Brain Abscess

OVERVIEW: What every practitioner needs to know

Are you sure your patient has a brain abscess? What should you expect to find?

  • Although uncommon, brain abscesses can be associated with death or devastating permanent neurologic deficit, and thus, require prompt diagnosis and treatment. A brain abscess is a focal area of cerebritis secondary to bacterial or, less commonly, fungal or protozoal infection that develops into a collection of pus surrounded by a vascular capsule. Origin of infection is most often secondary to spread from a continguous site of sinusitis, otitis, or periodontal inflammation. Neuroimaging by contrast-enhanced CT scan or MRI is the preferred diagnostic modality, and initial treatment consists of broad spectrum parenteral antibiotics and surgical drainage.
  • Clinical presentation is variable, in part related to the pathogen, method of entry into the brain parenchyma, and specific anatomical location. However, up to 75% of presentations are acute with symptom onset of less than 2 weeks. Notably, the signs and symptoms are usually more indicative of mass effect and intracerebral edema and less so of a febrile infection. Headache is observed in the majority of patients; fever is absent in about 50%. The minority present with the classic triad of headache, fever, and focal neurological deficit. Non-specific symptoms, such as nausea and vomiting, are more common and have been reported in up to 85% in some series.
  • Frontal lobe abscesses are often associated with drowsiness, inattention, and generalized cognitive slowing. Cerebellar abscesses may produce ataxia, dsymetria, and nystagmus. Intrasellar abscesses can simulate pituitary tumors, and focal brain stem abscesses can cause facial weakness or hemiparesis mimicking a stroke.

How did the patient develop a brain abscess? What was the primary source from which the infection spread?

Location of the abscess within the brain typically provides clue to the site of origin. As most brain abscesses are from a contiguous focus of infection, areas of the cortex adjacent to otitis or sinusitis are commonly affected. Depending on the severity of infection, spread through bone or tissue can be observed or otherwise indirectly through valveless emissary veins or retrograde thrombophlebitis.

  • Contiguous anatomic spread: Otitis, in particular, may lead to tracking infection through cochlear or vestibular aqueducts and the internal auditory canal. As a result, the majority of brain abscesses from an otogenic source are located in the temporal lobes, and, similarly, although cerebellar abscesses are uncommon, up to 90% are otogenic. In contrast, brain abscess of the frontal lobe is almost exclusively due to sinusitis. Alternative forms of contiguous spread occur after penetrating trauma, such as accidental injury or neurosurgical procedures.
  • Hematogenous abscesses: In general, brain abscess due to hematogenous seeding from a distant source is uncommon. However, 25% of cases of brain abscess occur in children younger than 4 years of age, and, in this age group, there is a large contribution of hematogenous spread due to congenital cyanotic heart disease. Multiple abscesses, particularly in the distribution of the middle cerebral artery, should prompt concern for sites of infection outside the ears and paranasal sinuses. Pulmonary infections, including empyema, lung abscess, and bronchiectasis are hematogenous sources of brain abscess. Intra-abdominal and pelvic infections have been reported less often as a source of brain abscess, and endocarditis as a cause of brain abscess remains surprisingly rare. Given the relative poor encapsulation of hematogenous abscesses, higher mortality is observed.
  • Cryptogenic: Upward of 20% of abscesses remain cryptogenic, perhaps as consequence of asymptomatic pulmonary arteriovenous malformations.

Which individuals are of greater risk of developing a brain abscesses?

Changes in antibiotic treatment of sinusitis and otitis media have largely contributed to the rarity of brain abscess, reported as 1,500-2,500 cases per year in the United States. Predisposing conditions are listed in Table I.

