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Brain Abscess

Pathogenesis of Brain Abscess

Brain abscess is a focal, intracerebral infection that begins as a localized area of cerebritis and develops into a collection of pus surrounded by a well-vascularized capsule. The leading etiologic agents of brain abscess are the streptococcal strains and S. aureus, although a myriad of other organisms has also been reported.

Pathogenic mechanisms of brain abscess formation. Fig.1 Pathogenic mechanisms of brain abscess formation. (Brouwer, 2014)

The most common source of microbial infection remains direct or indirect cranial infection arising from the paranasal sinuses, middle ear, and teeth. Other routes include seeding of the brain from distant sites of infection in the body or penetrating trauma to the head. Following brain abscess resolution patients may experience long-term complications including seizures, loss of mental acuity, and focal neurological defects that are lesion site dependent. Controlling the intensity and/or duration of the anti-bacterial immune response in the brain may allow for the effective elimination of bacteria while minimizing damage to surrounding brain tissue.

Immunopathogenesis of brain abscess. Fig.2 Immunopathogenesis of brain abscess. (Kielian, 2004)

Clinical Presentation of Brain Abscess

An abscess can primarily present in four basic syndromes viz: focal mass expansion, intracranial hypertension, diffuse destruction, and focal neurological deficit. There are marked variations in clinical symptoms and signs. Headache, changes in the level of consciousness, nausea and/or vomiting, and high fever are the most common manifestations. Brain abscesses may be unicentric or multifocal. A majority, about 90% brain abscess result from pericranial infection, and many who are hematology nous-borne are multifocal, especially from cyanotic congenital heart disease. Majority of the abscesses were in the frontal, temporal, and posterior fossa region.

Brain Abscess and Neuroinflammation

The immune response elicited can destroy the surrounding normal brain tissue. Recent research focus on a two-signal model of recognition, mediated by Toll-like receptors (TLR) and Nod-like receptors (NLR). TLR2 regulates bacterial burdens, immune infiltrates, and inflammatory mediator production during brain abscess development. NLR forms the inflammasome, the functional structure responsible for pro-interleukin-1b (pro-IL-1b) and pro-IL-18 processing, which when activated, IL-1b and IL-18, are implicated in the physiopathology of many neurogenerative disorders as well in CNS infection (e.g., bacterial meningitis, HIV-associated dementia, and brain abscess).

Scientists using a mouse model of brain abscess, founded that astrocyte GJ communication was significantly attenuated in regions immediately surrounding the abscess margins and progressively increased to levels typical of the uninfected brain with increasing distance from the abscess proper. Since CNS is not capable of robust regeneration that would be required to resolve the widespread parenchymal damage characteristic of brain abscess, it is essential that the immune response must be tightly regulated to effectively eradicate bacteria while limiting the extent of bystander damage to surrounding brain tissue.

Diagnosis of Brain Abscess

Brain abscess development can be divided into four stages: 1) early cerebritis (1-4 days); 2) late cerebritis (4-10 days); 3) early capsule formation (11-14 days); and 4) late capsule formation (>14 days). Staging of brain abscesses in humans has been based on findings obtained during CT or MRI scans.

Neuroimaging, usually a CT scan with contrast, is essential to diagnose a BA. CT facilitates early detection, exact localization, and accurate characterization, determination of the number, size, and staging of the abscess. It also detects hydrocephalus, raised intracranial pressure (ICP), edema, and associated infections like subdural empyema, ventriculitis and thus helps in treatment planning, in the assessment of the adequacy of treatment and sequential follow-up.

Imaging studies of brain abscess. Fig.3 Imaging studies of brain abscess. (Brouwer, 2014)

Products of Brain Abscess Research

Target name Product name Cat. No
TLR2 Rabbit TLR2/CD282 Antibody NAB-2102-MP816
NLR Mouse Anti-Human NLRP3 Monoclonal Antibody (Clone Cryo-2) NAB2105337SL
IL-18 Recombinant Mouse IL-18 (Asn36-Ser192) Protein, Carrier Free NPP201097LS

Brain abscess continues to be a formidable challenge despite the introduction of newer and effective antimicrobial chemotherapy and radiological and neurosurgical technology. As a leading international biotechnology company, Creative Biolabs focuses on research in neuroscience. Our team of highly qualified and experienced technical staff will work with you to develop and deliver analytical solutions for brain abscess research. Please feel free to contact us for detailed information.

References

  1. Brouwer, M.C.; et al. Brain abscess. New England Journal of Medicine. 2014, 371(5): 447-456.
  2. Kielian, T. Immunopathogenesis of brain abscess. J Neuroinflammation. 2004, 1: 16.
For Research Use Only. Not For Clinical Use.
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