The most common organisms causing bacterial cerebral abscess are virulent streptococci, many of which are anaerobic or microaerophilic. These organisms are often found in combination with other anaerobes (polymicrobial), notably Bacteroides, Fusobacterium, and Prevotella and less often, Propionibacterium (diphtheroids), and may be combined with Hemophilus species, Enterobacteriaceae, such as E. coli and Proteus. Staphylococci also commonly cause brain abscess, but pneumococci, meningococci, and H. influenzae rarely do. In addition, the gram-positive higher bacteria Actinomyces and Nocardia and certain fungi discussed later, notably Candida, Mucor, and Aspergillus, are isolated in some cases.
The type of organism tends to vary with the source of the abscess; staphylococcal abscesses are usually a consequence of accidental or surgical trauma, sometimes of endocarditis, especially in intravenous drug abusers; abscesses originating from otitic infections usually contain oropharyngeal flora including anaerobes and enteric organisms; and anaerobic streptococci are commonly metastatic from the lung and paranasal sinuses. Predisposing to nocardial brain abscess is pulmonary nocardial infection, often in immunosuppressed patients; this diagnosis is doubtful without a pneumonic infiltrate. In immunosuppressed patients, brain abscess is usually from a nonbacterial organism; fungi and parasites (toxoplasmosis) prevail although Mycobacteria are common and Listeria and melioidosis occurs but constitute special cases of an encephalitic disorder with small abscesses. Thus knowledge of the antecedent history enables one to institute appropriate therapy while awaiting the results of bacterial and fungal cultures.
Localized inflammatory exudate, septic thrombosis of vessels, and aggregates of degenerating leukocytes represent the early reaction to bacterial invasion of the brain. Surrounding the necrotic tissue are macrophages, astroglia, microglia, and many small veins, some of which show endothelial hyperplasia, contain fibrin, and are cuffed with polymorphonuclear leukocytes. There is interstitial edema in the surrounding white matter. At this stage, which is rarely observed postmortem, the lesion is poorly circumscribed and tends to enlarge by a coalescence of inflammatory foci. The term cerebritis is loosely applied to this local suppurative encephalitis or immature abscess.
Within several days, the intensity of the reaction begins to subside and the infection tends to become delimited. The center of the abscess takes on the character of pus; at the periphery, fibroblasts proliferate from the adventitia of newly formed blood vessels and form granulation tissue, which is readily identified pathologically within 2 weeks of the onset of the infection but it is evident earlier as restriction of diffusion on MRI (see Fig. 31-2). As the abscess becomes more chronic, the granulation tissue is replaced by collagenous connective tissue. It has also been noted, both in experimental animals and in humans, that the capsule of the abscess is not of uniform thickness, frequently being thinner on its medial (paraventricular) aspect. These factors account for the propensity of cerebral abscesses to spread deeply into the white matter and to produce daughter abscesses or a chain of abscesses and extensive surrounding cerebral edema. In some instances, the process culminates in a catastrophic rupture into the ventricles.