meningitis

Definition

Meningitis is a potentially fatal inflammation of the meninges, the thin, membranous covering of the brain and the spinal cord. Meningitis is most commonly caused by infection (by bacteria, viruses, or fungi), although it can also be caused by bleeding into the meninges, cancer, diseases of the immune system, and an inflammatory response to certain types of chemotherapy or other chemical agents. The most serious and difficult-to-treat types of meningitis tend to be those caused by bacteria.

Description

Meningitis is a particularly dangerous infection because of the very delicate nature of the brain. Brain cells are some of the only cells in the body that, once killed, will not regenerate themselves. Therefore, if enough brain tissue is damaged by an infection, serious, life-long handicaps will remain.

In order to learn about meningitis, it is important to have a basic understanding of the anatomy of the brain. The meninges are three separate membranes, layered together, which encase the brain and spinal cord:

• The dura is the toughest, outermost layer, and is closely attached to the inside of the skull.
• The middle layer, the arachnoid, is important because of its involvement in the normal flow of the cerebrospinal fluid (CSF), a lubricating and nutritive fluid that bathes both the brain and the spinal cord.
• The innermost layer, the pia, helps direct blood vessels into the brain.
• The space between the arachnoid and the pia contains CSF, which helps insulate the brain from trauma. Many blood vessels course through this space.

CSF, produced within specialized chambers deep inside the brain, flows over the surface of the brain and spinal cord. This fluid serves to cushion these relatively delicate structures, as well as supplying important nutrients for brain cells. CSF is reabsorbed by blood vessels located within the meninges. A careful balance between CSF production and reabsorption is important to avoid the accumulation of too much CSF.

Because the brain is enclosed in the hard, bony case of the skull, any disease that produces swelling will be damaging to the brain. The skull cannot expand at all, so when the swollen brain tissue pushes up against the skull's hard bone, the brain tissue becomes damaged and may ultimately die. Furthermore, swelling on the right side of the brain will not only cause pressure and damage to that side of the brain, but by taking up precious space within the tight confines of the skull, the left side of the brain will also be pushed up against the hard surface of the skull, causing damage to the left side of the brain as well.

Another way that infections injure the brain involves the way in which the chemical environment of the brain changes in response to the presence of an infection. The cells of the brain require a very well-regulated environment. Careful balance of oxygen, carbon dioxide, sugar (glucose), sodium, calcium, potassium, and other substances must be maintained in order to avoid damage to brain tissue. An infection upsets this balance, and brain damage can occur when the cells of the brain are either deprived of important nutrients or exposed to toxic levels of particular substances.

The cells lining the brain's tiny blood vessels (capillaries) are specifically designed to prevent many substances from passing into brain tissue. This is commonly referred to as the blood-brain barrier. The blood-brain barrier prevents various substances that could be poisonous to brain tissue (toxins), as well as many agents of infection, from crossing from the blood stream into the brain tissue. While this barrier is obviously an important protective feature for the brain, it also serves to complicate treatment in the case of an infection by making it difficult for medications to pass out of the blood and into the brain tissue where the infection is located.

— Rosalyn Carson-DeWitt, MD

Inflammation of the meninges of the brain and the spinal cord, most often caused by a bacterial or viral infection and characterized by fever, vomiting, intense headache, and stiff neck.

Inflammation of the meninges. Certain types of meningitis are associated with distinctive abnormalities in the cerebrospinal fluid. With certain types of meningitis, especially bacterial, the causative organism can usually be recovered from the fluid. See also Meninges.

Meningeal inflammation in most cases is caused by invasion of the cerebrospinal fluid by an infectious organism. Noninfectious causes also occur. For example, in immune-mediated disorders antigen-antibody reactions can cause meningeal inflammation. Other noninfectious causes of meningitis are the introduction into the cerebrospinal fluid of foreign substances such as alcohol, detergents, chemotherapeutic agents, or contrast agents used in some radiologic imaging procedures. Meningeal inflammation brought about by such foreign irritants is called chemical meningitis. Inflammation also can occur when cholesterol-containing fluid or lipid-laden material leaks into the cerebrospinal fluid from some intracranial tumors.

Bacterial meningitis is among the most feared of human infectious diseases because of its possible seriousness, its rapid progression, its potential for causing severe brain damage, and its frequency of occurrence. Most cases of bacterial meningitis have an acute onset. Common clinical manifestations are fever, headache, vomiting, stiffness of the neck, confusion, seizures, lethargy, and coma. Symptoms of brain dysfunction are caused by transmission of toxic materials from the infected cerebrospinal fluid into brain tissue and the disruption of arterial perfusion and venous drainage from the brain because of blood vessel inflammation. These factors also provoke cerebral swelling, which increases intracranial pressure. Before antibiotics became available, bacterial meningitis was almost invariably fatal. See also Antibiotic.

Most types of acute bacterial meningitis are septic-borne in that they originate when bacteria in the bloodstream (bacteremia, septicemia) gain entrance into the cerebrospinal fluid. Meningitis arising by this route is called primary bacterial meningitis. Secondary meningitis is that which develops following direct entry of bacteria into the central nervous system, which can occur at the time of neurosurgery, in association with trauma, or through an abnormal communication between the external environment and the cerebrospinal fluid.

Many viruses can cause meningeal inflammation, a condition referred to as viral aseptic meningitis. The most common viral causes include the enteroviruses, the various herpesviruses, viruses transmitted by arthropods, the human immunodeficiency virus type I (HIV-1), and formerly, the mumps virus. If the virus attacks mainly the brain rather than the spinal cord, the disorder is termed viral encephalitis. See also Animal virus; Arboviral encephalitides; Enterovirus; Herpes.

Fungal, parasitic, and rickettsial meningitis are less common in the United States than are bacterial and viral. These infections are more likely to be subacute or chronic than those caused by bacteria or viruses; in most cases, the meningeal inflammation is associated with brain involvement. An acute form of aseptic meningitis can occur in the spirochetal diseases, syphilis and Lyme disease. See also Lyme disease; Medical mycology; Medical parasitology; Rickettsioses; Syphilis.

Any infection or inflammation of the membranes covering the brain and spinal cord. It usually is a purulent infection and involves the fluid of the subarachnoid space. The most common causes in adults are bacterial infection with Streptococcus pneumoniae, Neisseria meningitidis, or Haemophilus influenzae. Aseptic meningitis may be caused by chemical irritation, neoplasms, or viruses.

Definition

Meningitis is a potentially fatal inflammation of the meninges, the thin, membranous covering of the brain and the spinal cord. Meningitis is most commonly caused by infection by bacteria, viruses, or fungi, although it can also be caused by bleeding into the meninges, cancer, diseases of the immune system, and an inflammatory response to certain types of chemotherapy or other chemical agents. The most serious and the most difficult to treat types of meningitis tend to be those caused by bacteria.

