rate occurring in heart and heart-lung transplant recipients (1.17%).8

mised immune systems. In solid organ transplant recipients, brain abscess has been associated with high-dose corticosteroids, the number of episodes of rejection, age younger than 10 years or older than 40 years, neutropenia, cadaveric transplant, uremia (in kidney transplant recipients), retransplantation procedures, major subsequent operations, and multiorgan failure.8,23,24 In the setting of bone marrow transplantation, prolonged neutropenia and the use of immunosuppressive agents have been found to increase the risk of brain abscess.7 Latent infection with Toxoplasma gondii places individuals with T cellrelated immune deficiencies, such as AIDS, at significant risk for development of toxoplasmic encephalitis. It is estimated that 10 to 40% of AIDS patients in the United States are latently infected, and without prophylaxis, 25 to 50% go on to develop toxoplasmic encephalitis.5

BRAIN ABSCESSCALFEE, WISPELWEY Table 1. Etiological Organism and Empirical Therapy of Brain Abscess Based on Source of Infection
Source Paranasal sinusitis Organism Microaerophilic and anaerobic streptococci, Haemophilus sp., Bacteroides sp. (non-fragilis), and Fusobacterium sp. Bacteroides sp. (including B. fragilis), streptococci, Pseudomonas aeruginosa, and Enterobacteriaceae Streptococci and Bacteroides fragilis Viridans streptococci or S. aureus Streptococcus sp., Actinomyces sp., and Fusobacterium sp. Enterobacteriaceae and Pseudomonaceae Streptococcus sp., Enterobacteriaceae, and anaerobes Staphylococcus aureus, Clostridium sp., and Enterobacteriaceae Staphylococci, Enterobacteriaceae, and Pseudomonaceae Streptococci Antimicrobial Therapy Penicillin or a third-generation cephalosporin (cefotaxime or ceftriaxone) plus metronidazole Penicillin plus metronidazole plus ceftazidime Penicillin plus metronidazole Nafcillin or vancomycin plus metronidazole plus third-generation cephalosporin Penicillin plus metronidazole plus ceftazidime Penicillin plus metronidazole plus ceftazidime Ceftazidime plus metronidazole plus penicillin Nafcillin or vancomycin plus third-generation cephalosporin Vancomycin plus ceftazidime Penicillin or third-generation cephalosporin plus metronidazole

Otitis media and mastoiditis

Dental infections Endocarditis Pyogenic lung infection Urinary sepsis Intra-abdominal source Penetrating head trauma Neurosurgical procedure Cyanotic congenital heart disease

As in bone marrow transplantation, pyogenic bacteria are unusual causes of brain abscess in the solid organ transplant recipient.8 Aspergillus is the most commonly isolated pathogen among patients in the acutely immunosuppressed state that occurs in the early posttransplantation period. In the more chronically immunosuppressed solid organ transplant recipient, the microbiology of brain abscess changes to include T. gondii, N. asteroides, Candida species, Mucoraceae, and, less commonly, L. monocytogenes. Among patients with AIDS, T. gondii has been considered the most common cause of an intracranial mass lesion. This is typically the result of reactivation of latent disease. Early in the epidemic, toxoplasmic encephalitis occurred in 3 to 10% of all AIDS patients in the United States. This represents approximately 30% of those identified to be at risk because of serologic evidence of previous infection with Toxoplasma.5,26 The incidence of toxoplasmic encephalitis has markedly de-

creased, in part because of highly active antiretroviral treatment as well as administration of trimethoprimsulfamethoxazole as prophylaxis against Pneumocystis carinii pneumonia.27,28 This decrease in toxoplasmic disease has resulted in an increase in the proportion of CNS mass lesions that are caused by primary central nervous system lymphoma (PCNSL) and progressive multifocal leukoencephalopathy (PML). These processes, related to Epstein-Barr virus (EBV) and JC virus, respectively, may now be at least as common as toxoplasmic encephalitis in the human immunodeficiency virus (HIV)infected patient. Other pathogens isolated from brain abscesses within this group include C. neoformans, N. asteroides, Candida species and other fungi, mycobacteria (Mycobacterium tuberculosis and atypical mycobacteria), and Listeria.

