What is meningitis?
Meningitis is an infection of the membranes (meninges) surrounding the brain and spinal cord. Meningitis can be caused by a bacterial, fungal or viral infection. Meningitis can be acute, with a quick onset of symptoms, it can be chronic, lasting a month or more, or it can be mild or aseptic. Anyone experiencing symptoms of meningitis should see a doctor immediately.
What is bacterial meningitis?
Acute bacterial meningitis is the most common form of meningitis. Approximately 80 percent of all cases are acute bacterial meningitis. Bacterial meningitis can be life threatening. The infection can cause the tissues around the brain to swell. This in turn interferes with blood flow and can result in paralysis or even stroke.
What causes bacterial meningitis?
The bacteria most often responsible for bacterial meningitis are common in the environment and can also be found in your nose and respiratory system without causing any harm. Sometimes meningitis occurs for no known reason. Other times it occurs after a head injury or after you have had an infection and your immune system is weakened.
Who gets bacterial meningitis?
Children between the ages of one month and two years are the most susceptible to bacterial meningitis. Adults with certain risk factors are also susceptible. You are at higher risk if you abuse alcohol, have chronic nose and ear infections, sustain a head injury or get pneumococcal pneumonia. You are also at higher risk if you have a weakened immune system, have had your spleen removed, are on corticosteroids because of kidney failure or have a sickle cell disease.
Additionally, if you have had brain or spinal surgery or have had a widespread blood infection you are also a higher risk for bacterial meningitis. Outbreaks of bacterial meningitis also occur in living situations where you are in close contact with others, such as college dormitories or military barracks.
What are the symptoms of bacterial meningitis?
You want to watch for high fever, headaches, and an inability to lower your chin to your chest due to stiffness in the neck. In older children and adults, you may see confusion, irritability, increasing drowsiness. Seizures and stroke may occur. In young children, the fever may cause vomiting and they may refuse to eat. Young children may become very irritable and cry. There may be seizures. Also, because the fluid around the skull may become blocked their heads may swell. The onset of symptoms is fast, within 24 hours. If allowed to progress, you can die from bacterial meningitis.
How is bacterial meningitis diagnosed?
It is important that you seek immediate medical assistance if you suspect meningitis. Your doctor will conduct a physical exam. Your doctor will look for a purple or red rash on the skin. Your doctor will check your neck for stiffness and will exam hip and knee flexion. Your doctor will have to decide if the cause is bacterial, viral or fungal and will have to analyze your spinal fluid so a spinal tap will be ordered. Your blood and urine may also be analyzed as well as the mucous from your nose and throat.
How is bacterial meningitis treated?
Bacterial meningitis is treated with antibiotics. A general intravenous antibiotic with a corticosteroid to bring down the inflammation may be prescribed even before all the test results are in. When the specific bacteria are identified, your doctor may decide to change antibiotics. In addition to antibiotics, it will be important to replenish fluids lost from loss of appetite, sweating, vomiting and diarrhea.
Can bacterial meningitis be cured?
There is a 10 percent death rate from bacterial meningitis but if diagnosed and treated early enough, most people recover.
Are there ever complications?
Unfortunately, if treatment is not undergone immediately, there may be permanent damage. Seizures, mental impairment and paralysis may be life long.
Is bacterial meningitis contagious?
You should encourage anyone who you have come into close contact with to seek preventative treatment. Anyone who you have had casual contact should not be affected.
Is there a vaccine for bacterial meningitis?
Yes, a vaccine is available, and the Centers for Disease Control and Prevention has specific guidelines regarding who should receive the vaccine.
The CDC recommends the meningococcal vaccine for:
All children and adolescents ages 11 through 18 College freshmen living in dormitories Military recruits Scientists routinely exposed to meningococcal bacteria Anyone traveling to or living in a part of the world where the disease is common, such as Africa
Anyone with a damaged spleen or who has had his or her spleen removed Anyone who has terminal complement component deficiency (an immune system disorder)
The CDC does not recommend the vaccine for:
Anyone who has ever had a severe (life threatening) allergic reaction to a previous dose of meningococcal vaccine. Anyone who has a severe (life threatening) allergy to any vaccine component. Tell your doctor if you have any severe allergies. The CDC recommends that the following individuals wait before receiving the vaccine or talk further with their doctor about the need for the vaccine: Anyone who is moderately or severely ill at the time of their scheduled appointment to receive their shot should wait until they recover. Anyone who has ever had Guillain-Barre syndrome should discuss getting the vaccine with his or her doctor. Pregnant women should only get the vaccine if it is clearly needed. Discuss the need with your doctor.
General Meningitis Questions
Q: What is meningitis?
A: Meningitis is an inflammation of the membranes that cover the brain and spinal cord. People sometimes refer to it as spinal meningitis. Meningitis is usually caused by a viral or bacterial infection. Knowing whether meningitis is caused by a virus or bacterium is important because the severity of illness and the treatment differ depending on the cause. Viral meningitis is generally less severe and clears up without specific treatment. But bacterial meningitis can be quite severe and may result in brain damage, hearing loss, or learning disabilities. For bacterial meningitis, it is also important to know which type of bacteria is causing the meningitis because antibiotics can prevent some types from spreading and infecting other
the patient should see a doctor immediately. Before the 1990s. A: Bacterial meningitis can be treated with a number of effective antibiotics. confusion. and sleepiness. Other symptoms may include nausea. The spinal fluid is obtained by performing a spinal tap. headache. Today. Infants with meningitis may appear slow or inactive. The diagnosis is usually made by growing bacteria from a sample of spinal fluid. Top of Page
Bacterial Meningitis Questions
Q: How is bacterial meningitis diagnosed?
A: Early diagnosis and treatment are very important.Q: What are the signs and symptoms of meningitis?
people. This vaccine has reduced the number of cases of Hib infection and the number of related meningitis cases. If symptoms occur. As the disease progresses. or be feeding poorly. Hib vaccine is now given to all children as part of their routine immunizations. discomfort looking into bright lights. Identification of the type of bacteria responsible is important for selection of correct antibiotics. headache. In newborns and small infants. however. patients of any age may have seizures. It is important. in which a needle is inserted into an area in the lower back where fluid in the spinal canal can be collected. or they may take 1 to 2 days. vomiting. and neck stiffness may be absent or difficult to detect. the classic symptoms of fever. Streptococcus pneumoniae andNeisseria meningitidis are the leading causes of bacterial meningitis. Haemophilus influenzae type b (Hib) was the leading cause of bacterial meningitis. A: High fever. These symptoms can develop over several hours. have vomiting. that
Q: Can bacterial meningitis be treated?
. and stiff neck are common symptoms of meningitis in anyone over the age of 2 years. be irritable.
Also. Fortunately. This can occur through coughing. against some serogroups of N. the bacteria are not spread by casual contact or by simply breathing the air where a person with meningitis has been. However. This is known as prophylaxis. should receive prophylaxis in these cases. People who qualify as close contacts of a person with meningitis caused by N. meningitidis and many types of Streptococcus pneumoniae.
A: Yes. although the risk is higher among the elderly. The bacteria can mainly be spread from person to person through the exchange of respiratory and throat secretions.
Q: Are there vaccines against bacterial meningitis?
A: Yes. or anyone with direct contact with a patient's oral secretions (such as a boyfriend or girlfriend) would be considered at increased risk of getting the infection. some forms of bacterial meningitis are contagious. sometimes the bacteria that cause meningitis have spread to other people who have had close or prolonged contact with a patient with meningitis caused by Neisseria meningitidis (also called meningococcal meningitis) or Hib. kissing. People in the same household or daycare center.
. none of the bacteria that cause meningitis are as contagious as things like the common cold or the flu. and sneezing. Prophylaxis for household contacts of someone with Hib disease is only recommended if there is 1 household contact younger than 48 months who has not been fully immunized against Hib or an immunocompromised child (a child with a weakened immune system) of any age is in the household. meningitidisshould receive antibiotics to prevent them from getting the disease. there are vaccines against Hib. The entire household. regardless of age. The vaccines are safe and highly effective. Appropriate antibiotic treatment of most common types of bacterial meningitis should reduce the risk of dying from meningitis to below 15%.Q: Is bacterial meningitis contagious?
treatment be started early in the course of the disease.