Description

Meningitis is a particularly dangerous infection because of the very delicate nature of the brain. Brain cells are some of the only cells in the body that, once killed, will not regenerate themselves. Therefore, if enough brain tissue is damaged by an infection, then serious lifelong handicaps will remain.

In order to learn about meningitis, it is important to have a basic understanding of the anatomy of the brain. The meninges are three separate membranes, layered together, which encase the brain and spinal cord:

• The dura is the toughest, outermost layer, and is closely attached to the inside of the skull.
• The middle layer, the arachnoid, is important because of its involvement in the normal flow of the cerebrospinal fluid (CSF), a lubricating and nutritive fluid that bathes both the brain and the spinal cord.
• The innermost layer, the pia, helps direct blood vessels into the brain.
• The space between the arachnoid and the pia contains CSF, which helps insulate the brain from trauma. Many blood vessels, as well as peripheral and cranial nerves course through this space.

CSF, produced within specialized chambers deep inside the brain, flows over the surface of the brain and spinal cord. This fluid serves to cushion these relatively delicate structures, as well as supplying important nutrients for brain cells. CSF is reabsorbed by blood vessels located within the meninges. A careful balance between CSF production and reabsorption is important to avoid the accumulation of too much CSF.

Because the brain is enclosed in the hard, bony case of the skull, any disease that produces swelling will be damaging to the brain. The skull cannot expand at all, so when the swollen brain tissue pushes up against the skull's hard bone, the brain tissue becomes damaged and the blood supply is compromised, and this tissue may ultimately die. Furthermore, swelling on the right side of the brain will not only cause pressure and damage to that side of the brain, but by taking up precious space within the tight confines of the skull, the left side of the brain will also be pushed up against the hard surface of the skull, causing damage to the left side of the brain, as well.

Another way that infections injure the brain involves the way in which the chemical environment of the brain changes in response to the presence of an infection. The cells of the brain require a very well-regulated environment. Careful balance of oxygen, carbon dioxide, sugar (glucose), sodium, calcium, potassium, and other substances must be maintained in order to avoid damage to brain tissue. An infection upsets this balance, and brain damage can occur when the cells of the brain are either deprived of important nutrients or exposed to toxic levels of particular substances.

The cells lining the brain's tiny blood vessels (capillaries) are specifically designed to prevent many substances from passing into brain tissue. This is commonly referred to as the blood-brain barrier. The blood-brain barrier prevents various substances that could be poisonous to brain tissue (toxins), as well as many agents of infection, from crossing from the blood stream into the brain tissue. While this barrier is obviously an important protective feature for the brain, it also serves to complicate treatment in the case of an infection by making it difficult for medications to pass out of the blood and into the brain tissue where the infection is located.

Causes & Symptoms

The most common infectious causes of meningitis vary according to an individual's age, habits, living environment, and health status. While nonbacterial types of meningitis are more common, bacterial meningitis is more potentially life-threatening. Three bacterial agents are responsible for about 80% of all bacterial meningitis cases. These bacteria are Haemophilus influenzae type b, Neisseria meningitidis (causing meningococcal meningitis), and Streptococcus pneumoniae (causing pneumococcal meningitis).

In newborns, the most common agents of meningitis are those that are contracted from the newborn's mother, including Group B streptococci (becoming an increasingly common infecting organism in the newborn period), Escherichia coli, and Listeria monocytogenes. The highest incidence of meningitis occurs in babies under a month old, with an increased risk of meningitis continuing through about two years of age.

Older children are more frequently infected by bacteria, including Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae.

Adults are most commonly infected by either S. pneumoniae or N. meningitidis, with pneumococcal meningitis the more common. Certain conditions predispose to this type of meningitis, including alcoholism and chronic upper respiratory tract infections (especially of the middle ear, sinuses, and mastoids).

N. meningitidis is the only organism that can cause epidemics of meningitis. For instance, cases have been reported when a child in a crowded day care situation or a military recruit in a crowded training camp has fallen ill with meningococcal meningitis.

There have been case reports in recent years of meningitis caused by Streptococcus bovis, an organism that is ordinarily found in the digestive tract of such animals as cows and sheep; and Pasteurella multocida, an organism that usually infects rabbits. Other atypical cases of meningitis include several caused by the anthrax bacillus. These cases have a high mortality rate.

Viral causes of meningitis include the herpes simplex virus, the mumps and measles viruses (against which most children are protected due to mass immunization programs), the virus that causes chickenpox, the rabies virus, and a number of viruses that are acquired through the bites of infected mosquitoes.

A number of medical conditions predispose individuals to meningitis caused by specific organisms. Patients with AIDS (acquired immunodeficiency syndrome) are more prone to getting meningitis from fungi, as well as from the agent that causes tuberculosis. Patients who have had their spleens removed, or whose spleens are no longer functional (as in the case of patients with sickle cell disease) are more susceptible to other infections, including meningococcal and pneumococcal meningitis.

The majority of meningitis infections are acquired by transmission through the blood. A person may have another type of infection (for instance, infection of the lungs, throat, or tissues of the heart) caused by an organism that can also cause meningitis. If this initial infection is not properly treated, the organism will continue to multiply, find its way into the blood stream, and be delivered in sufficient quantities to invade past the blood-brain barrier. Direct spread occurs when an organism spreads to the meninges from infected tissue next to or very near the meninges. This can occur, for example, with a severe, poorly treated ear or sinus infection.

Patients who suffer from skull fractures possess abnormal openings to the sinuses, nasal passages, and middle ears. Organisms that usually live in the human respiratory system without causing disease can pass through openings caused by such fractures, reach the meninges, and cause infection. Similarly, patients who undergo surgical procedures or who have had foreign bodies surgically placed within their skulls (such as tubes to drain abnormal amounts of accumulated CSF) have an increased risk of meningitis.

Organisms can also reach the meninges via an uncommon but interesting method called intraneural spread. This involves an organism invading the body at a considerable distance away from the head, spreading along a nerve, and using that nerve as a sort of ladder into the skull, where the organism can multiply and cause meningitis. Herpes simplex virus is known to use this type of spread, as is the rabies virus.

The classic symptoms of meningitis (particularly of bacterial meningitis) include fever, headache, vomiting, sensitivity to light (photophobia), irritability, severe fatigue (lethargy), stiff neck, and a reddish purple rash on the skin. Untreated, the disease progresses with seizures, confusion, and eventually coma.

A very young infant may not show the classic signs of meningitis. Early in infancy, a baby's immune system is not yet developed enough to mount a fever in response to infection, so fever may be absent. However, checking an infant's temperature to see if it is high or low could be an indication. Some infants with meningitis have seizures as their only identifiable symptom. Similarly, debilitated elderly patients may not have fever or other identifiable symptoms of meningitis.