CLINICAL PRESENTATION
Table 2. Microbiology of Central Nervous System Mass Lesions in Immunocompromised Patients
T-Cell Dysfunction Toxoplasma gondii Nocardia asteroides Cryptococcus neoformans Mycobacteria Listeria monocytogenes Primary CNS lymphoma (EBV associated) Progressive multifocal leukoencephalopathy (JC virus) Neutropenia Aspergillus species Candida species Mucoracae Enterobacteriaceae Pseudomonas aeruginosa

The classic presentation of a brain abscess is described as a triad of fever, headache, and focal neurologic deficits, but this combination of findings is seen in less than 50% of patients with a brain abscess.1,2,4,13,14,25 The presenting symptoms and signs are relatively nonspecific and are dependent upon the location and size of the abscess(es), the underlying immune status of the host, and the organism(s) involved. Common signs and symptoms identified at presentation are listed in Table 3. Because patients with most brain abscesses present with fairly nonspecific complaints and findings, the diagnosis of brain abscess should at least be considered in any

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SEMINARS IN NEUROLOGY VOLUME 20, NUMBER 3 2000 Table 3. Common Presenting Signs and Symptoms in Brain Abscess
Sign or Symptom Fever Headache Focal neurologic deficit Altered level of consciousness Seizure Nausea/vomiting Papilledema Nuchal rigidity Frequency (%) 3775 5694 4975 10100 12.547 3177 6.350 11

DIAGNOSIS The diagnosis of brain abscess is made by computed tomography (CT) or magnetic resonance imaging (MRI) and stereotactic biopsy. As already described, the clinical presentation can be nonspecific. Cerebrospinal fluid (CSF) analysis demonstrates normal or only nonspecific abnormalities. Not only does lumbar puncture fail to provide a specific diagnosis, it also places the patient at risk of cerebral or cerebellar herniation if intracranial pressure is elevated. Therefore, lumbar puncture is contraindicated, in general, in patients with a brain abscess. An exception to this rule is HIV-infected patients with small lesions without mass effect who either have no serologic evidence of previous Toxoplasma infection or have been treated with trimethoprimsulfamethoxazole as prophylaxis against P. carinii pneumonia. In these patients, sampling of CSF for polymerase chain reaction (PCR) testing for EBV DNA and JC virus DNA can often be safely performed to rule out PCNSL and PML.27 The development of CT and MRI has significantly improved the ability to diagnose and treat brain abscesses. CT allows much earlier detection and better localization than older imaging modalities. In fact, prior to the routine use of CT in evaluating patients with brain abscess, only 1 to 15% of cases were thought to involve

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patient presenting with fever, headache, and focal neurologic deficits. Brain abscesses occurring in the immunosuppressed host are more likely to have an occult presentation than those in the immunocompetent host because of a reduced inflammatory response to the infectious process.9 Several series of bone marrow and solid organ transplant recipients with brain abscesses have shown fever in 83 to 93% of cases, altered level of consciousness in 43 to 50%, cranial nerve abnormalities in 31%, and headache in 7%.7,8 Again, a relationship between the causative organism and the clinical presentation has been described. In one study of bone marrow transplant patients, 16% overall were asymptomatic; however, among the patients with candidal abscesses, 32% were asymptomatic.7 Among AIDS patients with toxoplasmic encephalitis, headache occurs in 78%, altered level of consciousness in 71%, fever in 63%, nausea and/or vomiting in 34%, and seizures in 10%.29

