Pathogenesis, clinical manifestations, and diagnosis of brain abscess

Author
Frederick S Southwick, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Anna R Thorner, MD
Last literature review version 18.3: septiembre 2010 | This topic last updated: abril 12, 2010 (More)
INTRODUCTION Brain abscess is a focal collection within the brain parenchyma, which can arise as a complication of
a variety of infections, trauma, or surgery.
The pathogenesis, clinical manifestations, and diagnosis of brain abscess will be presented here. The treatment and
prognosis of this disease are discussed separately. (See "Treatment and prognosis of brain abscess".)
PATHOGENESIS Bacteria can invade the brain either by direct spread, which accounts for 20 to 60 percent of cases,
or through hematogenous seeding [1]. Bacteremic spread typically causes multiple lesions [2].
Direct spread The direct spread of organisms from a contiguous site usually causes a single brain abscess. Primary
infections that can directly spread to the cerebral cortex include [3-7]:
Subacute and chronic otitis media and mastoiditis (spread to the inferior temporal lobe and cerebellum)
Frontal or ethmoid sinuses (spread to the frontal lobes)
Dental infection (usually spreads to the frontal lobes)
Brain abscess as a complication of ear infections has decreased in frequency, especially in developed countries [6,7]. By
contrast, brain abscess arising from a sinus infection remains an important consideration in both adults and children
[3,4,8].
Bullet wounds to the brain can result in necrotic tissue and leave metal fragments that can serve as a nidus for infection.
Other foreign bodies that have been associated with brain abscesses include a pencil tip lodged in the eye and a lawn
dart [9,10]. In these cases, brain abscess may develop many years after the injury. In addition, brain abscess can
occasionally result from facial trauma.
Brain abscess can also complicate neurosurgical procedures. Development of brain abscess after neurosurgery may be
delayed [11,12]. For example, in one report of two cases of brain abscess following surgery for vestibular schwannoma
(acoustic neuroma), one patient developed subtle neurologic findings three months after the surgery; the second
presented with seizures 15 months after the original surgery, which had been complicated by a Pseudomonas aeruginosa
meningitis [11].
Hematogenous spread Brain abscesses associated with bacteremia usually result in multiple abscesses that are
most commonly located in the distribution of the middle cerebral artery [2]. Abscesses usually form at the grey-white
matter junction where micro infarction damages the blood-brain barrier.
Conditions that lead to hematogenous seeding of the brain include [2,13-18]:
Chronic pulmonary infections, such as lung abscess and empyema, often in hosts with bronchiectasis or cystic
fibrosis
Skin infections
Pelvic infections
Intraabdominal infections
Esophageal dilation and endoscopic sclerosis of esophageal varices
Bacterial endocarditis (brain abscess complicates 2 to 4 percent of cases)
Cyanotic congenital heart diseases (most common in children)
Intrapulmonary right-to-left shunting in patients with pulmonary arteriovenous malformations. Up to 10 percent
of patients with pulmonary arteriovenous malformations develop brain abscesses. Since 70 to 90 percent of patients with
pulmonary arteriovenous malformations have underlying hereditary hemorrhagic telangiectasia, these patients often have
a history of recurrent nosebleeds and visible mucocutaneous telangiectasias. (See "Pulmonary AVMs, including
hereditary hemorrhagic telangiectasia: Etiology and clinical features" and "Hereditary hemorrhagic telangiectasia (Osler-
Weber-Rendu syndrome)".)
No primary site or underlying condition can be identified in 20 to 40 percent of patients with brain abscess depending
upon the series [19-21].
The location of a brain abscess reflects the site of the primary infection that spreads to the cerebral cortex. These
locations in the brain in order of decreasing frequency are [22]:
Frontal or temporal lobes
Frontal-parietal
Parietal
Cerebellar
Occipital
There may be features of the bacteria that contribute to the pathogenesis of brain abscess, although these have not been
extensively explored. As an example, Citrobacter spp have been observed to cause both meningitis and brain abscess in
neonates; in vitro, Citrobacter freundii was shown to be capable of invading human brain microvascular endothelial cells
[23].
Pathology An understanding of the pathology of brain abscess is required for the interpretation of computed
tomographic (CT) scan and magnetic resonance imaging (MRI) findings. The histologic changes depend upon the age of
the infection [24]. The early lesion (first one to two weeks) is poorly demarcated and is associated with localized edema.
There is evidence of acute inflammation but no tissue necrosis. This early stage is commonly called cerebritis. After two
to three weeks, necrosis and liquefaction occur, and the lesion becomes surrounded by a fibrotic capsule.
