|Classification according to ICD-10|
|G01||Meningitis in bacterial diseases classified elsewhere|
|G02||Meningitis in other infectious and parasitic diseases classified elsewhere|
|G03||Meningitis due to other and unspecified causes|
|ICD-10 online (WHO version 2019)|
A meningitis ( plural meningitis ; German meningitis , inflammation of the meninges formerly also, disease-like meningism ) is an inflammation of the brain and spinal cord , so the sheaths of the central nervous system (CNS). It can be caused by viruses , bacteria or other microorganisms, but it can also occur as a result of non-infectious stimuli. Since bacterial meningitis is fundamentally life-threatening due to the immediate proximity of the inflammation to the brain and spinal cord, meningitis is always a medical emergency until a bacterial cause has been safely excluded.
The most common symptoms of meningitis are headache and neck stiffness combined with fever , confusion or loss of consciousness , nausea, and sensitivity to light and loud noises. Children in particular can show unspecific symptoms such as irritability and drowsiness, especially in the initial phase. A characteristic rash is considered an indication of the presence of meningococcal meningitis.
Usually, the presence of the disease is by analyzing cerebrospinal fluid , which by means of a lumbar puncture , confirmed is removed or excluded. Meningitis is treated by giving antibiotics in good time and, if necessary, with antiviral substances. Corticosteroids can be helpful in preventing complications. Meningitis, especially if it is not recognized and treated in time, can be fatal or lead to serious sequelae such as deafness , epilepsy , hydrocephalus or cognitive impairment. Vaccinations exist to protect against certain meningitis pathogens. Meningitis caused by certain pathogens such as Haemophilus influenzae type B or meningococcal meningitis are notifiable diseases.
Meningitis is usually caused by the pathogen, i.e. an infectious disease . In most cases, infections with viruses, bacteria , fungi or parasites can be detected. Meningitis can also be caused by a number of non-infectious mechanisms. All forms in which no bacterial pathogen can be detected are generally referred to as aseptic meningitis . This is the case with non-infectious or viral causes (see lymphocytic choriomeningitis , early summer meningoencephalitis ), but also with previously treated bacterial meningitis in which bacteria are no longer found in the meninges , or also with infections near the meninges (such as sinusitis ). A endocarditis (infection of the heart valve with seeding of bacteria in the blood stream) may also be the cause of aseptic meningitis be. The aseptic meningitis is also of pathogens from the family of spirochetes , including that of syphilis ( Treponema pallidum ) and Lyme disease ( Borrelia burgdorferi ) are triggered. Even malaria , fungi (eg, Cryptococcus neoformans with immunodeficiency syndromes such as AIDS ) and amoebas (such as Naegleria fowleri from so contaminated drinking water) are known as triggers.
Dependence of the type of meningitis on age
As a general rule, it depends on the age of the patient which pathogens preferentially cause meningitis.
In premature babies and infants up to the age of 3 months is often Streptococcus agalactiae found. In particular, subtype III of Lancefield group B ( group B streptococci , GBS) is the cause of meningitis in neonatal sepsis , especially within the first few weeks of life . These pathogens have their natural reservoir in the gastrointestinal tract . However, the vagina (of the mother) can also be colonized with GBS intermittently, chronically or temporarily. Escherichia coli are also found in this age group , which also colonize the gastrointestinal tract. Newborns and immunocompromised patients can also contract Listeria monocytogenes (especially serotype IVb), a pathogen that also occurs epidemically .
Older children are more likely to develop Neisseria meningitidis (meningococci), Streptococcus pneumoniae (pneumococci, serotypes 6, 9, 14, 18 and 23) and children under five years of age are more likely to develop Haemophilus influenzae type B ( Haemophilus influenzae b infection ).
In adults, N. meningitidis and S. pneumoniae together cause about 80% of all meningitis cases. With increasing age (after the age of 50) L. monocytogenes is found more frequently .
Special cases: traumatic brain injury, cerebral shunt, cochlear implant, anatomical defects, disorders of the immune system
After a recent traumatic brain injury , bacteria from the nasal cavity can pass into the meningeal space.
Patients with a cerebral shunt have a similarly increased risk of infection . In these cases there are frequent infections with staphylococci , pseudomonads and gram-negative pathogens. These germs can also be found in patients with an immunodeficiency .
Sometimes cochlear implant placement or head and neck infections such as acute otitis media or mastoiditis can lead to meningitis. With cochlear implants, the risk of pneumococcal meningitis is significantly increased.