multiple lesions. Now it is recognized that up to 50% of cases have multiple abscesses.30 The classic CT appearance of a mature brain abscess is that of a ringenhancing mass lesion with a hypodense center that is frequently surrounded by a substantial amount of edema. The early cerebritis stages of brain abscess, however, enhance diffusely. The typical ring-enhancing appearance is not evident until the capsule forms during the later stages of development.31 CT is highly sensitive (>95%) in detecting this type of lesion. Unfortunately, ring-enhancing lesions seen on CT images are not specific for brain abscess; cystic and necrotic neoplastic lesions, hematomas, and infarcted brain tissue may have the same CT characteristics. The development of MRI has further enhanced the radiographic diagnosis of brain abscess. T1-weighted images demonstrate a hypointense abscess center, and T2-weighted images reveal an isointense or hyperintense abscess center. On T1-weighted images after gadolinium, there is enhancement of the abscess capsule. On T2-weighted MRI, the capsule is hypointense surrounded by a hyperintense area of edema. MRI is better than CT at evaluating the brainstem and the early cerebritis stage of brain abscess formation. Other noninvasive diagnostic techniques have shown greater specificity than CT and MRI in the evaluation of CNS mass lesions. Single photon emission computed tomography (SPECT) with thallium-201 has been used for patients with AIDS to distinguish accurately between PCNSL, with which focal uptake of thallium occurs (Fig. 1), and infectious abscesses, specifically those caused by T. gondii, which characteristically demonstrate no uptake of thallium.32,33 Perfusion MRI demonstrates increased regional blood flow in PCNSL compared with decreased regional blood flow in toxoplasmosis. Positron emission tomography (PET) using [18F]fluorodeoxyglucose has yielded similarly impressive results.34,35 In fact, one study found PET scanning to be 100% sensitive and specific in distinguishing neoplastic from nonneoplastic lesions. Magnetic resonance spectroscopy has been evaluated for use in discriminating neoplastic from infectious CNS lesions. In vitro and in vivo studies that have included mostly immunocompetent subjects have produced encouraging results.3642 Further evaluation and wider availability of these newer diagnostic tools will probably produce significant improvements in the initial noninvasive evaluation of CNS mass lesions. Although imaging procedures that may bring improved specificity to the radiologic diagnosis of brain abscess may soon be widely available, the currently available imaging modalities (CT and MRI) still lack the specificity needed to establish a definitive diagnosis and determine the causative organism(s). A surgical procedure is frequently required for diagnosis. In the past, surgical excision was often used. Today, stereotactic CTguided needle aspiration of lesions provides a less invasive alternative to total excision for the diagnosis and treatment of brain abscess. This procedure is well tolerated with a morbidity of 0 to 1% and mortality of 0.2% in nonHIV-infected patients.1,43 In HIV-infected patients morbidity and mortality rates of 12% and 2%,

BRAIN ABSCESSCALFEE, WISPELWEY

Figure 1. (A) Gadolinium-enhanced T1weighted MRI image of advanced HIV-infected patient revealing complex parietal mass lesion. (B) T2-weighted image of the same patient further characterizing the mass effect and edema. Some cuts revealed involvement of corpus callosum. (C) Thallium-201 SPECT reveals focal uptake of thallium at site of MRI image (side A) consistent with the diagnosis of central nervous system lymphoma.

respectively, have been reported.27 Specimens obtained during aspiration should be evaluated with Grams stain, aerobic and anaerobic bacterial cultures, mycobacterial stains and cultures, and fungal stains and cultures. Pathologic examination is also often useful. The diagnostic approach just described is also used in the immunosuppressed patient. Risks associated with invasive procedures may be higher in certain subsets of these patients, such as individuals with thrombocytopenia. Because of the high likelihood of toxoplasmic disease in HIV-infected patients with multiple lesions on CT or MRI and serologic evidence of previous Toxoplasma exposure, empirical treatment for Toxoplasma encephalitis rather than confirmation by aspiration has frequently been recommended.44 The diagnosis is then confirmed by observing the clinical and radiographic response to treat-

ment. Biopsy is often reserved for patients with atypical presentations, negative Toxoplasma serology, or single lesions on CT or MRI. This approach, however, has been called into question because of the changing epidemiology of CNS mass lesions in patients with AIDS. As more and more patients are treated with prophylactic regimens, less and less intracranial mass lesions in AIDS patients are due to toxoplasmosis. The recommendation that HIVinfected individuals with enhancing intracranial mass lesions and serologic evidence of previous Toxoplasma exposure be empirically treated with sulfadiazine and pyrimethamine is being reevaluated. Imaging studies may be less sensitive in immunosuppressed patients. For example, CT images revealed abnormalities in only 70% of bone marrow transplant patients with confirmed brain abscesses.7 Bone marrow

