Meningitis is an acute inflammation of the protective film covering the brain and spinal cord, known collectively as the meninges. The most common symptoms are fever, headache, and neck stiffness. Other symptoms include confusion or altered consciousness, vomiting, and an inability to tolerate mild or loud noises. Young children often show only nonspecific symptoms, such as irritability, drowsiness, or poor feeding. If there is a rash, it may indicate a particular cause of meningitis; for example, meningitis caused by meningococcal bacteria may be accompanied by a distinctive rash.
Inflammation can be caused by viral infections, bacteria, or other microorganisms, and less frequently by certain drugs. Meningitis can be life-threatening because of the proximity of inflammation to the brain and spinal cord; therefore, this condition is classified as a medical emergency. Lumbar punctures can diagnose or rule out meningitis. The needle is inserted into the spinal canal to collect samples of cerebrospinal fluid (CSF), which envelops the brain and spinal cord. CSF is checked in a medical laboratory.
Some forms of meningitis can be prevented by immunization with meningococcal, mumps, pneumococcal, and Hib vaccines. Giving antibiotics to people with significant exposure to certain types of meningitis may also be helpful. The first treatment in acute meningitis consists of administering antibiotics and sometimes antiviral drugs. Corticosteroids can also be used to prevent complications from excessive inflammation. Meningitis can cause serious long-term consequences such as deafness, epilepsy, hydrocephalus, or cognitive deficits, especially if not treated quickly.
By 2015 meningitis occurs in about 8.7 million people worldwide. This resulted in 379,000 deaths - down from 464,000 deaths in 1990. With the right treatment the risk of death in bacterial meningitis is less than 15%. Outbreaks of bacterial meningitis occur between December and June of each year in the sub-Saharan Africa region known as the meningitis belt. Smaller epidemics can also occur in other regions of the world. The word meningitis comes from the Greek ?????? meninx , "membrane" and medical suffix -itis , "inflammation".
Video Meningitis
Signs and symptoms
Clinical features
In adults, the most common meningitis symptoms are severe headache, occurring in nearly 90% of cases of bacterial meningitis, followed by nuchal stiffness (inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classical triage of diagnostic signs consists of nuchal rigidity, sudden high fever, and changes in mental status; However, these three features are only 44-46% of cases of bacterial meningitis. If none of these three signs, acute meningitis is highly unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noise). Young children often do not show the symptoms mentioned earlier, and may just be irritable and look unhealthy. Fontanel (the soft spot on the top of the baby's head) can be prominent in infants up to 6 months old. Another feature that differentiates meningitis from less severe disease in children is leg pain, cold extremities, and abnormal skin tone.
Nuchal stiffness occurs in 70% of meningitis bacteria in adults. Other signs include the presence of a positive Kernig mark or a Brudzi sign? Skiing. Kernig marks are assessed with people lying on their backs, with their hips and knees flexed to 90 degrees. In someone with a positive Kernig mark, the pain restricts the extension of the passive knee. A positive Brudzinski sign occurs when neck flexion causes knee flexion and involuntary hips. Although the Kernig and Brudzinski marks are equally used for meningitis screening, the sensitivity of these tests is limited. However, they have a very good specificity for meningitis: signs are rare in other diseases. Another test, known as "jerk acceleration maneuver" helps determine whether meningitis is present in those who report fever and headache. A person is required to turn his head horizontally quickly; if this does not make the headache worse, meningitis is not possible.
Other problems can produce symptoms similar to those above, but from non-meningitic causes. This is called meningism or pseudomeningitis.
Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis") can be distinguished from meningitis by other causes by rapidly spreading petechia rashes, which may precede other symptoms. The rash consists of many irregular ("petechiae") irregular spots on the stem, lower extremities, mucous membranes, conjunctiva, and (sometimes) the palms or soles of the feet. The rash usually does not turn pale; redness is not lost when pressed with fingers or glasses. Although this rash is not necessarily present in meningococcal meningitis, this rash is relatively specific for this disease; it, however, sometimes occurs in meningitis due to other bacteria. Other clues about the cause of meningitis may be signs of skin diseases of the hands, feet and mouth and genital herpes, both related to various forms of viral meningitis.