Damage due to meningitis occurs from a variety of phenomena. The action of infectious agents on the brain tissue is one direct cause of damage. Other types of damage may be due to the mechanical effects of swelling and compression of brain tissue against the bony surface of the skull. Swelling of the meninges may interfere with the normal absorption of CSF by blood vessels, causing accumulation of CSF and damage from the resulting pressure on the brain. Interference with the brain's carefully regulated chemical environment may cause damaging amounts of normally present substances (carbon dioxide, potassium) to accumulate. Inflammation may cause the blood-brain barrier to become less effective at preventing the passage of toxic substances into brain tissue.

Diagnosis

A number of techniques are used when examining a patient suspected of having meningitis to verify the diagnosis. Certain manipulations of the head (lowering the head, chin towards chest, for example) are difficult to perform and painful for a patient with meningitis.

The most important test used to diagnose meningitis is the lumbar puncture (LP), commonly called a spinal tap. Lumbar puncture involves the insertion of a thin needle into a space between the vertebrae in the lower back and the withdrawal of a small amount of CSF. The CSF is then examined under a microscope to look for bacteria or fungi. Normal CSF contains set percentages of glucose and protein. These percentages will vary with bacterial, viral, or other causes of meningitis. For example, bacterial meningitis causes a smaller than normal percentage of glucose to be present in CSF, as the bacteria are essentially "eating" the host's glucose, and using it for their own nutrition and energy production. Normal CSF should contain no infection-fighting cells (white blood cells), so the presence of white blood cells in CSF is another indication of meningitis. Some of the withdrawn CSF is also put into special lab dishes to allow growth of the suspected infecting organism, which can then be identified more easily. Special immunologic and serologic tests may also be used to help identify the infectious agent.

In rare instances, CSF from a lumbar puncture cannot be examined because the amount of swelling within the skull is so great that the pressure within the skull (intracranial pressure) is extremely high. This pressure is always measured immediately upon insertion of the LP needle. If it is found to be very high, no fluid is withdrawn because doing so could cause herniation of the brain stem. Herniation of the brain stem occurs when the part of the brain connecting to the spinal cord is thrust through the opening at the base of the skull into the spinal canal. Such herniation will cause compression of those structures within the brain stem that control the most vital functions of the body (breathing, heart beat, consciousness). Death or permanent debilitation follows herniation of the brain stem.

Treatment

Because meningitis is a potentially deadly condition, doctors should be contacted immediately for diagnosis and treatment. Alternative treatments should be used only to support the recovery process following appropriate antibiotic treatments, or used concurrently with antibiotic treatments.

General Recommendations

Patients should be well rested in bed, preferably in a darkened room. They should be given lots of fluids and nutritious foods. Patients should avoid processed foods and those with high fat and sugar content. Fats are difficult to digest in severely ill patients; sugar tends to depress the immune system and impede recovery process. Patients should also take vitamin A (up to 10,000 IU per day), B-complex vitamins (up to 1,500 mg per day), and vitamin C (up to 2 g per day) to help keep the body strong and prevent future infections. Additionally, the patient may consider taking other antioxidants, essential fatty acids (EFAs), and/or participate in therapies, such as massage therapy and movement therapies (e.g., t'ai chi).

Other Treatments

Alternative therapies, such as homeopathy, traditional Chinese medicine, and Western herbal medicine may help patients regain their health and build up their immune systems. The recovering individual, under the direction of a professional alternative therapist, may opt to include mushrooms into his or her diet to stimulate immune function. Contact an experienced herbalist or homeopathic practitioner for specific remedies.

Allopathic Treatment

Antibiotics are the first line of treatment for bacterial meningitis. In recent years, however, doctors have turned to such newer medications as vancomycin or the fluoroquinolones to treat bacterial meningitis because strains of S. pneumoniae and N. meningitidis have emerged that are resistant to penicillin and the older antibiotics. Because of the effectiveness of the blood-brain barrier in preventing the passage of substances into the brain, medications must be delivered directly into the patient's veins (intravenously) at very high doses. Antiviral drugs (acyclovir) may be helpful in shortening the course of viral meningitis, and antifungal medications are available as well. Patients who develop seizures will require medications to halt the seizures and prevent their return.

Expected Results

Viral meningitis is the least severe type of meningitis, and patients usually recover with no long-term effects from the infection. Bacterial infections, however, are much more severe, and progress rapidly. Without very rapid treatment with the appropriate antibiotic, the infection can swiftly lead to coma and death in less than a day's time. While death rates from meningitis vary depending on the specific infecting organism, the overall death rate is just under 20%.

The most frequent long-term effects of meningitis include deafness and blindness, which may be caused by the compression of specific nerves and brain areas responsible for the senses of hearing and sight. Some patients develop permanent seizure disorders, requiring lifelong treatment with antiseizure medications. Scarring of the meninges may result in obstruction of the normal flow of CSF, causing abnormal accumulation of CSF. This may be a chronic problem for some patients, requiring the installation of shunt tubes to drain the accumulation regularly.

Some cases of sudden and unexplained death in adults have been attributed to rapidly developing meningitis.

Prevention

Prevention of meningitis primarily involves the appropriate treatment of other infections an individual may acquire, particularly those that have a track record of seeding to the meninges (such as ear and sinus infections). Preventive treatment with antibiotics is sometimes recommended for the close contacts of an individual who is ill with meningococcal or H. influenzae type b meningitis. A meningococcal vaccine exists, and is sometimes recommended to individuals who are traveling to very high risk areas. A vaccine for H. influenzae type b is now given to babies as part of the standard array of childhood immunizations.

Resources

Books

"Meningitis." The Medical Advisor: The Complete guide to Alternative & Conventional Treatments. Home Edition. Richmond, VA: Time Life Inc., 1997.

Ray, C. George. "Central Nervous System Infections." In Sherris Medical Microbiology: An Introduction to Infectious Diseases, edited by Kenneth J. Ryan. Norwalk, CT: Appleton and Lange, 1994.

Swartz, Morton N. "Bacterial Meningitis." In Cecil Textbook of Medicine, edited by J. Claude Bennett and Fred Plum. Philadelphia: W.B. Saunders, 1996.

Periodicals

Aronin, S. I. "Current Pharmacotherapy of Pneumococcal Meningitis." Expert Opinion on Pharmacotherapy 3 (February 2002): 121–129.

Black, M., and D. I Graham. "Sudden Unexplained Death in Adults Caused by Intracranial Pathology." Journal of Clinical Pathology 55 (January 2002): 44–50.

Green, B. T., K. M. Ramsey, and P. E. Nolan. "Pasteurella multocida Meningitis: Case Report and Review of the Last 11 Years." Scandinavian Journal of Infectious Disease 34 (2002): 213–217.

Meissner, Judith W. "Caring for Patients With Meningitis." Nursing (July 1995): 50+.

Schuchat, Anne, et al. "Bacterial Meningitis in the United States in 1995." New England Journal of Medicine (October 2, 1997).

Tasyaran, M. A., O. Deniz, M. Ertek, and K. Cetin. "Anthrax Meningitis: Case Report and Review." Scandinavian Journal of Infectious Diseases 34 (2002): 66–67.

