Pathogenesis

Bacteria reach the brain parenchyma via the bloodstream, by direct extension from an adjacent focus of infection or by implantation through wounds as a result of trauma or neurosurgery. In about 15% of cases the source of infection cannot be identified. Haematogenous spread has been implicated in approximately 25% of cases. The most common primary foci are endocarditis and pulmonary infections. Brain abscesses resulting from haematogenous spread are often multifocal and more frequently involve middle cerebral artery territory. Congenital cyanotic heart disease and pulmonary suppuration (for example, bronchiectasis or lung abscess) are associated with an increased frequency of brain abscess. Sinusitis, otitis, and dental abscess are the most commonly implicated foci of infection that result in direct spread of infection to the brain parenchyma and subdural space. With improved treatment of these conditions the incidence of suppurative complications has declined. Spread of infection beyond the dural barrier is unusual in bacterial meningitis, but when it occurs is often secondary to gram negative organisms. Penetrating head injuries, particularly those secondary to gunshot wounds or associated with bone fragments, are occasionally associated with brain abscess. There is also a small risk following neurosurgical procedures.

The risk of brain abscess increases with immunosuppression, particularly that associated with the use of high dose corticosteroids, repeated episodes of rejection, and prolonged neutropenia in bone marrow/stem cell and solid organ transplant patients.

Experimental data indicate that bacteria cannot set up a nidus of infection in normal, undamaged brain and an area of devitalised or ischaemic tissue is a prerequisite. Generally it is believed that either a thrombophlebitis spreads from contiguous infection or that microinfarction from emboli or hypoxaemia produces a microscopic area of necrosis in which infection can become established. This is followed by cerebritis, with surrounding oedema of white matter; next the centre of cerebritis becomes necrotic and enlarges, capsule formation begins with the appearance of fibroblasts and neovascular change at the periphery, reactive astrocytosis, and surrounding oedema. Thereafter capsular development and thickening occurs.147 The time course is variable and may be as short as three weeks.

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