Table I.
Predisposing condition[common pathogens] Empiric antimicrobial regimen
Community acquired otitis media, mastoiditis, sinusitis[Streptococci 60-70%, Bacteroides and Prevotella species 20-40%, less commonly Enterobacteriaceae] Penicillin-G plus metronidazole
Dental infection[Streptococci, anaerobes including Fusobacterium and Actinomyces] Penicillin-G plus metronidazole
Post-neurosurgery or penetrating trauma[Staphylococcus aureus including MRSA, Staphylococcus epidermidis, Enterobacteriaceae, Pseudomonas aeruginosa, anaerobes including Clostridium species] Vancomycin plus anti-pseudomonal cephalosporin plus metronidazoleORVancomycin plus meropenem
Lung abscess, empyema +/- suspicion for Nocardia species[Streptococci, anaerobes including Fusobacterium, Actinomyces, Bacteroides and Prevotella, rare Enterobacteriaceae, rare community acquired MRSA] Vancomycin plus third-generation cephalosporin plus metronidazole+/- trimethoprim sulfamethoxazoleORVancomycin plus meropenem
HIV infection (CD4<100 or not on Toxoplasma prophylaxis), anti-Toxoplasma IgG positive or pending[Community acquired bacterial pathogens, Toxoplasma gondii, Cryptococcus neoformans, Mycobacterium species, Listeria monocytogenes] Third-generation cephalosporin plus metronidazole plus pyrimethamine (with folinic acid) plus sulfadiazine+/- ampicillin (particularly if prodrome of meningoencephalitis and brain stem location of abscess)Usually withhold empiric antifungal or antimycobacterial treatment until other pathogens ruled out
Neutropenia or diabetic ketoacidosis with sinusitis[Community acquired bacterial pathogens, Pseudomonas aeruginosa, Aspergillus, Candida, Mucorales, Scedosporium species] Vancomycin plus anti-pseudomonal cephalosporin plus metronidazoleORVancomycin plus meropenemANDAmphotericin B deoxycholate (or liposomal amphotericin B) plus voriconazole

See Table II for recommended doses and alternative treatment.

Table II.
Organism Antibiotic Dose Alternative
Streptococci Penicillin GCeftriaxoneCefotaxime 20-24 mil. units/d (divided Q4H)2-4 g/d (divided Q12H)12 g/d (divided Q6H) Vancomycin 15-20 mg/kg (divided Q12H)
Staphylococcus auerusMethicillin sensitive (MSSA)Methicillin resistant (MRSA) Nafcillin or oxacillinVancomycin Nafcillin 9-12 g/d (divided Q12H)Vancomycin 15-20 mg/kg (divided Q12H) Vancomycin 15-20 mg/kg (divided Q12H)Trimethoprim-sulfa (if sensitive); 15-20 mg/kg(trimethroprim)(divided Q6H)
Fusobacterium spp. Penicillin G 20-24 mil. units/d (divided Q4H) Clindamycin 2.4-4.8g/d (divided Q6H)
Prevotella spp. Metronidazole 30 mg/kg (divided Q6H) Clindamycin 2.4-4.8g/d (divided Q6H)
L. monocytogenes Ampicillin 2 g/d (divided Q4H) Trimethoprim-sulfa 15-20 mg/kg (trimethroprim) (divided Q6H)
H. influenzae CeftriaxoneCefotaxime 2-4 g/d (divided Q12H)12 g/d (divided Q6H) Aztreonam 6-8g/d (divided Q6-8H)Trimethoprim-sulfa 15-20 mg/d (trimethroprim) (divided Q6H)
Enterobacteriaceae CeftriaxoneCefotaxime 2-4 g/d (divided Q12H)12 g/d (divided Q6H) Aztreonam 6-8g/d (divided Q6-8H)Trimethoprim-sulfa 15-20 mg/kg (trimethroprim) (divided Q6H)
P. aeruginosa CeftazadimeCefepime 6g/d (divided Q8H)6g/d (divided Q8H) Meropenem 6g/d (divided Q8H)Aztreonam 6-8g/d (divided Q6-8H)
Actinomyces spp. Penicillin G 20-24 mil. units/d (divided Q4H) Clindamycin 2.4-4.8g/d (divided Q6H)
Nocardia spp. Trimethoprim-sulfa 15-20 mg/kg (trimethroprim) (divided Q6H) Meropenem 6g/d (divided Q8H) or ImipenemAmikacin 15 mg/kg (divided Q8H)Ceftriaxone or CefotaximeMinocycline
M. tuberculosis Isoniazid + Rifampin + Pyrazinamide + Ethambutol 300 mg (Q24) + 600-900 mg (Q24) + 15-30 mg/kg (Q24) + 15 mg/kg (Q24) —-
Candida spp. Amphotericin B deoxycholateLiposomal amphotericin B 0.6-1.0 mg/kg (Q24H)5 mg/kg (Q24H) Fluconazole 800 mg (Q24H)
Aspergillus spp. Voriconazole 8 mg/kg (divided Q12H) Amphotericin B deoxycholate 1.0 mg/kg (Q24H)Liposomal amphotericin B 5 mg/kg (Q24H)Posaconazole 800 mg (divided Q6-8H)
Mucorales (Zygomycetes) spp. Amphotericin B deoxycholateLiposomal amphotericin B 1.0 mg/kg (Q24H)5 mg/kg (Q24H) Posaconazole 800 mg (divided Q6-8H)1
Scedosporium spp. Voriconazole 8 mg/kg (divided Q12H) Posaconazole 800 mg (divided Q6-8H)
Cryptococcus neoformans Amphotericin B deoxycholateLiposomal amphotericin B+ Flucytosine 2 0.6-1.0 mg/kg (Q24H)5 mg/kg (Q24H)100 mg/kg flucytosine (divided Q6H) Fluconazole 800 mg (Q24H)
Toxoplasma gondii Pyramethamine + sulfadiazine 25-75 g (Q24H) + 4-6 g (divided Q6H) Pyramethamine 25-75 g (Q24H) + Clindamycin 2.4-4.8g/d (divided Q6H)Pyramethamine 25-75 g (Q24H) + AtovoquoneDapsoneTrimethoprim-sulfa 15-20 mg/d (trimethroprim) (divided Q6H)