Initial complication
Additional problems can occur in the early stages of the disease. This may require special care, and sometimes indicates severe illness or a worse prognosis. Infection can trigger sepsis, systemic inflammatory response syndrome, decreased blood pressure, rapid heart rate, low or abnormal low temperature, and rapid breathing. Very low blood pressure can occur at an early stage, especially but not exclusively in meningococcal meningitis; this can lead to insufficient blood supply to other organs. Disseminated intravascular coagulation, excessive activation of blood clots, can block blood flow to organs and paradoxically increase the risk of bleeding. Limb gangrene can occur in meningococcal disease. Severe meningococcal and pneumococcal infections can cause an adrenal gland haemorrhage, which causes the Waterhouse-Friderichsen syndrome, which is often fatal.
Brain tissue can swell, pressure inside the skull can be increased and the swollen brain may experience herniation through the skull base. This may be noticed by decreased levels of consciousness, loss of pupil light reflex, and abnormal posture. Inflammation of the brain tissue can also block the normal flow of CSF around the brain (hydrocephalus). Seizures can occur for various reasons; in children, generalized seizures occur in the early stages of meningitis (in 30% of cases) and do not necessarily indicate an underlying cause. Seizures can occur due to increased pressure and from areas of inflammation in brain tissue. Focal seizures (seizures involving one leg or body part), persistent seizures, slow onset seizures and seizures that are difficult to control with medication show worse long-term outcomes.
Meninges inflammation can cause cranial nerve abnormalities, a group of nerves arising from the brain stem that supplies the head and neck region and which control, among other functions, eye movement, facial muscles, and hearing. Visual symptoms and hearing loss may persist after episodes of meningitis. Inflammation of the brain (encephalitis) or blood vessels (cerebral vasculitis), as well as the formation of blood clots in the blood vessels (cerebral venous thrombosis), all may cause weakness, loss of sensation, or abnormal movement or function of the body part supplied by the affected part of the brain.
Maps Meningitis
Cause
Meningitis is usually caused by infection of microorganisms. Most infections are caused by viruses, with bacteria, fungi, and protozoa being the next most common cause. This may also be the result of various non-infectious causes. The term aseptic meningitis refers to cases of meningitis where no bacterial infection can be demonstrated. This type of meningitis is usually caused by a virus but may be due to a partially treated bacterial infection, when the bacteria disappears from the meninges, or pathogens infecting the space adjacent to the meninges (eg sinusitis). Endocarditis (an infection of the heart valve that spreads small groups of bacteria through the bloodstream) can cause aseptic meningitis. Aseptic meningitis can also occur due to infection of spirochetes, a group of bacteria including Treponema pallidum (causes of syphilis) and Borrelia burgdorferi (known to cause Lyme disease). Meningitis can be found in cerebral malaria (malaria infecting the brain) or amoebic meningitis, meningitis due to infection with amoeba such as Naegleria fowleri , contracted from fresh water sources.
Bacteria
The types of bacteria that cause bacterial meningitis vary according to the age group of the infected individual.
- In premature and newborn infants up to the age of three months, a common cause is group B streptococcus (subtype III which usually inhabits the vagina and is primarily the cause during the first week of life) and bacteria usually inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Listeria monocytogenes (IVb serotype) is transmitted by the mother before birth and may cause meningitis in the newborn.
- Older children are more frequently affected by Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those who toddlers with Haemophilus influenzae type B (in countries that do not offer vaccinations).
- In adults, Neisseria meningitidis and Streptococcus pneumoniae together cause 80% of cases of bacterial meningitis. The risk of infection with Listeria monocytogenes increases in people over 50 years. The introduction of the pneumococcal vaccine has lowered rates of pneumococcal meningitis in children and adults.
