Untreated, bacterial meningitis is almost always fatal. Viral meningitis, in contrast, tends to resolve spontaneously and is rarely fatal. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the person and the underlying cause. Of newborns, 20–30% may die from an episode of bacterial meningitis. This risk is much lower in older children, whose mortality is about 2%, but rises again to about 19–37% in adults. Risk of death is predicted by various factors apart from age, such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid, the severity of the generalized illness, a decreased level of consciousness or an abnormally low count of white blood cells in the CSF. Meningitis caused by "H. influenzae" and meningococci has a better prognosis than cases caused by group B streptococci, coliforms and "S. pneumonia". In adults, too, meningococcal meningitis has a lower mortality (3–7%) than pneumococcal disease.

In children there are several potential disabilities which may result from damage to the nervous system, including sensorineural hearing loss, epilepsy, learning and behavioral difficulties, as well as decreased intelligence. These occur in about 15% of survivors. Some of the hearing loss may be reversible. In adults, 66% of all cases emerge without disability. The main problems are deafness (in 14%) and cognitive impairment (in 10%).

Tuberculous meningitis in children continues to be associated with a significant risk of death even with treatment (19%), and a significant proportion of the surviving children have ongoing neurological problems. Just over a third of all cases survives with no problems.

The types of bacteria that cause bacterial meningitis vary according to the infected individual's age group.

- In premature babies and newborns up to three months old, common causes are "group B streptococci" (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and bacteria that normally inhabit the digestive tract such as "Escherichia coli" (carrying the K1 antigen). "Listeria monocytogenes" (serotype IVb) is transmitted by the mother before birth and may cause meningitis in the newborn.

- Older children are more commonly affected by "Neisseria meningitidis" (meningococcus) and "Streptococcus pneumoniae" (serotypes 6, 9, 14, 18 and 23) and those under five by "Haemophilus influenzae" type B (in countries that do not offer vaccination).

- In adults, "Neisseria meningitidis" and "Streptococcus pneumoniae" together cause 80% of bacterial meningitis cases. Risk of infection with "Listeria monocytogenes" is increased in persons over 50 years old. The introduction of pneumococcal vaccine has lowered rates of pneumococcal meningitis in both children and adults.

Recent skull trauma potentially allows nasal cavity bacteria to enter the meningeal space. Similarly, devices in the brain and meninges, such as cerebral shunts, extraventricular drains or Ommaya reservoirs, carry an increased risk of meningitis. In these cases, the persons are more likely to be infected with Staphylococci, Pseudomonas, and other Gram-negative bacteria. These pathogens are also associated with meningitis in people with an impaired immune system. An infection in the head and neck area, such as otitis media or mastoiditis, can lead to meningitis in a small proportion of people. Recipients of cochlear implants for hearing loss are more at risk for pneumococcal meningitis.

Tuberculous meningitis, which is meningitis caused by "Mycobacterium tuberculosis", is more common in people from countries in which tuberculosis is endemic, but is also encountered in persons with immune problems, such as AIDS.

Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system. Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is a skull fracture, particularly fractures that affect the base of the skull or extend towards the sinuses and petrous pyramids. Approximately 59% of recurrent meningitis cases are due to such anatomical abnormalities, 36% are due to immune deficiencies (such as complement deficiency, which predisposes especially to recurrent meningococcal meningitis), and 5% are due to ongoing infections in areas adjacent to the meninges.

Survivors of "Haemophilus" meningitis may experience permanent damage caused by inflammation around the brain, mostly involving neurological disorders. Long-term complications include brain damage, hearing loss, and mental retardation. Other possible long-term effects are reduced IQ, cerebral palsy, and the development of seizures. Children that survive the disease are more often held back in school, and are more likely to require special education services. Negative long-term effects are more likely in subjects whose treatments were delayed, as well as in subjects who were given antibiotics to which the bacteria was resistant. Ten percent of survivors develop epilepsy, while close to twenty percent of survivors develop hearing loss ranging from mild loss to deafness. About 45% of survivors experience no negative long-term effects.

The disease is associated with high rates of mortality and severe morbidity.

It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall.