MICROBIOLOGY Case reports implicate a wide variety of organisms as the cause of brain abscess [10,25-30]. The
pathogens involved differ depending upon the site of the primary infection (table 1), the age of the patient (with case
series reflecting differences in infecting microorganisms between children and adults), and the immune status of the host
[30,31]. Immunocompromised patients can have a broad array of organisms, including fungi, as the etiology of a brain
abscess, whereas bacterial species are most common in immunocompetent individuals [32,33]. The organism(s)
recovered from a brain abscess frequently provide a clue about the primary site of infection and any potential
undiagnosed underlying conditions in the host.
Anaerobic pathogens Anaerobic bacteria are common constituents of brain abscesses. These organisms generally
originate from the normal mouth flora and are most commonly associated with solitary brain abscesses originating from
otorhinolaryngeal infections [34]. However, intraabdominal or pelvic infections can occasionally lead to bacteremia with an
anaerobic organism that seeds the cerebral cortex. The anaerobes in such cases usually reflect colonic or female genital
tract flora. The most frequent anaerobes cultured from a brain abscess include: anaerobic streptococci, Bacteroides spp.
(including B. fragilis), Prevotella melaninogenica, Propionibacterium, Fusobacterium, Eubacterium, Veillonella, and
Actinomyces [31,34].
Aerobic pathogens Aerobic gram-positive cocci are also frequently encountered and include: viridans streptococci,
Streptococcus milleri, microaerophilic streptococci, Streptococcus pneumoniae (rare), and Staphylococcus aureus
[16,26]. S. aureus is a frequent pathogen in brain abscess following trauma or a neurosurgical procedure [19]. Cases of
community-acquired methicillin-resistant S. aureus have been described [35]. (See "Epidemiology of methicillin-resistant
Staphylococcus aureus infection in adults".)
S. milleri (also called S. anginosus) is particularly common; this organism possesses proteolytic enzymes that predispose
to necrosis of tissue and the formation of abscesses [36]. Rarely, the gram-positive rod Rhodococcus equi has been
associated with brain abscesses, primarily in immunocompromised patients but also in one reported immunocompetent
patient [37]. (See "Group C and group G streptococcal infection" and"Microbiology; pathogenesis; and epidemiology of
Rhodococcus equi infections".)
Aerobic gram-negative rods can be recovered from a brain abscess following neurosurgery or head trauma or when an
otogenic infection is the source. When gram-negative rods are isolated, Klebsiella pneumoniae, Pseudomonas spp.,
Escherichia coli, and Proteus spp. are most common. Less common pathogens include Haemophilus aphrophilus,
Actinobacillus actinomycetemcomitans, Salmonella, and Enterobacter spp. [38,39]. (See "Epidemiology and clinical
features of Gram-negative bacillary meningitis".)
Klebsiella pneumoniae brain abscess with or without meningitis can occur as a manifestation of metastatic infection that is
associated with community-acquired primary liver abscess. This syndrome is primarily seen in Southeast Asia, particularly
Taiwan. This disorder is discussed in detail separately. (See "Invasive liver abscess syndrome caused by Klebsiella
pneumoniae", section on 'Metastatic infection'.)
Immunocompromised hosts The range of organisms, particularly opportunistic pathogens, is considerably broader in
the immunocompromised host with a brain abscess [32,40]. Toxoplasma gondii can reactivate when the cell-mediated
immune system becomes compromised. (See "Toxoplasmosis in HIV-infected patients".)
Listeria can result in single or multiple brain or brainstem abscesses particularly in patients receiving corticosteroids [41].
Mortality is three times higher in patients with Listeria as compared to those with brain abscesses caused by other
bacteria [42]. (See "Clinical manifestations and diagnosis of Listeria monocytogenes infection", section on 'CNS
infection'.)
Nocardia asteroides, a common soil organism, can enter the bloodstream via the lungs and seed the cerebral cortex [43].
(See "Basic biology and epidemiology of nocardiosis" and "Clinical manifestations and diagnosis of nocardiosis".)
Aspergillus [44], Cryptococcus neoformans, and Coccidioides immitis also can enter through the lungs and subsequently
invade the cerebral cortex. (See "Clinical features and diagnosis of invasive aspergillosis" and"Clinical manifestations and
diagnosis of cryptococcal meningoencephalitis in HIV seronegative patients" and"Coccidioidal meningitis".)