Recent skull trauma may potentially allow bacterial nostrils to enter the meningeal space. Similarly, devices in the brain and meninges, such as cerebral shunt, extraventricular or Ommaya dams, carry an increased risk of meningitis. In this case, people are more likely to be infected with Staphylococci, Pseudomonas, and other Gram-negative bacteria. This pathogen is also associated with meningitis in people with immune system disorders. Infections of the head and neck areas, such as otitis media or mastoiditis, can cause meningitis in a small number of people. The cochlear implant receptor for hearing loss is more at risk for pneumococcal meningitis.
Meningitis tuberculosis, which is caused by meningitis Mycobacterium tuberculosis , is more common in people from countries where tuberculosis is endemic, but it is also encountered in people with immune problems, such as AIDS.
Recurrent bacterial meningitis may be caused by persistent anatomical defects, either congenital or acquired, or by immune system disorders. Anatomical abnormalities allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is a skull fracture, especially a fracture that affects the base of the skull or extends toward the petrous sinus and pyramid. Approximately 59% of cases of recurrent meningitis are due to anatomical abnormalities, 36% caused by immune deficiency (such as complement deficiency, predisposing primarily to recurrent meningococcal meningitis), and 5% due to ongoing infection in adjacent areas of meningitis..
Viral
The virus that causes meningitis includes enteroviruses, herpes simplex virus (generally type 2, which produces mostly genital wounds, less common type 1), varicella zoster virus (known for causing smallpox and nerve rash), mumps virus, HIV, and LCMV. Mollaret meningitis is a recurrent form of chronic herpes meningitis; allegedly caused by herpes simplex virus type 2.
Mushroom
There are a number of risk factors for fungal meningitis, including the use of immunosuppressants (such as after organ transplant), HIV/AIDS, and loss of immunity associated with aging. It is rare in those with normal immune systems but has occurred with drug contamination. Symptoms of onset are usually more gradual, with headache and fever being present for at least several weeks before diagnosis. The most common fungal meningitis is cryptococcal meningitis due to Cryptococcus neoformans . In Africa, cryptococcal meningitis is now the most common cause of meningitis in some studies, and it accounts for 20-25% of AIDS-related deaths in Africa. Other less common fungal pathogens that can cause meningitis include: Coccidioides immitis , Histoplasma capsulatum , Blastomyces dermatitidis , and Candida type.
Parasitic
The cause of parasites is often assumed when there is dominance of eosinophils (a type of white blood cell) in CSF. The most commonly involved parasites are Angiostrongylus cantonensis , Gnathostoma spinigerum , Schistosoma , as well as conditions of cysticercosis, toxocariasis, baylisascariasis, paragonimiasis, and the number of rare infections and noninfectious condition.
Not contagious
Meningitis can occur as a result of some non-infectious causes: cancer spread to meninges (malignant or neoplastic meningitis) and certain drugs (especially non-steroidal anti-inflammatory drugs, antibiotics and intravenous immunoglobulins). It can also be caused by several conditions of inflammation, such as sarcoidosis (later called neurosarcoidosis), connective tissue disorders such as systemic lupus erythematosus, and certain forms of vasculitis (inflammatory conditions of blood vessel walls), such as BehÃÆ'§et's disease. Epidermoid cysts and dermoid cysts can cause meningitis by releasing irritating matter into subarachnoid space. Rarely, migraine can cause meningitis, but this diagnosis is usually only done when other causes have been removed.
Mechanism
Meninges consist of three membranes that, together with cerebrospinal fluid, cover and protect the brain and spinal cord (central nervous system). The pia mater is a very fine impermeable membrane firmly attached to the surface of the brain, following all the small contours. The arachnoid mater (so named because of its spider-web-like appearance) is a bag that is loose at the top of the pia mater. Subarachnoid space separates the arachnoid membrane and pia mater and is filled with cerebrospinal fluid. The outermost membrane, dura mater, is a thick, durable membrane, attached to the arachnoid membrane and the skull.
