Meningitis is an acute inflammation of the protective membranes
covering the brain and spinal cord, known collectively as the
meninges. The most common symptoms are fever, headache, and neck
stiffness. Other symptoms include confusion or altered
consciousness, vomiting, and an inability to tolerate light or loud
noises. Young children often exhibit only nonspecific symptoms,
such as irritability, drowsiness, or poor feeding. If a rash is
present, it may indicate a particular cause of meningitis; for
instance, meningitis caused by meningococcal bacteria may be
accompanied by a characteristic rash.
The inflammation may be caused by infection with viruses, bacteria, or
other microorganisms, and less commonly by certain drugs.
Meningitis can be life-threatening because of the inflammation's
proximity to the brain and spinal cord; therefore, the condition is
classified as a medical emergency. A lumbar puncture can
diagnose or exclude meningitis. A needle is inserted into the
spinal canal to collect a sample of cerebrospinal fluid (CSF), that
envelops the brain and spinal cord. The CSF is examined in a medical
Some forms of meningitis are preventable by immunization with the
meningococcal, mumps, pneumococcal, and Hib vaccines. Giving
antibiotics to people with significant exposure to certain types of
meningitis may also be useful. The first treatment in acute
meningitis consists of promptly giving antibiotics and sometimes
Corticosteroids can also be used to prevent
complications from excessive inflammation.
Meningitis can lead
to serious long-term consequences such as deafness, epilepsy,
hydrocephalus, or cognitive deficits, especially if not treated
In 2015 meningitis occurred in about 8.7 million people worldwide.
This resulted in 379,000 deaths – down from 464,000 deaths in
1990. With appropriate treatment the risk of death in
bacterial meningitis is less than 15%. Outbreaks of bacterial
meningitis occur between December and June each year in an area of
sub-Saharan Africa known as the meningitis belt. Smaller outbreaks
may also occur in other areas of the world. The word meningitis is
from Greek μῆνιγξ meninx, "membrane" and the medical suffix
1 Signs and symptoms
1.1 Clinical features
1.2 Early complications
4.1 Blood tests and imaging
4.2 Lumbar puncture
6.1 Bacterial meningitis
6.2 Viral meningitis
6.3 Fungal meningitis
11 External links
Signs and symptoms
Neck stiffness, Texas meningitis epidemic of 1911–12
In adults, the most common symptom of meningitis is a severe headache,
occurring in almost 90% of cases of bacterial meningitis, followed by
nuchal rigidity (the inability to flex the neck forward passively due
to increased neck muscle tone and stiffness). The classic triad of
diagnostic signs consists of nuchal rigidity, sudden high fever, and
altered mental status; however, all three features are present in only
44–46% of bacterial meningitis cases. If none of the three
signs are present, acute meningitis is extremely unlikely. Other
signs commonly associated with meningitis include photophobia
(intolerance to bright light) and phonophobia (intolerance to loud
noises). Small children often do not exhibit the aforementioned
symptoms, and may only be irritable and look unwell. The fontanelle
(the soft spot on the top of a baby's head) can bulge in infants aged
up to 6 months. Other features that distinguish meningitis from
less severe illnesses in young children are leg pain, cold
extremities, and an abnormal skin color.
Nuchal rigidity occurs in 70% of bacterial meningitis in adults.
Other signs include the presence of positive
Kernig's sign or
Kernig's sign is assessed with the person lying
supine, with the hip and knee flexed to 90 degrees. In a person
with a positive Kernig's sign, pain limits passive extension of the
knee. A positive Brudzinski's sign occurs when flexion of the neck
causes involuntary flexion of the knee and hip. Although Kernig's sign
and Brudzinski's sign are both commonly used to screen for meningitis,
the sensitivity of these tests is limited. They do, however,
have very good specificity for meningitis: the signs rarely occur in
other diseases. Another test, known as the "jolt accentuation
maneuver" helps determine whether meningitis is present in those
reporting fever and headache. A person is asked to rapidly rotate the
head horizontally; if this does not make the headache worse,
meningitis is unlikely.