Other fungal pathogens causing brain abscess in the immunocompromised host include Candida spp, the fungi that
cause zygomycosis (mucormycosis), Cladosporium trichoides and Curvularia spp. (See "Mucormycosis (zygomycosis)".)
Fungal infections of the brain usually result in multiple brain abscesses, and the outcome is usually poor [33].
HIV-infected patients Individuals infected with the human immunodeficiency virus (HIV) frequently develop infections
of the cerebral cortex. The differential diagnosis of central nervous system infections in the HIV-infected patient is
discussed separately. (See "Approach to HIV-infected patients with central nervous system lesions" and "AIDS-
associated cryptococcal meningoencephalitis".)
Immigrants Parasites are the most common etiology of brain abscess in individuals who previously lived outside the
United States. Cysticercosis due to Taenia solium infection represents 85 percent of brain infections in Mexico City [45].
(See "Clinical manifestations and diagnosis of cysticercosis".)
Other parasites that can cause brain abscess or infection include: Entamoeba histolytica, Schistosoma japonicum, and
Paragonimus species [29]. Salmonella brain abscess has also been described in a traveler [25]. (See "Epidemiology;
pathogenesis; and clinical features of schistosomiasis" and "Paragonimiasis", section on 'Cerebral
paragonimiasis' and "Extraintestinal Entamoeba histolytica amebiasis", section on 'Brain abscess'.)
CLINICAL MANIFESTATIONS The manifestations of brain abscess initially tend to be nonspecific, resulting in a delay
in establishing the diagnosis [8,19]. The diagnosis is made at a mean of 13 to 14 days after the onset of symptoms [1]. A
number of other infectious and noninfectious entities are in the differential diagnosis of brain abscess (table 2).
Symptoms Headache is the most common symptom of a brain abscess although it is obviously also one of the most
common medical complaints. (See "Evaluation of headache in adults".)
The pain is usually localized to the side of the abscess, and its onset can be gradual or sudden. The pain tends to be
severe and not relieved by aspirin or other over-the-counter pain medications. In patients with cyanotic heart disease and
headache, brain abscess must always be excluded.
Neck stiffness occurs in 15 percent of patients with brain abscess. This complaint is most commonly associated with
occipital lobe abscess or an abscess that has leaked into a lateral ventricle. Changes in mental status (lethargy
progressing to coma) are indicative of severe cerebral edema and are a poor prognostic sign (see below). Vomiting
generally develops in association with increased intracranial pressure [1].
Physical examination Fever is not a reliable indicator of brain abscess since only 45 to 50 percent of patients have
this sign [46]. Focal neurologic deficits are observed in 50 percent of patients and generally occur days to weeks after the
onset of headache (table 3). Seizures develop in 25 percent of cases and can be the first manifestation of brain abscess
[46]. Grand mal seizures are particularly common in frontal abscesses.
Third and sixth cranial nerve deficits indicate raised intracranial pressure. Papilledema is a late manifestation of cerebral
edema and usually takes several days to develop. This finding is observed in approximately 25 percent of patients.
DIAGNOSIS In the setting of focal symptoms (eg, unilateral headache) or signs (eg, unilateral cranial nerve deficits,
hemiparesis) or the finding of papilledema, a lumbar puncture (LP) is contraindicated [47]. Decompression of the
cerebrospinal fluid (CSF) pressure below the tentorium in association with asymmetric cerebral edema results in
brainstem herniation in 1.5 to 30 percent of cases [1,19,48-50]. CT scan with contrast or MRI should be performed prior to
LP in this circumstance to exclude a focal cerebral lesion. Blood cultures should be drawn (positive in 15 percent of
cases) and empiric parenteral antibiotic therapy initiated before CT scan or MRI. If the study is negative, an LP can then
be performed.
Computed tomographic scan CT scan is not as sensitive as MRI for the diagnosis of brain abscess but can
frequently be obtained more easily on an emergent basis. When looking for a brain abscess, this study must be
performed with a contrast agent. The lesion has different appearances depending upon its age [24]:
Early cerebritis appears as an irregular area of low density that does not enhance following contrast injection.
As cerebritis evolves; the lesion enlarges with thick and diffuse ring enhancement following contrast injection.
The ring of contrast enhancement represents breakdown of the blood brain barrier and the development of an
inflammatory capsule.
The precontrast scan reveals a faint area of higher density than the surrounding edematous brain by the time
the lesion has matured and become encapsulated. The contrast study for these late lesions demonstrates a thin ring
which may not be uniform in thickness and is often less prominent on the medial surface, adjacent to the white matter,
where vascularity is reduced.