In bacterial meningitis, bacteria reach the meninges via either of the two main routes: through the bloodstream or through direct contact between the meninges and the nasal or skin cavity. In most cases, meningitis follows the invasion of blood flow by organisms that live on the mucosal surface such as the nasal cavity. This is often in turn preceded by a viral infection, which breaks down the normal barrier provided by the mucosal surface. Once the bacteria have entered the bloodstream, they enter the subarachnoid space in places of vulnerable blood-brain barrier - such as the choroid plexus. Meningitis occurs in 25% of newborns with bloodstream infections due to group B streptococci; This phenomenon is less common in adults. Direct contamination of the cerebrospinal fluid may arise from an internal device, a skull fracture, or nasopharyngeal or nasal sinus infection that has formed a channel with subarachnoid space (see above); sometimes, congenital defects of the dura mater can be identified.
The large-scale inflammation occurring in the subarachnoid space during meningitis is not a direct result of bacterial infection, but it can largely be attributed to the immune system response to bacterial entry into the central nervous system. When the components of the bacterial cell membrane are identified by the brain's immune cells (astrocytes and microglia), they respond by releasing large amounts of cytokines, mediators such as hormones that recruit other immune cells and stimulate other tissues to participate in the immune response.. The blood-brain barrier becomes more permeable, leading to "vasogenic" cerebral edema (brain swelling due to leakage of fluid from blood vessels). Large amounts of white blood cells enter CSF, causing inflammation of the meninges and causing "interstitial" edema (swelling due to fluid between cells). In addition, the walls of the blood vessels themselves become inflamed (cerebral vasculitis), leading to decreased blood flow and edema of the third type, "thexotoxic" edema. Three forms of cerebral edema all lead to increased intracranial pressure; along with the low blood pressure that is common in acute infections, it is more difficult for the blood to enter the brain, resulting in brain cells deprived of oxygen and apoptosis (programmed cell death).
It is known that antibiotic administration may initially exacerbate the process described above, by increasing the amount of bacterial cell membrane products released through bacterial destruction. Special treatments, such as the use of corticosteroids, are aimed at reducing the immune system's response to this phenomenon.
Diagnosis
Test and blood imaging
If a person is suspected of having meningitis, a blood test is performed to indicate inflammation (eg C-reactive protein, full blood count), as well as blood cultures.
The most important test in identifying or excluding meningitis is the analysis of cerebrospinal fluid through lumbar puncture (LP, spinal tap). However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or intracranial pressure (ICP) elevated, as it may cause brain herniation. If a person is at risk of developing mass ICP or injury (recent head injury, known immune system problems, local neurological signs, or evidence on raised ICP examination), CT scan or MRI is recommended before lumbar puncture. This applies to 45% of all adult cases. If CT or MRI is required before LP, or if LP proves difficult, professional guidance suggests that antibiotics should be given in advance to prevent delay in treatment, especially if this may be longer than 30 minutes. Often, a CT scan or MRI is done at a later stage to assess the complications of meningitis.
In the form of severe meningitis, blood electrolyte monitoring may be important; eg, hyponatremia often occurs in bacterial meningitis. The causes of hyponatremia, however, are controversial and may include dehydration, inappropriate antidiuretic hormone secretion (SIADH), or overly aggressive intravenous fluid administration.
Lumbar puncture
The lumbar puncture is performed by positioning the person, usually lying on the side, applying local anesthesia, and inserting the needle into the dural sac (the 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 usually between 6 and 18 cm water (cmH 2 O); in meningitis bacteria, the pressure usually increases. In cryptococcal meningitis, intracranial pressure increases significantly. Initial appearance of the fluid may prove an indication of the nature of the infection: cloudy CSF shows higher levels of protein, white and red blood cells and/or bacteria, and therefore may indicate bacterial meningitis.