Other problems can produce symptoms similar to those above, but from
non-meningitic causes. This is called meningism or pseudomeningitis.
Meningitis caused by the bacterium
Neisseria meningitidis (known as
"meningococcal meningitis") can be differentiated from meningitis with
other causes by a rapidly spreading petechial rash, which may precede
other symptoms. The rash consists of numerous small, irregular
purple or red spots ("petechiae") on the trunk, lower extremities,
mucous membranes, conjuctiva, and (occasionally) the palms of the
hands or soles of the feet. The rash is typically non-blanching; the
redness does not disappear when pressed with a finger or a glass
tumbler. Although this rash is not necessarily present in
meningococcal meningitis, it is relatively specific for the disease;
it does, however, occasionally occur in meningitis due to other
bacteria. Other clues on the cause of meningitis may be the skin
signs of hand, foot and mouth disease and genital herpes, both of
which are associated with various forms of viral meningitis.
Charlotte Cleverley-Bisman developed severe meningococcal meningitis
as a young child; in her case, the petechial rash progressed to
gangrene and required amputation of all limbs. She survived the
disease and became a poster child for a meningitis vaccination
campaign in New Zealand.
Additional problems may occur in the early stage of the illness. These
may require specific treatment, and sometimes indicate severe illness
or worse prognosis. The infection may trigger sepsis, a systemic
inflammatory response syndrome of falling blood pressure, fast heart
rate, high or abnormally low temperature, and rapid breathing. Very
low blood pressure may occur at an early stage, especially but not
exclusively in meningococcal meningitis; this may lead to insufficient
blood supply to other organs. Disseminated intravascular
coagulation, the excessive activation of blood clotting, may obstruct
blood flow to organs and paradoxically increase the bleeding risk.
Gangrene of limbs can occur in meningococcal disease. Severe
meningococcal and pneumococcal infections may result in hemorrhaging
of the adrenal glands, leading to Waterhouse-Friderichsen syndrome,
which is often fatal.
The brain tissue may swell, pressure inside the skull may increase and
the swollen brain may herniate through the skull base. This may be
noticed by a decreasing level of consciousness, loss of the pupillary
light reflex, and abnormal posturing. The inflammation of the brain
tissue may also obstruct the normal flow of CSF around the brain
Seizures may occur for various reasons; in
children, seizures are common in the early stages of meningitis (in
30% of cases) and do not necessarily indicate an underlying cause.
Seizures may result from increased pressure and from areas of
inflammation in the brain tissue.
Focal seizures (seizures that
involve one limb or part of the body), persistent seizures, late-onset
seizures and those that are difficult to control with medication
indicate a poorer long-term outcome.
Inflammation of the meninges may lead to abnormalities of the cranial
nerves, a group of nerves arising from the brain stem that supply the
head and neck area and which control, among other functions, eye
movement, facial muscles, and hearing. Visual symptoms and
hearing loss may persist after an episode of meningitis.
Inflammation of the brain (encephalitis) or its blood vessels
(cerebral vasculitis), as well as the formation of blood clots in the
veins (cerebral venous thrombosis), may all lead to weakness, loss of
sensation, or abnormal movement or function of the part of the body
supplied by the affected area of the brain.
Meningitis is typically caused by an infection with microorganisms.
Most infections are due to viruses, with bacteria, fungi, and
protozoa being the next most common causes. It may also result from
various non-infectious causes. The term aseptic meningitis refers
to cases of meningitis in which no bacterial infection can be
demonstrated. This type of meningitis is usually caused by viruses but
it may be due to bacterial infection that has already been partially
treated, when bacteria disappear from the meninges, or pathogens
infect a space adjacent to the meninges (e.g. sinusitis). Endocarditis
(an infection of the heart valves which spreads small clusters of
bacteria through the bloodstream) may cause aseptic meningitis.
Aseptic meningitis may also result from infection with spirochetes, a
group of bacteria that includes
Treponema pallidum (the cause of
Borrelia burgdorferi (known for causing Lyme disease).