A recurrent bacterial meningitis can also by anatomical defects ( congenital or acquired) or also by disturbances of the immune system caused. Anatomical defects can create a connection between the external environment and the nervous system. Therefore, the most common cause of recurrent meningitis is skull fracture , particularly fractures of the base of the skull and those involving the paranasal sinuses or temporal bone . A literature review of 363 cases of recurrent meningitis showed that 59% of the cases are caused by anatomical anomalies, 36% occur in the context of an immune deficiency (e.g. coagulation disorders , which mainly lead to recurrent meningococcal meningitis) and 5% due to the Account of persistent infections in the areas adjacent to the meninges.
The so-called tuberculous meningitis, i.e. meningitis due to an infection with the pathogen Mycobacterium tuberculosis , occurs more frequently in countries where tuberculosis is widespread, but is also observed in people with an immunodeficiency disease, such as AIDS .
Bacteria such as meningococci or Haemophilus influenzae tend to lead to purulent meningitis ( meningitis purulent ). Depending on the main localization of spreading a distinction is the hood or convexity of the basal meningitis . In the former, the purulent infiltrate is found over the cerebral hemispheres (especially frontoparietal), in the latter, preferably in the area of the brain base.
Although neurotropic viruses predominantly cause encephalitis , some virus species can also cause meningoencephalitis, encephalomyelitis, and meningitis. To differentiate it from classic bacterial meningitis, viral meningitis is also referred to as lymphocytic meningitis . Few viruses cause exclusively meningitis like the rodent-borne lymphocytic choriomeningitis (LCMV) virus . Meningitis as a mixed form or as an advanced course of infection is most frequently caused by enteroviruses such as the Coxsackie virus and the ECHO viruses in immunocompetent adults . Infections or reactivations of various herpes viruses can also manifest as meningitis, such as herpes simplex virus 1 , more rarely herpes simplex virus 2 , human herpes virus 6 and human herpes virus 7 . The herpes simplex viruses are the only viral pathogens that can also cause chronic meningitis. In severe cellular immunodeficiency (for example after a bone marrow transplant or in AIDS in stage C3) the cytomegalovirus and the Epstein-Barr virus can also trigger meningoencephalitis or meningitis. These also occur as typical complications with infections with the measles virus , the mumps virus and the rubella virus . In hantaviruses and parvovirus B19 , a meningeal involvement is described. As part of a fresh infection, the human immunodeficiency virus can cause encephalitis as well as meningitis ( acute retroviral syndrome ). Various viruses ( arboviruses ) transmitted by arthropods such as mosquitoes and ticks can cause encephalitis as well as meningitis. They include the TBE virus , Japanese encephalitis virus (→ Japanese encephalitis ), West Nile virus , Rift valley fever virus (→ Rift valley fever ), dengue virus and various subtypes of the sand fly fever virus (→ phlebotomus fever ) such as Tuscany -Virus .
A parasitic cause is often assumed when eosinophilia is found in the cerebrospinal fluid . The rat lungworm ( Angiostrongylus cantonensis ) and other roundworms such as Gnathostoma spinigerum are most common ; a treatment with albendazole carried out is questionable. Tuberculosis , syphilis , cryptococcosis and coccidioidomycosis are considered to be rare exclusion diagnoses . Also, cysticercosis can be the cause of chronic lymphocytic meningitis.
Non-infectious forms of meningitis
Non-infectious meningitis can occur as a result of various processes: through the spread of cancer cells to the meninges in the sense of a " meningiosis neoplastica " and as a side effect of certain drugs, especially non-steroidal anti -inflammatory drugs , antibiotics and intravenous immunoglobulins . Non-infectious meningitis can also be caused by inflammatory diseases such as sarcoid (neurosarcoidosis) or connective tissue diseases such as systemic lupus erythematosus or as a result of certain types of inflammatory diseases of the vascular wall such as Behçet's disease. An epidermoid cyst or dermoid cyst can cause meningitis by releasing inflammatory substances into the subarachnoid space. A Mollaret meningitis is a syndrome of recurrent episodes of aseptic meningitis. It is possibly caused by type 2 herpes simplex virus . In rare cases, migraines can cause meningitis, but this diagnosis is only acceptable if all other possible causes have been ruled out beforehand.
Meningitis, also known as cerebrospinal meningitis (epidemica) , affects all three layers of the meninges which, together with cerebrospinal fluid ( Liquor cerebrospinalis ), enclose and protect the brain and spinal cord. The innermost layer of the meninges, the pia mater , is a delicate, impermeable layer that is firmly connected to the surface of the brain and spinal cord and also encloses all furrows. The middle layer, the arachnoid or cobweb skin, sits loosely on the pia mater and "skips" the furrows of the brain. The gap between the two layers is called the subarachnoid space . It is filled with cerebrospinal fluid and, because it lies outside the CNS, is also called the external fluid space. The outermost layer of the meninges lies close to both the arachnoid and the skull bone. It is known as the dura mater .