Use only after response to amphotericin B has been documented.

Some clinicians use an amphotericin B formulation combined with 800 mg fluconazole rather than flucytosine.

  • Post sinusitis/otitis: Otogenic brain abscesses usually occur in a bimodal distribution in patients younger than 10 years of age and patients older than 40 years of age, whereas paranasal abscesses occur more commonly from adolescence to early adulthood. Streptococci, anaerobes less commonly enterobacteriaceae, are causative.
  • Post dental infection: This is enriched for streptococci and anaerobes as causative pathogens.
  • HIV/decreased cell mediated immunity: This is less common bacteria, such as Listeria monocytogenes, and non-bacterial abscesses from protozoa (e.g., Toxoplasma gondii), fungi (e.g., Cryptococcus neoformans), or mycobacteria (e.g., Mycobacterium tuberculosis).
  • Post neurosurgery or penetrating trauma: This is enriched for staphylococci, enterobacteriaceae, and Pseudmonas aeruginosa.
  • Neutropenia: This is enriched for Candida species, but also other invasive fungal pathogens.
  • Diabetic ketoacidosis: This is associated with invasive fungal pathogens, including the Mucorales, Aspergillus species, and Scedosporium species.

Beware: there are other diseases that can mimic a brain abscess:

  • Subdural empyema
  • Cranial epidural abscess
  • Suppurative dural venous thrombophlebitis
  • Intracranial bleed
  • Ischemic stroke
  • Non-infectious space occupying lesion (e.g., tumor, particularly in immunocompromised host)

What laboratory studies should you order and what should you expect to find?

Results consistent with the diagnosis

Unfortunately laboratory tests are non-specific. Lumbar puncture is contraindicated in those with suspected or confirmed brain abscess because of risk of brain herniation.

  • White blood cell (WBC): Only 10% of patients with brain abscess have a leukocytosis greater than 20,000, and in 40% the WBC is normal.
  • ESR and C-reactive protein: These may be moderately increased.
  • Blood cultures: In all patients suspected of brain abscess, blood cultures should be obtained prior to antibiotic therapy, and, in those with possible hematogenous source, such as lung abscess, blood cultures may be diagnostic.
  • Anti-Toxoplasma IgG antibody: This should be checked in patients suspected of central nervous system (CNS) toxoplasmosis, as more than 95% of patients with AIDS and CNS toxoplasmosis have titers ranging from 1:8 to greater than 1:1024. The rare patient with CNS toxoplasmosis will have an undetectable IgG. However, a positive titer in the presence of a radiographically compatible lesion should prompt an empiric trial of antibiotic therapy for Toxoplasma.
  • Serum cryptococcal antigen: In the HIV infected patient in whom C. neoformans is suspected and lumbar puncture is contraindicated in the setting of possible cryptococcoma, a serum antigen testing may be diagnostic.

Results that confirm the diagnosis

  • Abscess culture: Purulent drainage from the abscess at the time of surgical drainage should be sent for culture for aerobic and anaerobic bacteria, fungi, and mycobacteria and is diagnostic. Histopathologic staining of infected brain tissue may be confirmatory.

What imaging studies will be helpful in making or excluding the diagnosis of brain abscess?