Meningitis may be encountered in cerebral malaria (malaria infecting
the brain) or amoebic meningitis, meningitis due to infection with
amoebae such as Naegleria fowleri, contracted from freshwater
See also: Neonatal infection
Streptococcus pneumoniae- A causative bacteria of meningitis.
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
Older children are more commonly affected by Neisseria meningitidis
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).
Neisseria meningitidis and Streptococcus pneumoniae
together cause 80% of bacterial meningitis cases. Risk of infection
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
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.
Viruses that cause meningitis include enteroviruses, herpes simplex
virus (generally type 2, which produces most genital sores; less
commonly type 1), varicella zoster virus (known for causing chickenpox
and shingles), mumps virus, HIV, and LCMV. Mollaret's meningitis
is a chronic recurrent form of herpes meningitis; it is thought to be
caused by herpes simplex virus type 2.
There are a number of risk factors for fungal meningitis, including
the use of immunosuppressants (such as after organ transplantation),
HIV/AIDS, and the loss of immunity associated with aging. It
is uncommon in those with a normal immune system but has occurred
with medication contamination. Symptom onset is typically more
gradual, with headaches and fever being present for at least a couple
of weeks before diagnosis. The most common fungal meningitis is
cryptococcal meningitis due to Cryptococcus neoformans. In Africa,
cryptococcal meningitis is now the most common cause of meningitis in
multiple studies, and it accounts for 20–25% of AIDS-related
deaths in Africa. Other less common fungal pathogens which can
cause meningitis include: Coccidioides immitis, Histoplasma
capsulatum, Blastomyces dermatitidis, and Candida species.
A parasitic cause is often assumed when there is a predominance of
eosinophils (a type of white blood cell) in the CSF. The most common
parasites implicated are Angiostrongylus cantonensis, Gnathostoma
spinigerum, Schistosoma, as well as the conditions cysticercosis,
toxocariasis, baylisascariasis, paragonimiasis, and a number of rarer
infections and noninfective conditions.
Meningitis may occur as the result of several non-infectious causes:
spread of cancer to the meninges (malignant or neoplastic
meningitis) and certain drugs (mainly non-steroidal
anti-inflammatory drugs, antibiotics and intravenous
immunoglobulins). It may also be caused by several inflammatory
conditions, such as sarcoidosis (which is then called
neurosarcoidosis), connective tissue disorders such as systemic lupus
erythematosus, and certain forms of vasculitis (inflammatory
conditions of the blood vessel wall), such as Behçet's disease.
Epidermoid cysts and dermoid cysts may cause meningitis by releasing
irritant matter into the subarachnoid space. Rarely, migraine
may cause meningitis, but this diagnosis is usually only made when
other causes have been eliminated.
The meninges comprise three membranes that, together with the
cerebrospinal fluid, enclose and protect the brain and spinal cord
(the central nervous system). The pia mater is a very delicate
impermeable membrane that firmly adheres to the surface of the brain,
following all the minor contours. The arachnoid mater (so named
because of its spider-web-like appearance) is a loosely fitting sac on
top of the pia mater. The subarachnoid space separates the arachnoid
and pia mater membranes and is filled with cerebrospinal fluid. The
outermost membrane, the dura mater, is a thick durable membrane, which
is attached to both the arachnoid membrane and the skull.
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 in turn
preceded 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 vulnerable—such as the choroid plexus.
Meningitis occurs in 25% of newborns with bloodstream infections due
to group B streptococci; this phenomenon is less common in adults.
Direct contamination of the cerebrospinal fluid 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 entry of bacteria into the central nervous system. When
components of the bacterial cell membrane are identified by the immune
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 walls of the blood vessels themselves become
inflamed (cerebral vasculitis), which leads to decreased blood flow
and a third type of edema, "cytotoxic" edema. The three forms of
cerebral edema all lead to 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,
consequently brain cells are deprived of oxygen and undergo apoptosis
(programmed cell death).