Magnetic resonance imaging MRI should be performed with gadolinium diethylenetriamine peta-acetic acid. This
agent increases the T1 intensity and causes more prominent enhancement of lesions than CT scan. Compared to CT
scan, MRI:
Is more sensitive for early cerebritis
Is more sensitive for detecting satellite lesions
More accurately estimates the extent of central necrosis, ring enhancement, and cerebral edema
Better visualizes the brainstem
Diffusion-weighted MR imaging (DWI) is capable of differentiating ring-enhancing lesions due to brain abscess from
neoplastic lesions [51]. Abscesses are usually hyperintense on DWI (indicating restricted diffusion, characteristic of
viscous materials, such as pus), while neoplastic lesions are hypointense or show variable hyperintensity that is lower
than the intensity seen with an abscess [52].
Lumbar puncture As discussed above, this test is contraindicated in a patient with focal symptoms or signs. However,
an LP has been inadvertently performed in a number of cases. In one study of 65 patients with brain abscess that
underwent lumbar puncture, the CSF pattern was variable [50]. The mean protein level was 250 mg/dL (range 90 to 425
mg/dL); mean glucose level 39 mg/dL (range, 11 to 58 mg/dL); and mean white cell count 4407 per microL (range, 80 to
5006 per microL). Rarely, the CSF formula resembles bacterial meningitis, which indicates rupture of the abscess into the
ventricle [53]. When this occurs, the PMN count can be as high as 160,000/microL with accompanying hypoglycorrhachia
and an elevated protein. In patients with presumed meningitis who respond poorly to antibiotics, MRI should be performed
and may reveal an unsuspected brain abscess that has ruptured into the ventricle [54].
Culture The specimen obtained from stereotactic CT-guided aspiration or surgery should be sent for Gram's stain,
aerobic, anaerobic, mycobacterial, and fungal culture. In addition, special stains including an acid-fast stain for
mycobacteria, modified acid-fast stain for Nocardia, and fungal stains should be performed to aid in the identification of
the etiologic agent.
Serology Serology, anti-Toxoplasma immunoglobulin G (IgG) antibody in blood and anticysticercal antibodies on CSF
specimens, can aid in the diagnosis of Toxoplasma gondii or neurocysticercosis infections. (See "Toxoplasmosis in HIV-
infected patients" and "Clinical manifestations and diagnosis of cysticercosis".)
Histopathology Definitive diagnosis of brain abscess and frequently the identification of the etiologic agent is made by
pathologic examination of brain tissue obtained by open or stereotactic brain biopsy.
16S ribosomal sequencing In one study, 16S ribosomal DNA polymerase chain reaction amplification increased the
number of bacterial species isolated from brain abscesses as compared with standard culture; several species had not
been identified previously [55]. Further studies will be required to determine the significance of the identification of these
newly identified bacteria associated with brain abscesses [56].
SUMMARY AND RECOMMENDATIONS
Brain abscess is a focal collection within the brain parenchyma, which can arise as a complication of a variety of
infections, trauma, or surgery. Bacteria can invade the brain either by direct spread or through hematogenous seeding.
(See 'Introduction' above and 'Pathogenesis' above.)
The direct spread of organisms from a contiguous site usually causes a single brain abscess. Primary infections
that can directly spread to the cerebral cortex include subacute and chronic otitis media and mastoiditis (spread to the
inferior temporal lobe and cerebellum), frontal or ethmoid sinusitis (spread to the frontal lobes), and dental infection
(usually spreads to the frontal lobes). (See 'Direct spread' above.)
Brain abscesses associated with bacteremia usually result in multiple abscesses that are most commonly
located in the distribution of the middle cerebral artery. (See 'Hematogenous spread' above.)
A wide variety of organisms may cause brain abscess. The pathogens involved differ depending upon the site
of the primary infection (table 1). (See 'Microbiology' above.)
The manifestations of brain abscess initially tend to be nonspecific, resulting in a delay in establishing the
diagnosis. In addition, a number of other infectious and noninfectious entities are in the differential diagnosis of brain
abscess (table 2). (See 'Clinical manifestations' above.)
In the setting of focal symptoms (eg, unilateral headache) or signs (eg, unilateral cranial nerve deficits,
hemiparesis) or the finding of papilledema, a lumbar puncture (LP) is contraindicated, as brainstem herniation may occur
in 1.5 to 30 percent of cases when LP is performed in a patient with a brain abscess. (See'Diagnosis' above.)
