Lymphocytic choriomeningitis is not a commonly reported infection in humans, though most infections are mild and are often never diagnosed. Serological surveys suggest that approximately 1–5% of the population in the U.S. and Europe has antibodies to LCMV. The prevalence varies with the living conditions and exposure to mice, and it has been higher in the past due to lower standards of living. The island of Vir in Croatia is one of the biggest described endemic places of origin of LCMV in the world, with IFA testing having found LCMV antibodies in 36% of the population. Individuals with the highest risk of infection are laboratory personnel who handle rodents or infected cells. Temperature and time of year is also a critical factor that contributes to the number of LCMV infections, particularly during fall and winter when mice tend to move indoors. Approximately 10–20% of the cases in immunocompetent individuals are thought to progress to neurological disease, mainly as aseptic meningitis. The overall case fatality rate is less than 1% and people with complications, including meningitis, almost always recover completely. Rare cases of meningoencephalitis have also been reported. More severe disease is likely to occur in people who are immunosuppressed.

More than 50 infants with congenital LCMV infection have been reported worldwide. The probability that a woman will become infected after being exposed to rodents, the frequency with which LCMV crosses the placenta, and the likelihood of clinical signs among these infants are still poorly understood. In one study, antibodies to LCMV were detected in 0.8% of normal infants, 2.7% of infants with neurological signs and 30% of infants with hydrocephalus. In Argentina, no congenital LCMV infections were reported among 288 healthy mothers and their infants. However, one study found that two of 95 children in a home for people with severe mental disabilities had been infected with this virus. The prognosis for severely affected infants appears to be poor. In one series, 35% of infants diagnosed with congenital infections had died by the age of 21 months.

Transplant-acquired lymphocytic choriomeningitis proves to have a very high morbidity and mortality rate. In the three clusters reported in the U.S. from 2005 to 2010, nine of the ten infected recipients died. One donor had been infected from a recently acquired pet hamster while the sources of the virus in the other cases were unknown.

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."

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:

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.

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.

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.

Although meningitis is a notifiable disease in many countries, the exact incidence rate is unknown. In 2013 meningitis resulted in 303,000 deaths – down from 464,000 deaths in 1990. In 2010 it was estimated that meningitis resulted in 420,000 deaths, excluding cryptococcal meningitis.

Bacterial meningitis occurs in about 3 people per 100,000 annually in Western countries. Population-wide studies have shown that viral meningitis is more common, at 10.9 per 100,000, and occurs more often in the summer. In Brazil, the rate of bacterial meningitis is higher, at 45.8 per 100,000 annually. Sub-Saharan Africa has been plagued by large epidemics of meningococcal meningitis for over a century, leading to it being labeled the "meningitis belt". Epidemics typically occur in the dry season (December to June), and an epidemic wave can last two to three years, dying out during the intervening rainy seasons. Attack rates of 100–800 cases per 100,000 are encountered in this area, which is poorly served by medical care. These cases are predominantly caused by meningococci. The largest epidemic ever recorded in history swept across the entire region in 1996–1997, causing over 250,000 cases and 25,000 deaths.

Meningococcal disease occurs in epidemics in areas where many people live together for the first time, such as army barracks during mobilization, college campuses and the annual Hajj pilgrimage. Although the pattern of epidemic cycles in Africa is not well understood, several factors have been associated with the development of epidemics in the meningitis belt. They include: medical conditions (immunological susceptibility of the population), demographic conditions (travel and large population displacements), socioeconomic conditions (overcrowding and poor living conditions), climatic conditions (drought and dust storms), and concurrent infections (acute respiratory infections).

There are significant differences in the local distribution of causes for bacterial meningitis. For instance, while "N. meningitides" groups B and C cause most disease episodes in Europe, group A is found in Asia and continues to predominate in Africa, where it causes most of the major epidemics in the meningitis belt, accounting for about 80% to 85% of documented meningococcal meningitis cases.

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.

The best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella.

Many viral infections of the central nervous system occur in seasonal peaks or as epidemics, whereas others, such as herpes simplex encephalitis, are sporadic. In endemic areas it is mostly a disease of children, but as the disease spreads to new regions, or nonimmune travelers visit endemic regions, nonimmune adults are also affected.

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.

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

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.

Prevention of neonatal meningitis is primarily intrapartum (during labor) antibiotic prophylaxis (prevention) of pregnant mothers to decrease chance of early-onset meningitis by GBS. For late-onset meningitis, prevention is passed onto the caretakers to stop the spread of infectious microorganisms. Proper hygiene habits are first and foremost, while stopping improper antibiotic use; such as over-prescriptions, use of broad spectrum antibiotics, and extended dosing times will aid prevention of late-onset neonatal meningitis. A possible prevention may be vaccination of mothers against GBS and "E. coli", however, this is still under development.

While the "Haemophilus influenzae" bacteria is unable to survive in any environment outside of the human body, humans can carry the bacteria within their bodies without developing any symptoms of the disease. It spreads through the air when an individual carrying the bacteria coughs or sneezes. The risk of developing "Haemophilus" meningitis is most directly related to an individual's vaccination history, as well as the vaccination history of the general public. Herd immunity, or the protection that unvaccinated individuals experience when the majority of others in their proximity are vaccinated, does help in the reduction of meningitis cases, but it does not guarantee protection from the disease. Contact with other individuals with the disease also vastly increases the risk of infection. A child in the presence of family members sick with "Haemophilus" meningitis or carrying the bacteria is 585 times more likely to catch "Haemophilus" meningitis. Additionally, siblings of individuals with the Haemophilus influenzae meningitis receive reduced benefits from certain types of immunization. Similarly, children under two years of age have a greater risk of contracting the disease when attending day care, especially in their first month of attendance, due to the maintained contact with other children who might be asymptomatic carriers of the Hib bacteria.