It is recognized that administration of antibiotics may initially
worsen the process outlined above, by increasing the amount of
bacterial cell membrane products released through the destruction of
bacteria. Particular treatments, such as the use of corticosteroids,
are aimed at dampening the immune system's response to this
CSF findings in different forms of meningitis
Type of meningitis
often > 300/mm³
normal or high
PMNs, < 300/mm³
Blood tests and imaging
If someone is suspected of having meningitis, blood tests are
performed for markers of inflammation (e.g. C-reactive protein,
complete blood count), as well as blood cultures.
The most important test in identifying or ruling out meningitis is
analysis of the cerebrospinal fluid through lumbar puncture (LP,
spinal tap). However, lumbar puncture is contraindicated if there
is a mass in the brain (tumor or abscess) or the intracranial pressure
(ICP) is elevated, as it may lead to brain herniation. If someone is
at risk for either a mass or raised ICP (recent head injury, a known
immune system problem, localizing neurological signs, or evidence on
examination of a raised ICP), a CT or MRI scan is recommended prior to
the lumbar puncture. This applies in 45% of all adult
cases. If a CT or MRI is required before LP, or if LP proves
difficult, professional guidelines suggest that antibiotics should be
administered first to prevent delay in treatment, especially if
this may be longer than 30 minutes. Often, CT or MRI
scans are performed at a later stage to assess for complications of
In severe forms of meningitis, monitoring of blood electrolytes may be
important; for example, hyponatremia is common in bacterial
meningitis. The cause of hyponatremia, however, is controversial
and may include dehydration, the inappropriate secretion of the
antidiuretic hormone (SIADH), or overly aggressive intravenous fluid
Gram stain of meningococci from a culture showing Gram negative (pink)
bacteria, often in pairs
A lumbar puncture is done by positioning the person, usually lying on
the side, applying local anesthetic, and inserting a needle into the
dural sac (a sac around the spinal cord) to collect cerebrospinal
fluid (CSF). When this has been achieved, the "opening pressure" of
the CSF is measured using a manometer. The pressure is normally
between 6 and 18 cm water (cmH2O); in bacterial
meningitis the pressure is usually elevated. In cryptococcal
meningitis, intracranial pressure is markedly elevated. The
initial appearance of the fluid may prove an indication of the nature
of the infection: cloudy CSF indicates higher levels of protein, white
and red blood cells and/or bacteria, and therefore may suggest
The CSF sample is examined for presence and types of white blood
cells, red blood cells, protein content and glucose level. Gram
staining of the sample may demonstrate bacteria in bacterial
meningitis, but absence of bacteria does not exclude bacterial
meningitis as they are only seen in 60% of cases; this figure is
reduced by a further 20% if antibiotics were administered before the
sample was taken.
Gram staining is also less reliable in particular
infections such as listeriosis.
Microbiological culture of the sample
is more sensitive (it identifies the organism in 70–85% of cases)
but results can take up to 48 hours to become available. The
type of white blood cell predominantly present (see table) indicates
whether meningitis is bacterial (usually neutrophil-predominant) or
viral (usually lymphocyte-predominant), although at the beginning
of the disease this is not always a reliable indicator. Less commonly,
eosinophils predominate, suggesting parasitic or fungal etiology,
The concentration of glucose in CSF is normally above 40% of that in
blood. In bacterial meningitis it is typically lower; the CSF glucose
level is therefore divided by the blood glucose (
CSF glucose to serum
glucose ratio). A ratio ≤0.4 is indicative of bacterial
meningitis; in the newborn, glucose levels in CSF are normally
higher, and a ratio below 0.6 (60%) is therefore considered
abnormal. High levels of lactate in CSF indicate a higher
likelihood of bacterial meningitis, as does a higher white blood cell
count. If lactate levels are less than 35 mg/dl and the
person has not previously received antibiotics then this may rule out
Various other specialized tests may be used to distinguish between
different types of meningitis. A latex agglutination test may be
positive in meningitis caused by Streptococcus pneumoniae, Neisseria
Escherichia coli and group B
streptococci; its routine use is not encouraged as it rarely leads to
changes in treatment, but it may be used if other tests are not
diagnostic. Similarly, the limulus lysate test may be positive in
meningitis caused by
Gram-negative bacteria, but it is of limited use
unless other tests have been unhelpful. Polymerase chain reaction
(PCR) is a technique used to amplify small traces of bacterial DNA in
order to detect the presence of bacterial or viral DNA in
cerebrospinal fluid; it is a highly sensitive and specific test since
only trace amounts of the infecting agent's DNA is required. It may
identify bacteria in bacterial meningitis and may assist in
distinguishing the various causes of viral meningitis (enterovirus,
herpes simplex virus 2 and mumps in those not vaccinated for
Serology (identification of antibodies to viruses) may be
useful in viral meningitis. If tuberculous meningitis is
suspected, the sample is processed for Ziehl-Neelsen stain, which has
a low sensitivity, and tuberculosis culture, which takes a long time
to process; PCR is being used increasingly. Diagnosis of
cryptococcal meningitis can be made at low cost using an India ink
stain of the CSF; however, testing for cryptococcal antigen in blood
or CSF is more sensitive, particularly in people with AIDS.
