By Dr. Keertana Anne and Dr. Elena Perez
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Core
Meningitis is a condition caused by acute inflammation of the leptomeninges (the two thin inner layers of the meninges). These are the pia and arachnoid mater, which surround the brain and spinal cord.
Diagram - The meningeal layers surrounding the brain. The pia and arachnoid mater are inflamed in patients with meningitis
Source illustration: OpenStax, source, CC BY 4.0.
The causes of meningitis can be split into infectious or non-infectious.
Infectious causes can include localised bacterial, viral or fungal infections or systemic infections (infections affecting the whole body) such as tuberculosis, syphilis or Lyme disease.
Non-infectious causes can be as a result of cancer, drugs (non-steroidal anti-inflammatory drugs, known as NSAIDs, and certain antibiotics), or secondary to systemic disorders (conditions affecting the whole body). An example is sarcoidosis, in which small clumps of inflammatory cells form in organs.
In the UK, viral meningitis is more common than bacterial meningitis. However, bacterial meningitis is more serious and is associated with high levels of morbidity and mortality and therefore requires urgent recognition and treatment. The causative organism of bacterial meningitis depends on a multitude of factors, primarily the age of the patient.
- In neonates (babies in their first 28 days of life): Escherichia coli, Group B streptococcus and Listeria monocytogenes. Neonatal meningitis has a very high morbidity and mortality rate.
- In children aged 3 months and older, important causes include Neisseria meningitidis and Streptococcus pneumoniae. Haemophilus influenzae type b is less common where vaccination is widespread.
- In adults, the most common causes are Streptococcus pneumoniae and Neisseria meningitidis. Listeria monocytogenes is also a cause, and people with risk factors for it are given an extra antibiotic (amoxicillin) to cover it.
Meningococcal bacteria, which are usually carried harmlessly in the back of the nose and throat, are spread by respiratory droplets and secretions. Spread is most likely after prolonged close contact. This is why close contacts of a person with meningococcal disease (infection with Neisseria meningitidis) or Haemophilus influenzae type b may need prophylactic treatment (preventive antibiotics). See the section on management of contacts below.
In bacterial meningitis, the infection can spread to the meninges via two separate routes: via the bloodstream (bacteraemia), and when there is any direct contact between the meninges and the nasal cavity or skin.
Bacteraemic spread starts with bacteria colonising (living in) the nasopharynx, the space at the back of the nose and throat. From there, bacteria can enter the blood and invade the meninges, especially where the blood-brain barrier (the tightly sealed lining of the brain’s blood vessels, which controls what enters the brain) is thin or damaged. An example is the choroid plexus (the tissue that makes cerebrospinal fluid). The bacteria cause a localised inflammation through the central nervous system’s immune defences: astrocytes (support cells) and microglia (immune cells). This inflammation increases the permeability of the blood-brain barrier, making it leakier.
Direct contact with the meninges can arise from traumatic events, iatrogenic infection spread (infection caused by medical care, for example after inserting a device that stays in the body, such as a drain) or congenital defects.
Patients with meningitis commonly present with a severe headache and neck stiffness, although not all features are present in every patient. Some may also have an altered mental state, with neurological symptoms such as confusion, irritability and drowsiness. Other symptoms may include fever, photophobia (discomfort or pain caused by bright light), nausea and vomiting and a non-blanching rash (a rash that does not fade when pressed).
Headache and neck stiffness are harder to identify in babies and young children, and neck stiffness is less common in babies. Parents may just complain that their child is feverish, irritable, vomiting or refusing feeds. Clinicians must have a high suspicion of bacterial meningitis when examining a young child with a suspected acute infection.
The patient’s whole body should always be appropriately exposed and examined when suspecting meningitis, to investigate and assess for the non-blanching rash. This rash appears as red or purple spots that do not fade when pressed. Petechiae are spots smaller than 2 mm across, and purpura are spots larger than 2 mm. They form when blood leaks out of inflamed capillaries, which have become leaky (permeable).
