Brain Abscess Clinical Presentation

Updated: Mar 02, 2021
  • Author: Itzhak Brook, MD, MSc; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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In about two thirds of patients with brain abscess, symptoms are present for 2 weeks or less. The clinical course ranges from indolent to fulminant.

Most symptoms are a result of the size and location of the space-occupying lesion or lesions.

The triad of fever, headache (often severe and on the side of the abscess), and focal neurologic deficit occurs in less than half of patients. The frequency of common symptoms and signs is as follows: [1]

  • Headache - 70%

  • Mental status changes (may indicate cerebral edema) - 65%

  • Focal neurologic deficits - 65%

  • Fever - 50%

  • Seizures - 25-35%

  • Nausea and vomiting - 40%

  • Nuchal rigidity - 25%

  • Papilledema - 25%

A suddenly worsening headache, followed by emerging signs of meningismus, is often associated with rupture of the abscess.



The clinical manifestations of brain abscess are initially nonspecific, which can lead to delay in diagnosis. Brain abscess usually manifests as symptoms of a space-occupying lesion. The symptoms and signs include the following:

  • Low-grade or high-grade fever

  • Persistent headache (often localized)

  • Drowsiness

  • Confusion

  • Stupor

  • General or focal seizures

  • Nausea and vomiting

  • Focal motor or sensory impairments

  • Papilledema

  • Ataxia

  • Hemiparesis

  • Neck stiffness

Localized neurologic signs are eventually found in most patients. The signs and/or symptoms are a direct function of the intracranial location of the abscess, as follows:

  • Cerebellar abscess - Nystagmus, ataxia, vomiting, and dysmetria

  • Brainstem abscess - Facial weakness, headache, fever, vomiting, dysphagia, and hemiparesis

  • Frontal abscess - Headache, inattention, drowsiness, mental status deterioration, motor speech disorder, hemiparesis with unilateral motor signs, and grand mal seizures

  • Temporal lobe abscess - Headache, ipsilateral aphasia (if in the dominant hemisphere), and visual defects

  • Occipital abscess- Neck rigidity

In the initial stages of the infection, an abscess can manifest as a nonspecific form of encephalitis accompanied by signs of increased intracranial pressure.

The headache associated with brain abscess can gradually develop or suddenly emerge and is often localized to the abscess' side. It is often severe and is not relieved by mild pain medications.

Papilledema may develop in older child and adults, and younger infants may exhibit bulging fontanels. This is a late expression of cerebral edema.

A ruptured brain abscess may produce purulent meningitis associated with signs of neurologic damage.

Vomiting commonly develops in association with increased intracranial pressure. Changes in mental status (lethargy progressing to coma) suggest severe cerebral edema.

Specific clinical symptoms are characteristic of some pathogens.



The microbial etiology of brain abscess depends on the patient's age, site of primary infection, and the patient's immune status. [19, 20]

Anaerobic and microaerophilic cocci and gram-negative and gram-positive anaerobic bacilli are the most important isolates. A significant number of brain abscesses are polymicrobic. [19, 20, 21, 22, 23]

Oral flora anaerobes generally originate from infected ears and sinuses and abdominal anaerobes (Bacteroides fragilis group) reach the intracranial cavity through bacteremia.

The predominant organisms include the following:

  • Staphylococcus aureus, including methicillin-resistant [24]
  • Aerobic, anaerobic, and microaerophilic streptococci, including alpha-hemolytic streptococci,  Streptococcus anginosus (milleri) group ( Streptococcus anginosus, Streptococcus constellatus, and Streptococcus intermedius)
  • Prevotella and Fusobacterium species and B fragilis
  • Enterobacteriaceae ( Klebsiella pneumoniae, Escherichia coli, Enterobacter species, and Proteus species) [25]
  • Pseudomonas species
  • Other anaerobes: (Veillonella, Eubacterium, Cutibacterium (formerly  Propionibacterium) , 
  • Methanobrevibacter oralis,  Methanobrevibacter smithii. [26]  

Less common causes include the following:

  • Haemophillus influenzae
  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Haemophilus aphrophilus
  • Other Enterobacteriacae (Enterobacter species, Actinobacillus, actinomycetemcomitans, and Salmonella species)
  • Burkholderia pseudomallei (also known as Pseudomonas pseudomallei) [27]
  • Actinobacillus actinomycetemcomitans
  • Actinomyces
  • Nocardia asteroides
  • Mycobacterium species
  • Fungi (eg, Aspergillus, Candida, Cryptococcus, Mucorales, Coccidioides, Histoplasma capsulatum, Blastomyces dermatitidis, Bipolaris, Exophiala dermatitidis, Curvularia pallescense, Ochronosis gallopava, Ramichloridium mackenziei)
  • Protozoa (eg, Toxoplasma gondii, Entamoeba histolytica, Trypanosoma cruzi, Schistosoma, Paragonimus)
  • Helminths (eg, Taenia solium)
  • Toxoplasma gondii
  • Pseudallescheria boydii

Co-infection with bacterial, viral, and fungal organisms can occur. [28]

The following organisms are associated with certain predisposing conditions: [29]

  • Sinus and dental infections - Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli (eg, Prevotella, Porphyromonas, Bacteroides, Fusobacterium, Cutibacterium (formerly  Propionibacterium), microaerophilic streptococci (mainly Streptococcus milleri), Haemophillus, S aureus, Enterobacteriaceae) [21]
  • Ear infections (including mastoiditis) - Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli, Haemophillus, Pseudomonas, and Enterobacteriaceae [30]
  • Pulmonary infections - Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli (eg, Prevotella, Porphyromonas, Bacteroides), Fusobacterium, Actinomyces, Nocardia [13]
  • Endocarditis - Alpha hemolytic streptococci, S aureus
  • Congenital heart disease - Aerobic and microaerophilic streptococci, S aureus
  • Liver abscess or diabetes mellitus (reported in Southeast Asia) - Klebsiella pneumoniae [31]
  • Penetrating head trauma - S aureus, aerobic streptococci, Enterobacteriaceae, Clostridium spp.
  • Esophageal dilatation- Peptostrepotoccocci spp., Streptococcus milleri, and Eschericia coli ,  [32]
  • Neurosurgical procedures- S aureus, Pseudomonas, Enterobacter, Propionibacterium acnes [33, 34]
  • Neonates - Citrobacter [35]
  • Urinary tract-Pseudomonas, Enterobacteriaceae, Enterobacter
  • Transplantation - Aspergillus, Candida, Cryptococcus, Mucorales, Nocardia, T gondii [12]
  • Immunocompromised - Aerobic gram-negative bacilli, T gondii, Nocardia asteroids, Listeria monocytogenes, Aspergillus, Cryptococcus, Coccidioides immitis, Candida, Mucorales [36, 37, 38]
  • HIV infection - T gondii, Mycobacterium, Cryptococcus, Nocardia, L monocytogenes [14]
  • Living, visiting, or immigrating from an endemic area: Taenia solium (causing cysticercosis), Schistosoma japonicum, Entamoeba histolytica, and Paragonimus species.

Al Masalma et al performed a 16S rDNA-based metagenomic analysis of cerebral abscesses and identified 80 distinct bacterial taxa, including 44 not previously described in brain abscess. Therefore, microbial flora of brain abscesses is far from being fully known and is differentially distributed depending on the abscess etiology. Further studies are warranted to determine the significance of the identification of the newly recovered bacteria associated within brain abscesses. [39]