A diagnostic and therapeutic difficulty is "partially treated
meningitis", where there are meningitis symptoms after receiving
antibiotics (such as for presumptive sinusitis). When this happens,
CSF findings may resemble those of viral meningitis, but antibiotic
treatment may need to be continued until there is definitive positive
evidence of a viral cause (e.g. a positive enterovirus PCR).
Histopathology of bacterial meningitis: autopsy case of a person with
pneumococcal meningitis showing inflammatory infiltrates of the pia
mater consisting of neutrophil granulocytes (inset, higher
Meningitis can be diagnosed after death has occurred. The findings
from a post mortem are usually a widespread inflammation of the pia
mater and arachnoid layers of the meninges.
tend to have migrated to the cerebrospinal fluid and the base of the
brain, along with cranial nerves and the spinal cord, may be
surrounded with pus – as may the meningeal vessels.
For some causes of meningitis, protection can be provided in the long
term through vaccination, or in the short term with antibiotics. Some
behavioral measures may also be effective.
Bacterial and viral meningitis are contagious, but neither is as
contagious as the common cold or flu. Both can be transmitted
through droplets of respiratory secretions during close contact such
as kissing, sneezing or coughing on someone, but cannot be spread by
only breathing the air where a person with meningitis has been.
Viral meningitis is typically caused by enteroviruses, and is most
commonly spread through fecal contamination. The risk of infection
can be decreased by changing the behavior that led to transmission.
Since the 1980s, many countries have included immunization against
Haemophilus influenzae type B in their routine childhood vaccination
schemes. This has practically eliminated this pathogen as a cause of
meningitis in young children in those countries. In the countries in
which the disease burden is highest, however, the vaccine is still too
expensive. Similarly, immunization against mumps has led to a
sharp fall in the number of cases of mumps meningitis, which prior to
vaccination occurred in 15% of all cases of mumps.
Meningococcus vaccines exist against groups A, B, C, W135 and
Y. In countries where the vaccine for meningococcus group
C was introduced, cases caused by this pathogen have decreased
substantially. A quadrivalent vaccine now exists, which combines
four vaccines with the exception of B; immunization with this ACW135Y
vaccine is now a visa requirement for taking part in Hajj.
Development of a vaccine against group B meningococci has proved much
more difficult, as its surface proteins (which would normally be used
to make a vaccine) only elicit a weak response from the immune system,
or cross-react with normal human proteins. Still, some
countries (New Zealand, Cuba,
Norway and Chile) have developed
vaccines against local strains of group B meningococci; some have
shown good results and are used in local immunization schedules.