Contrast-enhanced CT scan or MRI are the standard of care for brain abscess diagnosis:

  • Computed tomography (CT): The advent of rapid neuroimaging has improved both the diagnosis and the treatment outcome in patients suspected of brain abscess. CT allows imaging of intracranial structures, as well as the paranasal sinuses, mastoids, and middle ear. CT must be performed with contrast, and, when contraindicated, MRI is preferred. Contrast allows visualization of the characteristic abscess appearance of a hypodense center with peripheral ring enhancement. Adjacent to the enhancement is a variable amount of hypodense edema. In the later stages of infection with more intact encapsulation, contrast does not penetrate as well and may not differentiate a hypodense center. After surgical aspiration of an abscess, CT appearance of improvement may lag by several weeks. CT $$$
  • Magnetic resonance imaging (MRI): MRI is the preferred diagnostic procedure when available. More sensitive than CT in visualizing the early edema pattern of new abscess formation, MRI also better differentiates the central necrosis of brain abscess from other non-infected fluid accumulations. MRI can best distinguish spread of infection to the ventricles and subarachnoid space as well. Gadolinium enhancement offers capsular enhancement on T1-weighted images, whereas T2-weighted images highlight the surrounding edema with high intensity signal. Additional patterns on imaging that may provide pathogen-specific clues include: multiple lesions with marked edema and mass effect in HIV-infected patients with toxoplasmosis cerebral infarct with minimal contrast enhancement in immunosuppressed patients with aspergillosis sinus opacification, erosion of bone or fascial planes, or cavernous sinus involvement in rhinocerebral mucormycosis. MRI $$$$
  • CT scan of the brain $1000-2000, $$$; MRI $2000-3000, $$$$; costs will vary by institution

What consult service or services would be helpful for making the diagnosis and assisting with treatment?

If you decide the patient has a brain abscess, what therapies should you initiate immediately?

  • Management of brain abscess is a best approached in multidisciplinary coordination involving neuroradiologists, neurosurgeons, and infectious disease and critical care specialists.
  • General treatment approach: All patients presenting with seizure, focal neurologic deficit, or altered level of consciousness should prompt concern for brain abscess and, thus, trigger evaluation with contrast-enhanced CT scan or MRI. Lumbar puncture should be delayed until a space-occupying lesion is excluded. If neuroimaging is delayed and clinical symptoms progress, then blood cultures for bacteria and fungi should be obtained and empiric antibacterial therapy begun. Once a possible brain abscess is identified by neuroimaging, neurosurgical evaluation should be obtained. If an additional focus is found within the paranasal sinus or middle ear, consultation with an otolaryngologist is recommended.
  • Principles of anti-infective therapy: Once an abscess has been aspirated or blood cultures have been drawn in the setting of clinical deterioration, empiric antibiotic therapy should cover pathogens of the patient’s predisposing condition. Only after culture and susceptibilities are known is antibiotic therapy able to be narrowed.
  • Given the frequency of streptococci in community acquired brain abscess, an empiric regimen should always include high-dose penicillin-G or a third-generation cephalosporin. A third-generation cephalosporin is preferred given the additional broad gram-negative coverage.
  • In almost every setting with suspicion of bacterial abscess, metronidazole or equivalent anaerobic coverage should be added to the regimen given the relatively high percentage of Bacteriodes fragilis isolated and the delayed growth on culture. Metronidazole also targets Prevotella species, attains high intracerebral concentrations, and is not affected by concomitant corticosteroids.
  • Other predisposing conditions require more tailored therapy.
  • Duration of parenteral antibiotic therapy is 6-8 weeks but should be managed in consultation with an infectious disease specialist. Antibiotic duration cannot be determined based on contrast-enhanced CT scan resolution alone, as nodular lesions may persist 4-6 weeks after successful completion of therapy.

1. Anti-infective agents

If I am not sure what pathogen is causing the infection what anti-infective should I order?