The Meningitis Research Foundation is conducting a study to see if new genomic techniques can the speed, accuracy and cost of diagnosing meningitis in children in the UK. The research team will develop a new method to be used for the diagnosis of meningitis, analysing the genetic material of microorganisms found in CSF (cerebrospinal fluid). The new method will first be developed using CSF samples where the microorganism is known, but then will be applied to CSF samples where the microorganism is unknown (estimated at around 40%) to try and identify a cause.

The most common causes of viral meningitis in the United States are non-polio enteroviruses. The viruses that cause meningitis are typically acquired from sick contacts. However, in most cases, people infected with viruses that may cause meningitis do not actually develop meningitis.

Viruses that can cause meningitis include:

Because it is a bacterial disease, the primary method of treatment for "Haemophilus" meningitis is anti-bacterial therapy. Common antibiotics include ceftriaxone or cefotaxime, both of which can combat the infection and thus reduce inflammation in the meninges, or the membranes that protect the brain and spinal cord. Anti-inflammatories such as corticosteroids, or steroids produced by the body to reduce inflammation, can also be used to fight the meningeal inflammation in an attempt to reduce risk of mortality and reduce the possibility of brain damage.

Late-onset meningitis is most likely infection from the community. Late onset meningitis may be caused by other Gram-negative bacteria and "staphylococcal" species. In developing countries "Streptococcus pneumoniae" accounts for most cases of late onset.

In early-onset neonatal meningitis, acquisition of the bacteria is from the mother before the baby is born or during birth. The most common bacteria found in early-onset are group B "Streptococcus" (GBS), "Escherichia coli", and "Listeria monocytogenes". In developing countries, Gram-negative enteric (gut) bacteria are responsible for the majority of early onset meningitis.

Persons with component deficiencies in the final common complement pathway (C3,C5-C9) are more susceptible to "N. meningitidis" infection than complement-satisfactory persons, and it was estimated that the risk of infection is 7000 times higher in such individuals. In addition, complement component-deficient populations frequently experience frequent meningococcal disease since their immune response to natural infection may be less complete than that of complement non-deficient persons.

Inherited properdin deficiency also is related, with an increased risk of contracting meningococcal disease. Persons with functional or anatomic asplenia may not efficiently clear encapsulated "Neisseria meningitidis" from the bloodstream Persons with other conditions associated with immunosuppression also may be at increased risk of developing meningococcal disease.

Ameobic pathogens exist as free-living protozoans. Nevertheless, these pathogens cause rare and uncommon CNS infections. N. fowleri produces primary amebic meningoencephalitis (PAM). The symptoms of PAM are indistinguishable from acute bacterial meningitis. Other amebae cause granulomatous amebic encephalitis (GAE), which is a more subacute and can even a non-symptomatic chronic infection. Ameobic meningoencephalitis can mimic a brain abscess, aseptic or chronic meningitis, or CNS malignancy.

The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further ten months. Steroids help reduce the risk of death in those without HIV. Steroids can be used in the first six weeks of treatment, A few people may require immunomodulatory agents such as thalidomide. Hydrocephalus occurs as a complication in about a third of people with TB meningitis. The addition of aspirin may reduce or delay mortality, possibly by reducing complications such as infarcts.

Tuberculous meningitis is also known as TB meningitis or tubercular meningitis. Tuberculous meningitis is "Mycobacterium tuberculosis" infection of the meninges—the system of membranes which envelop the central nervous system.

Aseptic meningitis, or sterile meningitis, is a condition in which the layers lining the brain, the meninges, become inflamed and a pyogenic bacterial source is not to blame. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g., Kernig's sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF) obtained via lumbar puncture (normally being fewer than five visible leukocytes per microscopic high-power field).

The term "aseptic" is frequently a misnomer, implying a lack of infection. On the contrary, many cases of aseptic meningitis represent infection with viruses or mycobacteria that cannot be detected with routine methods. While the advent of polymerase chain reaction has increased the ability of clinicians to detect viruses such as enterovirus, cytomegalovirus, and herpes virus in the CSF, many viruses can still escape detection. Additionally, mycobacteria frequently require special stains and culture methods that make their detection difficult. When CSF findings are consistent with meningitis, and microbiologic testing is unrevealing, clinicians typically assign the diagnosis of aseptic meningitis—making it a relative diagnosis of exclusion.