In bacterial meningitis, the pathogens can reach the meninges via the blood (haemotogenic) or migrate there directly from the mucous membranes of the nasal cavity or the skin . This is usually preceded by a viral infection that damages the normally existing protective function of the mucous membranes. Once the bacteria are in the blood, they can enter the subarachnoid space via areas in which the blood-brain or blood-liquor barrier is less pronounced (such as the choroid plexus ). Meningitis in newborns is due to haematogenous spread of group B streptococci in 25% of cases. This is less common in adults. Cause an immediate spreading of germs into the cerebrospinal fluid may be introduced medical equipment, but also a skull fracture, or an infection of the nasopharynx ( nasopharynx ) or of the paranasal sinuses , a fistula have been formed with the subarachnoid space. Occasionally, a congenital dura mater defect can also be responsible.
The term aseptic meningitis describes a syndrome that is characterized by an acute occurrence of meningeal irritation, fever and CSF pleocytosis. Typically, there is no growth of a pathogen in a bacterial culture. In most aseptic meningitis, the inflammation of the meninges is caused by enteroviruses and herpes simplex type 2 viruses. If one examines the virally caused meningitis, enteroviruses are found to be the cause in up to 90% of cases. Enteroviruses make up around half of the pathogens identified in children. Therefore, viral meningitis is often called aseptic meningitis. Other authors simply explain that aseptic meningitis is always present when the inflammation of the meninges is not caused by a pus-causing pathogen. The term is usually used for a form of meningitis in which a benign course is observed without the inflammation spreading to the brain parenchyma. However, the term “drug-induced aseptic meningitis” (DIAM) is also subsumed under the term. Medicines that can produce the appearance of meningitis are mainly non-steroidal anti-inflammatory drugs, antibiotics and intravenous antibodies. Aseptic meningitis as a result of vaccination was recently observed in a mumps epidemic in the United States and Canada. Tumors are an increasingly common cause of aseptic meningitis. In this context one speaks in the Anglo-Saxon-speaking area of a "neoplastic meningitis". The decisive factor for naming the disease as meningitis is the observation that the tumor cells that migrate into the subarachnoid space lead to an irritation of the meninges, which creates the clinical picture of mild meningitis. In rare cases, rheumatoid arthritis or neuroborreliosis can be associated with aseptic meningitis. Occasionally there are epidemics of aseptic meningitis. Such an epidemic was recently observed in Latvia. It was caused by the Coxsackie virus.
The generalized inflammation that occurs in meningitis in the subarachnoid space is by no means the direct consequence of the germ multiplication, but rather the result of the complex immune response as a result of the germ colonization . This immune response consists primarily in the production of cytokines by astrocytes and microglia . This stimulates other components of the immune system . As a result, the blood-brain barrier is disturbed , which can be accompanied by swelling of the brain (vasogenic brain edema ). The changed permeability of the cerebral vessels not only causes fluid to pass into the brain tissue, but also a penetration of leukocytes into the CSF space. These contribute significantly to the inflammatory process and interstitial brain edema by releasing further cytokines and remains of dead bacteria. This also leads to inflammation of the walls of the cerebral vessels ( cerebral vasculitis ), which contributes to cytotoxic cerebral edema and a disruption of cerebral blood flow. The three types of cerebral edema that occur in meningitis now lead to increased intracranial pressure and reduced blood flow to the brain, with the consequence of programmed cell death of nerve cells . The synopsis of these processes explains the observation that the clinical condition of patients with meningitis can initially worsen if the patients are treated with an antibiotic . This is due to the increased release of bacterial endotoxins into the CSF space. The administration of corticosteroids can alleviate these processes.
Clinical signs and symptoms
In adults, an intense headache is the most common symptom of the disease and occurs in over 90% of all cases of bacterial meningitis. It is usually accompanied by a stiff neck ( meningism ), which is found in 70% of adult patients with bacterial meningitis. Other clinical signs that are common in meningitis are photophobia and sensitivity to noise . The classic symptom triad of meningitis consists of neck stiffness, high fever and a decreased level of consciousness . However, this triad is only found in about 45% of cases of bacterial meningitis. If none of the three clinical signs are present, meningitis is very unlikely.