CSF samples are examined for the presence and type of white blood cells, red blood cells, protein levels and glucose levels. Gram staining of the sample may show bacteria in bacterial meningitis, but no bacteria do not exclude bacterial meningitis because they are seen in only 60% of cases; This number is reduced by 20% â € <â € The concentration of glucose in CSF is usually above 40% of that in the blood. In bacterial meningitis is usually lower; CSF glucose levels are divided by blood glucose (CSF glucose against serum glucose ratio). The ratio <= 0.4 is indicative of bacterial meningitis; in newborns, glucose levels in CSF are usually higher, and a ratio below 0.6 (60%) is therefore considered abnormal. High levels of lactate in CSF suggest a higher likelihood of bacterial meningitis, as well as higher white blood cell counts. If the lactate level is less than 35 mg/dl and the person has never received antibiotics, then this can rule out meningitis bacteria. Other special tests can be used to differentiate between different types of meningitis. Latex agglutination tests may be positive for meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and group B streptococcus ; regular use is not recommended as it rarely leads to changes in treatment, but may be used if other tests are not diagnostic. Similarly, a lysate limulus test may be positive in meningitis caused by Gram-negative bacteria, but its use is limited unless other tests do not help. Polymerase chain reaction (PCR) is a technique used to strengthen small traces of bacterial DNA to detect the presence of bacterial or viral DNA in cerebrospinal fluid; this is a very sensitive and specific test because it only tracks the number of DNA infectious agents needed. It can identify bacteria in bacterial meningitis and can help differentiate various causes of viral meningitis (enterovirus, herpes simplex virus 2 and mumps in those not vaccinated for this). Serology (identification of antibodies against viruses) may be useful in viral meningitis. If suspected tuberculosis meningitis, samples are processed for low-sensitivity Ziehl-Neelsen staining, and tuberculosis cultures, which take a long time to process; PCR is increasingly used. The diagnosis of cryptococcal meningitis can be done at low cost using Indian ink stains from CSF; However, testing of cryptococcal antigens in the blood or CSF is more sensitive, especially in people with HIV. Diagnostic and therapeutic difficulties are "partially treated meningitis", in which there are symptoms of meningitis after receiving antibiotics (as for alleged sinusitis). When this occurs, CSF findings may be similar to viral meningitis, but antibiotic treatment may need to be continued until there is definite positive evidence of viral causes (eg positive enterovirus PCR). Postmortem
Meningitis can be diagnosed after death occurs. Findings from post mortem are usually widespread inflammation of the pia mater and the arachnoid layer of the meninges. Neutrophil granulocytes tend to migrate to the cerebrospinal fluid and brain stem, along with the cranial nerves and spinal cord, may be surrounded by pus - as are the meningeal vessels.
Prevention
For some causes of meningitis, protection can be given in the long term through vaccination, or in the short term with antibiotics. Some behavioral actions may also be effective.
Behavior
Bacterial meningitis and viruses are contagious, but not as infectious as colds or the common cold. Both can be transmitted through droplets of respiratory secretions during close contact such as kissing, sneezing or coughing in a person, but can not spread by just breathing the air in which a person with meningitis has occurred. Viral meningitis is usually caused by enteroviruses, and is most commonly spread through fecal contamination. The risk of infection may decrease by altering the behavior that causes transmission.
Vaccinations
Since the 1980s, many countries have included immunization against Type B haemophilus influenzae in their routine childhood vaccination scheme. This has practically eliminated these pathogens as a cause of meningitis in children in these countries. In countries where the burden of disease is highest, however, the vaccine is still too expensive. Similarly, immunization against mumps has led to a sharp decline in the number of mumps of meningitis, which before vaccination occurred in 15% of all cases of mumps.