. and pia mater. bacteria. the free encyclopedia
Classification and external resources
Meninges of the central nervous system: dura mater.Meningitis
From Wikipedia. ICD-10 ICD-9 DiseasesDB G00–G03 320–322 22543
MedlinePlus 000680 eMedicine MeSH med/2613 emerg/309emerg/390 D008581
Meningitis is inflammation of the protective membranes covering the brain and spinal cord. Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord. or other microorganisms. and less commonly by certain drugs. therefore the condition is classified as a medical emergency. arachnoid. known collectively as the meninges. The inflammation may be caused by infection withviruses.
corticosteroid drugs can also be used to prevent complications from overactive inflammation. especially if not treated quickly. onlynonspecific symptoms may be present. pneumococci or mumps virus infections) may be prevented byimmunization. vomiting. meningitis caused by meningococcal bacteria may be accompanied by a characteristic rash. it may indicate a particular cause of meningitis.The most common symptoms of meningitis are headache and neck stiffness associated withfever. Sometimes. and an inability to tolerate light (photophobia) or loud noises (phonophobia). confusion or altered consciousness. In some situations. The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs.
. especially in small children. Meningitis can lead to serious long-term consequences such asdeafness. such as irritability and drowsiness. If a rash is present.Some forms of meningitis (such as those associated with meningococci. A lumbar puncture may be used to diagnose or exclude meningitis. for instance. the fluid that envelops the brain and spinal cord. hydrocephalus and cognitive deficits. The CSF is then examined in a medical laboratory. Haemophilus influenzae type B. epilepsy. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF).
1 Behavioral o 5.4 Parasitic o 2.3 Postmortem 5 Prevention o 5.5 Non-infectious 3 Mechanism 4 Diagnosis o 4.2 Early complications 2 Causes o 2.2 Steroids o 6.1 Blood tests and imaging o 4.2 Bacterial meningitis 6.Contents
1 Signs and symptoms o 1.2 Pharmaceutical 6 Treatment o 6.3 Viral o 2.2.1 Initial treatment o 6.2 Lumbar puncture o 4.1 Bacterial o 2.3 Viral meningitis o 6.2.1 Antibiotics 6.4 Fungal meningitis 7 Prognosis 8 Epidemiology 9 History 10 See also 11 References
.2 Aseptic o 2.1 Clinical features o 1.
and an abnormal skin color.
. meningitis is unlikely. if this does not make the headache worse. Although Kernig's and Brudzinski's signs are both commonly used to screen for meningitis. cold extremities. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. however. all three features are present in only 44–46% of all cases of bacterial meningitis. Another test. and may only be irritable and look unwell. They do. the sensitivity of these tests is limited. Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis. Other features that might distinguish meningitis from less severe illnesses in young children are leg pain. In infants up to 6 months of age. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). The classic triad of diagnostic signs consists of nuchal rigidity. with the hip and knee flexed to 90 degrees. a severe headache is the most common symptom of meningitis – occurring in almost 90% of cases of bacterial meningitis. The patient is told to rapidly rotate his or her head horizontally.
12 External links
In adults. sudden high fever. however. Small children often do not exhibit the aforementioned symptoms. known as the "jolt accentuation maneuver" helps determine whether meningitis is present in patients reporting fever and headache. bulging of the fontanelle (the soft spot on top of a baby's head) may be present. Kernig's sign is assessed with the patient lying supine. pain limits passive extension of the knee. and altered mental status. Other signs of meningisminclude the presence of positive Kernig's sign or Brudzinski's sign. Texas Meningitis Epidemic of 1911–12. meningitis is extremely unlikely. In a patient with a positive Kernig's sign. have very good specificity for meningitis: the signs rarely occur in other diseases. If none of the three signs is present. followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness).
high or abnormally low temperature and rapid breathing. the excessive activation of blood clotting. The rash is typically non-blanching: the redness does not disappear when pressed with a finger or a glass tumbler. this may lead to insufficient blood supply to other organs. foot and mouth disease and genital herpes. This may be noticed by a decreasing level of consciousness. The patient.fast heart rate. and sometimes indicate severe illness or worse prognosis. and abnormal posturing. it is relatively specific for the disease. with increasing pressure inside the skull and a risk of swollen brain tissue causing herniation.
People with meningitis may develop additional problems in the early stages of their illness. occasionally occur in meningitis due to other bacteria. The brain tissue may swell. lower extremities. it does. Very low blood pressure may occur early.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. irregular purple or red spots ("petechiae") on the trunk.Charlotte Cleverley-Bisman. Although this rash is not necessarily present in meningococcal meningitis. These may require specific treatment. The rash consists of numerous small. The infection may trigger sepsis. loss of the pupillary light reflex. both of which are associated with various forms of viral meningitis. In meningococcal disease. Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands. conjuctiva. leading to Waterhouse-Friderichsen syndrome. mucous membranes.  Other clues as to the nature of the cause of meningitis may be the skin signs ofhand. may cause both the obstruction of blood flow to organs and a paradoxical increase of bleeding risk. Disseminated intravascular coagulation. a systemic inflammatory response syndrome of falling blood pressure. Inflammation of the brain tissue may also obstruct the normal flow of CSF
A severe case of meningococcal meningitis in which the petechial rash progressed to gangrene and requiredamputation of all limbs. and (occasionally) the palms of the hands or soles of the feet. survived the disease and became a poster child for a meningitis vaccination campaign in New Zealand. especially but not exclusively in meningococcal illness. which is often lethal. gangrene of limbs can occur.
meningitidis and S. can lead
. as well as infections by pseudomonas and other Gramnegative bacilli. 
Meningitis is usually caused by infection from viruses or microorganisms. see below). or abnormal movement or function of the part of the body supplied by the affected area in the brain. In adults. Since the pneumococcal vaccine was introduced. Streptococcus pneumoniae (serotypes 6. It may also result from various non-infectious causes. 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 those that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Similarly. In a small proportion of people. Seizures may result from increased pressure and from areas of inflammation in the brain tissue. with bacteria. in children. Visual symptoms and hearing loss may persist after an episode of meningitis (see below). and parasites being the next most common causes. Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space. The inflammation of the meninges may lead to abnormalities of the cranial nerves. rates of pneumococcal meningitis have declined in children and adults. In these cases. individuals with a cerebral shunt or related device (such as an extraventricular drain or Ommaya reservoir) are at increased risk of infection through those devices. facial muscles and hearing. Most cases are due to infection with viruses. Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. monocytogenes in those over 50 years old.around the brain (hydrocephalus).
The types of bacteria that cause bacterial meningitis vary by age group. 14. persistent seizures. among other functions. an infection in the head and neck area. however. infections with staphylococci are more likely. Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis). with increased risk ofL. Focal seizures (seizures that involve one limb or part of the body). Older children are more commonly affected by Neisseria meningitidis (meningococcus). 9. loss of sensation. a group of nerves arising from the brain stem that supply the head and neck area and control eye movement. may all lead to weakness. 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination. seizures are common in the early stages of meningitis (30% of cases) and do not necessarily indicate an underlying cause. In premature babies and newborns up to three months old. fungi. pneumoniae together cause 80% of all cases of bacterial meningitis. Seizures may occur for various reasons. N. such as otitis media or mastoiditis. late-onset seizures and those that are difficult to control with medication are indicators of a poorer long-term outcome. The same pathogens are also more common in those with an impaired immune system. as well as the formation of blood clots in the veins (cerebral venous thrombosis).
a type of bacteria that includes Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (known for causing Lyme disease). is typically seen in people with immune deficiency such as AIDS. Recurrent bacterial meningitis may be caused by persisting anatomical defects. as well as the conditions cysticercosis. due to Cryptococcus neoformans. but it may be due to bacterial infection that has already been partially treated. e. particularly fractures that affect the base of the skull or extend towards the sinuses and petrous pyramids. meningitis due to infection with Mycobacterium tuberculosis. Endocarditis (infection of the heart valves with spread of small clusters of bacteria through the bloodstream) may cause aseptic meningitis. A literature review of 363 reported cases of recurrent meningitis showed that 59% of cases are due to such anatomical abnormalities. Meningitis may be encountered in cerebral malaria (malaria infecting the brain). is contracted from freshwater sources. sinusitis).