  • Community acquired, HIV negative, no prior neurosurgical procedure: Recommend a third-generation cephalosporin, such as cefotaxime 3-4 grams every 8 hours or ceftriaxone 2 gram every 12 hours plus metronidazole at 7.5 mg/kg (usually 500 mg) every 6 hours. If a dental infection is the confirmed source, then high dose penicillin G (24 million units daily) can be substituted for the cephalosporin.
  • Post-neurosurgery or penetrating trauma: Recommend an anti-pseudomonal cephalosporin, such as cefepime at 2 grams every 8 hours or ceftazadime at 2 grams every 8 hours plus metronidazole at 7.5 mg/kg (usually 500 mg) every 6 hours. Additionally, vancomycin should be added at 15-20 mg/kg every 12 hours given the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) and Staphylococcus epidermidis. Alternatively, a carbapenem, such as meropenem at 2 grams every 8 hours can be substituted for the anti-pseudomonal cephalosporin and metronidazole. Meropenem may be preferred, depending on the local resistance patterns of multidrug-resistant Enterobacteriaceae. Imipenem, although used successfully in the treatment of abscesses, including those from Nocardia species, is associated with an increased risk of seizures.
  • HIV positive, neuroimaging suspicious for CNS toxoplasmosis, anti-Toxoplasma IgG antibody positive or pending: Recommend additional empiric therapy with pyrimethamine, given as single loading dose of 75-100 mg followed by 25-50 mg daily dose, plus sulfadiazine at 1 gram every 6 hours. Folinic acid is also given at 10 mg daily to prevent pyrimethamine induced bone marrow suppression. Clindamycin can be substituted for sulfadiazine and given at 600 mg (intravenous) every 6 hours. In patients with a single enhancing lesion in whom primary CNS lymphoma is a strong consideration or in those with an undetectable anti-Toxoplasma IgG, brain biopsy is recommended. Single-photon emission computed tomography (SPECT) has been used to differentiate CNS lymphoma in this situation but can be confounded by tumor age and presence of a necrotic central focus of some lymphoma lesions. In the case of more characteristic multiple enhancing lesions in an HIV-positive patient with an undetectable anti-Toxoplasma IgG, an empiric trial of 2 weeks of anti-Toxoplasma therapy prior to brain biopsy has been advocated.
  • Lung abscess and/or suspicion of Nocardia species: Recommend, in addition to treatment for community acquired brain abscess, vancomycin at 15-20 mg/kg every 12 hours given the slight enrichment for certain strains of community-acquired MRSA to form lung abscess and trimethoprim-sulfamethoxazole at 5 mg/kg every 6 hours. Alternatives to trimethoprim-sulfamethoxazole for the treatment of confirmed CNS nocardiosis include imipenem, amikacin, minocycline, or linezolid. Successful combination regimens for immunocompromised hosts with Nocardia brain abscess have included imipenem and a sulfonamide or amikacin. Species identification of Nocardia is important, as antimicrobial susceptibility will vary. In contrast to other bacterial brain abscesses, if Nocardia is confirmed in an immunocompromised host, antibiotic duration should be continued for up to 12 months.
  • Neutropenia and fungal brain abscess suspected: A low threshold for empiric antifungal therapy must be maintained in certain clinical scenarios in the immunocompromised host, but, in confirmed fungal brain abscess, surgical excision is paramount. An amphotericin B preparation, such as amphotericin B deoxycholate at 0.6-1.0 mg/kg daily or liposomal amphotericin B at 5 mg/kg daily, will adequately cover brain abscesses from Candida species and most endemic fungi. If Aspergillus is suspected, voriconazole at 4 mg/kg every 12 hours is preferred and successful combination therapy of voriconazole with an amphotericin B preparation or an echinocandin has been demonstrated. Thus, a reasonable empiric strategy if Aspergillus is suspected would be a combination of an amphotericin B preparation and voriconazole pending surgical excision, histopathology, and culture. Although an amphotericin B preparation is the drug of most activity against mucormycosis, aggressive surgical excision and debridement is most curative when the Mucorales are suspected given the ability to invade blood vessels leading to local tissue infarction and impenetrability of medication. Scedosporium species demonstrate in vitro resistance to amphotericin, and voriconazole has been reported to be beneficial, especially when combined with prompt and complete surgical drainage.
  • The majority of patients require surgery. Consensus exists that all lesions greater than 2.5 cm should be excised or stereotactically aspirated. Specimens should be sent for culture and histopathology.
  • Craniotomy: Open craniotomy is often not necessary but is more commonly employed in cases of traumatic abscess to assure removal of all foreign material or to debride bone fragments. Posterior fossa abscesses also likely require an open approach because of greater risk of herniation with evolving mass effect. Ventriculostomy is occasionally required if evidence exists for marked increased intracranial pressure due to obstructive hydrocephalus, ventricular rupture, or other uncontrolled mass effect.
  • Aspiration: Indications for closed drainage are more controversial. If a patient is stable with an accessible abscess, then prompt aspiration prior to antibiotic therapy may allow specific bacteriologic diagnosis and, therefore, the narrowest of spectrum of long-term antibiotic exposure. However, aspiration during an early cerebritis stage may risk hemorrhage.