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.

Adenovirus can cause severe necrotizing pneumonia in which all or part of a lung has increased translucency radiographically, which is called Swyer-James Syndrome. Severe adenovirus pneumonia also may result in bronchiolitis obliterans, a subacute inflammatory process in which the small airways are replaced by scar tissue, resulting in a reduction in lung volume and lung compliance.

Although epidemiologic characteristics of the adenoviruses vary by type, all are transmitted by direct contact, fecal-oral transmission, and occasionally waterborne transmission. Some types are capable of establishing persistent asymptomatic infections in tonsils, adenoids, and intestines of infected hosts, and shedding can occur for months or years. Some adenoviruses (e.g., serotypes 1, 2, 5, and 6) have been shown to be endemic in parts of the world where they have been studied, and infection is usually acquired during childhood. Other types cause sporadic infection and occasional outbreaks; for example, epidemic keratoconjunctivitis is associated with adenovirus serotypes 8, 19, and 37. Epidemics of febrile disease with conjunctivitis are associated with waterborne transmission of some adenovirus types, often centering on inadequately chlorinated swimming pools and small lakes. ARD is most often associated with adenovirus types 4 and 7 in the United States. Enteric adenoviruses 40 and 41 cause gastroenteritis, usually in children. For some adenovirus serotypes, the clinical spectrum of disease associated with infection varies depending on the site of infection; for example, infection with adenovirus 7 acquired by inhalation is associated with severe lower respiratory tract disease, whereas oral transmission of the virus typically causes no or mild disease. Outbreaks of adenovirus-associated respiratory disease have been more common in the late winter, spring, and early summer; however, adenovirus infections can occur throughout the year.

"Ad14 (for adenovirus serotype 14), has caused at least 140 illnesses in New York, Oregon, Texas and Washington, according to a report from the Centers for Disease Control and Prevention. The illness made headlines in Texas in September 2007, when a so-called "boot camp flu" sickened hundreds at Lackland Air Force Base in San Antonio. A 19-year-old trainee died."

Several adenoviruses, including Ad5, Ad9, Ad31, Ad36, Ad37, and SMAM1, have at least some evidence of causation of obesity in animals, adipogenesis in cells, and/or association with human obesity. To date, the most thorough investigations have been conducted for adenovirus serotype 36 (Adv36).

Fungal meningitis may be caused by the following (and also other) types of fungi:

- "Candida" - "C. albicans" is the most common "Candida" species causing CNS infection.

- "Coccidioides" - it is endemic to southwestern United States and Mexico. A third of patients presenting with disseminated coccidioidomycosis have developed meningitis.

- "Histoplasma" - occurs in bird and bat droppings and is endemic in parts of the United States, South, and Central America. CNS involvement occurs in 10-20% of disseminated histoplasmosis cases.

- "Blastomyces" - occurs in soil rich in decaying organic matter in the Midwest United States. Meningitis is an unusual manifestation of blastomycosis and can be very difficult to diagnose.

- "Cryptococcus" (Cryptococcal meningitis) - it is thought to be acquired through inhalation of soil contaminated with bird droppings. "C. neoformans" is the most common pathogen to cause fungal meningitis.

- "Aspergillus" - "Aspergillus" infections account for 5% of CNS fungal infections.

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.

Common causes of viral pneumonia are:

- "Influenza virus" A and B

- "Respiratory syncytial virus" (RSV)

- "Human parainfluenza viruses" (in children)

Rarer viruses that commonly result in pneumonia include:

- "Adenoviruses" (in military recruits)

- "Metapneumovirus"

- "Severe acute respiratory syndrome virus" (SARS coronavirus)

- "Middle East respiratory syndrome virus" (MERS coronavirus)

Viruses that primarily cause other diseases, but sometimes cause pneumonia include:

- "Herpes simplex virus" (HSV), mainly in newborns or young children

- "Varicella-zoster virus" (VZV)

- "Measles virus"

- "Rubella virus"

- "Cytomegalovirus" (CMV), mainly in people with immune system problems

- "Smallpox virus"

- "dengue virus"

The most commonly identified agents in children are "respiratory syncytial virus", "rhinovirus", "human metapneumovirus", "human bocavirus", and "parainfluenza viruses".

HIV-infected individuals are likely to be at increased risk for meningococcal disease; HIV-infected individuals who wish to reduce their risk of meningococcal disease may receive primary immunization against meningococcal disease. Although efficacy of meningitis A,C,Y and W-135 vaccines have not been evaluated in HIV-infected individuals to date, HIV-infected individuals 11–55 years of age may receive primary immunization with the conjugated vaccine. Vaccination against meningitis does not decrease CD4+ T-cell counts or increase viral load in HIV-infected individuals, and there has been no evidence that the vaccines adversely affect survival.

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.

Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.

A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene "CCR5" gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of "CCR5" made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.