. paragonimiasis. Schistosoma. or by disorders of the immune system. The most common cause of recurrent meningitis is skull fracture.toxocariasis. Recipients of cochlear implants for hearing loss are at an increased risk of pneumococcal meningitis. with disappearance of the bacteria from the meninges. Anatomical defects allow continuity between the external environment and the nervous system. or by infection in a space adjacent to the meninges (e. which predisposes especially to recurrent meningococcal meningitis). This is usually due to viruses.g. 36% due to immune deficiencies (such as complement deficiency. either congenital or acquired. herpes simplex virus type 2 (and less commonly type 1). Gnathostoma spinigerum. HIV. The most common parasites implicated are Angiostrongylus cantonensis. is more common in those from countries wheretuberculosis is common. and a number of rarer infections and noninfective conditions. Aseptic meningitis may also result from infection withspirochetes. Tuberculous meningitis. varicella zoster virus(known for causing chickenpox and shingles).g.to meningitis. Amoebic meningitis. but is also encountered in those with immune problems. meningitis due to infection with amoebae such as Naegleria fowleri.
A parasitic cause is often assumed when there is a predominance of eosinophils (a type of white blood cell) in the CSF.
Viruses that can cause meningitis include enteroviruses. baylisascariasis. Fungal meningitis. and LCMV. such as AIDS. mumps virus. and 5% due to ongoing infections in areas adjacent to the meninges.
The term aseptic meningitis refers loosely to all cases of meningitis in which no bacterial infection can be demonstrated.
When components of the bacterial cell membrane are identified by the immune cells of the brain (astrocytes and microglia). and is filled with cerebrospinal fluid. is a thick durable membrane. The arachnoid mater (so named because of its spider-web-like appearance) is a loosely fitting sac on top of the pia mater. but this diagnosis is usually only made when other causes have been eliminated. the dura mater. It may also be caused by several inflammatory conditions such as sarcoidosis (which is then called neurosarcoidosis). and certain forms of vasculitis (inflammatory conditions of the blood vessel wall) such as Behçet's disease.  Direct contamination of the cerebrospinal fluid may arise from indwelling devices. which is attached to both the arachnoid membrane and the skull. migraine may cause meningitis. In most cases. Meningitis occurs in 25% of newborns with bloodstream infections due to group B streptococci. This is often in turn preceded by viral infections. Rarely. antibiotics and intravenous immunoglobulins). together with the cerebrospinal fluid. Mollaret's meningitis is a syndrome of recurring episodes of aseptic meningitis. The subarachnoid space separates the arachnoid and pia mater membranes. The outermost membrane. they enter the subarachnoid space in places where theblood-brain barrier is vulnerable—such as the choroid plexus. it is thought to be caused by herpes simplex virus type 2.
The meninges comprise three membranes that. congenital defects of the dura mater can be identified. Once bacteria have entered the bloodstream. The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection but can rather largely be attributed to the response of the immune system to the entrance of bacteria into the central nervous system. In bacterial meningitis. they respond by releasing large amounts of cytokines. or infections of the nasopharynx or the nasal sinuses that have formed a tract with the subarachnoid space (see above). connective tissue disorders such as systemic lupus erythematosus. 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. skull fractures.Non-infectious
Meningitis may occur as the result of several non-infectious causes: spread of cancer to the meninges (malignant meningitis) and certaindrugs (mainly non-steroidal anti-inflammatory drugs. meningitis follows invasion of the bloodstream by organisms that live upon mucous surfaces such as the nasal cavity. following all the minor contours. hormone-like mediators that recruit other immune cells and stimulate other tissues to participate in an immune
. Epidermoid cysts and dermoid cysts may cause meningitis by releasing irritant matter into the subarachnoid space. occasionally. The pia mater is a very delicate impermeable membrane that firmly adheres to the surface of the brain. enclose and protect the brain and spinal cord (thecentral nervous system). which break down the normal barrier provided by the mucous surfaces. this phenomenon is less common in adults.
leading to "vasogenic" cerebral edema (swelling of the brain due to fluid leakage from blood vessels).
CSF findings in different forms of meningitis
Type of meningitis Glucose
PMNs. often > 300/mm³
normal or high
mononuclear. causing inflammation of the meninges. The three forms of cerebral edema all lead to an increased intracranial pressure. the walls of the blood vessels themselves become inflamed (cerebral vasculitis). < 300/mm³
mononuclear and PMNs. and leading to "interstitial" edema (swelling due to fluid between the cells). this means that it is harder for blood to enter the brain. "cytotoxic" edema.response. It is recognized that administration of antibiotics may initially worsen the process outlined above. together with the lowered blood pressure often encountered in acute infection. and brain cells are deprived of oxygen and undergo apoptosis (automated cell death). The blood-brain barrier becomes more permeable. In addition. < 300/mm³
. such as the use of corticosteroids. which leads to a decreased blood flow and a third type of edema. Particular treatments. by increasing the amount of bacterial cell membrane products released through the destruction of bacteria. are aimed at dampening the immune system's response to this phenomenon. Large numbers of white blood cells enter the CSF.
When this has been achieved. However.g. complete blood count). applying local anesthetic. 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. a CT or MRI scan is recommended prior to the lumbar puncture. due to a combination of factors including dehydration. The pressure is normally between 6 and 18 cm water (cmH2O). as well as blood cultures. the "opening pressure" of the CSF is measured using a manometer. and therefore may suggest bacterial meningitis. professional guidelines suggest that antibiotics should be administered first to prevent delay in treatment. a known immune system problem. the inappropriate excretion of the antidiuretic hormone (SIADH). The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP. for example. as it may lead to brain herniation.
. or if LP proves difficult. If a CT or MRI is required before LP. lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated. hyponatremia is common in bacterial meningitis. localizing neurological signs. spinal tap). or overly aggressive intravenous fluid administration.Malignant
tests and imaging
In someone suspected of having meningitis.
A lumbar puncture is done by positioning the patient. In severe forms of meningitis. If someone is at risk for either a mass or raised ICP (recent head injury. Often. monitoring of blood electrolytes may be important. in bacterial meningitis the pressure is typically elevated. Creactive protein. and inserting a needle into the dural sac (a sac around the spinal cord) to collect cerebrospinal fluid (CSF). or evidence on examination of a raised ICP). usually lying on the side. This applies in 45% of all adult cases. CT or MRI scans are performed at a later stage to assess for complications of meningitis. blood tests are performed for markers of inflammation (e. especially if this may be longer than 30 minutes.
but it may be used if other tests are not diagnostic. PCR is being used increasingly. and tuberculosis culture. proteincontent and glucose level. 
. A latex agglutination test may be positive in meningitis caused by Streptococcus pneumoniae. It may identify bacteria in bacterial meningitis and may assist in distinguishing the various causes of viral meningitis (enterovirus. its routine use is not encouraged as it rarely leads to changes in treatment.6 (60%) is therefore considered abnormal. in the newborn. the CSF glucose level is therefore divided by the blood glucose (CSF glucose to serum glucose ratio). The type of white blood cell predominantly present (see table) indicates whether meningitis is bacterial (usually neutrophil-predominant) or viral (usually lymphocyte-predominant). red blood cells. High levels of lactate in CSF indicate a higher likelihood of bacterial meningitis. the sample is processed for Ziehl-Neelsen stain. it is a highly sensitive and specific test since only trace amounts of the infecting agent's DNA is required. Haemophilus influenzae. Serology (identification of antibodies to viruses) may be useful in viral meningitis. testing for cryptococcal antigen in blood or CSF is more sensitive. the limulus lysate test may be positive in meningitis caused by Gram-negative bacteria. The concentration of glucose in CSF is normally above 40% of that in blood. as does a higher white blood cell count. If tuberculous meningitis is suspected. and a ratio below 0. Similarly. although in the beginning of the disease this is not always a reliable indicator. In bacterial meningitis it is typically lower. 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. glucose levels in CSF are normally higher. this figure is reduced by a further 20% if antibiotics were administered before the sample was taken. which takes a long time to process. Gram staining of the sample may demonstrate bacteria in bacterial meningitis. A ratio ≤0. among others. herpes simplex virus 2 and mumps in those not vaccinated for this).4 is indicative of bacterial meningitis. Less commonly. suggesting parasitic or fungal etiology. but it is of limited use unless other tests have been unhelpful. however. and Gram staining is also less reliable in particular infections such aslisteriosis. but absence of bacteria does not exclude bacterial meningitis as they are only seen in 60% of cases. Escherichia coli and group B streptococci. eosinophils predominate. which has a low sensitivity. Neisseria meningitidis. 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.  Diagnosis of cryptococcal meningitis can be made at low cost using an India ink stain of the CSF. often in pairs
The CSF sample is examined for presence and types of white blood cells.  Various more specialized tests may be used to distinguish between various types of meningitis. particularly in persons with AIDS.Gram stain of meningococci from a culture showing Gram negative (pink) bacteria.
