- Venous to arterial shunting: The bypass of pulmonary capillary circulation of a patient’s blood is a common reason for bacteria to gain access to the brain’s circulation. This is seen in congenital heart disease (23, 30, 51, 62, 74,109), pulmonary disease such as chronic infection (51), persisting left superior vena cava (43), and AVMs of the pulmonary circulation (17, 65).
- Bacteremia: Bacteremia from any source has been associated with brain abscesses. Some examples include endocarditis, skin folliculitis, and osteomyelitis (51).
- Abscesses with epicenter at gray-white junction: The sources of hematogenous dissemination can lead to metastatic brain abscesses, especially at the junction between the gray and white matter (1, 30, 74, 127, 103, 109).
- MCA distribution: Abscesses that are the result of hematogenous spread from distant sources may have a distribution that reflects the cerebral arterial supply, most commonly that of the MCA (31).
Contiguous spread of infection
- Otitis media and mastoiditis: This is a common source for abscesses, particularly in the emerging world (38, 78, 86).
- Sinusitis: Sinusitis is a common source for abscesses in the frontal and temporal lobes. It occurs by spread through bridging venous circulation from the sinuses to the dura (30, 109).
- Meningitis: Meningitis is a particular risk for neonates and infants (33, 85, 125).
- Dental infections: The role of odontogenic infection in the pathogenesis of brain abscess has been described. Dental pathology and/or treatments have been linked to a small number of brain abscesses as possible sources of infection in children (122, 141).
- Congenital tracts communicating skin with CNS: Direct communication with the CSF through a congenital dermal sinus tract can result in abscess formation (96, 99).
Penetrating traumatic injury to CNS
- Traumatic introduction of infection: A penetrating object is commonly colonized with bacteria that can seed any tissue it contacts. In the CNS penetration can lead to an abscess. Additionally, infection of contiguous tissue can spread into the CNS to cause an abscess.
Complication of neurosurgical procedure
- Complication of a surgery: Any infection occurring in an operative bed or within foreign material left after a neurosurgical procedure can lead to the development of an abscess when it is not treated in a timely fashion.
- Immunodeficiency: This is a common cause of brain abscesses is an immunocompromised patient.
- Unknown etiology: In a large proportion of cases (15–30%), the cause is unknown.
Stages in abscess development
A brain abscess is an intraparenchymal infection that commences as a localized area of cerebritis evolving through various stages into a collection of encapsulated purulent material (14).
- Early cerebritis stage: The early cerebritis stage constitutes the first 3 days of the infection. On the introduction of bacteria, a localized area of inflammation develops. This inflammatory process is primarily composed of polymorphonuclear leukocytes, lymphocytes, and plasma cells that have migrated from the blood vessels. As the infection progresses, the inflammatory cells accumulate in the adventitia of blood vessels in the region of the infection. At this stage the lesion is an ill-defined infiltration of inflammatory cells and vasodilation. The lesion usually has peripheral edema.
- Late cerebritis stage: The late cerebritis stage occurs between days 4 and 9 of the infection. The necrotic center enlarges as enzymes are released from the inflammatory cells, and pus and acellular debris begin to coalesce. At the margins of the necrosis a zone of inflammatory cells, large foamy macrophages, and fibroblasts accumulate. The fibroblasts begin to form a reticulin network around the area of necrosis. There is associated proliferation of new blood vessels around the area of infection, and cerebral edema is usually at its maximum during this phase.
- Early capsule formation stage: Between days 10 and 14 the necrotic center begins to shrink due to macrophage engulfment of the acellular debris. Fibroblasts continue to accumulate, and mature collagen begins to develop from the reticulin network that has been laid down around the infection. Cerebral edema begins to diminish, and reactive astrocytes become apparent in the surrounding brain tissue. The pathological characteristics of this stage are necrosis and liquefaction of the central area, with the formation of a distinct, thin-walled capsule of fibroblasts.
- Late capsule formation stage: After day 14 the lesion is a fully developed brain abscess, and it can be divided into five histologically distinct zones. Zone 1 is the necrotic center with inflammatory cells and acellular debris. Zone 2 is composed of inflammatory cells, macrophages, and fibroblasts. Zone 3 is a fully mature collagen capsule. Zone 4 contains neovasculature with continued perivascular cuffing, and zone 5 demonstrates edematous cerebral tissue with reactive astrocytosis and reactive gliosis. The pathological characteristic of this stage is the fully formed, thick collagenous abscess capsule.
Microbiology of brain abscesses
- Gram-positive cocci most common: Gram-positive cocci are the most common causative agents found in pediatric brain abscesses, followed by gram-negative bacilli (30, 44, 66, 109).
- Methecillin-resistant Staphylococcus increasing problem: There are increasing rates of methicillin- resistant Staphylococcus aureus in nosocomial infections, shunts, and penetrating trauma-related brain abscesses in children (12, 51).
- 10–20% sterile cultures: Relatively high rates of sterile cultures, varying between 10% and 20%, are reported in the literature. These rates may be explained by prior antibiotic treatment, the difficulty in isolating anaerobic microorganisms, or inadequate sampling technique (12).
- Anaerobic bacteria increasingly isolated: With the improvement of microbiological laboratory techniques, anaerobic bacteria are now more commonly (40–100% of cases) detected (12).
- Neonatal abscesses due to deficient immunoglobulins: Most abscesses in neonates are thought to be related to a deficiency of placentally transferred immunoglobulin and complement.
- Opportunistic and fungal organisms in immunocompromised patients: Fungal pathogens are found more frequently in immunocompromised patients (51). HIV-positive patients must be examined carefully for opportunistic organisms (such as Toxoplasma gondii).
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