Tunkel, A. R., and W. M. Scheld. "Treatment of Bacterial Meningitis." Current Infectious Disease Reports 4 (February 2002): 7–16.

Vilarrasa, N., A. Prats, M. Pujol, et al. "Streptococcus bovis Meningitis in a Healthy Adult Patient." Scandinavian Journal of Infectious Diseases 34 (2002): 61–62.

Organizations

American Academy of Neurology. 1080 Montreal Avenue, St. Paul, MN 55116. (612) 695-1940. .

Meningitis Foundation of America. 7155 Shadeland Station, Suite 190, Indianapolis, IN 46256-3922. (800) 668-1129. .

[Article by: Mai Tran; Rebecca J. Frey, PhD]

Definition

Meningitis is a serious inflammation of the meninges, the membranes (lining) that surround the brain and spinal cord. It can be of bacterial, viral, or fungal origin.

Description

Meningitis is usually the result of a viral or bacterial infection. Viral meningitis, also called aseptic meningitis, is generally less severe and often disappears without specific treatment, while bacterial meningitis can be quite serious and may result in brain damage, hearing loss, or learning disabilities in children. The infection may even cause death.

Bacterial meningitis is either monococcal or pneumococcal, depending on the type of bacteria responsible for the infection. Meningitis caused by Haemophilus influenzae and related strains (A, B C, Y, and W135) is also called meningococcal meningitis. Similarly, meningitis due to Streptococcus pneumoniae is also called pneumococcal meningitis.

Transmission

Most types of meningitis are contagious. A person may be exposed to meningitis bacteria when someone with meningitis coughs or sneezes. The bacteria can also spread through kissing or sharing eating utensils or a toothbrush.

Demographics

According to the National Institute of Neurological Disorders and Stroke (NINDS), some 6,000 cases of pneumococcal meningitis are reported in the United States each year. Meningococcal meningitis is common in minors ages two to 18. Each year about 2,600 people get this highly contagious disease. High-risk groups include infants under the age of one year, people with suppressed immune systems, travelers to foreign countries where the disease is endemic, and college students and Army recruits who reside in dormitories and other close quarters. Between 10 and 15 percent of cases are fatal, with another 10 to 15 percent involving brain damage and other serious side effects.

Causes and Symptoms

The bacteria which cause bacterial meningitis live in the back of the nose and throat region and are carried by 10 to 25 percent of the population. They cause meningitis when they get into the bloodstream and travel to the meninges.

At least 50 kinds of bacteria can cause bacterial meningitis. According to the Centers for Disease Control (CDC), before the 1990s, Haemophilus influenzae type b (Hib) was the leading cause of bacterial meningitis, but subsequent vaccines given to all children as part of their routine immunizations have reduced the occurrence of the disease due to H. influenzae. As of 2004, Streptococcus pneumoniae and Neisseria meningitidis were the leading causes of bacterial meningitis.

In newborns, the most common agents of meningitis are those that are contracted from the newborn's mother, including Group B streptococci (becoming an increasingly common infecting organism in the newborn period), Escherichia coli, and Listeria monocytogenes. The highest incidence of meningitis occurs in babies less than a month old, with an increased risk of meningitis continuing through about two years of age.

Older children are more frequently infected by the bacteria Haemophilus influenzae, Neisseria meningitidis, and Streptococci pneumoniae.

Most cases of viral meningitis are caused by enteroviruses (viruses that typically cause stomach flu). However, many other types of viruses, such as the herpes simplex virus, the mumps and measles viruses (against which most children are protected due to mass immunization programs), the virus that causes chickenpox, the rabies virus, and a number of viruses that are acquired through the bites of infected mosquitoes.

Meningitis symptoms include high fever, headache, and stiff neck in children over the age of two years. These symptoms can develop over several hours, or they may take one to two days. Other symptoms may include nausea, vomiting, discomfort looking into bright lights, confusion, and sleepiness. In some cases, a rash may be present. In newborns and small infants, these symptoms may be absent or difficult to detect, and the infant may only appear slow or inactive, or be irritable, have vomiting, or be feeding poorly. As the disease progresses, patients of any age may also have seizures.

When to Call the Doctor

Parents should call a doctor if a child has a temperature above 101°F (38.5°C). If any meningitis symptoms occur, the child should see a doctor immediately, as early diagnosis and treatment are very important for a successful outcome.

Diagnosis

Viral meningitis often remains undiagnosed because its symptoms are similar to those of the common flu. As for bacterial meningitis, the diagnosis is established by growing bacteria from a sample of spinal fluid. The spinal fluid is obtained by performing a lumbar puncture (also called a spinal tap), in which a needle is inserted into an area in the lower back where fluid in the spinal canal is readily accessible.

Treatment

Bacterial meningitis treatment usually involves intravenous administered antibiotics, for a minimum of four days. The type of meningitis contracted will determine the specific antibiotic used. It is imperative that treatment start as early as possible, in order to avoid brain damage and death.

Viral meningitis cases usually resolve without complications, but typically, antibiotics are ineffective in treating it, so none are prescribed. The child will be told to get as much rest as he or she can. If the child has pain related to the disease such as headaches or other body pains, medication can be used to treat it.

Prognosis

The long-term outlook for children who develop bacterial meningitis varies significantly. The outcome depends on the child's age, the bacteria causing the infection, complications, and the treatment the child receives. The complications of bacterial meningitis can be severe and include neurological problems such as hearing loss, visual impairment, seizures, and learning disabilities. The heart, kidneys, and adrenal glands may also be affected. Although some children develop long-lasting problems, most children who receive prompt diagnosis and treatment recover fully.

The majority of cases of viral meningitis resolve with no complications.

Prevention

Many children as of 2004 routinely receive vaccines against meningitis, starting at about two months of age. Immunizations are recommended by the American Academy of Pediatrics and many other organizations. If a child has not been vaccinated, parents should talk to their doctor about the Hib and pneumococcal (Prevnar 7) vaccines.

Vaccines are available for both meningococcal and pneumococcal meningitis. Specifically, there are vaccines against Hib and against some strains of N. meningitidis and many types of Streptococcus pneumoniae. The vaccines against Hib are very safe and highly effective. There is a vaccine that protects against four strains of N. meningitidis, but it is not routinely used in the United States. There are also vaccines to prevent meningitis due to S. pneumoniae, which can also prevent other forms of infection due to S. pneumoniae.

Parents should teach children to wash their hands often, especially before they eat and after using the bathroom, or after petting animals. They should be taught how to wash their hands vigorously, covering both the front and back of each hand with soap and rinsing thoroughly under running water.

Parental Concerns

Some forms of bacterial meningitis are contagious. The bacteria are spread through coughing, kissing, and sneezing. Fortunately, the bacteria that cause meningitis are not as contagious as the common cold or the flu, and they are not spread by casual contact or by simply breathing the air where a person with meningitis has been. However, people in the same household or daycare center, or anyone with direct contact with a patient's oral secretions is considered at increased risk of acquiring the infection.