MRI is the imaging study of choice in brain abscess as it is more sensitive than the CT scan. Diffusion-weighted
MR imaging (DWI) is, in addition, more capable of differentiating ring-enhancing lesions due to brain abscess from
neoplastic lesions. (See 'Magnetic resonance imaging' above.)
The specimen obtained from stereotactic CT-guided aspiration or surgery should be sent for Gram's stain,
aerobic, anaerobic, mycobacterial, and fungal cultures, special stains, and histopathology. (See'Diagnosis' above.)
Patients at risk for parasitic brain abscess should have serology of blood and/or CSF sent for diagnostic testing.
(See 'Serology' above.)
Microbiologic pathogens in brain abscesses, according to major
primary source of infection
Source of infection Pathogens
Paranasal sinuses Streptococcus (especially S. milleri), Haemophilus,
Bacteroides, Fusobacterium
Odontogenic sources Streptococcus, Bacteroides, Prevotella, Fusobacterium,
Haemophilus
Otogenic sources Enterobacteriaceae, Streptococcus, Pseudomonas,
Bacteroides
Lungs Streptococcus, Fusobacterium, Actinomyces
Urinary tract Pseudomonas, Enterobacter
Penetrating head trauma Staphylococcus aureus, Enterobacter, Clostridium
Neurosurgical procedure Staphylococcus, Streptococcus, Pseudomonas,
Enterobacter
Endocarditis Viridans streptococcus, S. aureus
Congenital cardiac malformations (especially
right-to-left shunts)
Streptococcus
Reproduced with permission from: Friedlander, RM, Gonzalez, RG, Afridi, NA, Pfannl, R. Case 16-
2003 A 58-year-old woman with left-sided weakness and a right frontal brain mass. N Engl J
Med 2003; 348:2125. Copyright 2003 Massachusetts Medical Society.

Differential diagnosis of brain abscess
Epidural and subdural empyema
Septic dural sinus thrombosis
Mycotic cerebral aneurysms
Septic cerebral emboli with associated infarction
Acute focal necrotizing encephalitis (most commonly due to herpes simplex virus)
Metastatic or primary brain tumors
Pyogenic meningitis

Neurologic deficits in brain abscess by location
Temporal lobe
Werincke's aphasia
Homonymous superior quadranopsia
Mild contralateral facial muscle weakness
Frontal lobe
Drowsy
Inattentive
Disturbed judgment
Mutism
Seizures
Presence of grasp, suck and snout reflexes
Contralateral hemiparesis (when the abscess is large)
Parietal lobe
Impaired position sense, two point discrimination and stereognosis
Focal sensory and motor seizures
Homonymous hemianopsia
Impaired opticokinetic nystagmus
Cerebellar
Ataxia
Nystagmus (coarser on gaze toward the lesion)
Ipsilaterial incoordination of arm and leg movements with intention tremor
Brainstem
Facial weakness and dysphagia
Multiple other cranial nerve palsies
Contralateral hemiparesis







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Treatment and prognosis of brain abscess
Author
Frederick S Southwick, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Anna R Thorner, MD
Last literature review version 18.3: septiembre 2010 | This topic last updated: junio 8, 2009 (More)
INTRODUCTION Brain abscess is a focal collection within the brain parenchyma, which can arise as a complication of
a variety of infections, trauma, or surgery. Successful treatment of a brain abscess requires a high index of suspicion for
the infection, which can have subtle presentations, and frequently requires a combination of drainage and antimicrobial
therapy. A summary of key steps in management is provided in Table 1 (table 1).
The treatment and prognosis of brain abscess will be presented here. The pathogenesis, clinical manifestations, and
diagnosis of this disease are discussed separately. (See "Pathogenesis, clinical manifestations, and diagnosis of brain
abscess".)
THERAPY Successful management of a brain abscess usually requires a combination of antibiotics and surgical
drainage for both diagnostic and therapeutic purposes [1-3].
Antibiotics A number of drugs can be chosen depending upon the likely origin of the abscess and the probable
pathogen(s) involved. These antibiotics include:
Penicillin G covers most mouth flora including both aerobic and anaerobic streptococci. However, the
emergence of penicillinase-producing anaerobes (eg, B. fragilis, Prevotella) is a potential limitation of penicillin therapy.
Metronidazole readily penetrates brain abscesses; intralesional concentrations have been found to be 40
microgram/mL. This drug has excellent bactericidal activity against many anaerobes but is not active against aerobic
organisms including microaerophilic streptococci. Given the excellent intralesional concentrations and the high probability
of anaerobes, many experts recommend administering this agent to most patients with brain abscess.
