Acute Bacterial Meningitis Pathophysiology

Acute Bacterial Meningitis

    * Introduction
    * Pathophysiology
    * Clinical
    * Diagnosis
    * Treatment

Pathophysiology
Pathogenesis mechanism comprises the following steps: nasopharyngeal colonization, invasion of nasopharyngeal epithelial cells, invasion of blood flow, blood brain barrier crossing and replication inside the subarachnoid space. Neisseria meningitidis and Streptococcus pneumoniae are part of the normal flora of the nasal epithelium and does not produce any disease only when the host immune system is compromised and the bacteria enter the bloodstream. Invasion involves shunting epithelial secretory immunoglobulin A ciliary mechanisms and avoid cleaning. Venous Sinuses of the dura mater and choroid plexus is the major route of invasion of the central nervous system. Once the bacteria have entered the subarachnoid space, they find a favorable environment for development, with small resources subarachnoid space defense.
Humoral host defense mechanisms (activity-dependent immunoglobulin and complement activation) are almost nonexistent in the subarachnoid space. Phagocytosis of pathogenic bacteria in cerebrospinal fluid is ineffective. With the multiplication of bacteria in the subarachnoid space will produce meninges inflammation, inflammation that is responsible for the clinical syndrome of bacterial meningitis. Inflammation of the subarachnoid space is induced by constituents of bacteria. Effects of inflammation meningiene and enter the bacterial multiplication resulting in increased permeability of blood brain barrier, cerebral edema vasogen, darkening the normal flow of cerebrospinal fluid, cerebral vasculitis, increased intracranial pressure, decreased cerebral blood flow, hypoxia and acidosis cortical cerebrospinal fluid.
Pathologically speaking exudate in subarachnoid space is one that has a typical appearance, yellow-gray or yellowish, more abundant in tanks at the base of the brain and the external surface of the cerebral hemispheres. Exudate tends to accumulate in the basal cisterns and extends along the spinal cord and along the spinal and cranial nerve sheaths.
Microscopic examination of the exudate reveals a large number of neutrophils and bacteria. After several days of infection subarahnoid vessel walls become inflamed, meningeene veins dilate and focal necrosis may complicate the vascular wall. Sometimes it can cause a hemorrhagic stroke caused by cortical trombozarea cortical veins and dural sinuses. One week after infection, neutrophils leave the place of the component exudate macrophages. Nuclei of neurons and glial cells nuclei shrink perivascular space infiltrates with neutrophils and lymphocytes. Increased intracranial pressure is the result of blocking the opening of Magendie, and intracranial pressure too high increases the risk of cerebral edema combined with cerebellar tonsils hernierii life-threatening.