DISEASES OF CENTRAL NERVOUS SYSTEM-1

DISEASES OF CENTRAL NERVOUS SYSTEM-1

Meningitis

Meningitis is an infection of the meninges, the thin lining that surrounds the brain and the spinal cord. There are reports that the causative agent, Neisseria meningitidis (the meningococcus), was first identified in 1887.

Infection within the subarachnoid space or through out the leptomininges is referred to as meningitis. Based on the host’s response to the invading microorganism, meningitis is divided into two major categories: Purulent and Aseptic meningitis.

PURULENT MENINGITIS

A patient with purulent meningitis will typically have marked acute inflammatory exudates with large numbers of polymorpholonuclear cells. Frequently the underlying CNS tissue, in particular the ventricles, may be involved. If the ventricles become involved, then this process is referred to as ventriculitis. These infections are frequently cased by bacteria.

Pathogenesis

The outcome of a host-microbe interaction depends on the characteristics of both the host and the microorganism. An important host defense mechanism of the CNS is the blood-brain barrier; the choroids plexus, arachnoid’s membrane and the cerebral microvascular endothelium are the key structures. Because of the unique structural properties of the vascular endothelium, such as continuous intercellular tight junctions, this barrier minimizes the passage of infectious agents into CSF in addition to regulating the transport of plasma proteins, glucose, and electrolytes.

Age

Age of the host and other underlying host factors also contribute to whether and individual will be predisposed to develop meningitis or not. Neonates have the highest prevalence of meningitis cases. This is probably due to their immature immune system, the organisms present in the colonized female vaginal tract, and the increased permeability of the blood –brain barrier of newborns. Lack of demonstrable humoral antibody against Haemophilus influenzae type [b] in children has been associated with increased incidence of meningitis. Before the age of widespread vaccination, most children developed measurable antibody by around age 5. Also adults without the necessary antibody to Neisseria meningitidis could be linked to epidemic meningitis-especially those who live in crowded areas/conditions (e.g. military barracks, high school/college dormitories). N. meningitidis has been associated with epidemic meningitis.

Because the respiratory tract is the primary portal of entry for many etiologic agents of meningitis, factors that predispose adults to meningitis are often the same as those that increase the likelihood that the adult will develop pneumonia or other respiratory tract infections/colonization. Alcoholism, splenectomy, diabetes mellitus, and immunosuppression contribute to increased risk. Patients with prosthetic devices- particularly central nervous system shunts are also at risk of developing meningitis.

For organisms to reach CNS-primarily through blood borne route, host defense mechanism must be overcome. Most cases of meningitis caused by bacteria share a similar pathogenesis. A successful meningeal pathogen must first sequentially colonize and cross the host’s mucosal epithelium and then enter and survive in the bloodstream. The most common causes of the meningitis possess the ability to evade the host’s defense mechanism at each of these levels. For example clinical isolates of the Strep. Pneumoniae and N. meningitidis secrete IgA proteases (enzymes) that destroy the action of the host’s secretory IgA, thereby facilitating bacterial attachment to the epithelium. In addition, all of the most common etiologic agents of bacterial meningitis possess an antiphagocytic capsule that helps the organisms evade the destruction by the host’s immune system.

Organisms appear to enter the CNS by interacting and subsequently breaking down the blood-brain barrier at the level of microvascular endothelium. To date one of the least understood processes in the pathogenesis of meningitis is how the organisms cross this barrier into the subarachnoid space. Nevertheless, there appear to be specific bacterial surface components, such as pili, that facilitate adhesion of the organisms to the microvascular endothelial cells and subsequent penetration into the CSF. Organisms can enter through-1) loss of capillary integrity by disrupting tight junctions of the blood-brain barrier, -2) transport within circulating phagocytic cells, or -3) by crossing the endothelial cell lining within endothelial cell vacuoles. After gaining access, the organism multiplies within the CSF, a site initially free of antimicrobial antibodies or phagocytic cells.


Clinical manifestations:
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