2. Next list other therapeutic modalities.

  • Corticosteroids: Dexamethasone has a limited role in prevention of impending cerebral herniation in an abscess causing significant mass effect prior to surgical evacuation. Corticosteroids may delay entry of antibiotics into the CNS, slow capsule formation and clearance of bacteria, and alter appearance of follow-up neuroimaging. Thus, prolonged use of corticosteroids beyond surgical drainage should be avoided.
  • Anticonvulsants: Although seizures do not affect the overall mortality rate, they may occur in 10-25% of cases of brain abscess, and an anticonvulsant is recommended in the early course of therapy.
  • Post-surgical/intensive care monitoring: It is recommended that all patients undergoing non-operative management and those in the early post-operative period following aspiration or excision be observed in a neuro-intensive care setting. Potential for rapid changes in intracranial pressure warrant scheduled neurologic examination and vital sign measurement, usually every hour in the early post-operative period. Antibiotic administration may need to be dose adjusted for change in kidney function. Fever or leukocytosis should not only prompt consideration of the brain abscess, but also hospital acquired infections, including Clostridium difficile, which has led to poor outcome in otherwise successfully treated brain abscesses.

What complications could arise as a consequence of a brain abscess?

What should you tell the family about the patient’s prognosis?

  • Case fatality rates have dropped to 0-25% in the era of improved neuroimaging, more effective antibiotic therapy, and new surgical techniques.
  • Predictors of poor response include delay in diagnosis, multiple abscesses or localization to the posterior fossa, a fungal pathogen, ventricular rupture (80-100% mortality), and Glasgow Coma Scale less than 12 on presentation.
  • Long-term neurologic sequelae develop in 30-50%.

What pathogens are responsible for this disease?

Brain abscess is usually a monomicrobial process, although 30% may have a mixed bacterial infection. Although bacteria predominate, less commonly fungal or protozoal species may cause brain abscess, but the pathogens are highly dependent on the predisposing infection or host immunodeficiency.

Streptococci are the most common of bacterial species, are found in the presence of other bacteria when mixed, and are commonly oropharyngeal in origin. The milleri group of Streptococci, including anginosus, constellatus, and intermedius, have a particular predisposition for deep abscess formation, the brain being no exception (see Table I). Enterobacteriaciae and anaerobes are also prevalent, found in 40% of cases. The anaerobes, such as Prevotella and Bacteroides species, arise in the presence of contiguous dental abscess or more distant lung abscess or empyema. Staphylococcus aureus is found in 10-15% of isolates, is usually of pure culture, and is additionally notable for association with penetrating trauma or infective endocarditis.

With proliferation of broad-spectrum antimicrobial use, immunosuppressive therapy for malignancy or organ transplantation, and hyperalimentation, fungal brain abscesses have become more prevalent. Candida species are more prevalent and can cause micro-abscesses and even a diffuse nodular gliosis pattern of disease. Cerebral aspergillosis warrants mention in discussion of the neutropenic host, and brain involvement may occur in up to 20% of invasive disease. Mucormycosis is observed in patients with diabetes and ketoacidosis, hematologic malignancy, or corticosteroid use and usually cause brain abscess as an extension of destructive rhinocerebral disease.

In contrast, brain abscess with Scedosporium apiospermum may be observed in immunocompetent hosts, usually after exposure to contaminated water, as reported following near-drowning episodes, but has also been associated with pulmonary or intravenous catheter infection.

How do these pathogens cause disease?

Pathogenic stages of brain abscess have been divided into histologic categories depending on the stage of infection:

  • early cerebritis (1-3 days)
  • late cerebritis (4-9 days)
  • early capsule formation (10-13) days
  • late capsule formation (14 days onward)

Early cerebritis is marked by bacteria visible on Gram stain, acute inflammation, and marked edema. As macrophages and fibroblasts surround the lesion, the center becomes necrotic in the late cerebritis stage. A thickened collagen capsule begins to form as the necrotic center regresses in the early capsule stage. Edema has usually regressed by the late capsular stage. In animal models of brain abscess, certain pathogens are observed to be more virulent. For example, Staphylococcus aureus develops a greater degree of necrosis, and the time to capsule formation is extended, likely because of α-toxin formation.