Further indications of meningism are positive Kernig , Brudzinski and Lasègue signs : Patients are often found lying in bed with their legs drawn up and unable to straighten their knees (Kernig's sign). If there is an involuntary pulling of the legs when the head is bent forward, it is called the Brudzinski sign. Passive bending of the extended leg in the hip joint up to an angle of 45 ° can lead to sharp pain shooting into the leg from the back (Lasègue sign). The sensitivity of these tests, which are often used in everyday clinical practice, is not very high. Kernig and Brudzinski signs, however, have a high specificity , which means that they rarely occur in other diseases. Another test, the jolt accentuation maneuver, can also be helpful: if the patient shakes their head horizontally and quickly back and forth (as when saying no) and this does not worsen the headache, meningitis is unlikely.
Young children often have no characteristic symptoms, they are sometimes just irritable and sickly. Infants up to six months of age sometimes have a bulging fontanel , pain in the legs, cold extremities, and paleness.
If the meningitis is caused by the bacterium Neisseria meningitidis (meningococcal meningitis), then this can be characterized by the appearance of a purpura if the bacteria spread through the blood . This skin appearance consists of numerous small irregular red or purple spots (extensive bleeding under the skin) on the trunk, lower extremities, mucous membranes, conjunctiva and occasionally the palms of the hands or soles of the feet. Although the rash does not always occur in meningococcal meningitis, it is quite specific for the disease, but it also occurs in other pathogens. Characteristic skin rashes are also found in meningitis forms caused by the causative agents of hand-foot-mouth disease and in herpes simplex meningoencephalitis.
Patients with meningitis can experience particular complications in the early stages of the disease. These complications require special treatment and sometimes indicate an unfavorable prognosis. The infection can cause sepsis with a systemic inflammatory response syndrome with drop in blood pressure , tachycardia , abnormal body temperature, and tachypnea . The drop in blood pressure can occur early in the course of the disease, particularly in meningococcal meningitis, and can lead to circulatory disorders in various organs. A consumption coagulation disorder is the result of excessive coagulation activation and can, on the one hand, disrupt the blood supply to entire organs and, on the other hand, significantly increase the risk of bleeding. With meningococcal meningitis, gangrene of the extremities can develop. Infections with meningococci and pneumococci can cause hemorrhage in the adrenal gland resulting in Waterhouse-Friderichsen syndrome , which is often fatal. Another problem is the development of cerebral edema , with increasing intracranial pressure and the risk of entrapment due to the swelling of the brain. This can be accompanied by a decreased level of consciousness with a deterioration in the pupillary reflexes , breathing difficulties and an abnormal posture. An infection of the brain tissue can also lead to an obstruction of the CSF flow, resulting in hydrocephalus . Epileptic seizures can occur for a variety of reasons; they are a common early complication in children (30% of cases) and provide no indication of the underlying disorder. Seizures sometimes start in areas of the brain that are compressed or inflamed. Partial seizures (these are types of seizures that lead to motor discharges in an extremity or in parts of the body), a seizure status, late-onset seizures and those that are difficult or impossible to control with medication are indicative of an unfavorable long-term prognosis. Meningitis can also impair the cranial nerves and thus impair the control of eye, face and head movements, swallowing and hearing. Visual disturbances and hearing loss can be persistent after meningitis. The problem is occurring on the disease after calcification of the cochlea ( cochlear ), therefore, should be made during and after a meningitis meshed hearing tests in order in appropriate cases at an early stage deafness, a cochlear implant to enable that is not always possible after the ossification. Inflammation of the brain tissue ( encephalitis ) or the cerebral vessels ( cerebral vasculitis ) as well as the development of a sinus or cerebral vein thrombosis can lead to a focal neurological deficit with paralysis, sensory disorders and movement disorders in the areas of the body supplied by the affected brain regions.
|Lower forms||glucose||Protein content||Cell count|
often> 300 / mm³
|Acutely viral||normal||normal or increased||
<300 / mm³
PMNs, <300 / mm³
|mushroom||humiliated||elevated||<300 / mm³|
Blood tests and imaging tests
If meningitis is suspected, the blood is examined for changes that are typical of inflammation (for example, the concentration of C-reactive protein , the blood count or the white blood cell count and in the blood culture ). The most important test to confirm or dismiss a suspicion of meningitis is to examine the cerebrospinal fluid obtained with a lumbar puncture . The lumbar puncture is contraindicated in the case of masses in the brain (for example tumors or abscesses) or if there is an increase in intracranial pressure, because the brain can become trapped. In order to be able to avoid this risk, a computed tomography or magnetic resonance tomography of the skull is indicated in advance if the patient has an appropriate medical history , which is necessary in up to 45% of cases. An ultrasound scan of the head can also help make the diagnosis in infants and young children. If an imaging examination is necessary prior to a lumbar puncture, preventive antibiotic treatment is recommended to avoid delaying the start of treatment. Imaging techniques are often used to better assess the development of complications during treatment. If the course is severe, the blood electrolytes should always be monitored , since in these cases hyponatremia can occur as a result of Schwartz-Bartter syndrome or as a side effect of infusion therapy.