Aseptic meningitis can result from non-infectious causes as well. it can be a relatively infrequent side effect of medications, or be a result of an autoimmune disease. There is no formal classification system of aseptic meningitis except to state the underlying cause, if known. The absence of bacteria found in the spinal fluid upon spinal tap, either through microscopic examination or by culture, usually differentiates aseptic meningitis from its pyogenic counterpart.

"Aseptic meningitis", like non-gonococcal urethritis, non-Hodgkin lymphoma and atypical pneumonia, merely states what the condition is not, rather than what it is. Terms such as viral meningitis, bacterial meningitis, fungal meningitis, neoplastic meningitis and drug-induced aseptic meningitis can provide more information about the condition, and without using one of these more specific terms, it is difficult to describe treatment options or prognosis.

Individuals with a weak immune system are most at risk. This includes individuals taking immunosuppressive medication, cancer patients, HIV patients, premature babies with very low birth weight, the elderly, etc.

People who are at an increased risk of acquiring particular fungal infections in general may also be at an increased risk of developing fungal meningitis, as the infection may in some cases spread to the CNS. People residing in the Midwestern United States, and Southwestern United States and Mexico are at an increased risk of infection with "Histoplasma" and "Coccidioides", respectively.

Although for a long time, the cause of Mollaret's meningitis was not known, recent work has associated this problem with herpes simplex viruses, which cause cold sores, occular herpes as well as genital herpes.

Cases of Mollaret's resulting from varicella zoster virus infection, diagnosed by polymerase chain reaction (PCR), have been documented. In these cases, PCR for herpes simplex was negative.

Some patients also report frequent shingles outbreaks. Varicella zoster virus, which causes chickenpox and shingles is part of the herpes family, and is sometimes called "herpes zoster virus". CNS epidermoid cysts can give rise to Mollaret's meningitis especially with surgical manipulation of cyst contents.

A familial association, where more than one family member had Mollaret's, has been documented.

Meningitis A,C,Y and W-135 vaccines can be used for large-scale vaccination programs when an outbreak of meningococcal disease occurs in Africa and other regions of the world. Whenever sporadic or cluster cases or outbreaks of meningococcal disease occur in the US, chemoprophylaxis is the principal means of preventing secondary cases in household and other close contacts of individuals with invasive disease. Meningitis A,C,Y and W-135 vaccines rarely may be used as an adjunct to chemoprophylaxis,1 but only in situations where there is an ongoing risk of exposure (e.g., when cluster cases or outbreaks occur) and when a serogroup contained in the vaccine is involved.

It is important that clinicians promptly report all cases of suspected or confirmed meningococcal disease to local public health authorities and that the serogroup of the meningococcal strain involved be identified. The effectiveness of mass vaccination programs depends on early and accurate recognition of outbreaks. When a suspected outbreak of meningococcal disease occurs, public health authorities will then determine whether mass vaccinations (with or without mass chemoprophylaxis) is indicated and delineate the target population to be vaccinated based on risk assessment.

Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for "Candida" meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for "Aspergillus" and coccidioidal infections is poor.

The number of new cases a year of acute encephalitis in Western countries is 7.4 cases per 100,000 population per year. In tropical countries, the incidence is 6.34 per 100,000 per year. The incidence of Encephalitis has not changed much over time, with an incidence of encephalitis in the US of 250,000 from 2005 to 2015. Approximately seven per 100,000 patients were hospitalized for encephalitis in the US during this time. In 2015, encephalitis was estimated to have affected 4.3 million people and resulted in 150,000 deaths worldwide. Herpes simplex encephalitis has an incidence of 2–4 per million population per year.

Identification of poor prognostic factors include thrombocytopenia, cerebral edema, status epilepticus, and thrombocytopenia. In contrast, a normal encephalogram at the early stages of diagnosis is associated with high rates of survival.

Death occurs in about 10% of cases and people do well about 70% of the time. This is a large improvement from the 1960s due to improved ability to image the head, better neurosurgery and better antibiotics.