The Meningococcus vaccine exists against groups A, B, C, W135 and Y. In countries where the vaccine for meningococcal group C is introduced, the cases caused by these pathogens have dropped substantially. Quadrivalent vaccine now exists, which combines four vaccines with the exception of B; immunization with the ACW135Y vaccine is now a visa requirement to take part in the Hajj. The development of vaccines against meningococci B group proved much more difficult, because the surface protein (which is usually used to make the vaccine) only generates a weak response from the immune system, or reacts cross with normal human proteins. However, several countries (New Zealand, Cuba, Norway, and Chile) have developed vaccines against local strains of group B meningococci; some have shown good results and are used in local immunization schedules. Two new vaccines, both approved in 2014, are effective against a broader range of B group meningococci strains. In Africa, to date, the approach to prevention and control of the meningococcal epidemic is based on early disease detection and mass vaccination of emergency reactive populations at risk with A/C bivalent A/C or trivalent A/C/W135 polysaccharide, despite the introduction of MenAfriVac (group A meningococcus vaccine) has shown effectiveness in young people and has been described as a model for product development partnerships in resource-limited settings.
Regular vaccination against Streptococcus pneumoniae with pneumococcal conjugate vaccine (PCV), which is active against seven common serotypes of these pathogens, significantly reduces the incidence of pneumococcal meningitis. Pneumococcal polysaccharide vaccine, which includes 23 strains, is only given to certain groups (eg those who have undergone splenectomy, surgical removal of the spleen); does not generate significant immune responses in all recipients, eg. little child. Childhood vaccinations with Bacillus Calmette-Guà ©  © rin have been reported to significantly reduce TB meningitis levels, but the effectiveness of waning in adulthood has led to better vaccine search.
Antibiotics
Short-term antibiotic antibiotics are another prevention method, especially meningococcal meningitis. In the case of meningococcal meningitis, preventive treatment in close contact with antibiotics (eg rifampicin, ciprofloxacin or ceftriaxone) may reduce the risk of acquiring the condition, but not protect against future infections. Resistance to rifampicin has been noted to increase after use, which has led some to suggest to consider other agents. While antibiotics are often used in an attempt to prevent meningitis in those with basilar skull fractures there is not enough evidence to determine whether these are beneficial or harmful. This applies to those with or without CSF leakage.
Management
Meningitis is potentially life-threatening and has a high mortality rate if untreated; delay in treatment has been associated with worse outcomes. Thus, treatment with broad-spectrum antibiotics should not be delayed while confirmatory tests are underway. If meningococcal disease is suspected in primary care, guidelines recommend that benzylpenicillin be administered before transfer to the hospital. Intravenous fluids should be given if hypotension (low blood pressure) or shock are present. It is unclear whether intravenous fluids should be given regularly or whether this should be restricted. Given that meningitis can lead to a number of early serious complications, routine medical reviews are recommended to identify these complications early and to include the person into an intensive care unit if deemed necessary.
Mechanical ventilation may be necessary if the level of consciousness is very low, or if there is evidence of respiratory failure. If there are signs of increased intracranial pressure, steps to monitor the pressure can be taken; this will allow optimization of cerebral perfusion pressure and various treatments to reduce intracranial pressure with drugs (eg mannitol). Seizures are treated with anticonvulsants. Hydrocephalus (CSF obstruction flow) may require insertion of a temporary or long-term drainage device, such as a cerebral shunt.
bacterial meningitis
Antibiotics
Empirical antibiotics (treatment without a definitive diagnosis) should be initiated immediately, even before lumbar puncture results and CSF analysis are known. The initial treatment options depend largely on the type of bacteria that cause meningitis in certain places and populations. For example, in England empirical treatment consists of third-generation cephalosporins such as cefotaxime or ceftriaxone. In the United States, where resistance to cefalosporin is increasingly found in streptococci, the addition of vancomycin to preliminary treatment is recommended. Chloramphenicol, either alone or in combination with ampicillin, however, seems to work well.