The ‘glass test’ or the ‘tumbler test’ can be used to assess whether the rash blanches under pressure. The presence of this rash can indicate meningococcal septicaemia (a serious blood infection with Neisseria meningitidis), and the patient should be managed rapidly. The rash can be harder to see on brown or black skin. Check paler areas, such as the palms, the soles of the feet, the roof of the mouth, the whites of the eyes and the inside of the eyelids.
Image - A purpuric rash. These are spots larger than 2 mm, and can be seen in patients with meningococcal septicaemia. The rash is non-blanching
Creative commons source by Hektor [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]
Two physical signs that can be elicited in meningitis are Kernig’s and Brudzinski’s signs. A positive sign is thought to be due to meningeal irritation (inflammation of the meninges). These signs often miss meningitis: in a study of 297 adults with suspected meningitis, each sign was positive in only 5% of those who had meningitis. A negative sign does not rule meningitis out.
- Kernig’s Sign - The patient is unable to straighten their leg when the hip is flexed to 90 degrees.
- Brudzinski’s Sign - When the patient’s neck is flexed, their knees and hips will also flex.
Bacterial Meningitis vs Meningococcal Septicaemia
It is important to differentiate between bacterial meningitis and meningococcal septicaemia.
Bacterial meningitis is an acute infection of the meninges caused by bacteria, which can include Neisseria meningitidis as well as other organisms listed above. While the primary site of infection is the meninges, patients may also show systemic features of infection.
Meningococcal septicaemia is bloodstream infection with Neisseria meningitidis causing sepsis. Organisms carried in the nasopharynx may invade the bloodstream and then reach the meninges; septicaemia can occur with or without meningitis. A non-blanching petechial or purpuric rash is an important warning sign of systemic infection, but its absence does not exclude meningococcal disease.
Before beginning any specific investigations for meningitis, the patient should be screened for any signs of meningococcal septicaemia. If there are any, treat the person urgently for sepsis, following the NICE guidelines on suspected sepsis. Take blood tests, including blood cultures, and start intravenous ceftriaxone (an antibiotic) within 1 hour of arrival at hospital.
All patients with suspected meningitis (especially bacterial) should have a lumbar puncture (a needle inserted into the lower back to collect cerebrospinal fluid) if it is safe. Do not do one if there are signs that might mean raised intracranial pressure (raised pressure inside the skull). These include new focal neurological signs (problems coming from one area of the brain, including seizures), abnormal pupil reactions and a very low or falling level of consciousness. A lumbar puncture is also not done if there is extensive or rapidly spreading purpura, or infection where the needle would go in. Shock, breathing problems, uncontrolled seizures and a bleeding risk are treated first. Brain scans are not routinely needed before a lumbar puncture. When a scan is needed, take bloods and give antibiotics first.
The cerebrospinal fluid (CSF) collected is sent to the lab. The lab looks for any causative organisms using Gram staining (a stain that sorts bacteria into two groups by their cell wall), culture and sensitivity testing (which antibiotics work against them) and PCR (polymerase chain reaction, a test that detects the genetic material of a pathogen). It also checks the biochemistry of the fluid: protein, glucose and lactate levels.
The lumbar puncture also allows clinicians to rule out a diagnosis of a subarachnoid haemorrhage, which can present similarly (see our article on Subarachnoid Haemorrhage).
The table below shows the results that may come back from the lumbar puncture.
Table - Typical CSF patterns in bacterial meningitis, viral meningitis and subarachnoid haemorrhage. Patterns may overlap and require clinical interpretation; glucose should be assessed alongside a paired blood glucose concentration. For suspected subarachnoid haemorrhage, follow the time-dependent NICE investigation pathway: visible blood or yellow discolouration alone does not establish the diagnosis.
Based on the original SimpleMed table by Dr. Keertana Anne; revised clinical summary. Meningitis patterns checked against WHO 2025, Table 3.1; SAH investigation checked against NICE NG228.
Normal CSF from a lumbar puncture is clear, with normal glucose, low protein levels and no abnormal cell types.