Ceftriaxone covers most aerobic and microaerophilic streptococci (and can be used in place of penicillin) but
also covers many Enterobacteriaceae as well, which can cause brain abscess particularly in association with chronic ear
or sinus infections or following penetrating trauma. Cefotaxime provides similar coverage.
Ceftazidime or cefepime should be used when brain abscess complicates a neurosurgical procedure or in
cases in which the abscess culture grows P. aeruginosa.
Oxacillin, nafcillin, or vancomycin should be included when brain abscess follows penetrating head trauma or
craniotomy, or when S. aureus bacteremia is documented. Vancomycin should be particularly considered for post-
neurosurgery patients, in hospital-associated infections, and in communities where community-associated methicillin-
resistant S. aureus is common until culture and susceptibility results are available.
Aminoglycosides, erythromycin, tetracyclines, clindamycin, and first generation cephalosporins should not be used to
treat brain abscess because these drugs do not cross the blood brain barrier at high concentrations.
Empiric therapy We recommend the empiric antimicrobial regimen be based on the presumptive source of the
abscess and Gram stain results if available.
For patients with a brain abscess arising from an oral, otogenic, or sinus source (eg, chronic otitis or mastoiditis; site of
abscess usually temporal lobe or cerebellum; frontal or ethmoid sinusitis; site of abscess usually frontal lobe), we
recommend treatment with:
Metronidazole (15 mg/kg IV as a loading dose, followed by 7.5 mg/kg IV every eight hours; not to exceed 4 g
per day) PLUS either penicillin G (20 to 24 million units per day IV in six equally divided doses) for a suspected oral focus,
or ceftriaxone (2 g IV every 12 hours) OR cefotaxime (2 g IV every four to six hours) for a suspected sinus or otogenic
source.
For patients with a brain abscess from hematogenous spread (eg, bacteremia, endocarditis; multiple abscesses in middle
cerebral artery distribution), we recommend treatment with:
Vancomycin (30 mg/kg IV daily in two equally divided doses adjusted for renal function) for empiric coverage of
methicillin-resistant Staphylococcus aureus. If susceptibility testing reveals methicillin-sensitive S.
aureus, vancomycin should be replaced with nafcillin (2 g IV every four hours) or oxacillin (2 g IV every four hours) since
these agents have better CNS penetration than vancomycin. Metronidazole and ceftriaxone orcefotaxime, dosed as
above, may be added for initial empiric coverage if the bacteriology is uncertain.
For brain abscess in postoperative neurosurgical patients, we recommend treatment with:
Vancomycin (30 mg/kg IV daily in two equally divided doses adjusted per renal function) PLUS ceftazidime (2 g
IV every eight hours) or cefepime (2 g IV every eight hours). If susceptibility testing reveals methicillin-sensitive S.
aureus, vancomycin should be replaced with nafcillin (2 g IV every four hours) or oxacillin (2 g IV every four hours) since
these agents have better CNS penetration than vancomycin.
For brain abscess following penetrating trauma, we recommend treatment with:
Vancomycin (30 mg/kg IV daily in two equally divided doses adjusted per renal function) PLUS
either ceftriaxone (2 g IV every 12 hours) or cefotaxime (2 g IV every four to six hours). If susceptibility testing reveals
methicillin-sensitive S. aureus, vancomycin should be replaced with nafcillin (2 g IV every four hours) or oxacillin (2 g IV
every four hours) since these agents have better CNS penetration than vancomycin.
Subsequent treatment When the etiologic agent(s) has been identified by culture, treatment regimens should be
simplified and directed to that pathogen(s).
Duration of therapy The duration of antibiotics for brain abscess is prolonged, usually six to eight weeks. The duration
of therapy should be guided by follow up assessment of clinical course and imaging studies; antibiotic therapy is
continued until there is a good clinical response and resolution of the CT or MRI findings. Contrast enhancement at the
site of the abscess may persist for several months [3]. Thus, this finding alone is not an indication for continued antibiotic
treatment or for surgical exploration.
Surgery The neurosurgeon needs to be contacted at the time of initial diagnosis of a brain abscess. Needle aspiration
and surgical excision have both been used to treat brain abscess, and are also required for diagnosis, prior to the
initiation of antibiotic therapy if possible. An exception may be when a brain abscess occurs in the setting of bacteremia,
in which case empiric antibiotic therapy is based upon the results of blood culture.
Aspiration Needle aspiration is generally preferable to surgical excision since the neurologic sequelae are reduced.