Awareness of the symptoms and signs of meningitis, especially the rash which may accompany meningococcal meningitis is very important.

Resources

Books

Leigh, Jenny. A Dr. Spot Casebook: George Has Meningitis. London: Haldane & Mason, 2003.

Routh, Kristina. Meningitis (Just the Facts). Chicago: Heineman Library, 2004.

Tunkel, Allan R. Bacterial Meningitis. Philadelphia: Lippincott Williams & Wilkins, 2001.

Periodicals

Anderson, V., et al. "Cognitive and executive function 12 years after childhood bacterial meningitis: effect of acute neurologic complications and age of onset." Journal of Pediatrics & Psychology 29, no. 2 (March 2004): 67–81.

Gupta, S., and A. B. Tuladhar. "Does early administration of dexamethasone improve neurological outcome in children with meningococcal meningitis?" Archives of Disease in Childhood 89, no. 1 (January 2004): 82–83.

Hvidd, A., and M. Melhye. "Impact of routine vaccination with a conjugate Haemophilus influenzae type b vaccine." Vaccine 22, no. 3–4 (January 2004): 378–82.

Posfay-Barbe, K. M., and E. R. Wald. "Pneumococcal vaccines: do they prevent infection and how?" Current Opinions in Infectious Diseases 17, no. 3 (June 2004): 177–84.

Spach, D. H. "New issues in bacterial meningitis in adults. Antibiotic resistance has complicated treatment." Postgraduate Medicine 114, no. 5 (November 2004): 43–50.

Organizations

Meningitis Foundation of America. 6610 North Shadeland Avenue, Suite 200, Indianapolis, IN 46220–4393. Web site: www.musa.org.

National Institute of Allergy and Infectious Diseases (NIAID). National Institutes of Health, 6610 Rockledge Drive, MSC 6612, Bethesda, MD 20892–6612. Web site: www.meningitis.org.

National Meningitis Foundation. 22910 Chestnut Road, Lexington Park, MD 20653. Web site: www.nmaus.org.

Meningitis Research Foundation. Midland Way, Thornbury, Bristol BS35 2BS, UK. Web site: www.meningitis.org.

Web Sites

"Meningococcal Disease Homepage." Centers for DiseaseControl and Prevention. Available online at www.cdc.gov/ncidod/dbmd/diseaseinfo/meningococcal_g.htm (accessed October 25, 2004).

[Article by: Monique Laberge, Ph.D.]

For more information on meningitis, visit Britannica.com.

Inflammation of the meninges. the membranes surrounding the brain and spinal cord. Meningitis may be of bacterial or viral origin. It can be associated with a head injury, such as a depressed skull fracture, sustained during a contact or collision sport. Symptoms include headache, fever, and neck stiffness.

Inflammation of the meninges of the brain or spinal cord, most often resulting from a bacterial or viral infection.

Inflammation of the meninges. When the inflammatory process affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis or meningitis proper. It is also classified as fibrinous, hemorrhagic, purulent or eosinophilic, depending on the principal reaction of the tissues.
The term meningitis does not refer to a specific disease entity but rather to the pathological condition of inflammation of the tissues of the meninges. The etiological agent can be anything that activates the inflammatory process, including both pathogenic and nonpathogenic organisms, such as bacteria, viruses and fungi; chemical toxins such as lead and arsenic; contrast media used in myelography; and metastatic malignant cells.
In animals there are no specific meningitides, most cases of meningitis occurring as secondary complications to other diseases and having a bacterial etiology. Clinical signs seen commonly include fever, cutaneous hyperesthesia and rigidity of the muscles of the neck and forelimbs. A cerebrospinal fluid tap should assist in the diagnosis.

• Beagle m. — see beagle pain syndrome.
• Bernese Mountain Dog m. — an acute, aseptic nonsuppurative meningitis seen in young Bernese Mountain Dogs of unknown etiology.
• cerebrospinal m. — an inflammation of the brain and spinal cord; it may be caused by many different organisms.
• Pug m. — see Pug meningoencephalitis.
• spinal m. — inflammation of the meninges of the spinal cord.

Meningitis
Classification and external resources
Meninges of the central nervous system: dura mater, arachnoid, and pia mater.
ICD-10	G00.–G03.
ICD-9	320–322
DiseasesDB	22543
MedlinePlus	000680
eMedicine	med/2613 emerg/309 emerg/390
MeSH	D008581

Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges.^[1] The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs.^[2] 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.^[1][3]

The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia). Sometimes, especially in small children, only nonspecific symptoms may be present, such as irritability and drowsiness. 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.^[1][4]

A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory.^[3] The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation.^[3][4] Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly.^[1][4] Some forms of meningitis (such as those associated with meningococci, Haemophilus influenzae type B, pneumococci or mumps virus infections) may be prevented by immunization.^[1]

Contents 1 Signs and symptoms 1.1 Clinical features 1.2 Early complications 2 Causes 2.1 Bacterial 2.2 Aseptic 2.3 Viral 2.4 Non-infectious 3 Mechanism 4 Diagnosis 4.1 Blood tests and imaging 4.2 Lumbar puncture 4.3 Postmortem 5 Treatment 5.1 Initial treatment 5.2 Bacterial meningitis 5.2.1 Antibiotics 5.2.2 Steroids 5.3 Viral and fungal meningitis 6 Prognosis 7 Epidemiology 8 Prevention 9 History 10 References 11 External links

Signs and symptoms

Clinical features

In adults, a severe headache is the most common symptom of meningitis – occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness).^[5] 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 all cases of bacterial meningitis.^[5][6] If none of the three signs is present, meningitis is extremely unlikely.^[6] 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 looking unwell.^[1] In infants up to 6 months of age, bulging of the fontanelle (the soft spot on top of a baby's head) may be present. Other features that might distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and abnormal skin color.^[7]

Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis.^[6] Other signs of meningism include the presence of positive Kernig's sign or Brudzinski's sign. Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient 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 and Brudzinski's signs are both commonly used to screen for meningitis, the sensitivity of these tests is limited.^[6][8] They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases.^[6] Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in patients reporting fever and headache. The patient is told to rapidly rotate his or her head horizontally; if this does not make the headache worse, meningitis is unlikely.^[6]

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.^[7] 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.^[1] Other clues as to the nature of 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.^[9]

Early complications

A severe case of meningococcal meningitis in which the petechial rash progressed to gangrene and required amputation of all limbs. The patient, Charlotte Cleverley-Bisman, survived the disease and became a poster child for a meningitis vaccination campaign in New Zealand.

