Pathophysiology of Meningitis

         Meningitis is generally as a result of the spread of disease in the organ or other body tissues. Viral / bacterial hematogenous spread to lining of the brain, for example in disease pharyngitis, tonsillitis, pneumonia, Bronchopneumonia and endocarditis. The spread of bacteria / viruses can also be continuitatum of inflammation of the organ or tissue that is near the lining of the brain, eg, brain abscess, otitis media, mastoiditis, cavernous sinus thrombosis and Sinusitis. The spread of germs can also occur as a result of head trauma with fracture open brain surgery or complications. Invasion of germs into space Subarachnoid cause an inflammatory reaction in the pia mater and the arachnoid, CSS (liquid Cerebrospinal) and the ventricle system.

        At first, small meningeal blood vessels and is undergoing hyperemia; in a very short time it has spread leukocyte cells polymorphonuclear into the subarachnoid space then formed exudate. In some days the formation of lymphocytes and histiocytes, and in the second week, formed plasma cells. Exudate formed consisting of two layers, the outer containing polymorphonuclear leukocytes and fibrin, whereas in the inner layers are macrophages.

      Inflammatory process in addition to the arteries also occurs in veins in the cortex and can lead to thrombosis, cerebral infarction, cerebral edema and degeneration neuronneuron. Thrombosis and perineural exudate organization that fibrino - purulent cause cranial abnormalities. In meningitis caused by viruses, fluid Cerebrospinal Meningitis seemed clear than that caused by bacteria.

     There is a main line where the agent of infection (bacteria, viruses, fungi, parasites) can reach the central nervous system (CNS) and causing meningeal disease. Initially, agent colonizes infection or form a focal infection in the host. This colonization can form on the skin infections, ear infections, dental, nasopharynx, respiratory tract, gastrointestinal tract or urinary tract. Most meningeal pathogens transmitted through the route respiratory.

The colonization of the area , the organisms penetrate the host defense against the submucosa (eg , physical barriers, local immunity, phagocytes / macrophages) and gain access to the central nervous system through :
( 1 ) invasion into the circulation of the blood (bacteremia, viremia, fungemia, and parasitemia) and subsequent hematogenous are released into the central nervous system, where it is the mode most often spread to most of the agent (eg, meningococcus, cryptococcal, syphilitic, and pneumococcal meningitis) ;
( 2 ) neuronal damage (eg, olfactory nerve and peripherals) with agent causes eg, Naegleria fowleri, Gnathostoma spinigerum ; or
( 3 ) direct contact (eg, sinusitis, otitis media, congenital malformations, trauma , intracranial direct inoculation during manipulation).

         Once inside the central nervous system , infectious agents will be able to survive because of host defense (eg, immunoglobulins, neutrophils, complement components) is limited in this body compartment. The existence and replication agents are controlled and do not encourage a meningeal inflammatory cascade.

         Key pathophysiology of meningitis, including the important role of cytokines (eg, tumor necrosis factor- alpha [ TNF - alpha ] , interleukin [ IL ] -1) , chemokines ( IL - 8 ) , and other proinflammatory molecules in the pathogenesis of neuronal damage during pleocytosis and bacterial meningitis. Increased concentrations of TN- alpha, IL-1, IL-6 , and IL-8 in the cerebrospinal fluid are typical findings of bacterial meningitis patient.

      Port de entry: mostly come through the respiratory tract, causing respiratory infections. The gastrointestinal or urinary tract is also a route of infection. Further focal infection occurs. Of focal infection will penetrate the submucosa and reach the central nervous system through : invasion into the blood circulation, eg from damaged nerves and peripheral nerves olfactorius. Port de other entry is the direct contact of the focal infection sinusitis, otitis media or from congenital malformations, trauma, direct inoculation moment, head surgery.