 By changing behavior to prevent the causes of transmission.
Meningitis can be diagnosed after death has occurred. Neither are as contagious as the common cold orflu. When this happens.
Histopathology of bacterial meningitis: autopsy case of a patient with pneumococcal meningitis showing inflammatory infiltrates of the pia mater consisting of neutrophil granulocytes (inset. but cannot be spread by only breathing the air where a person with meningitis has been. sneezing or coughing on someone. or in the short term with antibiotics. along with cranial nerves and the spinal cord. and is most commonly spread through fecal contamination. infection by viruses and bacteria can be prevented.
For some causes of meningitis.
. a positive enterovirus PCR). but antibiotic treatment may need to be continued until there is definitive positive evidence of a viral cause (e. Viral meningitis is typically caused byEnteroviruses.g. prophylaxis can be provided in the long term with vaccine. The findings from a post mortem are usually a widespread inflammation of the pia mater and arachnoid layers of the meninges covering the brain and spinal cord. where there are meningitis symptoms after receiving antibiotics (such as for presumptive sinusitis). higher magnification). CSF findings may resemble those of viral meningitis. Both can be transmitted through droplets of respiratory secretions during close contact such as kissing.
Bacterial and viral meningitis are contagious. Neutrophil granulocytes tend to have migrated to the cerebrospinal fluid and the base of the brain. may be surrounded withpus—as may the meningeal vessels.A diagnostic and therapeutic conundrum is the "partially treated meningitis".
rifampicin. significantly reduces the incidence of pneumococcal meningitis.
. small children. which covers 23 strains. The pneumococcal polysaccharide vaccine. many countries have included immunization against Haemophilus influenzae type B in their routine childhood vaccination schemes. immunization against mumps has led to a sharp fall in the number of cases of mumps meningitis. or cross-react with normal human proteins. those who have had a splenectomy. cases caused by this pathogen have decreased substantially. some have shown good results and are used in local immunization schedules. Short-term antibiotic prophylaxis is also a method of prevention. though the introduction of MenAfriVac (meningiococcus group A vaccine) has demonstrated effectiveness in young people and has been described as a model for product development partnerships in resource-limited settings. particularly of meningococcal meningitis.  A quadrivalent vaccine now exists. Still. In the countries where the disease burden is highest. Routine vaccination against Streptococcus pneumoniae with the pneumococcal conjugate vaccine (PCV).  Meningococcus vaccines exist against groups A. W135 and Y. C. but its waning effectiveness in adulthood has prompted a search for a better vaccine. In Africa.Since the 1980s.g. the surgical removal of the spleen). This has practically eliminated this pathogen as a cause of meningitis in young children in those countries. the vaccine is still too expensive. which prior to vaccination occurred in 15% of all cases of mumps. ciprofloxacin or ceftriaxone) can reduce their risk of contracting the condition. Immunization with the ACW135Y vaccine against four strains is now a visa requirement for taking part in the Hajj. Cuba.g. Norway and Chile) have developed vaccines against local strains of group B meningococci. In countries where the vaccine for meningococcus group C was introduced. Development of a vaccine against group B meningococci has proved much more difficult. is only administered in certain groups (e. Childhood vaccination with Bacillus Calmette-Guérin has been reported to significantly reduce the rate of tuberculous meningitis. which is active against seven common serotypes of this pathogen. which combines all four vaccines. until recently. as its surface proteins (which would normally be used to make a vaccine) only elicit a weak response from the immune system. however. it does not elicit a significant immune response in all recipients. In cases of meningococcal meningitis.g. some countries (New Zealand. prophylactic treatment of close contacts with antibiotics (e. but does not protect against future infections. Similarly. 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. e.
 as well as admission to an intensive care unit if deemed necessary. regular medical review is recommended to identify these complications early.g. addition of vancomycin to the initial treatment is recommended. or if there is evidence of respiratory failure. Given that meningitis can cause a number of early severe complications. For instance. Once the Gram stain results become available. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place. even before the results of the lumbar puncture and CSF analysis are known. measures to monitor the pressure may be taken. For instance. one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis. such as acerebral shunt. inthe United Kingdom empirical treatment consists of a third-generation cefalosporin such ascefotaxime or ceftriaxone.
Empiric antibiotics (treatment without exact diagnosis) must be started immediately. If meningococcal disease is suspected in primary care. this would allow the optimization of the cerebral perfusion pressure and various treatments to decrease the intracranial pressure with medication (e. whether the infection was preceded by head injury. Intravenous fluids should be administered if hypotension (low blood pressure) or shock are present. Seizures are treated withanticonvulsants. mannitol). in young children and those over 50 years of age.Empirical therapy may be chosen on the basis of the age of the patient. If there are signs of raised intracranial pressure. and the broad type of bacterial cause is
. Thus treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted. as well as those who are immunocompromised. guidelines recommend that benzylpenicillin be administered before transfer to hospital.
Structural formula of ceftriaxone. Hydrocephalus (obstructed flow of CSF) may require insertion of a temporary or longterm drainage device. In the USA. delay in treatment has been associated with a poorer outcome. addition of ampicillin is recommended to coverListeria monocytogenes. where resistance to cefalosporins is increasingly found in streptococci. whether the patient has undergone neurosurgery and whether or not a cerebral shunt is present. Mechanical ventilation may be needed if the level of consciousness is very low.Meningitis is potentially life-threatening and has a high mortality rate if untreated.
influenzae and only if given prior to the first dose of antibiotics. For an antibiotic to be effective in meningitis. influenzae meningitis. Even in high-income countries. Thus.known. it may be possible to change the antibiotics to those likely to deal with the presumed group of pathogens. A 2010 analysis of previous studies has shown that the benefit from steroids may not be as significant as previously found. those with tuberculous meningitis are typically treated for a year or longer. Most of the antibiotics used in meningitis have not been tested directly on meningitis patients in clinical trials. While tuberculosis of the lungs is typically treated for six months. and is greatest in cases of H.  and adverse neurological outcomes. Given that most of the benefit of the treatment is confined to those with pneumococcal meningitis. but also reach the meninges in adequate quantities. it must not only be active against the pathogenic bacterium. some guidelines suggest that dexamethasone be discontinued if another cause for meningitis is identified. The likely mechanism is suppression of overactive inflammation. corticosteroids are recommended in the treatment of pediatric meningitis if the cause is H. the incidence of which has decreased dramatically since the introduction of the Hib vaccine. Professional guidelines therefore recommend the commencement of dexamethasone or a similar corticosteroid just before the first dose of antibiotics is given.
Adjuvant treatment with corticosteroids (usually dexamethasone) has been shown in some studies to reduce rates of mortality. the benefit of corticosteroids is only seen when they are given prior to the first dose of antibiotics. and continued for four days. empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism and its sensitivities to antibiotics.  In tuberculous meningitis there is a strong evidence base for treatment with corticosteroids.  Adjuvant corticosteroids have a different role in children than in adults. whereas other uses are controversial. Though the benefit of corticosteroids has been demonstrated in adults as well as in children from high-income countries. severe hearing loss and neurological damage in adolescents and adults from high income countries which have low rates of HIV. The results of the CSF culture generally take longer to become available (24–48 hours). although this evidence is restricted to those without AIDS. the reason for this discrepancy is not clear.
. Tuberculous meningitis requires prolonged treatment with antibiotics. The one possible significant benefit is reduction of hearing loss in survivors. Rather. the relevant knowledge has mostly derived from laboratory studies in rabbits. Once they do. their use in children from low-income countries is not supported by evidence. some antibiotics have inadequate penetrance and therefore have little use in meningitis.
learning and behavioral difficulties. Some of the hearing loss may be reversible. This risk is much lower in older children. With treatment.