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SEMINARS IN NEUROLOGY VOLUME 20, NUMBER 3 2000

transplant recipients with low total white blood cells (WBCs) or lymphocyte counts frequently have no notable edema or contrast enhancement on CT and MR imaging.45 This may reflect a diminished inflammatory and/or immunologic response to the infectious process. Neuroimaging is typically normal in Candida meningoencephalitis. TREATMENT An approach that combines both medical and surgical management is recommended in most cases of brain abscess. Drainage of abscesses plays an important therapeutic as well as diagnostic role. Commonly accepted treatment guidelines include aspiration or excision of all lesions that are larger than 2.5 cm in diameter or that are causing a mass effect. Stereotactic CT-guided aspiration is typically considered to be the procedure of choice for primary drainage of brain abscesses, but this remains somewhat controversial. If immediate surgery is planned, preoperative antibiotics should be withheld so as not to sterilize cultures. Imaging studies should be repeated at least once every 1 to 2 weeks during treatment. Imaging should be repeated immediately if clinical deterioration occurs. Abscess lesions that are demonstrated to have enlarged or that fail to respond to treatment on follow-up imaging should undergo repeated aspiration. Although a medical-surgical approach is considered in most cases to be the standard of care, initial treatment with antibiotics alone may be recommended for a small subset of patients.46 This group includes clinically stable patients who are felt to be high risk for surgical intervention or who have concomitant meningitis, ependymitis, hydrocephalus requiring a shunt, deep or dominant lesions, or multiple distantly located abscesses. In the cases in which medical therapy alone is used, broad-spectrum antibiotics providing coverage of the most likely organisms involved should be initiated. Blood cultures should be obtained prior to starting treatment. Imaging studies should be repeated weekly during the first 2 weeks of treatment or sooner if clinical deterioration occurs. Imaging should then be performed every 2 weeks until the completion of a 6 to 8 week course of antibiotics and then every 2 to 4 months for 1 year to monitor for disease recurrence. The initial choice of antibiotics must be empirical while awaiting the results of microbiological testing of the aspirated material. Agents that provide antimicrobial coverage of the most likely pathogens and that achieve adequate concentrations within the brain parenchyma should be used (Table 1). In the nonimmunosuppressed patient a combination of vancomycin (adult dose: 1 g every 12 hours), metronidazole (adult dose: 500 mg every 6 hours), and cefotaxime (adult dose: 1 to 2 g every 4 to 8 hours, maximum dose 12 g/day) is often recommended. Obviously, adjustments of or additions to this empirical regimen should be made on the basis of clinical history and the primary site of infection, if known. The antibiotic regimen is later tailored to the specific organisms isolated in culture. Duration of antimicrobial therapy in brain abscess is largely empiri-

cal. A 6- to 8-week course of parenteral therapy is usually recommended. Abscesses treated by surgical excision may require a shorter duration of treatment, but this recommendation is largely based on anecdotal evidence. The additional benefit of oral antimicrobial agents after completion of a full course of intravenous antibiotics is unproved. Empirical treatment in the immunosuppressed patient with brain abscess must take into account the patients specific immune defect. As already discussed, in the HIV-infected patient with multiple brain lesions and a positive serologic test for Toxoplasma, empirical therapy for toxoplasmic encephalitis with pyrimethamine and sulfadiazine is a common approach. Clindamycin can be substituted for the sulfa-allergic patient. Folinic acid should be administered with pyrimethamine. A response to treatment is rapid in most patients with toxoplasmic encephalitis, with a median response time of 5 days. The response rate is 74% by the seventh day and 91% by the end of the second week of treatment.44 If a response has not occurred within 2 weeks, biopsy should be performed to evaluate for other etiologies of the brain lesions, such as lymphoma. Biopsy should be considered at the time of presentation in HIV-infected patients with a negative serologic test for Toxoplasma and in patients who have received prophylactic therapy. As mentioned before, however, the decreasing incidence of toxoplasmic encephalitis and relative increases in PCNSL and PML have led some clinicians to pursue a definitive diagnosis more actively (using some combination of SPECT, perfusion MRI, biopsy, and PCR of CSF for EBV DNA and JC DNA) at the time of presentation. For neutropenic patients and those in the immediate posttransplantation period, empirical therapy for brain abscess should include amphotericin B because of the high frequency with which fungal infection, particularly aspergillosis, occurs in this population. Nocardial infections should be treated with a high-dose sulfonamide regimen (such as trimethoprim-sulfamethoxazole) and prophylactic treatment should be continued for at least 1 year after transplantation.47 HIV-infected patients treated for Nocardia infections should receive lifelong suppressive therapy after completing a full course of treatment for the acute infection.48 Because the use of steroids can result in decreased antibiotic penetration into the abscess cavity and in alteration of clinical and radiographic findings, adjunctive corticosteroids should be reserved for patients with elevated intracranial pressure caused by cerebral edema or to the mass lesion itself. The dose of steroids should be tapered as rapidly as possible. Anticonvulsant therapy is typically recommended in order to reduce the risk of seizures, which is greater than 90% in patients who do not receive prophylactic therapy.49 PROGNOSIS Prior to the advent of antimicrobial therapy, the mortality rate for brain abscesses approached 100%.19,5057 Subsequent to the development of effective antimicrobials, highly sensitive imaging procedures,

