Risk factors for meningitis include the following:

Age of 60 years or greater Age of 5 years or less Diabetes mellitus, renal or adrenal insufficiency, hypoparathyroidism, orcystic fibrosis Immunosuppression, which increases the risk of opportunistic infections and acute bacterial meningitis Human immunodeficiency virus (HIV) infection, which predisposes to bacterial meningitis caused by encapsulated organisms, primarily S pneumoniae, and opportunistic pathogens Crowding (eg, military recruits and college dorm residents), which increases the risk of outbreaks of meningococcal meningitis Splenectomy and sickle cell disease, which increase the risk of meningitis secondary to encapsulated organisms Alcoholism and cirrhosis Contiguous infection (eg, sinusitis) Dural defect (eg, traumatic, surgical, congenital) Thalassemia major Intravenous (IV) drug abuse Bacterial endocarditis Malignancy (increased risk of Listeria species infection) Meningitis is caused by the bacteria Neisseria meningitidis (known as "meningococcal meningitis") . In bacterial meningitis, bacteria reach the meninges by one of two main routes: through the bloodstream or through direct contact between the meninges and either the nasal cavity or the skin. In most cases, meningitis follows invasion of the bloodstream by organisms that live upon mucous surfaces such as the nasal cavity. This is often preceded further by viral infections, which break down the normal barrier provided by the mucous surfaces. Once bacteria have entered the bloodstream, they enter the subarachnoid space in places where the blood-brain barrier is vulnerablesuch as the choroid plexus. In the newborn, 25% of those with bloodstream infections due to group B streptococci experience meningitis; in adults this phenomenon is more uncommon.[1] Direct contamination of the cerebrospinal fluid (CSF) may arise from indwelling devices, skull fractures, or infections of the nasopharynx or the nasal sinuses that have formed a tract with the subarachnoid space (see above); occasionally, congenital defects of the dura mater can be identified. The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection but can rather largely be attributed to the response of the immune system to the entrance of bacteria into the central nervous system. When components of the bacterial cell membrane are identified by the immune system-related cells of the brain (astrocytes and microglia), they respond by releasing large amounts of cytokines, hormone-like mediators that recruit other immune cells and stimulate other tissues to participate in an immune response. The blood-brain barrier becomes more permeable, leading to "vasogenic" cerebral edema (swelling of the brain due to fluid leakage from blood vessels). Large numbers of white blood cells enter the CSF, causing inflammation of the meninges, and leading to "interstitial" edema (swelling due to fluid between the cells). In addition, the wall of the blood vessels themselves becomes inflamed (cerebral vasculitis), which leads to a decreased blood flow and a third type of edema, "cytotoxic" edema. The three different forms of cerebral edema all lead to an increased intracranial pressure; together with the lowered blood pressure often encountered in acute infection this means that it is harder for blood to enter the brain, and brain cells are deprived of oxygen and undergo apoptosis (automated cell death). Recently, there has been more evidence to suggest that a complicated network of cytokines, chemokines, proteolytic enzymes and oxidants are responsible for the entire inflammatory process which leads to necrosis (cell death). Genetic targeting and/or pharmacological blockages of these pathways may help to prevent diffuse (widespread) brain injury and therefore decrease mortality of meningitis.

It is recognized that antibiotics may initially worsen the process outlined above, by increasing the amount of bacterial cell membrane products released through the destruction of bacteria. Risk factors: Age. Most cases of viral meningitis occur in children younger than age 5. In the past, bacterial meningitis also usually affected young children. But since the mid-1980s, as a result of the protection offered by current childhood vaccines, the median age at which bacterial meningitis is diagnosed has shifted from 15 months to 25 years. Living in a community setting. College students living in dormitories, personnel on military bases, and children in boarding schools and child care facilities are at increased risk of meningococcal meningitis, probably because infectious diseases tend to spread quickly wherever large groups of people congregate. Pregnancy. If you're pregnant, you're at increased of contracting listeriosis an infection caused by listeria bacteria, which may also cause meningitis. If you have listeriosis, your unborn baby is at risk, too. Working with animals. People who work with domestic animals, including dairy farmers and ranchers, have a higher risk of contracting listeria, which can lead to meningitis. Compromised immune system. Factors that may compromise your immune system including AIDS, diabetes and use of immunosuppressant drugs also make you more susceptible to meningitis. Removal of your spleen, an important part of your immune system, also may increase your risk.

Infectious Agents like parasite, virus, bacteria, and fungus.

Initially, the infectious agent colonizes or establishes a localized infection in the host

Through infecting

Skin, nasopharynx, respiratory tract, gastrointestinal tract, or genitourinary tract

From this site, the organism invades the submucosa by circumventing host defenses, like physical barriers, local immunity, phagocytes/ macrophages by:

Invasion of the blood stream like bacteremia, viremia, fungemia, parasitemia

A retrograde neuronal pathway like olfactory and peripheral nerves

Direct contagious spread like sinusitis, and otitis media

MENINGITIS