Cerebrospinal fluid (liquor cerebrospinalis) is obtained by means of a lumbar puncture . The pressure in the subarachnoid space can then be measured, which is usually between 6 and 18 cm water column (cm H 2 O). With bacterial meningitis, the CSF pressure is usually increased. The macroscopic appearance of the cerebrospinal fluid allows conclusions to be drawn about the cause. Normally, CSF is clear, a cloudy to cloudy cerebrospinal cord fluid indicates increased protein levels, white and red blood cells and / or bacteria and thus bacterial meningitis. If the leukocyte count is very high ( pleocytosis ), the liquor can appear purulent.
The cerebrospinal fluid is examined microscopically for red and white blood cells and chemically for protein, lactate and glucose content . A gram stain can be used to detect bacteria. However, its absence does not rule out bacterial meningitis. In bacterial meningitis, bacteria are microscopically detectable in only 60% of the cases, and even only in 40% of previous antibiotics. The Gram stain for the detection of specific infections such as listeriosis is also unreliable. A bacterial culture of the sample is more sensitive, it can detect microorganisms in 70–85% of cases, but it takes up to 48 hours before the results are available. The distinction between white blood cells already gives clues as to whether bacterial ( neutrophilic granulocytes predominate) or viral ( lymphocytes predominate) meningitis is present. However, this finding is not very reliable in the early stages of the disease. Eosinophilic granulocytes predominate much less often , which indicates a parasitic or fungal infection.
"Aseptic meningitis" refers to meningitis regardless of the cause, if the liquor contains inflammatory cells, but no pathogens can be detected in the culture. This case can occur in the case of an infection with pathogens that are difficult to cultivate ( spirochetes such as Borrelia , treponemas or leptospira ; viruses; fungi; mycoplasmas ) or in non-infectious forms.
The glucose concentration in the cerebrospinal fluid is usually around 65% of the blood glucose value. The quotient of CSF glucose value and blood sugar value is typically lower in bacterial meningitis (quotient ≤ 0.4). In newborns, the CSF glucose value is higher and a quotient below 0.6 is considered to be pathological. Lactic acid (lactate) is a breakdown product of glucose if its metabolism is incomplete; it is therefore the opposite of the glucose concentration. A high level of lactate is more predictive of bacterial meningitis than an increase in white blood cells.
Numerous selective testing methods are used to identify the different types of meningitis. A latex test can be positive for Streptococcus pneumoniae , Neisseria meningitidis , Haemophilus influenzae , Escherichia coli and group B streptococci . However, its routine use is not recommended, as its result rarely leads to therapy adjustments. But it can be helpful when other testing methods fail. The Limulus amebocyte lysate test can also be positive for meningitis caused by gram-positive germs, but it should only be used if other test methods do not provide any usable results. The polymerase chain reaction can be used to replicate the DNA of viruses and bacteria in vitro so that even small amounts of pathogens in the cerebrospinal fluid can be recognized. The sensitivity and specificity of this examination are very high because traces of pathogen DNA are sufficient for identification. This examination can therefore be an essential aid in differentiating bacterial or viral pathogens (for example enteroviruses, herpes simplex 2 viruses and, in unvaccinated people, also mumps). Serological examinations ( antigen - antibody reactions in vitro) can be helpful in viral meningitis. If tuberculosis is suspected, either the Ziehl-Neelsen staining is used on the test material (low sensitivity), or cultures are set up (slow growth, therefore a result only after six weeks). Since both methods have considerable disadvantages, the polymerase chain reaction (PCR) is also being used more and more for this question. The diagnosis of cryptococcal meningitis can be made inexpensively with the help of negative staining with Indian ink. However, testing for cryptococcal antigen in blood or liquor is more sensitive, especially in AIDS patients.
A previously undetected but treated meningitis is a diagnostic and therapeutic puzzle, as meningitis symptoms are found in these cases after the patient has received an antibiotic - for example because of a sinus infection . Signs of viral meningitis can then be found in the CSF, but antibacterial treatment must be continued until viral meningitis has been confirmed by further measures (PCR).
Meningitis can be diagnosed even after death. There are extensive inflammatory changes in the pia mater and arachnoid in particular. Because neutrophils migrated into the liquor and the base of the brain (part of the brain close to the base of the skull) during lifetime, pus can be found on the cranial nerves, the spinal cord or the cerebral arteries .
