With a hematogenous infection in the course of a bacteremia, usually a single type of virulent bacterium gains entry to the cranial cavity. In the adult the most common spontaneous or community-acquired pathogenic organisms are pneumococcus (Streptococcus pneumoniae), meningococcus (Neisseria meningitidis), group B streptococcus, Listeria monocytogenes, and staphylococcus; in the neonate, Escherichia coli and group B streptococcus; in the infant and unvaccinated child, H. influenzae. By contrast, when septic material embolizes from infected lungs, pulmonary arteriovenous fistulas, or congenital heart lesions, or extends directly from ears or sinuses, more than one type of bacterial flora common to these sites may be transmitted. Such “mixed infections” pose difficult problems in therapy. Occasionally in these latter conditions, culture of the causative organisms may be unsuccessful, even from the pus of an abscess (mainly because of difficulty in culturing for anaerobic organisms and due to the prior use of antibiotics). Infections that follow neurosurgery or the insertion of a cranial appliance are usually staphylococcal or due to anaerobic gram negative organisms; a small number are a result of mixed flora, including anaerobic ones, or one of the enteric organisms. In determining the most likely invading organism, the age of the patient, the clinical setting of the infection (community-acquired, postsurgical, or nosocomial), the immune status of the patient, and evidence of systemic and local cranial disease all must be taken into account.
The Biology of Bacterial Meningitis
The immediate effect of bacteria or other microorganisms in the subarachnoid space is to cause an inflammatory reaction in the pia and arachnoid as well as in the cerebrospinal fluid (CSF). Because the subarachnoid space is continuous around the brain, spinal cord, and optic nerves, an infective agent gaining entry to any one part of the space allows it to spread rapidly to all of it, even its most remote recesses; in other words, meningitis is always cerebrospinal. Infection also reaches the ventricles, either directly from the choroid plexuses or by reflux through the foramina of Magendie and Luschka.
The first reaction to bacteria or their toxins is hyperemia of the meningeal venules and capillaries and an increased permeability of these vessels, followed shortly by exudation of protein and the migration of neutrophils into the pia and subarachnoid space. The subarachnoid exudate increases rapidly, particularly over the base of the brain; it extends into the sheaths of cranial and spinal nerves and, for a very short distance, into the perivascular spaces of the cortex. During the first few days, mature and immature neutrophils, many of them containing phagocytosed bacteria, are the predominant cells. Within a few days, lymphocytes and histiocytes increase gradually in numbers. During this time, there is exudation of fibrinogen, which is converted to fibrin after a few days. In the latter part of the second week, plasma cells appear and subsequently increase in number. At about the same time the cellular exudate becomes organized into two layers—an outer one, just beneath the arachnoid membrane, made up of neutrophils and fibrin, and an inner one, next to the pia, composed largely of lymphocytes, plasma cells, and mononuclear cells or macrophages. Although fibroblasts of the meninges begin to proliferate early, they are not conspicuous until later, when they take part in the organization of the exudate, resulting in fibrosis of the arachnoid and loculation of pockets of exudate.