Other investigations include basic observations, blood tests and a neurological assessment (see our article on the Reticular Formation for more information about neurological assessments). Blood tests include blood cultures, taken before antibiotics are given, and a whole-blood PCR test for meningococcus (Neisseria meningitidis) and pneumococcus (Streptococcus pneumoniae). A throat swab is also taken for meningococcal culture, preferably before antibiotics.
Managing the Patient
In all patients with meningitis, general management measures should take place. These include providing adequate pain relief, antipyretics (drugs that lower fever), fluid and nutritional support if required, placing them in a dark room to relieve any photophobia and positioning their head up.
Patients with bacterial meningitis need to be monitored more closely and treated aggressively due to the high mortality rate of the disease. All patients with suspected bacterial meningitis must be given empiric antibiotic therapy within 1 hour of arrival in hospital. Take blood samples, including blood cultures, first. Do the lumbar puncture before giving antibiotics unless it is not safe or would cause a clinically significant delay. If it would delay treatment, start antibiotic therapy immediately. The choice of antibiotic depends on the age of the patient and can vary based on local guidelines.
Corticosteroids, in the form of dexamethasone, are given to people over 3 months old with strongly suspected or confirmed bacterial meningitis. For babies aged 28 days to 3 months, get advice from an infection specialist. Give the first dose with or before the first dose of antibiotics if possible, but do not delay antibiotics to wait for dexamethasone. Once the cause is known, continue dexamethasone if it is pneumococcus or Haemophilus influenzae type b, and stop it for all other organisms. If no cause is found, get advice from an infection specialist on whether to continue. Corticosteroids are not routinely given for meningococcal disease.
Managing Contacts
Acute meningitis, meningococcal septicaemia and acute encephalitis are notifiable diseases in England (doctors must report any suspected case to public health teams, without waiting for laboratory confirmation). The other UK nations have their own similar rules. The local health protection team advises on which contacts need treatment. Close contacts of a person with meningococcal disease are offered prophylactic antibiotic treatment (antibiotics to prevent infection) as soon as possible, ideally within 24 hours of the diagnosis. Close contacts are people who had prolonged close contact in a household-type setting in the 7 days before the illness began. Examples are people living or sleeping in the same household, boyfriends or girlfriends, and university students sharing a kitchen in a hall of residence. People with only brief contact are included only if they were directly exposed to respiratory secretions (droplets from the nose and throat) around the time the person was admitted to hospital. The risk to a contact is low. It is highest in the first 7 days after the diagnosis and then falls sharply.
Vaccinations
Children and teenagers are offered routine NHS vaccines that protect against the main causes of meningitis. These include the MenB, MenACWY, pneumococcal, 6-in-1 (diphtheria, tetanus, whooping cough, polio, hepatitis B and Hib) and MMRV (measles, mumps, rubella and varicella) vaccines. Three of these programmes are described below.
- The Meningococcal group B (MenB) vaccine is given to babies at 8 weeks, 12 weeks and 1 year. Group B is the most common cause of meningococcal disease in people under 25. In England, group B caused 88.8% (309 of 348) of confirmed cases of all ages in 2025/26.
- The Haemophilus influenzae type b and meningococcal group C (Hib/MenC) booster at 1 year is no longer part of the routine schedule. Protection against Hib now comes from the 6-in-1 vaccine, given at 8, 12 and 16 weeks. Children born on or after 1 July 2024 also have a 4th dose at 18 months.
- The MenACWY vaccine protects against meningococcal groups A, C, W and Y. It was introduced because of an increase in cases of meningococcal group W disease. It is offered to children in school year 9, at age 13 or 14. Anyone who missed it at school can have it up to the age of 25. People under 25 who have not had it should ideally have it at least 2 weeks before starting college or university.
See our article on Childhood Immunisations for more information.
Most people with viral meningitis make a full recovery. Bacterial meningitis is rarer but more serious, and complications occur in up to 30% of children and up to one-third of adults. The complications are dependent on the extent of the damage done, how quickly treatment was given and which surrounding structures were affected.