People with meningitis may develop additional problems in the early stages of their 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 early, especially but not exclusively in meningococcal illness; this may lead to insufficient blood supply to other organs.^[1] Disseminated intravascular coagulation, the excessive activation of blood clotting, may cause both the obstruction of blood flow to organs and a paradoxical increase of bleeding risk. In meningococcal disease, gangrene of limbs can occur.^[1] Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often lethal.^[10]

The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain tissue getting trapped. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal positioning.^[4] Inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus).^[4] Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (30% of cases) and do not necessarily indicate an underlying cause.^[3] Seizures may result from increased pressure and from areas of inflammation in the brain tissue.^[4] 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 are indicators of a poorer long-term outcome.^[1]

The 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 control eye movement, facial muscles and hearing, among other functions.^[1][6] Visual symptoms and hearing loss may persist after an episode of meningitis (see below).^[1] 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 in the brain.^[1][4]

Causes

Meningitis is usually caused by infection by viruses or microorganisms. Most cases are due to infection with viruses,^[6] with bacteria, fungi, and parasites being the next most common causes.^[2] It may also result from various non-infectious causes.^[2]

Bacterial

The types of bacteria that cause bacterial meningitis vary by 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 those that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Older children are more commonly affected by Neisseria meningitidis (meningococcus), 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, see below).^[1][3] In adults, N. meningitidis and S. pneumoniae together cause 80% of all cases of meningitis, with increased risk of L. monocytogenes in those over 50 years old.^[3][4]

Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space. Similarly, 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. In these cases, infections with staphylococci are more likely, as well as infections by pseudomonas and other Gram-negative bacilli.^[3] The same pathogens are also more common in those with an impaired immune system.^[1] In a small proportion of people, an infection in the head and neck area, such as otitis media or mastoiditis, can lead to meningitis.^[3] Recipients of cochlear implants for hearing loss are at an increased risk of pneumococcal meningitis.^[11]

Tuberculous meningitis, meningitis due to infection with Mycobacterium tuberculosis, is more common in those from countries where tuberculosis is common, but is also encountered in those with immune problems, such as AIDS.^[12]

Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system.^[13] Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is skull fracture,^[13] particularly fractures that affect the base of the brain or extend towards the sinuses and petrous pyramids.^[13] A literature review of 363 reported cases of recurrent meningitis showed that 59% of cases are due to such anatomical abnormalities, 36% due to immune deficiencies (such as complement deficiency, which predisposes especially to recurrent meningococcal meningitis), and 5% due to ongoing infections in areas adjacent to the meninges.^[13]

Aseptic

The term aseptic meningitis refers loosely to all cases of meningitis in which no bacterial infection can be demonstrated. This is usually due to viruses, but it may be due to bacterial infection that has already been partially treated, with disappearance of the bacteria from the meninges, or by infection in a space adjacent to the meninges (e.g. sinusitis). Endocarditis (infection of the heart valves with spread of small clusters of bacteria through the bloodstream) may cause aseptic meningitis. Aseptic meningitis may also result from infection with spirochetes, a type of bacteria that includes Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (known for causing Lyme disease). Meningitis may be encountered in cerebral malaria (malaria infecting the brain). Fungal meningitis, e.g. due to Cryptococcus neoformans, is typically seen in people with immune deficiency such as AIDS. Amoebic meningitis, meningitis due to infection with amoebae such as Naegleria fowleri, is contracted from freshwater sources.^[2]

Viral

Viruses that can cause meningitis include enteroviruses, herpes simplex virus type 2 (and less commonly type 1), varicella zoster virus (known for causing chickenpox and shingles), mumps virus, HIV, and LCMV.^[9]

Non-infectious

Meningitis may occur as the result of several non-infectious causes: spread of cancer to the meninges (malignant meningitis)^[14] and certain drugs (mainly non-steroidal anti-inflammatory drugs, antibiotics and intravenous immunoglobulins).^[15] 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.^[2] Epidermoid cysts and dermoid cysts may cause meningitis by releasing irritant matter into the subarachnoid space.^[2][13] Mollaret's meningitis is a syndrome of recurring episodes of aseptic meningitis; it is now thought to be caused by herpes simplex virus type 2. Rarely, migraine may cause meningitis, but this diagnosis is usually only made when other causes have been eliminated.^[2]

Mechanism

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.^[1] 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.^[1]

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. 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 a decreased blood flow and a third type of edema, "cytotoxic" edema. The three forms of cerebral edema all lead to an 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, and brain cells are deprived of oxygen and undergo apoptosis (automated cell death).^[1]

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 phenomenon.^[1][4]

Diagnosis

CSF findings in different forms of meningitis^[16]

Type of meningitis	Glucose	Protein	Cells
Acute bacterial	low	high	PMNs, often > 300/mm³
Acute viral	normal	normal or high	mononuclear, < 300/mm³
Tuberculous	low	high	mononuclear and PMNs, < 300/mm³
Fungal	low	high	< 300/mm³
Malignant	low	high	usually mononuclear

Blood tests and imaging

In someone 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.^[3][17]

The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap).^[18] 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.^[3][17][19] This applies in 45% of all adult cases.^[4] 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,^[3] especially if this may be longer than 30 minutes.^[17][19] Often, CT or MRI scans are performed at a later stage to assess for complications of meningitis.^[1]

Lumbar puncture

A lumbar puncture is done by positioning the patient, 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);^[18] in bacterial meningitis the pressure is typically elevated.^[3][17] 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 bacterial meningitis.^[3]

Gram stain of meningococci from a culture showing Gram negative (pink) bacteria, often in pairs

The CSF sample is examined for presence and types of white blood cells, red blood cells, protein content and glucose level.^[3] 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, and Gram staining is also less reliable in particular infections such as listeria. 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.^[3] The type of white blood cell predominantly present predicts whether meningitis is due to bacterial or viral infection (see table).^[3]

The concentration of glucose in CSF is normally above 40% 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;^[18] in the newborn, glucose levels in CSF are normally higher, and a ratio below 0.6 (60%) is therefore considered abnormal.^[3] High levels of lactate in CSF indicate a higher likelihood of bacterial meningitis, as does a higher white blood cell count.^[18]

Various more specialized tests may be used to distinguish between various types of meningitis. A latex agglutination test may be positive in meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, 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.^[3] 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 this).^[9] Serology (identification of antibodies to viruses) may be useful in viral meningitis.^[9] 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.^[12] 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 persons with AIDS.^[20][21][22]

A diagnostic and therapeutic conundrum is the "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).^[9]

Postmortem

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 covering the brain and spinal cord. Neutrophil leucocytes 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.^[23]

Treatment

Initial treatment

Meningitis is potentially life-threatening and has a high mortality rate if untreated;^[3] delay in treatment has been associated with a poorer outcome.^[4] Thus treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted.^[19] If meningococcal disease is suspected in primary care, guidelines recommend that benzylpenicillin be administered before transfer to hospital.^[7] Intravenous fluids should be administered if hypotension (low blood pressure) or shock are present.^[19] Given that meningitis can cause a number of early severe complications, regular medical review is recommended to identify these complications early,^[19] as well as admission to an intensive care unit if deemed necessary.^[4]

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).^[4] Seizures are treated with anticonvulsants.^[4] Hydrocephalus (obstructed flow of CSF) may require insertion of a temporary or long-term drainage device, such as a cerebral shunt.^[4]

Bacterial meningitis

Antibiotics

Structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis.