Prevention and hygiene regulations
In the 1980s, vaccination against Haemophilus influenzae B was included in the recommended routine regimens for children in many countries , which means that this pathogen no longer plays a major role as a cause of meningitis in these countries (in contrast to the countries in which this vaccination is too expensive). Similarly, vaccination against mumps has also significantly reduced the number of cases of meningitis caused by this disease. Meningococcal vaccinations are available for groups A, C, W135 and Y and, since 2013, for group B.
In countries where vaccination against group C meningococci had been introduced, the number of new cases it triggered fell. Since 2007 the industry has offered a quadruple vaccine containing the above ingredients. Immunization with the quadruple vaccine ACW135Y is required for the issuance of a visa as part of an Islamic pilgrimage ( Hajj ).
In the Federal Republic of Germany, 385 cases of bacterial meningitis were reported in 2010, a third less than five years earlier. Around ten percent (31 cases) were fatal. Serogroups B and C predominate in Europe. Since 70 percent of meningitis diseases now occur in serogroup B, there was a prevention gap that had to be filled with an innovation. The development of a vaccine against serogroup B encountered particular complications. The capsule antigen showed great resemblance to a surface antigen on nerve cells. Only by means of the "reverse vaccinology" procedure were four components of the pathogen that are suitable for a vaccine determined. The corresponding clinical studies, carried out separately for the groups infants, adolescents and adults, all produced good results. All babies who had received at least two vaccinations developed antibody titers that were classified as protective. In the clinically included 1,631 adolescents aged 11 to 17, there were no serious complications and a good protective effect. A good protective effect was also achieved in the clinical study with adult laboratory workers who deal with infectious material. In January 2013, a meningococcal B vaccine was approved in Europe, which can be used in children from two months of age and in adults.
Vaccination against streptococcal pneumonia using the pneumococcal vaccine , which is effective against seven serotypes of the pathogen, clearly reduces the incidence of meningitis caused by pneumococci. The "pneumococcal polysaccharide vaccine", which covers 23 strains, is only administered in special cases. This includes patients with a removed spleen . This vaccination does not produce adequate immunity in some patients, especially children. There have been reports of a decrease in tuberculous meningitis in children vaccinated with Bacillus Calmette-Guérin . The insufficient effectiveness in adults is the reason for the search for a better alternative.
For the prophylaxis of neonatal sepsis due to group B streptococci (GBS), it is recommended in Germany to carry out a microbiological examination for GBS in all pregnant women between the 35 + 0 and 37 + 0 week of pregnancy. A smear from the vaginal introitus and anorectum already allows a statement to be made about the presumed GBS colonization status at the calculated delivery date. If GBS colonization is detected during the screening, no immediate antibiotic therapy should be carried out , but antibiotic prophylaxis at the time of delivery ( when labor begins or after rupture of the bladder). The drug of choice is penicillin G , which is given every four hours until delivery. Ampicillin is an effective alternative, but by promoting the development of resistance in gram-negative pathogens, it has disadvantages compared to penicillin from a neonatal point of view. If you are allergic to penicillin, cefazolin or a second generation cephalosporin should be used. In order to achieve the highest possible protective effect of antibiotic prophylaxis for the child, the first administration of the antibiotic to the mother should be more than four hours before the birth. In the case of a primary caesarean section without rupture of the bladder and without labor, antibiotic GBS prophylaxis can be dispensed with, as the risk of a child's GBS infection is low. Women who have already given birth to a child with GBS infection should generally receive prophylaxis with an antibiotic during childbirth. Screening can be dispensed with in these women. In some of these cases of meningitis, prevention can also be done long-term with vaccination and short-term with antibiotics.
In Germany, if there is a justified suspicion of meningococcal meningitis, the responsible health authorities must be informed. Patients must also be isolated for up to 24 hours after initiating adequate antibiotic therapy. Since the incubation period is usually 3–4 (max. 10) days, contact persons receive chemoprophylaxis, as standard rifampicin for two days. Alternatives are ciprofloxacin in adults and ceftriaxone in children. This will reduce the risk of the disease being passed on. But it does not protect against a future illness.
Meningitis is a potentially life-threatening condition and has a high mortality rate if left untreated. Delayed treatment is associated with a less favorable prognosis. For this reason, the start of treatment with a broad spectrum antibiotic (depending on the patient's age and comorbidities) should not wait until technical examinations (such as a CSF examination) confirm the diagnosis. If meningococcal meningitis is suspected, a calculated antibiotic therapy should be started before a microbiological culture result (with antibiogram) is received or penicillin G should be administered on site as an emergency treatment. In the event of dehydration with low blood pressure or symptoms of shock , fluids should be administered intravenously. Due to the manifold and serious complications of the disease, patients should be examined by a doctor frequently; in case of doubt, treatment in an intensive care unit is indicated. With awareness disturbed patients and respiratory failure one is ventilation necessary. If there are indications of increased intracranial pressure, this should be measured and measures to reduce intracranial pressure taken, for example with mannitol . Seizures can be treated with an anticonvulsant ; hydrocephalus may require the installation of an external ventricular drainage system or a ventriculo-peritoneal shunt system .