. mortality (risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause. but there are no clinical trials that have specifically addressed whether this treatment is effective. but rises again to about 19–37% in adults. as well as decreased intelligence. whose mortality is about 2%. Of the newborn patients. epilepsy. influenzae and meningococci has a better prognosis compared to cases caused by group B streptococci. bedrest. decreased level of consciousness or abnormally low count of white blood cells in the CSF. and frequent (ideally daily) lumbar punctures to relieve the pressure are recommended. In adults. Meningitis caused by H. such as amphotericin B andflucytosine. and analgesics. is treated with long courses of highly dosed antifungals. Risk of death is predicted by various factors apart from age. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs such as aciclovir. In adults. occur in about 15% of survivors. In children there are several potential disabilities which result from damage to the nervous system. the severity of the generalized illness. Raised intracranial pressure is common in fungal meningitis.Viral meningitis typically requires supportive therapy only. 20–30% may die from an episode of bacterial meningitis. such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid. or alternatively a lumbar drain. tends to resolve spontaneously and is rarely fatal.
Fungal meningitis. Mild cases of viral meningitis can be treated at home with conservative measures such as fluid. Viral meningitis tends to run a more benign course than bacterial meningitis. Viral meningitis.
Untreated. too. bacterial meningitis is almost always fatal. The main problems are deafness (in 14%) and cognitive impairment (in 10%). pneumonia. meningococcal meningitis has a lower mortality (3–7%) than pneumococcal disease. coliforms and S. such as cryptococcal meningitis. 66% of all cases emerge without disability. Sensorineural hearing loss. most viruses responsible for causing meningitis are not amenable to specific treatment. in contrast.
 no data ≤ 10 10–25 25–50 50–75 75–100 100–200 200–300 300–400
Demography of meningococcalmeningitis.000 inhabitants in 2002. meningitis belt epidemic zones sporadic cases only
Disability-adjusted life year for meningitis per 100.
These cases are predominantly caused by meningococci. Epidemics typically occur in the dry season (December to June). at 45. and occurs more often in the summer. and it seems that meningism was known to pre-Renaissance physicians such as Avicenna.000 cases and 25. and concurrent infections (acute respiratory infections). Sub-Saharan Africa has been plagued by large epidemics of meningococcal meningitis for over a century. The description of tuberculous meningitis. college campuses and the annual Hajjpilgrimage. which is poorly served by medical care. then called "dropsy in the brain". accounting for about 80% to 85% of documented meningococcal meningitis cases.000 annually in Western countries. Bacterial meningitis occurs in about 3 people per 100. is often attributed to Edinburgh physician Sir Robert Whytt in a posthumous report that appeared in 1768. Although the pattern of epidemic cycles in Africa is not well understood. Meningococcal disease occurs in epidemics in areas where many people live together for the first time. They include: medical conditions (immunological susceptibility of the population). For instance. causing over 250.000 annually. Attack rates of 100–800 cases per 100.000 deaths. leading to it being labeled the "meningitis belt". The largest epidemic ever recorded in history swept across the entire region in 1996–1997. 
Some suggest that Hippocrates may have realized the existence of meningitis. although the link with tuberculosis and its pathogen was not made until the next century. demographic conditions (travel and large population displacements). the rate of bacterial meningitis is higher. group A is found in Asia and continues to predominate in Africa. climatic conditions (drought and dust storms).000 are encountered in this area. such as army barracks during mobilization. the exact incidence rate is unknown. while N. dying out during the intervening rainy seasons. socioeconomic conditions (overcrowding and poor living conditions). and an epidemic wave can last two to three years. at 10.400–500 500–1000 1000–1500 ≥ 1500
Although meningitis is a notifiable disease in many countries.000. several factors have been associated with the development of epidemics in the meningitis belt. Population-wide studies have shown that viral meningitis is more common.
.9 per 100. where it causes most of the major epidemics in the meningitis belt. In Brazil. There are significant differences in the local distribution of causes for bacterial meningitis. meningitides groups B and C cause most disease episodes in Europe.8 per 100.
 The introduction in the late 20th century of Haemophilus vaccines led to a marked fall in cases of meningitis associated with this pathogen. Several other epidemics in Europe and the United States were described shortly afterward. African epidemics became much more common in the 20th century. The first report of bacterial infection underlying meningitis was by the Austrian bacteriologist Anton Weichselbaum. this was developed further by the American scientist Simon Flexner and markedly decreased mortality from meningococcal disease. who in 1887 described themeningococcus. The first recorded major outbreak occurred in Geneva in 1805.It appears that epidemic meningitis is a relatively recent phenomenon. In 1944. and the first report of an epidemic in Africa appeared in 1840. 
Infections of the central nervous system (CNS) can be divided into 2 broad categories: those primarily involving the meninges (meningitis) and those primarily confined to the parenchyma (encephalitis). antiserum was produced in horses.penicillin was first reported to be effective in meningitis. See the images of meningitis below. In 1906. Mortality from meningitis was very high (over 90%) in early reports.
.  and in 2002 evidence emerged that treatment with steroids could improve the prognosis of bacterial meningitis. starting with a major epidemic sweeping Nigeria and Ghana in 1905– 1908.
Edwin P. This axial T2-weighted magnetic
resonance image shows only mild ventriculomegaly.
. Courtesy of the
CDC/Dr.Pneumococcal meningitis in a patient with alcoholism. This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal effacement
Acute bacterial meningitis. Acute bacterial meningitis. Ewing. Jr.
which increase the risk of meningitis secondary to encapsulated organisms Alcoholism and cirrhosis Recent exposure to others with meningitis. which predisposes to bacterial meningitis caused by encapsulated organisms. with or without prophylaxis Contiguous infection (eg. congenital) Thalassemia major Intravenous (IV) drug abuse Bacterial endocarditis Ventriculoperitoneal shunt Malignancy (increased risk of Listeria species infection) Some cranial congenital deformities
.A delicate. military recruits and college dorm residents).A tough outer membrane Arachnoid . and opportunistic pathogens Crowding (eg. primarily S pneumoniae. weblike middle membrane Subarachnoid space . renal or adrenal insufficiency.bacterial meningitis. sinusitis) Dural defect (eg. axial T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows). orcystic fibrosis Immunosuppression.A lacy. This contrast-enhanced.
Meningitis is a clinical syndrome characterized by inflammation of the meninges. They consist of the following: Dura . which increases the risk of outbreaks of meningococcal meningitis Splenectomy and sickle cell disease. traumatic. 3 layers of membranes that enclose the brain and spinal cord. which increases the risk of opportunistic infections and acute bacterial meningitis Human immunodeficiency virus (HIV) infection. fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cord Risk factors for meningitis include the following:
Age of 60 years or greater Age of 5 years or less Diabetes mellitus. hypoparathyroidism. surgical.
(See Anatomy. which is more common and is defined as inflammation of the arachnoid tissue and subarachnoid space.) Meningitis is anatomically divided into inflammation of the dura. (See Etiology. however. meningitis may be classified as acute or chronic. meningitis manifests with meningeal symptoms (eg. photophobia).   The disease was uniformly fatal before the antimicrobial era.) The emergence of resistant bacterial strains has prompted changes in antibiotic protocols in some countries. (See Epidemiology. Depending on the duration of symptoms. it remains alarmingly high. meningitis may be concentrated at the base of the brain.Clinically. headache. but with the advent of antimicrobial therapy. Nonetheless.
. If not treated. including the United States. such as with fungal diseases and tuberculosis.)
Pyogenic (bacterial) meningitis consists of inflammation of the meninges and the underlying subarachnoid CSF. The organisms usually enter the meninges through the bloodstream from other parts of the body. as well as pleocytosis (an increased number of white blood cells) in the cerebrospinal fluid (CSF). and leptomeningitis. under certain conditions. (See Etiology and Clinical Presentation. which is less common. bacterial meningitis may lead to lifelong debility or death. Most cases of bacterial meningitis are localized over the dorsum of the brain. the overall mortality rate from bacterial meningitis has decreased. sometimes referred to as pachymeningitis.) Meningitis can also be divided into the following 3 general categories: Pyogenic (bacterial) Granulomatous Lymphocytic The most common cause of meningeal inflammation is irritation caused by bacterial or viral infections. nuchal rigidity. being approximately 25%.
This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis). with marked herniation and a prominent subdural empyema. neuronal cell protectants still hold only future promise as adjunctive therapy.
Subdural empyema and arterial infarct in a patient with bacterial meningitis. (See Treatment and Management and Medication. Numerous infectious and noninfectious causes of meningitis have been identified.