Empirical therapy can be chosen based on a person's age, whether the infection is preceded by a head injury, whether the person has undergone recent neurosurgery and whether there is a brain shunt or not. In young children and those over 50 years of age, as well as those who are immunocompromised, the addition of ampicillin is recommended to cover Listeria monocytogenes . Once the results of Gram staining are available, and a wide range of bacterial causes are known, it is possible to alter antibiotics for those who may be dealing with the group of suspected pathogens. CSF culture results usually take longer to be available (24-48 hours). Once they do so, empirical therapy can be transferred to specific antibiotic therapy targeted to specific causal organisms and antibiotic sensitivity. In order for antibiotics to be effective in meningitis, antibiotics should not only be active against pathogenic bacteria but also achieve sufficient meninges; some antibiotics have inadequate penetration and therefore have little use in meningitis. Most antibiotics used in meningitis have not been tested directly in people with meningitis in clinical trials. In contrast, relevant knowledge is largely derived from laboratory studies on rabbits. Meningitis of tuberculosis requires long-term treatment with antibiotics. While pulmonary tuberculosis is usually treated for six months, those with TB meningitis are usually treated for a year or more.
Steroids
Additional treatment with corticosteroids (usually dexamethasone) has shown some benefits, such as a reduction in hearing loss, and better short-term neurological outcomes in adolescents and adults from high-income countries with low HIV levels. Some studies have found a decrease in mortality rates while other studies do not. They also appear to be helpful in those with meningitis tuberculosis, at least in those who are HIV negative.
Therefore, professional guidelines recommend the commencement of the same dexamethasone or corticosteroid just before the first dose of antibiotics is given, and continued for four days. Given that most treatment benefits are limited to those with pneumococcal meningitis, some guidelines suggest that dexamethasone is discontinued if other causes for meningitis are identified. A possible mechanism is overactive activation of the inflammation.
Additional treatment with corticosteroids has a different role in children than in adults. Although the benefits of corticosteroids have been shown in adults as well as in children of high-income countries, their use in children from low-income countries is not supported by evidence; the reasons for this discrepancy are not clear. Even in high-income countries, the benefits of corticosteroids are only seen when given before the first dose of antibiotics, and the largest in the case of H. influenzae meningitis, an event that has declined 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 before the first dose of antibiotics; Other uses are controversial.
Viral meningitis
Viral meningitis usually requires supportive therapy only; most viruses responsible for causing meningitis can not receive special treatment. Viral meningitis tends to run more benign than bacterial meningitis. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs such as acyclovir, but no clinical trials specifically address whether the treatment is effective. Mild cases of viral meningitis can be treated at home with conservative measures such as fluid, bed rest, and analgesics.
Mushroom meningitis
Fungal meningitis, such as cryptococcal meningitis, is treated with high-dose antifungals, such as amphotericin B and flucytosine. Increased intracranial pressure is common in fungal meningitis, and frequent (ideally daily) lumbar puncture to relieve pressure is recommended, or as an alternative to lumbar drain.
Prognosis
Untreated, bacterial meningitis is almost always fatal. Viral meningitis, in contrast, tends to disappear spontaneously and is rarely fatal. With treatment, death (risk of death) from bacterial meningitis depends on the age of the person and the underlying cause. In newborns, 20-30% can die from episodes of bacterial meningitis. This risk is lower in older children, whose mortality is about 2%, but it increases again to about 19-37% in adults. The risk of death is predicted by a variety of factors regardless of age, such as pathogens and the time it takes for the pathogen to be cleared of cerebrospinal fluid, the severity of the common disease, the decreased level of consciousness or the abnormally low amount of white blood cells in CSF. Meningitis is caused by H. influenzae and meningococcus has a better prognosis than cases caused by streptococcal B, coliform and S. pneumonia groups. In adults too, meningococcal meningitis has a lower mortality (3-7%) than pneumococcal disease.