In the case of bacterial meningitis, treatment must be given immediately if it is suspected - i.e. without confirmation of the diagnosis. The antibiotic is selected primarily on the basis of an assumption about the causative germ (“blind”). In Great Britain , therefore, a cephalosporin such as cefotaxime is suspected of being administered, in the USA, due to increasing resistance, vancomycin is not uncommon . When choosing an antibiotic for initial therapy, consider the patient's age and whether the patient has suffered a head injury, neurosurgical operation, or a shunt system installed. In children, patients over 50 years of age and people who are immunocompromised, the addition of ampicillin is recommended to cover an infection with Listeria .
As soon as the result of a smear examination is available, the spectrum of pathogens can be narrowed down sufficiently to adjust the antibiotic therapy if necessary. The results of the CSF culture are usually only available after one or two days. Then the empirical therapy can be switched to a specific therapy, since the pathogen and its sensitivity are usually known. In order for antibiotics to be effective in meningitis, they must reach the meninges in sufficient quantities. Some antibiotics can not cross the blood-brain barrier and are therefore unsuitable for treating meningitis. The knowledge about the suitability of the corresponding medication mostly comes from animal experiments.
The treatment of tuberculous meningitis requires a sufficiently long antibiotic therapy. While tuberculostatics are usually given for six months in the case of pulmonary tuberculosis , these are extended to a year in the case of an infection of the meninges. If the patient does not also have AIDS, corticosteroids are also given.
The adjuvant treatment of meningitis with corticosteroids (usually dexamethasone ) reduces mortality and the risk of hearing loss and neurological impairment in adolescent and adult patients in Western countries with a low HIV infection rate. The presumed mechanism is the suppression of excessive inflammatory reactions.
The treatment guidelines therefore recommend the administration of dexamethasone or similar corticosteroids immediately before the first administration of antibiotics and further for four days. Since experience has shown that patients with pneumococcal infection benefit most from administration of corticosteroids, some authors advise discontinuing corticosteroids as soon as another pathogen has been identified.
Corticosteroids work differently in children and adults with meningitis. While both patient groups benefit in western countries, an advantage for children from poor countries has not been proven. The cause of this difference is unknown. In rich western countries, the benefit of adjuvant corticosteroid therapy has only been proven in cases of Haemophilus influenzae meningitis, and then only if started before antibiotic therapy. However, their incidence has decreased significantly since the introduction of the Haemophilus influenzae B vaccines. Some authors therefore recommend giving corticosteroids only in children with Haemophilus influenzae meningitis and then only if no antibiotics have been given beforehand. All other cases are judged controversially.
Viral meningitis usually only requires supportive treatment, since most viruses that cause meningitis are not amenable to causal therapy. Viral meningitis is usually more benign than bacterial meningitis. Herpes simplex virus infections and varicella zoster virus infections can respond to antivirals such as acyclovir , but there are no clinical studies that have examined the effectiveness of this measure. Mild courses of viral meningitis can also be treated on an outpatient basis with conservative measures (bed rest, painkillers and sufficient fluids).
The cryptococcal meningitis by means of high doses of antifungals such as amphotericin B or 5-fluorocytosine treated over a long period of time.
Viral meningitis tends to heal spontaneously and is rarely fatal. If left untreated, bacterial meningitis is almost always fatal. With treatment, the mortality ( lethality ) from bacterial meningitis depends on the age of the patient and the underlying cause. Newborn patients can die from bacterial meningitis in 20–30% of cases. The risk of dying is significantly lower in older children. Their mortality is only around 2%, but in adults it rises again to around 19–37%. The risk of dying from meningitis depends on other factors besides age. The pathogen and the time it takes for the organism to remove the pathogen from the liquor play a role. The general condition of the patient, the extent of the impaired consciousness and whether leukopenia is present are also decisive . Meningitis caused by Haemophilus influenzae or meningococci has a better prognosis than one caused by group B streptococci, coliforms, or pneumococci. In adults, the prognosis of meningococcal meningitis is more favorable (mortality of 3 to 7%) than diseases with pneumococci .