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1. Mamelak AN, Mampalam TJ, Obana WG, Rosenblum ML. Improved management of multiple brain abscesses: a combined surgical and medical approach. Neurosurgery 1995;36:7685 2. Nicolosi A, Hauser WA, Musicco M, Kurland LT. Incidence and prognosis of brain abscess in a defined population: Olmsted County, Minnesota, 19351981. Neuroepidemiology 1991;10: 122131 3. Sofianou D, Selviarides P, Sofianos E, Tsakris A, Foroglou G. Etiological agents and predisposing factors of intracranial abscesses in a Greek university hospital. Infection 1996;24: 144146 4. ODonoghue MA, Green HT, Shaw MD. Cerebral abscess on Merseyside 19801988. J Infect 1992;25:163172 5. Anonymous. Evaluation and management of intracranial mass lesions in AIDS: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 1998;50: 2126 6. Levy RM, Janssen RS, Bush TJ, Rosenblum ML. Neuroepidemiology of the acquired immunodeficiency syndrome. J Acquir Immune Defic Syndr 1988;1:314. 7. Hagensee ME, Bauwens JE, Kjos B, Bowden RA. Brain abscess following marrow transplantation: experience at the Fred Hutchinson Cancer Research Center, 19841992. Clin Infect Dis 1994;19:402408 8. Selby R, Ramirez CB, Singh R, et al. Brain abscess in solid organ transplant recipients receiving cyclosporine-based immunosuppression. Arch Surg 1997;132:304310 9. Conti DJ, Rubin RH. Infection of the central nervous system in organ transplant recipients. Neurol Clin 1988;6:241260 10. Gupta SK, Manjunath-Prasad KS, Sharma BS, et al. Brain abscess in renal transplant recipients: report of three cases. Surg Neurol 1997;48:284287

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and improved surgical techniques, the overall mortality for brain abscess has drastically decreased. Reports of case series have stated case fatality rates of 0 to 8%.1,30,42,5862 Mortality has consistently been shown to be related to mental status at the time of diagnosis, short duration of symptoms prior to diagnosis, and concurrent bacterial meningitis.2,4,13,14 The majority of survivors (66 to 94%) have no major residual neurologic deficits with the exception of seizure disorders, which occur in as high as 70% of patients.1,2,4 As stated before, toxoplasmic encephalitis in the HIV-infected patient typically responds well to treatment. However, recurrence rates of up to 26% have been reported.63 Persistent focal enhancement on imaging studies after initial treatment has been reported in a subpopulation of individuals at high risk for recurrence. Chronic suppressive therapy is recommended for the HIV-infected patient with a history of toxoplasmic encephalitis. The tremendous decrease in overall mortality from brain abscess is not evident within the transplant population. The mortality associated with brain abscess in bone marrow transplant recipients was 97% in one series and was unrelated to pathogen or mode of treatment.7 In this series, 56 of 58 patients died within 15 days of diagnosis, with an average of 4.2 days between diagnosis and death. A similar outcome is seen in solid organ transplant recipients, where overall mortality in brain abscess cases is 86% (85 to 100% in fungal abscesses and 75 to 90% in nocardial abscesses).8,24

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