In children there are some potential disabilities that may be caused by damage to the nervous system, including sensorineural hearing loss, epilepsy, learning and behavioral difficulties, and decreased intelligence. This occurs in about 15% of survivors. Some hearing loss may be reversible. In adults, 66% of all cases appear flawless. The main problems are deafness (in 14%) and cognitive impairment (in 10%).
Meningitis of tuberculosis in children continues to be associated with significant risk of death even with treatment (19%), and a significant proportion of surviving children have ongoing neurological problems. More than a third of all cases survive without problems.
Epidemiology
Although meningitis is a disease reported in many countries, the exact incidence rate is unknown. In 2013 meningitis resulted in 303,000 deaths - down from 464,000 deaths in 1990. In 2010 it was estimated that meningitis resulted in 420,000 deaths, excluding cryptococcal meningitis.
Bacterial meningitis occurs in about 3 people per 100,000 annually in Western countries. Studies throughout the population show that viral meningitis is more common, ie, 10.9 per 100,000, and more common in summer. In Brazil, the rate of bacterial meningitis is higher, at 45.8 per 100,000 per year. Sub-Saharan Africa has been plagued by a major epidemic of meningococcal meningitis for more than a century, causing it to be labeled a "meningitis belt". The epidemic usually occurs in the dry season (December to June), and epidemic waves can last two to three years, dying during the rainy season. The attack rate of 100-800 cases per 100,000 is found in this area, which is not well served by medical care. These cases are mostly caused by meningococcal. The largest epidemic ever recorded in history swept across the region in 1996-1997, causing more than 250,000 cases and 25,000 deaths.
Meningococcal disease occurs in epidemics in areas where many people live together for the first time, such as army barracks during mobilization, campuses, and annual Hajj pilgrimages. Although the pattern of the epidemic cycle in Africa is not well understood, several factors have been linked to the development of epidemics in the meningitis belt. They include: medical conditions (immunological susceptibility of the population), demographic conditions (travel and large population movements), socioeconomic conditions (population density and poor living conditions), climatic conditions (drought and dust storms), and concurrent infections (respiratory infections I).
There are significant differences in the local distribution of bacterial meningitis causes. For example, when N. meningitides groups B and C cause most episodes of disease in Europe, Group A is found in Asia and continues to dominate in Africa, where it causes most of the major epidemics in the meningitis belt, 80% to 85%. documented meningococcal meningococcal cases.
History
Some suggest that Hippocrates may have been aware of the existence of meningitis, and it seems that meningism is known by pre-Renaissance doctors such as Avicenna. Description of TB meningitis, later called "basalt in the brain", is often associated with Edinburgh physician Sir Robert Whytt in a posthumous report that appeared in 1768, although the association with tuberculosis and his pathogens was not made until the following century.
It seems that epidemic meningitis is a relatively new phenomenon. The first major outbreak was recorded in Geneva in 1805. Several other epidemics in Europe and the United States were described shortly thereafter, and the first report of the epidemic in Africa appeared in 1840. The epidemic in Africa became more common in the 20th century, beginning with the epidemic great sweeping Nigeria and Ghana in 1905-1908.
The first report of bacterial infections underlying meningitis was by Austrian bacteriologist Anton Weichselbaum, who in 1887 described meningococcus . Mortality from meningitis is very high (over 90%) in the initial report. In 1906, the antiserum was produced with horses; this was further developed by American scientist Simon Flexner and a marked reduction in mortality from meningococcal disease. In 1944, penicillin was first reported to be effective in meningitis. Introduction at the end of the 20th century Haemophilus vaccine led to a marked decline in cases of meningitis associated with this pathogen, and in 2002, evidence emerged that treatment with steroids could improve the prognosis of bacterial meningitis. World Day Meningitis is celebrated on 24 April every year.
References
External links
- Meningitis in Curlie (based on DMOZ)
- Meningitis Center for Disease Control and Prevention (CDC)
Source of the article : Wikipedia
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