Needle aspiration is preferred for speech areas and regions of the sensory or motor cortex and in comatose patients.
A Burr hole is placed and then needle aspiration is performed under CT or ultrasonography guidance. It is important that
the aspirate be cultured for aerobes and anaerobes, fungi, and Mycobacterium tuberculosis. If the abscess fails to change
in size or expands in diameter, it should be reaspirated.
Reports have emphasized an improved outcome with stereotactic guidance to improve the precision of needle aspiration
[4]. As an example, in one series of 29 patients treated with this approach, only 2 new neurological deficits developed
after surgery [4].
Under certain circumstances, drainage may be delayed or not required:
Early cerebritis without evidence of cerebral necrosis
Abscesses located in vital regions of the brain or those inaccessible to aspiration [5]
When the decision is made not to drain immediately, follow-up with sequential CT or MRI is critical. There are no specific
guidelines for timing of follow-up imaging. A repeat scan in 48 hours and at one week are typical, although any change in
clinical status requires immediate repeat imaging.
Surgical excision Surgical excision is a more radical approach that generally results in greater neurologic deficits and
now is infrequently performed. Excision may be the initial treatment of choice in the following circumstances:
Traumatic brain abscesses (to remove bone chips and foreign material)
Encapsulated fungal brain abscesses
Multiloculated abscesses
In addition, the following are indications for excision after initial aspiration and drainage [6]:
No clinical improvement within one week
Depressed sensorium
Signs of increased intracranial pressure
Progressive increase in the ring diameter of the abscess
Patients with multiloculated lesions are more likely to recur and may require a second operative procedure for cure [7].
The course of intravenous antibiotic therapy can be shortened to two to four weeks following excision compared with
drainage. Excised lesions are less likely to relapse than lesions that have only been drained [8].
Glucocorticoids Glucocorticoids should be used when substantial mass effect can be demonstrated on
imaging. Dexamethasone is administered at a loading dose 10 mg IV followed by 4 mg every six hours; the drug should
be discontinued as soon as possible.
The addition of glucocorticoids has a number of disadvantages including [9]:
Reduction in contrast enhancement on CT scan
Slowing of capsule formation
Increasing the risk of ventricular rupture
Decreasing the penetration of antibiotics into the abscess
PROGNOSIS AND OUTCOME Published mortality rates from brain abscess range from zero to 30 percent [10-14]. In
a large retrospective series from France of 96 patients with brain abscess, there was a significant difference in the
mortality rate from 1993 to 1999 compared to the period 1980 to 1992 (8 versus 30 percent); there was also a trend
toward earlier diagnosis and improved neurologic function in the more recent time period [12].
Poor prognostic factors for recovery from a brain abscess include [11]:
Rapid progression of the infection before hospitalization
Severe mental status changes on admission
Stupor or coma (60 to 100 percent mortality)
Rupture into the ventricle (80 to 100 percent mortality)
Neurologic sequelae, of which seizures are the most common, occur in 30 to 60 percent of patients [11]. Patients with
frontal brain abscess are particularly vulnerable to recurrent seizures.
SUMMARY AND RECOMMENDATIONS
Successful management of a brain abscess usually requires a combination of antibiotics and surgical drainage
(table 1). (See 'Therapy' above.)
The neurosurgeon needs to be contacted at the time of initial diagnosis of a brain abscess. Surgical drainage
generally is required for both diagnosis and treatment. (See 'Surgery' above.)
We recommend empiric antimicrobial therapy for all patients with a presumptive brain abscess (Grade 1B).
Antimicrobial therapy should be administered as soon as possible, although preferably after diagnostic aspiration. The
empiric antibiotic regimen is based upon the presumptive source of the abscess and Gram stain results if available.
(See 'Empiric therapy' above.)
When the etiologic agent(s) has been identified by culture, we recommend treatment regimens be simplified
and directed to that pathogen(s) (Grade 1B). (See 'Subsequent treatment' above.)
We recommend treatment for at least six to eight weeks, guided by follow up assessment of clinical course and
imaging studies for resolution of the CT or MRI findings (Grade 1B). (See 'Duration of therapy' above.)
We suggest glucocorticoids be used only when substantial mass effect can be demonstrated on a scan and the
mental status is significantly depressed (Grade 2C). (See 'Glucocorticoids' above.)
Mortality from brain abscess ranges from zero to 30 percent. (See 'Prognosis and outcome' above.)
Neurologic sequelae, of which seizures are the most common, occur in 30 to 60 percent of patients.