WHAT’S THE EVIDENCE: Diagnosis and management of brain abscess is based largely on case series and expert opinion

Abgrall, S, Rabaud, C, Constagliola, D. “Incidence and risk factors for toxoplasmic encephalitis in human immunodeficiency virus-infected patients before and during the highly active antiretroviral therapy era”. Clin Infect Dis. vol. 33. 2001. pp. 1747-55.

Beckham, JD, Tyler, KL.. “Neuro-intensive care in patients with acute CNS infections”. Neurotherap. vol. 9. 2012 Jan. pp. 124-38.

Cortez, KJ, Walsh, TJ., Scheld, WM, Whitley, RJ, Marra, CM. “Space-occupying fungal lesions”. Infections in the central nervous system. 2004. pp. 713-34.

Czartoski, T.. “Central nervous system infections in transplantation”. Curr Treat Options Neurol. vol. 8. 2006. pp. 193-201.

Dworzack, DL, Clarck, RB, Borkowski, WJ. “Pseudallescheria boydii brain abscess: association with near drowning and efficacy of high-dose, prolonged miconazole therapy in patients with multiple abscesses”. Medicine. vol. 68. 1989. pp. 218-24.

Hakan, T.. “Management of bacterial brain abscess”. Neurosurg Focus. vol. 24. 2008. pp. 1-7.

Hakan, T, Ceran, N, Erdem, I. “Bacterial brain abscesses: an evaluation of 96 cases”. J Infect. vol. 52. 2006. pp. 359-66.

Heilpern, KL, Lorber, B.. “Focal intracranial infections”. Infect Dis Clin North Am. vol. 10. 1996. pp. 879-98.

Kao, PT, Tseng, HK, Liu, CP. “Brain abscess: clinical analysis of 53 cases”. J Microbiol Immunol Infect. vol. 36. 2003. pp. 129-36.

Kastenbauer, S, Pfister, HW, Wispelwey, B, Scheld, WM, Whitley, RJ, Marra, CM. “Brain abscess”. Infections in the central nervous system. 2004. pp. 479-508.

Kielian, T, Cheung, A, Hickey, WF.. “Diminished virulence of an alpha-toxin mutant of Staphylococcus aureus in experimental brain abscess”. Infect Immun. vol. 69. 2001. pp. 6902-11.

Mathisen, GE, Johnson, JP.. “Brain abscess”. Clin Infect Dis. vol. 4. 1997. pp. 763-79.

Nadkarni, T, Goel, A.. “Aspergilloma of the brain: an overview”. J Postgrad Med. vol. 51. 2005. pp. S37-41.

Prasad, KN, Mishra, AM, Gupta, D. “Analysis of microbial etiology and mortality in patients with brain abscess”. J Infect. vol. 53. 2006. pp. 221-7.

Sifri, CD, Park, J, Helm, G. “Fatal brain abscess due to community-associated methicillin-resistant staphylococcus aureus strain USA300”. Clin Infect Dis. vol. 45. 2007. pp. 113-7.

Skiest, DJ.. “Focal neurological disease in patients with acquired immunodeficiency syndrome”. Clin Infect Dis. vol. 34. 2002. pp. 103-15.

Smith, SJ, Ughratdar, MacArthur DC.. “Never go to sleep on undrained pus: aretrospective review of surgery for intraparenchymal cerebral abscess”. Br J Neurosurg. vol. 23. 2009. pp. 412-7.

Troke, P, Aguirrebengoa, K, Artgea, C. “Treatment of scedosoporiosis with voriconazole: clinical experience with 107 patients”. Antimicrob Agents Chemother. vol. 52. 2008. pp. 1743-50.

Tseng, JH, Tsend, MY.. “Brain abscess in 142 patients: factors influencing outcome and mortality”. Surg Neurol. vol. 65. 2006. pp. 442-9.

Tunkel, AR., Mandell, GL, Bennett, JE, Dolin, R. “Brain Abscess”. Principles and practices of infectious diseases. 2010. pp. 1265-78.

Wang, HL, Seo, YH, LaSala, PR, Tarrand, JJ. “Nocardiosis in 132 patients with cancer: microbiological and clinical analyses”. Am J Clin Pathol. vol. 142. 2014 Oct. pp. 513-23.

Wispelwey, B, Petersen, KM., Schlossberg, D. “Intracranial Suppuration”. Clinical infectious diseases. 2008. pp. 531-40.