Empiric antibiotics (treatment without exact diagnosis) must 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. For instance, in the United Kingdom empirical treatment consists of a third-generation cefalosporin such as cefotaxime or ceftriaxone.^[17][19] In the USA, where resistance to cefalosporins is increasingly found in streptococci, addition of vancomycin to the initial treatment is recommended.^[3][4][17] Empirical therapy may be chosen on the basis of the age of the patient, whether the infection was preceded by head injury, whether the patient has undergone neurosurgery and whether or not a cerebral shunt is present.^[3] For instance, in young children and those over 50 years of age, as well as those who are immunocompromised, addition of ampicillin is recommended to cover Listeria monocytogenes.^[3][17] 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.^[3]

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.^[3] 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 meningitis patients in clinical trials. Rather, the relevant knowledge has mostly derived from laboratory studies in rabbits.^[3]

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.^[12] In tuberculous meningitis there is a strong evidence base for treatment with corticosteroids, although this evidence is restricted to those without AIDS.^[24]

Steroids

Adjuvant treatment with corticosteroids (usually dexamethasone) reduces rates of mortality, severe hearing loss and neurological damage in adolescents and adults from high income countries which have low rates of HIV.^[25] The likely mechanism is suppression of overactive inflammation.^[26] 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.^[17][19] 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.^[3][17]

Adjuvant 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 evidence; the reason for this discrepancy is not clear.^[27] 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,^[3][28] 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, whereas other uses are controversial.^[3]

Viral and fungal meningitis

Viral meningitis typically requires supportive therapy only; most viruses responsible for causing meningitis are not amenable to specific treatment. Viral meningitis tends to run a more benign course than bacterial meningitis. 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.^[9] Mild cases of viral meningitis can be treated at home with conservative measures such as fluid, bedrest, and analgesics.^[29] Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of highly dosed antifungals, such as amphotericin B and flucytosine.^[20][30]

Prognosis

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 patient and the underlying cause. Of the newborn patients, 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.^[1][4] 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,^[1] the severity of the generalized illness, decreased level of consciousness or abnormally low count of white blood cells in the CSF.^[4] Meningitis caused by H. influenza and meningococci has a better prognosis compared to cases caused by group B streptococci, coliforms and S. pneumoniae.^[1] In adults, too, meningococcal meningitis has a lower mortality (3–7%) than pneumococcal disease.^[4]

In children there are several potential disabilities which result from damage to the nervous system. Sensorineural hearing loss, epilepsy, learning and behavioral difficulties, as well as decreased intelligence, occur in about 15% of survivors.^[1] Some of the hearing loss may be reversible.^[31] In adults, 66% of all cases emerge without disability. The main problems are deafness (in 14%) and cognitive impairment (in 10%).^[4]

Epidemiology

Demography of meningococcal meningitis.     meningitis belt     epidemic zones     sporadic cases only

Although meningitis is a notifiable disease in many countries, the exact incidence rate is unknown.^[9] 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. In sub-Saharan Africa, large epidemics of meningococcal meningitis occur in the dry season, leading to it being labeled the "meningitis belt"; annual rates of 500 cases per 100,000 are encountered in this area, which is poorly served by medical care. These cases are predominantly caused by meningococci.^[6] The most recent epidemic, affecting Nigeria, Niger, Mali and Burkina Faso, started in January 2009 and is ongoing.^[32]

Meningococcal disease occurs in epidemics in areas where many people live together for the first time, such as army barracks during mobilization, college campuses^[1] and the annual Hajj pilgrimage.^[33]

There are significant differences in the local distribution of causes for bacterial meningitis. For instance, N. meningitides groups B and C cause most disease episodes in Europe, while group A meningococci are more common in China and amongst Hajj pilgrims. In the "meningitis belt" of Africa, group A and C meningococci cause most of the outbreaks. Group W135 meningococci have caused several recent epidemics in Africa and during the Hajj.^[34] These differences are expected to change further as vaccines against common strains are introduced.^[34]

Prevention

For some causes of meningitis, prophylaxis can be provided in the long term with vaccine, or in the short term with antibiotics.

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 where the disease burden is highest, however, the vaccine is still too expensive.^[34][35] 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.^[9]

Meningococcus vaccines exist against groups A, C, W135 and Y.^[36] In countries where the vaccine for meningococcus group C was introduced, cases caused by this pathogen have decreased substantially.^[34] A quadrivalent vaccine now exists, which combines all four vaccines. Immunization with the ACW135Y vaccine against four strains is now a visa requirement for taking part in the Hajj.^[33] 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.^[34][36] 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.^[36]

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.^[34][37] The pneumococcal polysaccharide vaccine, which covers 23 strains, is only administered in 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.^[37]

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.^[34]

Short-term antibiotic prophylaxis is also a method of prevention, particularly of meningococcal meningitis. In cases of meningococcal meningitis, prophylactic treatment of 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.^[17][38]

History

Some suggest that Hippocrates may have realized the existence of meningitis,^[6] and it seems that meningism was known to pre-Renaissance physicians such as Avicenna.^[39] 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.^[39][40] It appears that epidemic meningitis is a relatively recent phenomenon.^[41] The first recorded major outbreak occurred in Geneva in 1805.^[41][42] 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 sweeping Nigeria and Ghana in 1905–1908.^[41]

The first report of bacterial infection underlying meningitis was by the Austrian bacteriologist Anton Weichselbaum, who in 1887 described the meningococcus.^[43] 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.^[44][45] In 1944, penicillin was first reported to be effective in meningitis.^[46] The introduction in the late 20th century of Haemophilus vaccines led to a marked fall in cases of meningitis associated with this pathogen,^[35] and in 2002 evidence emerged that treatment with steroids could improve the prognosis of bacterial meningitis.^[26][27][45]

References

1. ^ ^{a b c d e f g h i j k l m n o p q r s t u v w x y} Sáez-Llorens X, McCracken GH (June 2003). "Bacterial meningitis in children". Lancet 361 (9375): 2139–48. doi:10.1016/S0140-6736(03)13693-8. PMID 12826449. 
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External links