(See'Prognosis and outcome' above.)
REFERENCES
1. Mathisen, GE, Johnson, JP. Brain abscess. Clin Infect Dis 1997; 25:763.
2. Chun, CH, Johnson, JD, Hofstetter, M, Raff, MJ. Brain abscess. A study of 45 consecutive cases. Medicine (Baltimore)
1986; 65:415.
3. Cavuoglu, H, Kaya, RA, Trkmenoglu, ON, et al. Brain abscess: analysis of results in a series of 51 patients with a
combined surgical and medical approach during an 11-year period. Neurosurg Focus 2008; 24:E9.
4. Duma, CM, Kondziolka, D, Lunsford, LD. Image-guided stereotactic management of non-AIDS-related cerebral infection.
Neurosurg Clin N Am 1992; 3:291.
5. Carpenter, JL. Brain stem abscesses: cure with medical therapy, case report, and review. Clin Infect Dis 1994; 18:219.
6. Ng, PY, Seow, WT, Ong, PL. Brain abscesses: review of 30 cases treated with surgery. Aust N Z J Surg 1995; 65:664.
7. Su, TM, Lan, CM, Tsai, YD, et al. Multiloculated pyogenic brain abscess: experience in 25 patients. Neurosurgery 2008;
62 Suppl 2:556.
8. Mampalam, TJ, Rosenblum, ML. Trends in the management of bacterial brain abscesses: a review of 102 cases over 17
years. Neurosurgery 1988; 23:451.
9. Quartey, GR, Johnston, JA, Rozdilsky, B. Decadron in the treatment of cerebral abscess. An experimental study. J
Neurosurg 1976; 45:301.
10. Schliamser, SE, Bckman, K, Norrby, SR. Intracranial abscesses in adults: an analysis of 54 consecutive cases. Scand J
Infect Dis 1988; 20:1.
11. Seydoux, C, Francioli, P. Bacterial brain abscesses: factors influencing mortality and sequelae. Clin Infect Dis 1992;
15:394.
12. Tattevin, P, Bruneel, F, Clair, B, et al. Bacterial brain abscesses: a retrospective study of 94 patients admitted to an
intensive care unit (1980 to 1999). Am J Med 2003; 115:143.
13. Yang, SY, Zhao, CS. Review of 140 patients with brain abscess. Surg Neurol 1993; 39:290.
14. Jansson, AK, Enblad, P, Sjlin, J. Efficacy and safety of cefotaxime in combination with metronidazole for empirical
treatment of brain abscess in clinical practice: a retrospective study of 66 consecutive cases. Eur J Clin Microbiol Infect
Dis 2004; 23:7.


Rapid empiric management of brain abscess

Empiric antibiotics
Immediately begin empiric antibiotics following sterotactic or open biopsy/aspiration to obtain a specimen for
Gram stain, culture, and pathology.
The antibiotic regimen is dependent on Gram stain, if available, and the likely source of abscess.
Origin of abscess Treatment regimen
Oral, otogenic, or
sinus source
Metronidazole (15 mg/kg IV as a loading dose, followed by 7.5 mg/kg IV every eight
hours) PLUS either penicillin G (20 to 24 million units per day IV in six equally
divided doses) for a suspected oral focus, or ceftriaxone (2 g IV every 12
hours) or cefotaxime (2 g IV every four to six hours) for a suspected sinus or
otogenic source
Hematogenous
spread
Vancomycin* (30 mg/kg IV daily in two equally divided doses adjusted per renal
function) for empiric coverage of methicillin-resistant Staphylococcus aureus.
Metronidazole may be added for anaerobic coverage
Postoperative
neurosurgical
patients
Vancomycin* (30 mg/kg IV daily in two equally divided doses adjusted per renal
function) PLUS either ceftazidime (2 g IV every eight hours) orcefepime (2 g IV
every eight hours)
Penetrating trauma Vancomycin* (30 mg/kg IV daily in two equally divided doses adjusted per renal
function) PLUS either ceftriaxone (2 g IV every 12 hours) orcefotaxime (2 g IV
every four to six hours)
Glucocorticoids
Glucocorticoids should be used when substantial mass effect can be demonstrated on imaging and the
mental status is significantly depressed.
Dexamethasone is administered at a loading dose of 10 mg IV followed by 4 mg every six hours.
* If susceptibility testing reveals methicillin-sensitive S. aureus, vancomycin should be
replaced with nafcillin (2 g IV every four hours) or oxacillin (2 g IV every four hours)
since these agents have better CNS penetration than vancomycin