Meningitis can also be also classified more specifically according to its etiology. and the absence of left mastoid air. Examples of common noninfectious
. an adjacent epidural empyema with marked dural enhancement (arrow). and the inflammation may evolve into the following conditions (see the images below):
Ventriculitis Empyema Cerebritis
Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows leftsided parenchymal hypoattenuation in the middle cerebral artery territory.) The specific infective agents that are involved in bacterial meningitis vary among different patient age groups.Apart from dexamethasone.
Approximately 75% of patients with bacterial meningitis present subacutely. for example.
For more information. Depending on the specific bacterial cause. any of the following: Pneumococcal meningitis Haemophilus influenzae meningitis Staphylococcal meningitis Meningococcal meningitis Tuberculous meningitis Unlike subacute (1-7 d) or chronic (>7 d) meningitis. the syndrome may be called. Depending on age and general condition. which have myriad infectious and noninfectious etiologies. and so they require emergency care. ideally within 30 minutes of emergency department (ED) presentation. with
.causes include medications (eg.)
Acute bacterial meningitis
Acute bacterial meningitis denotes a bacterial cause of this syndrome. Patients with acute bacterial meningitis may decompensate very quickly. This is usually characterized by an acute onset of meningeal symptoms and neutrophilic pleocytosis. see the following:
Meningococcal Meningitis Staphylococcal Meningitis Haemophilus Meningitis Tuberculous Meningitis
Subacute bacterial meningitis
Most bacterial meningitis is not acute. antibiotics) and carcinomatosis. nonsteroidal anti-inflammatory drugs [NSAIDs]. these gravely ill patients present acutely with signs and symptoms of meningeal inflammation and systemic infection of less than 24 hours' duration (and usually >12 hours’ duration). including antimicrobial therapy. acute meningitis (< 1 d) is almost always a bacterial infection caused by 1 of several organisms. (See Etiology.
it can be reclassified as a form of acute viral meningitis (eg. These ill patients still require urgent ED diagnosis and care to prevent further decompensation. a cause for meningitis is not apparent after initial evaluation and is therefore classified as aseptic meningitis. and amebic meningoencephalitis. herpes simplex virus [HSV] meningitis). and parasitic agents. fever.
Meningitis caused by nonbacterial organisms
Fungal and parasitic causes of meningitis are also termed according to their specific etiologic agent. the condition can also be caused by bacterial. mycobacterial. enterovirus meningitis. a specific viral etiology is identified in 55-70% of cases of aseptic meningitis.
. after an extensive workup. such as cryptococcal meningitis. These patients characteristically have an acute onset of meningeal symptoms.symptoms beginning several days prior.
If. the disease can be reclassified according to its etiology. and cerebrospinal pleocytosis that is usually prominently lymphocytic. aseptic meningitis is found to have a viral etiology. When the cause of aseptic meningitis is discovered. If appropriate diagnostic methods are performed.
In many cases. Go to Viral Meningitis for complete information on this topic. However. fungal. Histoplasmameningitis.
in meningitis. protein. lactate. and the underlying parenchyma is invaded by the inflammatory process. causes brain swelling and can eventually result in decreasing blood flow to parts of the brain. in turn. Replicating bacteria. This process. blood vessels become leaky and allow fluid. the pial barrier is not penetrated. and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis and account for the characteristic changes in CSF cell count. increasing numbers of inflammatory cells. white blood cells. When the body tries to fight the infection. Depending on the severity of bacterial meningitis. worsening the symptoms of infection. the pial barrier is broken. they are somewhat isolated from the immune system and can spread. However.
. pH. the inflammatory process may remain confined to the subarachnoid space. this protection is an advantage because the barrier prevents the body from attacking itself. and the underlying parenchyma remains intact. in more severe forms of bacterial meningitis. once bacteria or other organisms have found their way to the brain. the barrier can become a problem. However. and glucose in patients with this disease. cytokine-induced disruptions in membrane transport.
The brain is naturally protected from the body's immune system by a barrier the meninges create between the bloodstream and the brain. the problem can worsen. bacterial meningitis may lead to widespread cortical destruction. particularly when left untreated. Normally.Chronic meningitis is a constellation of signs and symptoms of meningeal irritation associated with CSF pleocytosis that persists for longer than 4 weeks. and other infection-fighting particles to enter the meninges and brain. Thus. In less severe forms.
the cycle of decreasing cerebral brain fluid (CBF). interstitial) significantly contributes to intracranial hypertension and a consequent decrease in cerebral blood flow. particularly to the basal cisterns. and inducing vasculitis and thrombophlebitis (causing local brain ischemia). and the products of bacterial degradation.Exudates extend throughout the CSF. Interstitial edema (secondary to obstruction of CSF flow.
The increased CSF viscosity resulting from the influx of plasma components into the subarachnoid space and diminished venous outflow lead to interstitial edema.
Intracranial pressure and cerebral brain fluid
One complication of meningitis is the development of increased intracranial pressure (ICP). Ongoing endothelial injury may result in vasospasm and thrombosis. with resultant hearing loss). and other cellular activation lead to cytotoxic edema. further compromising CBF. The ensuing cerebral edema (ie. obliterating CSF pathways (causing obstructive hydrocephalus). Anaerobic metabolism
. and may lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CBF. Without medical intervention. worsening cerebral edema. cytotoxic edema (swelling of cellular elements of the brain through the release of toxic factors from the bacteria and neutrophils). neutrophils. and the patient soon dies from systemic complications or from diffuse CNS ischemic injury. vasogenic. cranial nerve VIII. and vasogenic edema (increased blood brain barrier permeability) are all thought to play a role in the development of increased ICP. and increasing ICP proceeds unchecked. The pathophysiology of this complication is complex and may involve many proinflammatory molecules as well as mechanical elements. as in hydrocephalus). damaging cranial nerves (eg. cytotoxic.
IL-1. lymphocytes. interleukin [IL]-1). and microglial cells. peptidoglycan. such as the Toll-like receptors. and IL-8 are characteristic findings in patients with bacterial meningitis. and other proinflammatory molecules in the pathogenesis of pleocytosis and neuronal damage during occurrences of bacterial meningitis. In addition. IL-6. (Cytokine levels.) The proposed events involving these inflammation mediators in bacterial meningitis begin with the exposure of cells (eg. astrocytes. leukocytes. including those of IL-6. endothelial cells. astrocytes. tumor necrosis factor-alpha [TNF-alpha]. which contributes to increased lactate concentration and hypoglycorrhachia. previously known as endogenous pyrogen. this exposure incites the synthesis of cytokines and proinflammatory mediators. TNF-alpha is a glycoprotein derived from activated monocyte-macrophages. microglia. TNF-alpha.ensues. and interferon-gamma. IL-1. chemokines (IL-8). and meningeal macrophages) to bacterial products released during replication and death. Increased CSF concentrations of TNF-alpha. if this uncontrolled process is not modulated by effective treatment. have been found to be elevated in patients with aseptic meningitis. Eventually. TNF-alpha and IL-1 are most prominent among the cytokines that mediate this inflammatory cascade. hypoglycorrhachia results from decreased glucose transport into the spinal fluid compartment. is also produced primarily by activated mononuclear phagocytes and is responsible for the induction of
The role of cytokines and secondary mediators in bacterial meningitis
Key advances in understanding the pathophysiology of meningitis include insight into the pivotal roles of cytokines (eg. Data indicate that this process is likely initiated by the ligation of the bacterial components (eg. lipopolysaccharide) to pattern-recognition receptors. transient neuronal dysfunction or permanent neuronal injury results.
In experimental models of meningitis. The chemokine IL-8 mediates neutrophil chemoattractant responses induced by TNF-alpha and IL-1. the precise roles of all these secondary mediators in meningeal inflammation remain unclear. this contributes to vasogenic edema and elevated CSF protein levels. Many secondary mediators. they appear early during the course of disease and have been detected within 30-45 minutes of intracisternal endotoxin inoculation. either synergistically or independently. appears to participate in the induction of increased blood-brain barrier permeability. The net result of the above processes is vascular endothelial injury and increased blood-brain barrier permeability. neutrophils migrate from the bloodstream and penetrate the damaged blood-brain barrier. is believed to mediate the formation of thrombi and the activation of clotting factors within the vasculature. such as IL-6. IL-8. In response to the cytokines and chemotactic molecules.