• Meningitis at the Open Directory Project

v • d • e Pathology of the nervous system, primarily CNS (G00–G47, 320–349) Brain/ encephalopathy Inflammatory Encephalitis (Viral encephalitis, Herpesviral encephalitis) · Cavernous sinus thrombosis · Brain abscess (Amoebic) Degenerative Extrapyramidal and movement disorders Basal ganglia disease: Parkinsonism (Parkinson's disease, Postencephalitic parkinsonism)  · Neuroleptic malignant syndrome  · Pantothenate kinase-associated neurodegeneration · Progressive supranuclear palsy · Striatonigral degeneration · Hemiballismus · Huntington's disease · Olivopontocerebellar atrophy Dyskinesia: Dystonia (Spasmodic torticollis, Meige's, Blepharospasm) · Chorea (Choreoathetosis)  · Myoclonus (Myoclonic epilepsy) Essential tremor  · Restless legs  · Stiff person Dementia Alzheimer's (Early-onset)  · Frontotemporal dementia/Frontotemporal lobar degeneration (Pick's, Dementia with Lewy bodies) · Multi-infarct dementia Mitochondrial disease Leigh's Demyelinating autoimmune (Multiple sclerosis, Neuromyelitis optica, Schilder's disease) · hereditary (Adrenoleukodystrophy, Alexander, Canavan, Krabbe, ML, Pelizaeus-Merzbacher, VWM, MFC, CAMFAK syndrome) · Central pontine myelinolysis · Marchiafava-Bignami disease  · Alpers' Episodic/ paroxysmal Seizure/epilepsy Focal  · Generalised  · Status epilepticus  · Myoclonic epilepsy Headache Migraine (Familial hemiplegic)  · Cluster  · Vascular  · Tension Vascular Transient ischemic attack (Amaurosis fugax, Transient global amnesia) Cerebrovascular disease  · Stroke (MCA, ACA, PCA, Foville's, Millard-Gubler, Lateral medullary, Weber's, Lacunar stroke) Sleep disorders Insomnia  · Hypersomnia  · Sleep apnea (Obstructive, Ondine's curse)  · Narcolepsy  · Cataplexy  · Kleine-Levin  · Circadian rhythm sleep  · Delayed sleep phase  · Advanced sleep phase CSF Intracranial hypertension (Hydrocephalus/Normal pressure, Idiopathic intracranial hypertension) · Cerebral edema · Intracranial hypotension Other Brain herniation · Reye's  · Hepatic encephalopathy  · Toxic encephalopathy Spinal cord/ myelopathy Inflammatory Myelitis: Poliomyelitis · Demyelinating disease (Transverse myelitis) · Tropical spastic paraparesis Other Syringomyelia · Syringobulbia · Morvan's syndrome · Vascular myelopathy (Foix-Alajouanine syndrome) · Spinal cord compression Both/either Inflammatory Encephalomyelitis (Acute disseminated) Meningitis/Arachnoiditis: Bacterial (Tuberculous, Haemophilus, Pneumococcal) · Viral (Herpesviral) · Fungal (Cryptococcal) · Aseptic (Drug-induced) Meningoencephalitis Systemic atrophies SA Friedreich's ataxia · Ataxia telangiectasia MND UMN only: PLS · PP · HSP LMN only: PMA · PBP (Fazio-Londe, Infantile progressive bulbar palsy) · SMA (SMN-linked, Kennedy disease, SMAX2, DSMA1) both: ALS central nervous system navs: anat/physio/dev, noncongen/congen/neoplasia, symptoms+signs/eponymous, proc

v • d • e Inflammation Acute Plasma derived mediators Bradykinin · complement (C3, C5a, MAC) · coagulation (Factor XII, Plasmin, Thrombin) Cell derived mediators preformed: Lysosome granules · vasoactive amines (Histamine, Serotonin) synthesized on demand: cytokines (IFN-γ, IL-8, TNF-α, IL-1) · eicosanoids (Leukotriene B4, Prostaglandins) · Nitric oxide · Kinins Chronic Macrophage · Epithelioid cell · Giant cell · Granuloma Processes Traditional: Rubor · Calor · Tumor · Dolor (pain) · Functio laesa Modern: Acute-phase reaction/Fever · Vasodilation · Increased vascular permeability · Exudate · Leukocyte extravasation · Chemotaxis Specific types Nervous CNS (Encephalitis, Myelitis) · Meningitis (Arachnoiditis) · PNS (Neuritis) · eye (Dacryoadenitis, Scleritis, Keratitis, Choroiditis, Retinitis, Chorioretinitis, Blepharitis, Conjunctivitis, Iritis, Uveitis) · ear (Otitis, Labyrinthitis, Mastoiditis) Cardiovascular Carditis (Endocarditis, Myocarditis, Pericarditis) · Vasculitis (Arteritis, Phlebitis, Capillaritis) Respiratory upper (Sinusitis, Rhinitis, Pharyngitis, Laryngitis) · lower (Tracheitis, Bronchitis, Bronchiolitis, Pneumonitis, Pleuritis) · Mediastinitis Digestive mouth (Stomatitis, Gingivitis, Gingivostomatitis, Glossitis, Tonsillitis, Sialadenitis/Parotitis, Cheilitis, Pulpitis, Gnathitis) · tract (Esophagitis, Gastritis, Gastroenteritis, Enteritis, Colitis, Enterocolitis, Duodenitis, Ileitis, Caecitis, Appendicitis, Proctitis) · accessory (Hepatitis, Cholangitis, Cholecystitis, Pancreatitis) · Peritonitis Integumentary Dermatitis (Folliculitis) · Cellulitis · Hidradenitis Musculoskeletal Arthritis · Dermatomyositis · soft tissue (Myositis, Synovitis/Tenosynovitis, Bursitis, Enthesitis, Fasciitis, Capsulitis, Epicondylitis, Tendinitis, Panniculitis) Osteochondritis: Osteitis (Spondylitis, Periostitis) · Chondritis Urinary Nephritis (Glomerulonephritis, Pyelonephritis) · Ureteritis · Cystitis · Urethritis Reproductive female: Oophoritis · Salpingitis · Endometritis · Parametritis · Cervicitis · Vaginitis · Vulvitis · Mastitis male: Orchitis · Epididymitis · Prostatitis · Balanitis · Balanoposthitis pregnancy/newborn: Chorioamnionitis · Omphalitis Endocrine Insulitis · Hypophysitis · Thyroiditis · Parathyroiditis · Adrenalitis Lymphatic Lymphangitis · Lymphadenitis

This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)

Dansk (Danish)
n. - meningitis, hjernehindebetændelse

Nederlands (Dutch)
hersenvlies- ontsteking

Français (French)
n. - méningite

Deutsch (German)
n. - Meningitis, Hirnhautentzündung

Ελληνική (Greek)
n. - (παθολ.) μηνιγγίτιδα

Italiano (Italian)
meningite

Português (Portuguese)
n. - meningite (f) (Med.)

Русский (Russian)
менингит

Español (Spanish)
n. - meningitis

Svenska (Swedish)
n. - hjärnhinneinflammation

中文（简体）(Chinese (Simplified))
髓膜炎

中文（繁體）(Chinese (Traditional))
n. - 髓膜炎

한국어 (Korean)
n. - 뇌막염

日本語 (Japanese)
n. - 髄膜炎

العربيه (Arabic)
‏(الاسم) إلتهاب سحائي‏

עברית (Hebrew)
n. - ‮דלקת קרום המוח‬

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