Two new vaccines, both approved in 2014, are effective against a wider
range of group B meningococci strains. In Africa, until
recently, the approach for prevention and control of meningococcal
epidemics was based on early detection of the disease and emergency
reactive mass vaccination of the at-risk population with bivalent A/C
or trivalent A/C/W135 polysaccharide vaccines, though the
MenAfriVac (meningococcus group A vaccine) has
demonstrated effectiveness in young people and has been described as a
model for product development partnerships in resource-limited
Routine vaccination against
Streptococcus pneumoniae with the
pneumococcal conjugate vaccine (PCV), which is active against seven
common serotypes of this pathogen, significantly reduces the incidence
of pneumococcal meningitis. The pneumococcal polysaccharide
vaccine, which covers 23 strains, is only administered to certain
groups (e.g. those who have had a splenectomy, the surgical removal of
the spleen); it does not elicit a significant immune response in all
recipients, e.g. small children. Childhood vaccination with
Bacillus Calmette-Guérin has been reported to significantly reduce
the rate of tuberculous meningitis, but its waning effectiveness in
adulthood has prompted a search for a better vaccine.
Short-term antibiotic prophylaxis is another method of prevention,
particularly of meningococcal meningitis. In cases of meningococcal
meningitis, preventative treatment in close contacts with antibiotics
(e.g. rifampicin, ciprofloxacin or ceftriaxone) can reduce their risk
of contracting the condition, but does not protect against future
infections. Resistance to rifampicin has been noted to
increase after use, which has caused some to recommend considering
other agents. While antibiotics are frequently used in an attempt
to prevent meningitis in those with a basilar skull fracture there is
not enough evidence to determine whether this is beneficial or
harmful. This applies to those with or without a CSF leak.
Meningitis is potentially life-threatening and has a high mortality
rate if untreated; delay in treatment has been associated with a
poorer outcome. Thus, treatment with wide-spectrum antibiotics
should not be delayed while confirmatory tests are being
conducted. If meningococcal disease is suspected in primary care,
guidelines recommend that benzylpenicillin be administered before
transfer to hospital. Intravenous fluids should be administered if
hypotension (low blood pressure) or shock are present. It is not
clear whether intravenous fluid should be given routinely or whether
this should be restricted. Given that meningitis can cause a
number of early severe complications, regular medical review is
recommended to identify these complications early and to admit the
person to an intensive care unit if deemed necessary.
Mechanical ventilation may be needed if the level of consciousness is
very low, or if there is evidence of respiratory failure. If there are
signs of raised intracranial pressure, measures to monitor the
pressure may be taken; this would allow the optimization of the
cerebral perfusion pressure and various treatments to decrease the
intracranial pressure with medication (e.g. mannitol).
treated with anticonvulsants.
Hydrocephalus (obstructed flow of
CSF) may require insertion of a temporary or long-term drainage
device, such as a cerebral shunt.
Structural formula of ceftriaxone, one of the third-generation
cefalosporin antibiotics recommended for the initial treatment of
Empiric antibiotics (treatment without exact diagnosis) should be
started immediately, even before the results of the lumbar puncture
and CSF analysis are known. The choice of initial treatment depends
largely on the kind of bacteria that cause meningitis in a particular
place and population. For instance, in the
United Kingdom empirical
treatment consists of a third-generation cefalosporin such as
cefotaxime or ceftriaxone. In the USA, where resistance to
cefalosporins is increasingly found in streptococci, addition of
vancomycin to the initial treatment is recommended.
Chloramphenicol, either alone or in combination with ampicillin,
however, appears to work equally well.
Empirical therapy may be chosen on the basis of the person's age,
whether the infection was preceded by a head injury, whether the
person has undergone recent neurosurgery and whether or not a cerebral
shunt is present. In young children and those over 50 years of
age, as well as those who are immunocompromised, the addition of
ampicillin is recommended to cover Listeria monocytogenes. Once
the Gram stain results become available, and the broad type of
bacterial cause is known, it may be possible to change the antibiotics
to those likely to deal with the presumed group of pathogens. The
results of the CSF culture generally take longer to become available
(24–48 hours). Once they do, empiric therapy may be switched to
specific antibiotic therapy targeted to the specific causative
organism and its sensitivities to antibiotics. For an antibiotic to
be effective in meningitis it must not only be active against the
pathogenic bacterium but also reach the meninges in adequate
quantities; some antibiotics have inadequate penetrance and therefore
have little use in meningitis. Most of the antibiotics used in
meningitis have not been tested directly on people with meningitis in
clinical trials. Rather, the relevant knowledge has mostly derived
from laboratory studies in rabbits.