Bacterial seeding usually occurs by hematogenous spread. producing the profound neutrophilic pleocytosis characteristic of bacterial meningitis. from other parts of the body. Nitric oxide is a free radical molecule that can induce cytotoxicity when produced in high amounts. nitric oxide. PAF. In patients without an identifiable
. PGE2. are presumed to amplify this inflammatory event. a product of cyclooxygenase (COX). and platelet activation factor (PAF). Organisms typically enter the meninges through the bloodstream. prostaglandins (PGE2). In many patients. with its myriad biologic activities. leading to the entry of many blood components into the subarachnoid space. Both molecules have been detected in the CSF of individuals with bacterial meningitis.fever during bacterial infections. However. IL-6 induces acute-phase reactants in response to bacterial infection.
Acute leptomeningitis results in congestion and hyperemia of the piaarachnoid and distention of the subarachnoid space by the exudates. hematogenous seeding into distant sites occurs. including the CNS. Many meningitis-causing bacteria are carried in the nose and throat. basal cisterns. complement components) appear to be limited in this body compartment. and the presence of toxic mediators in the CSF. antibodies. local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. This process of meningeal inflammation has been an area of extensive investigation in recent years that has led to a better understanding of meningitis pathophysiology.
. the infectious agents likely survive because host defenses (eg. immunoglobulins.source of infection. often without symptoms in the carrier. complement-mediated bacterial killing. Most meningeal pathogens are transmitted through the respiratory route. and neutrophil phagocytosis). and cranial nerves. which extends throughout the CSF. Inflammations are characterized by polymorphonuclear cell infiltration and extensive fibrinous exudation. Bacterial seeding results in increased permeability of the bloodbrain barrier. cerebral edema. Once inside the bloodstream. The presence and replication of infectious agents remain uncontrolled and incite a cascade of meningeal inflammation. the infectious agent must escape immune surveillance (eg. presumably by damaging mucosal defenses. Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment. Once inside the CNS. as exemplified by the fact that Neisseria meningitidis (meningococcus) is carried nasopharyngeally and by the nasopharyngeal colonization with Streptococcus pneumoniae(pneumococcus). neutrophils. Subsequently. The specific pathophysiologic mechanisms by which the infectious agents gain access into the subarachnoid space remain unclear.
In bacterial meningitis. and the presence of toxic mediators in the CSF. the paucity of antibodies. When components of the bacterial cell membrane are identified by the immune system-related cells of the brain (astrocytes and microglia). Bacterial cell wall components initiate a cascade of complement. In the newborn. occasionally. In most cases. meningitis follows invasion of the bloodstream by organisms that live upon mucous surfaces such as the nasal cavity.Once in the CSF. The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection but can rather largely be attributed to the response of the immune system to the entrance of bacteria into the central nervous system. 25% of those with bloodstream infections due to group B streptococci experience meningitis. Direct contamination of the cerebrospinal fluid (CSF) may arise from indwelling devices. which break down the normal barrier provided by the mucous surfaces. This is often preceded further by viral infections. or infections of the nasopharynx or the nasal sinuses that have formed a tract with the subarachnoid space (see above). Once bacteria have entered the bloodstream. Meningitis is caused by the bacteria Neisseria meningitidis (known as "meningococcal meningitis") . congenital defects of the dura mater can be identified. and white blood cells allows the bacterial infection to flourish. they enter the subarachnoid space in places where the blood-brain barrier is vulnerable—such as the choroid plexus. cerebral edema.
.and cytokine-mediated events that result in increased permeability of the blood-brain barrier. skull fractures. in adults this phenomenon is more uncommon. 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. complement components.
such as the use of glucocorticoids. Genetic targeting and/or pharmacological blockages of these pathways may help to prevent diffuse (widespread) brain injury and therefore decrease mortality of meningitis. causing inflammation of the meninges. and brain cells are deprived of oxygen and undergo apoptosis (automated cell death). Particular treatments. there has been more evidence to suggest that a complicated network of cytokines. the wall of the blood vessels themselves becomes inflamed (cerebral vasculitis). "cytotoxic" edema. hormone-like mediators that recruit other immune cells and stimulate other tissues to participate in an immune response. The three different forms of cerebral edema all lead to an increased intracranial pressure. The blood-brain barrier becomes more permeable. which leads to a decreased blood flow and a third type of edema. are aimed at dampening the immune system's response to this phenomenon
. together with the lowered blood pressure often encountered in acute infection this means that it is harder for blood to enter the brain. and leading to "interstitial" edema (swelling due to fluid between the cells). by increasing the amount of bacterial cell membrane products released through the destruction of bacteria. In addition. leading to "vasogenic" cerebral edema (swelling of the brain due to fluid leakage from blood vessels). chemokines. Recently. Large numbers of white blood cells enter the CSF.they respond by releasing large amounts of cytokines. proteolytic enzymes and oxidants are responsible for the entire inflammatory process which leads to necrosis (cell death). It is recognized that antibiotics may initially worsen the process outlined above.
During the exam. your doctor may check for signs of infection around the head. chest or sinuses may reveal swelling or inflammation. which is collected during a procedure known as a spinal tap. These tests can also help your doctor look for infection in other areas of the body that may be associated with meningitis. the CSF fluid often shows a low sugar (glucose) level along with an increased white
.Tests and diagnosis
By Mayo Clinic staff Your family doctor or pediatrician can diagnose meningitis based on a medical history. You or your child may undergo the following diagnostic tests:
Blood cultures. A sample may also be placed on a slide to which stains are added (Gram's stain). Spinal tap (lumbar puncture). particularly bacteria. a physical exam and certain diagnostic tests. Imaging. In people with meningitis. then examined under a microscope for bacteria. ears. X-rays and computerized tomography (CT) scans of the head. Blood drawn from a vein is sent to a laboratory and placed in a special dish to see if it grows microorganisms. The definitive diagnosis of meningitis is often made by analyzing a sample of your cerebrospinal fluid (CSF). throat and the skin along the spine.
But it can also occur when bacteria directly invade the meninges. but the cause may also be a bacterial infection. It can take up to a week to get these test results. as a result of an ear or sinus infection or a skull fracture. Less commonly. This may provide results about your meningitis in as little as four hours and help to determine proper treatment. Bacterial meningitis Acute bacterial meningitis usually occurs when bacteria enter the bloodstream and migrate to the brain and spinal cord. he or she may order a DNA-based test known as a polymerase chain reaction (PCR) amplification to check for the presence of viral causes of meningitis. you may need additional tests. identifying the source of the infection is an important part of developing a treatment plan.
By Mayo Clinic staff
Meningitis usually results from a viral infection. If you have chronic meningitis caused by cancer or an inflammatory illness.blood cell count and increased protein. CSF analysis may also help your doctor identify the exact bacterium that's causing the illness. The most common include:
. If your doctor suspects meningitis. Because bacterial infections are the most serious and can be life-threatening. a fungal infection may cause meningitis. A number of strains of bacteria can cause acute bacterial meningitis.
and infections in late pregnancy may cause a baby to be stillborn or die shortly after birth. This infection is highly contagious. newborns and older adults tend to be more susceptible. But new Hib vaccines — available as part of the routine childhood immunization schedule in the United States — have greatly reduced the number of cases of this type of meningitis. Viral meningitis Each year. in dust and in foods that have become contaminated. hot dogs and luncheon meats. viruses cause a greater number of cases of meningitis than do bacteria. Neisseria meningitidis (meningococcus). When it occurs. Haemophilus influenzae (haemophilus). young children and adults in the United States.