Fungi and parasites may also cause the disease. Fungi and parasites are especially associated with immunocompromised patients. Other causes include: "Nocardia asteroides", "Mycobacterium", Fungi (e.g. "Aspergillus", "Candida", "Cryptococcus", "Mucorales", "Coccidioides", "Histoplasma capsulatum", "Blastomyces dermatitidis", "Bipolaris", "Exophiala dermatitidis", "Curvularia pallescens", "Ochroconis gallopava", "Ramichloridium mackenziei", "Pseudallescheria boydii"), Protozoa (e.g. "Toxoplasma gondii", "Entamoeba histolytica", "Trypanosoma cruzi", "Schistosoma", "Paragonimus"), and Helminths (e.g. "Taenia solium"). Organisms that are most frequently associated with brain abscess in patients with AIDS are poliovirus, "Toxoplasma gondii", and "Cryptococcus neoformans", though in infection with the latter organism, symptoms of meningitis generally predominate.

These organisms are associated with certain predisposing conditions:

- Sinus and dental infections—Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli (e.g. "Prevotella", "Porphyromonas", "Bacteroides"), "Fusobacterium", "S. aureus", and Enterobacteriaceae

- Penetrating trauma—"S. aureus", aerobic streptococci, Enterobacteriaceae, and "Clostridium" spp.

- Pulmonary infections—Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli (e.g. "Prevotella", "Porphyromonas", "Bacteroides"), "Fusobacterium", "Actinomyces", and "Nocardia"

- Congenital heart disease—Aerobic and microaerophilic streptococci, and "S. aureus"

- HIV infection—"T. gondii", "Mycobacterium", "Nocardia", "Cryptococcus", and "Listeria monocytogenes"

- Transplantation—"Aspergillus", "Candida", "Cryptococcus", "Mucorales", "Nocardia", and "T. gondii"

- Neutropenia—Aerobic gram-negative bacilli, "Aspergillus", "Candida", and "Mucorales"

Meningitis is a very common in children. Newborns can develop herpes virus infections through contact with infected secretions in the birth canal. Other viral infections are acquired by breathing air contaminated with virus-containing droplets exhaled by an infected person. Arbovirus infections are acquired from bites by infected insects (called epidemic encephalitis). Viral central nervous system infections in newborns and infants usually begin with fever. The inability of infants to communicate directly makes it difficult to understand their symptoms. Newborns may have no other symptoms and may initially not otherwise appear ill. Infants older than a month or so typically become irritable and fussy and refuse to eat. Vomiting is common. Sometimes the soft spot on top of a newborn's head (fontanelle) bulges, indicating an increase in pressure on the brain. Because irritation of the meninges is worsened by movement, an infant with meningitis may cry more, rather than calm down, when picked up and rocked. Some infants develop a strange, high-pitched cry. Infants with encephalitis often have seizures or other abnormal movements. Infants with severe encephalitis may become lethargic and comatose and then die. To make the diagnosis of meningitis or the diagnosis of encephalitis, doctors do a spinal tap (lumbar puncture) to obtain cerebrospinal fluid (CSF) for laboratory analysis in children.

Recurring Mollaret meningitis attacks will occur through the patient lifespan so long as the HSV virus is not managed. Patients have reported symptoms for as long as 30 years from first episode. Diet and stress management are key to keeping the HSV virus at bay.

Patients infected in solid organ transplants have developed a severe fatal illness, starting within weeks of the transplant. In all reported cases, the initial symptoms included fever, lethargy, anorexia and leukopenia, and quickly progressed to multisystem organ failure, hepatic insufficiency or severe hepatitis, dysfunction of the transplanted organ, coagulopathy, hypoxia, multiple bacteremias and shock. Localized rash and diarrhea were also seen in some patients. Nearly all cases have been fatal.

In May 2005, four solid-organ transplant recipients contracted an illness that was later diagnosed as lymphocytic choriomeningitis. All received organs from a common donor, and within a month of transplantation, three of the four recipients had died as a result of the viral infection. Epidemiologic investigation traced the source to a pet hamster that the organ donor had recently purchased from a Rhode Island pet store. Similar cases occurred in Massachusetts in 2008, and Australia in 2013. Currently, there is not a LCMV infection test that is approved by the Food and Drug Administration for organ donor screening. The "Morbidity and Mortality Weekly Report" advises health-care providers to "consider LCMV infection in patients with aseptic meningitis and encephalitis and in organ transplant recipients with unexplained fever, hepatitis, or multisystem organ failure."