Tuberculous meningitis requires
prolonged treatment with antibiotics. While tuberculosis of the lungs
is typically treated for six months, those with tuberculous meningitis
are typically treated for a year or longer.
Additional treatment with corticosteroids (usually dexamethasone) has
shown some benefits, such as a reduction of hearing loss, and better
short term neurological outcomes in adolescents and adults from
high-income countries with low rates of HIV. Some research has
found reduced rates of death while other research has not.
They also appear to be beneficial in those with tuberculosis
meningitis, at least in those who are
Professional guidelines therefore recommend the commencement of
dexamethasone or a similar corticosteroid just before the first dose
of antibiotics is given, and continued for four days.
Given that most of the benefit of the treatment is confined to those
with pneumococcal meningitis, some guidelines suggest that
dexamethasone be discontinued if another cause for meningitis is
identified. The likely mechanism is suppression of overactive
Additional treatment with corticosteroids have a different role in
children than in adults. Though the benefit of corticosteroids has
been demonstrated in adults as well as in children from high-income
countries, their use in children from low-income countries is not
supported by the evidence; the reason for this discrepancy is not
clear. Even in high-income countries, the benefit of
corticosteroids is only seen when they are given prior to the first
dose of antibiotics, and is greatest in cases of H. influenzae
meningitis, the incidence of which has decreased dramatically
since the introduction of the Hib vaccine. Thus, corticosteroids are
recommended in the treatment of pediatric meningitis if the cause is
H. influenzae, and only if given prior to the first dose of
antibiotics; other uses are controversial.
Viral meningitis typically only requires supportive therapy; most
viruses responsible for causing meningitis are not amenable to
Viral meningitis tends to run a more benign course
than bacterial meningitis.
Herpes simplex virus
Herpes simplex virus and varicella zoster
virus may respond to treatment with antiviral drugs such as aciclovir,
but there are no clinical trials that have specifically addressed
whether this treatment is effective. Mild cases of viral
meningitis can be treated at home with conservative measures such as
fluid, bedrest, and analgesics.
Fungal meningitis, such as cryptococcal meningitis, is treated with
long courses of high dose antifungals, such as amphotericin B and
flucytosine. Raised intracranial pressure is common in fungal
meningitis, and frequent (ideally daily) lumbar punctures to relieve
the pressure are recommended, or alternatively a lumbar drain.
Disability-adjusted life year
Disability-adjusted life year for meningitis per
100,000 inhabitants in 2004.
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
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
Demography of meningococcal meningitis.
sporadic cases only
Deaths from meningitis per million persons in 2012
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
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
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.
Some suggest that
Hippocrates may have realized the existence of
meningitis, and it seems that meningism was known to
pre-Renaissance physicians such as Avicenna. The description of
tuberculous meningitis, then called "dropsy in the brain", is often
attributed to Edinburgh physician Sir
Robert Whytt in a posthumous
report that appeared in 1768, although the link with tuberculosis and
its pathogen was not made until the next century.
It appears that epidemic meningitis is a relatively recent
phenomenon. The first recorded major outbreak occurred in Geneva
in 1805. Several other epidemics in Europe and the United
States were described shortly afterward, and the first report of an
epidemic in Africa appeared in 1840. African epidemics became much
more common in the 20th century, starting with a major epidemic
Ghana in 1905–1908.
The first report of bacterial infection underlying meningitis was by
the Austrian bacteriologist Anton Weichselbaum, who in 1887 described
the meningococcus. Mortality from meningitis was very high (over
90%) in early reports. In 1906, antiserum was produced in horses; this
was developed further by the American scientist
Simon Flexner and
markedly decreased mortality from meningococcal disease. In
1944, penicillin was first reported to be effective in meningitis.
The introduction in the late 20th century of
Haemophilus vaccines led
to a marked fall in cases of meningitis associated with this
pathogen, and in 2002, evidence emerged that treatment with
steroids could improve the prognosis of bacterial
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