Streptococcus pneumoniae (pneumococcus). Viral meningitis is usually mild and often clears on its own within two weeks. are most vulnerable. These bacteria can be found almost anywhere — in soil. ear infection (otitis media) or sinusitis. Many wild and domestic animals also carry the bacteria. Haemophilus influenzae type b (Hib) bacterium was the leading cause of bacterial meningitis in children. and may cause local epidemics in college dormitories. This bacterium is the most common cause of bacterial meningitis in infants. Contaminated foods have included soft cheeses. due to disease or medication effect. Listeria monocytogenes (listeria). although pregnant women. People with weakened immune systems. It affects mainly teenagers and young adults. boarding schools and military bases. Fortunately. Listeria can cross the placental barrier. most healthy people exposed to listeria don't become ill. Meningococcal meningitis commonly occurs when bacteria from an upper respiratory infection enter your bloodstream. Before the 1990s. This bacterium is another leading cause of bacterial meningitis. it tends to follow an upper respiratory infection. A group of viruses known as
. It more commonly causes pneumonia or ear or sinus infections.
http://www. fever. Other meningitis causes Meningitis can also result from noninfectious causes. Occasionally it can mimic acute bacterial meningitis. Viruses such as herpes simplex virus. These viruses tend to circulate in late summer and early fall.ebmedicine. Although acute meningitis strikes suddenly.enteroviruses are responsible for about 30 percent of viral meningitis cases in the United States. such as AIDS. joint aches and headache. sore throat. As many viral meningitis episodes never have a specific virus identified as the cause. the signs and symptoms of chronic meningitis — headaches. some types of cancer and inflammatory diseases such as lupus. This type of meningitis is rare. La Crosse virus. chronic meningitis develops over two weeks or more. vomiting and mental cloudiness — are similar to those of acute meningitis. The most common signs and symptoms of enteroviral infections are rash. such as drug allergies. It's lifethreatening if not treated with an antifungal medication. Nevertheless.JP G
. Fungal meningitis Fungal meningitis is relatively uncommon and causes chronic meningitis. West Nile virus and others also can cause viral meningitis. diarrhea. Chronic meningitis Chronic forms of meningitis occur when slow-growing organisms invade the membranes and fluid surrounding your brain. Cryptococcal meningitis is a common fungal form of the disease that affects people with immune deficiencies.net/media_library/aboutUs/Antibiotic%20Recommendations%20For%20The% 20Treatment%20Of%20Bacterial%20Meningitis%20Pediatric%20Emergency%20Medicine%20Practice.
clevelandclinic.org/wiki/Meningitis http://www.mayoclinic.medscape. Children under age 5.http://answers.com/health/meningitis/DS00118/DSECTION=causes
Predisposing/Precipitating Factors of Bacterial meningitis
Incidence of meningitis is high among Blacks and Native American. young people ages 18 to 24 and older adults are more likely to develop meningitis than the rest of the population.com/article/232915-overview#a0104 http://www. Eskimo and American Indian children are especially at risk of meningitis caused by the bacteria H.com/article/bacterial-meningitis http://emedicine.medscape. Male infants have a high incidence of gram-negative neonatal meningitis.gov/meningitis/about/faq. People with weakened or suppressed immune systems also are at higher
.wikipedia. influenzae risk.html http://my.aspx http://www. Black.yahoo.com/article/232915-overview http://en.bettermedicine.com/question/index?qid=20081106212728AAfHijP http://emedicine.cdc.org/disorders/meningitis/hic_bacterial_meningitis. and Streptococcus pneumoniae.
an important part of your immune system. Listeriosis can be transmitted from mother to fetus through the placenta. ranchers) and pregnant women are at increased risk for meningitis associated with listeriosis (disease transmitted from animals to humans via soil). you’re 20 times more likely to contract listeriosis..
. causing spontaneous abortion.People who work with domestic animals (e. diabetes and use of immunosuppressant drugs – also make you more susceptible to meningitis. If you have listeriosis. Other factors that may compromise your immune system – including AIDS. including dairy farmers and ranchers. College students living in dormitories. may also increase your risk. your unborn baby is at risk too.g. personnel on military bases and children in boarding schoolsand child-care facilities are at increased risk of meningococcal meningitis. If you’re pregnant. The disease is usually fatal in newborns. Removal of your spleen. Some studies have linked increased risk to smoking and drinking alcohol. which may suppress your body’s immune system. Also at higher risk of listeriosis are people who work with domestic animals. dairy farmers. an infection that may cause meningitis. mainly because infectious diseases tend to spread quickly wherever large groups of people congregate.
15 to 45 mg/dl) Decreased CSF glucose level (normal. 60 to 80 mg/dl. prostration. Other general manifestations related to infection may also be present. and photophobia.Signs & Symptoms of Bacterial Meningitis
The classic manifestations of meningitis are nuchal rigidity (rigidity of the neck). chills. but. influenza is frequently detected with this technique. Clients with bacterial meningitis demonstrate the following:
Moderately elevated CSF pressures Elevated CSF protein level (normal. fever. fever. Brudzinski’s sign and Kernig’s sign. Seizures may occur. H. the client appears acutely ill and confused. stuporous. such as headache. tachycardia. A petechial or hemorrhagic rash may develop. The CSF is cloudy. bacterial antigens can be determined. as the infection progresses. The client may be irritable at first. or comatose. Gram stain of the CSF reveals organisms in 70% to 80% of all cases. Diagnosis is made by lumbar puncture. and vomiting. When the organisms cannot be identified. or two thirds of the serum glucose value)
diagnosis from the
made CSF. with predominantly polymorphonuclear leukocytes. usually increased (100 to 10. meningitides. influenza and N.
manifestations and is confirmed by isolating the causative Empirical meningitis includes cephalosporins. The use
. Once the organism is known. rifampin. It is believed that the cephalosporins are more potent against the beta-lactamase organisms.
Elevated white blood cell count.
Health Promotion and Preventive Aspects for Bacterial Meningitis
Bacterial meningitis constitutes a medical emergency. 000/cm3). and vancomycin. Chloramphenicol and trimethoprimsulfamethoxazole are recommended for clients allergic to penicillin. antibiotics with greater sensitivity ma are used. Factors contributing to development of meningitis also need to be addressed. High doses of the appropriate antibiotic are usually prescribed for at least 10 days. Prognosis varies according to the causative organism. The empirical use of penicillin or ampicillin in the treatement of CNS infection is avoided because of the beta-lactamaseproducing H.
Residual neurologic deficits are rare in adults. Deaths most often occur in newborn infants and in older adults. brain and increased and ICP fluid attributable hydrocephalus. the blood-brain barrier recovers asinflammation subsides.
. swelling. Patient must be watched carefully for changed in neurologic function or other signs of worsening condition.
overload. Anticonvulsants may be prescribed for seizure prevention. Frequent assessment of the neurologic status is indicated to detect early manifestations of increasing ICP and seizures. seizures. Complications are rate but may include septic shock. However. Antibiotics are given intravenously. If untreated.of antibiotics has reduced the death rate to less than 5% for all types of bacterial meningitis. Adequate fluid and electrolyte balance must be maintained. so for short time antibiotics penetrate the CNS. it can be fatal within hours to days. inflammation inhibits the blood-brain barrier. vasomotor to collapse. and high doses are required to reach the CSF. A unique problem in treating CNS infection is that an intact blood-brain barrier prevents complete penetration of the antibiotic.
consciousness (LOC) and signs of increased ICP (plucking at the bedcovers. range-of-motion
Maintain adequate nutrition and elimination. all of which may signal an impending crisis. but avoid fluid overload because of the danger of cerebral edema. deteriorating LOC.
Position the patient carefully to prevent joint stiffness and neck pain. Watch for signs for cranial nerve involvement (ptosis. Maintain adequate fluid intake to avoid dehydration. To prevent constipation and minimize the risk of
. and altered respirations.
Be especially alert for a temperature increase up to 38. It may be necessary to provide small. Assist according with to planned positioning exercises. onsent of seizures. seizures. strabismus. antibiotics and other drugs. schedule. Turn him often.
Monitor fluid balance.V. and a change in motor function and vital signs).Nursing Considerations for Bacterial Meningitis
often. vomiting. frequent meals or to supplement meals with nasogastric tube or parenteral feedings. and diplopia). site often and change the sites according to hospital policy. 9o Celsius (102 F). Measure central venous pressure and intake and output accurately.V. check I. To avoid infiltration and phlebitis.
Watch for adverse effects of I.
increased ICP resulting from straining at stool. attempt to reorient him often. Reassure his family that the delirium and behavior changes caused by meningitis usually disappear.
Provide reassurance and support. If he’s deliberious or confused. give the patient a mild laxative or stool softener.
To help prevent development of meningitis. Follow strict sterile technique when treating patients with head wounds or skull fractures. Relieve headache with a nonopioid analgesic.
Give haemophilus influenza type B and pneumococcal vaccins to children. Give meningocococcal vaccine to college students.
Give prophylactic antibiotics to those who have been exposed to a patient with meningitis. fi a severe neurologic deficit appears permanent.
comfort. refer the patient o a rehabilitation program as soon as the acute phase of this illness has passed. Darkening the room may decrease photophobia. Maintain a quiet environment. The patient may be frightened by his illness and frequent lumbar punctures. such as aspirin or acetaminophen as ordered. teach patients with chronic sinusitis or other chronic infections and the importance of proper medical treatment.
. Give prophylactic antibiotics to those who have been exposed to a patient with meningitis.