Complications can include hearing or vision loss (either partial or total), behavioural problems and issues with memory, concentration, coordination and movement. Other complications include seizures and hydrocephalus (a build-up of cerebrospinal fluid in the brain). Disseminated infection (infection that has spread through the bloodstream), as seen in meningococcal disease, can also affect other organs such as bones, joints and the kidneys. Meningococcal disease can also cause skin scarring and amputations.
Encephalitis is a condition of inflammation of the brain parenchyma itself. A cause is not always found. When one is found, it is most often a viral infection. Less often, the immune system mistakenly attacks the brain (autoimmune encephalitis).
Examples of viral infections that cause encephalitis in the UK include:
- Herpes simplex virus (the most commonly identified cause of encephalitis), which also causes cold sores
- Varicella zoster virus, which causes chickenpox and shingles
- Mumps virus
- Measles virus
- Influenza
Worldwide, some viruses that cause encephalitis are spread by vectors (living things, such as insects, that carry an infection from one host to another). Examples are mosquitoes, which spread West Nile virus and Japanese encephalitis, and ticks, which spread tick-borne encephalitis. Rabies is spread by infected mammals.
Encephalitis and meningitis can both cause fever, headache and other overlapping symptoms. Sustained confusion or altered behaviour, focal neurological deficits and seizures suggest brain involvement. Focal deficits are problems caused by damage to one area of the brain, such as weakness of one side of the body or difficulty speaking. Seizures and altered mental state can also occur in bacterial meningitis, so seizures alone do not reliably distinguish the two conditions. Meningoencephalitis (inflammation of both the brain and the meninges) involves both.
The symptoms of encephalitis have many possible causes, so several tests may be needed to diagnose it. These include a brain scan (CT or MRI) and a lumbar puncture, with the CSF checked for signs of infection or an immune system problem. An EEG may also be done. A CT scan may be performed before the lumbar puncture if there are clinical features suggesting raised intracranial pressure.
Management of encephalitis is urgent and takes place in hospital. When herpes simplex encephalitis is suspected, antivirals (intravenous aciclovir) are given. Alongside this, antibiotics (commonly ceftriaxone) are given until bacterial meningitis has been ruled out. Other treatment depends on the cause.
Normal prion proteins (PrP) are found on the surface of cells in almost all body tissues, with the highest levels in brain and nerve cells. Their exact role is unknown, but they may help pass messages between some brain cells. PrP can misfold into an abnormal form, known as PrPSc (the scrapie form, named after the prion disease of sheep). In sporadic disease the trigger is unknown, but a normal prion protein may change into the abnormal form spontaneously. The abnormal form can also arise from the inheritance of a mutated gene, from eating contaminated food, or accidentally through medical or surgical treatment. Once present, it makes normal prion proteins misfold too, so it builds up in the brain.
Prions cause spongiform encephalopathies (diseases that damage the brain). These are named for the sponge-like appearance of the brain seen at autopsy (examination after death). This appearance results from neurone death caused by aggregation (clumping) of prions. Prion diseases affect several species. Examples include scrapie in sheep, bovine spongiform encephalopathy in cows (BSE or mad cow disease), Kuru in New Guinean tribes (believed to be transmitted through cannibalism) and Creutzfeldt-Jakob disease (CJD).
There are 4 main types of Creutzfeldt-Jakob disease. Sporadic CJD is the most common, accounting for about 8 in every 10 cases, and its trigger is unknown. Familial (inherited) CJD is caused by an inherited mutation in the gene that makes the prion protein. Variant CJD is likely to be caused by eating meat from cattle with BSE. Very rarely, variant CJD has been passed on by blood transfusion. Iatrogenic CJD is spread accidentally through medical or surgical treatment.
CJD causes brain damage that worsens rapidly. Symptoms include impaired memory, changes in personality, loss of muscle coordination and visual disturbances. In sporadic CJD, neurological symptoms come first and worsen over a few months. In variant CJD, psychological symptoms (changes in behaviour and emotions) usually come first, and the illness lasts longer. In the first 35 UK deaths, the median length of illness was 14 months. There is currently no cure for the disease and management is mainly supportive.
Edited by: Dr. Maddie Swannack
Reviewed by: Dr. Thomas Burnell and Dr. Marcus Judge
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