The bacteriological profile of brain abscess has changed significantly over the past 50 years. In the older literature, aerobic streptococci, pneu-mococci and Staphylococcus aureus predominated, with relatively few Gram-negative and anerobic infections reported [1,2]. More recent series have shown a significant increase in anerobic abscesses, the most common isolates being Bacteroides spp. and anerobic streptococci. The incidence of Gram-negative infections has also increased, sometimes comprising more than 20% of cases. Although most abscesses are caused by a single organism, mixed infections occur in up to 33% of cases, particularly otogenic abscesses. The incidence of negative cultures remains around 25%; however, the use of meticulous microbiological techniques can result in positive cultures in virtually 100% of brain abscesses, even in the face of antibiotic therapy .
The microbiological profile of a brain abscess is closely linked to the underlying etiology. Although the source of infection is usually apparent, a definitive underlying cause may be obscure in around 30% of patients. Anerobic organisms predominate in abscesses caused by underlying otogenic and dental infections, and are common in metastatic and cryptogenic abscesses. The most common organisms isolated from sinusitic abscesses include those that normally inhabit the para-nasal sinuses, including S. aureus, aerobic streptococci and Hemophilus influenzae, although anerobes may be identified in over 50% of sinusitic abscesses
Suppurative processes of the air sinuses are the most common underlying cause of brain abscess, which develops by direct intracranial extension or through retrograde thrombophlebitis of diploic or emissary veins [1,2,4]. Sinusitic and otogenic abscesses are usually solitary and located superficially. Metastatic abscesses develop following hematogenous dissemination of micro-organisms from a systemic infection. Common primary foci include skin pustules, pulmonary infections, acute divertic-ulitis, osteomyelitis, periodontal abscess and sub-acute bacterial endocarditis (SBE). Interestingly, transient bacteremia alone is unlikely to result in abscess formation, owing to inherent resistance of the blood-brain barrier to infection. Metastatic abscesses are often multiple and are distributed in a manner proportionate to regional CBF, the middle cerebral artery territory being the most common location. They tend to occur at the corticomedullary junction but can also occur deep in the parenchyma.
Cerebral abscess is a leading cause of morbidity in patients with cyanotic congenital heart disease (CHD) . Cardiac malformations that produce a right-to-left shunt allow bacteria to bypass the pulmonary capillary bed, where they are normally filtered. Additionally, longstanding hypoxemia results in polycythemia and increased blood viscosity that predispose to areas of microinfarction, thus providing favorable conditions for the growth of microorganisms. Curiously, endocarditis is not thought to be an important factor in the patho-genesis of these lesions and, unlike many metastatic abscesses, those associated with CHD are generally solitary.
Finally, post-traumatic or post-operative abscesses may occur following direct inoculation of bacteria into the brain. Post-traumatic abscesses tend to develop relatively soon following trauma, although some cases have been described as presenting many years following injury. Post-traumatic abscess can be prevented in large measure by early, aggressive debride-ment of necrotic non-viable tissue at the time of the injury. Post-operative abscesses usually result from organisms introduced at the time of
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