Meningitis can cause a number of sequelae in children. In up to 15% of the surviving children, sensorineural hearing loss , epilepsy , learning disabilities and behavioral problems as well as a reduced intelligence can be observed. This also has a negative impact on school and professional careers. The hearing loss can be reversible in some cases. In adults, around two thirds of cases are without consequential damage. Here mainly hearing loss (in 14% of cases) and cognitive deficits (in 10% of cases) occur.
Although meningitis is a reportable disease in many countries , exact epidemiological figures are not known. In western countries there are about 3 cases of bacterial meningitis per 100,000 people per year. Population studies have shown that viral meningitis is more common, with around 11 cases per 100,000 population per year, and that there is a peak in the disease in summer. In Brazil, the incidence rate is significantly higher at around 46 / 100,000 inhabitants per year. In sub-Saharan Africa , meningitis epidemics occur during the dry season with an incidence rate of 100 to 800 / 100,000 inhabitants per year. In Africa, these epidemics mainly start between December and June, can last two to three years and then end during the rainy season. The disease is mainly caused by meningococci. The largest known epidemic of this type occurred in 1996–1997. At that time, 250,000 people fell ill and 25,000 died. Meningococcal diseases occur in epidemic form when many people live together in large numbers for the first time. This occurs, for example, in barracked recruits during mobilization, in the first year of college or on pilgrimages such as the annual Hajj . Although the causes of recurring epidemics, as in Africa, are not well understood, various factors have been blamed for these occurrences. These include an increased willingness of the affected people to become ill, demographic conditions such as the high number of refugees, overpopulation, poverty, climatic conditions and recurrent respiratory infections .
There are significant regional differences in the occurrence of meningitis. In mening coccal meningitis in Europe, for example, Neisseria of groups B and C are predominantly found, while subtype A dominates in China and among pilgrims to Mecca. Subtypes A and C are mainly responsible for the diseases in the meningitis belt. The most recent epidemics in Africa and Saudi Arabia were caused by meningococci of group W135. It is expected that such regional differences will also occur in the future as a result of vaccination campaigns, among other things. The current outbreak of a meningitis epidemic in Africa has persisted since January 2009. West African countries are mainly affected. In the meantime, over 1,000 people have died and over 25,000 have fallen ill as part of this epidemic. It is currently the second most serious meningitis epidemic since 1996.
The writings of Hippocrates of Kos (* around 460 BC; † around 370 BC) contain numerous descriptions of disease states that are compatible with the clinical picture of meningitis. It is believed that medieval doctors like Avicenna were aware of the symptom of meningism. From the 17th and 18th centuries there are various reports of patients suffering from “brain fever” (“phrenitis”, “cephalitis”), whose symptom constellations partly suggest the presence of meningitis or encephalitis. In a work published posthumously in 1685, Thomas Willis described "Phrensy" (German: about "feverish delusion"), a meningitis symptomatology with meningism, opisthotonus and seizures, which he attributed to an inflammation of the meninges and compression of the brain. His records also include the description of a corresponding "epidemic fever" in 1661, which was probably a meningococcal epidemic. The first description of tubercular meningitis is attributed to the British doctor Robert Whytt from Edinburgh in 1768. This disease was called "cerebral addiction" at the time. However, the connection to the tuberculosis pathogen was only established about a hundred years later. Epidemic meningitis appears to be a largely modern phenomenon. The first known outbreak of the disease in the form of an epidemic is often given for the year 1805 in the Swiss city of Geneva and was first described scientifically in detail by Vieusseux . A short time later, more meningitis epidemics are described in Europe and the USA. In 1840 such an event was first known in North Africa, in Algeria. Outbreaks in Nigeria in 1905 and Ghana from 1906 to 1908 were possibly the first meningococcal epidemic in West Africa. The Austrian bacteriologist Anton Weichselbaum described bacterial meningitis for the first time in 1887 and named the pathogen "Meningococcus".
Mortality from meningitis was very high in the early reports (over 90%). The American scientist Simon Flexner produced an antiserum from horse blood in 1906 and thereby achieved a significant reduction in mortality. The effectiveness of penicillin in treating meningitis was first described in 1944 . The introduction of the Haemophilus vaccination at the end of the 20th century led to a significant decrease in the incidence of this pathogen. The most recent important advance in 2002 was the demonstration of the effectiveness of corticosteroid treatment in reducing complications in the early course of the disease.
In Germany, meningococcal meningitis is a reportable disease according to Section 6 (1) number 1 of the Infection Protection Act (IfSG). You are required to report by name in the event of suspicion, illness or death. The diagnosing doctors, etc., are obliged to report the illness ( Section 8 IfSG). In addition, the direct evidence of Neisseria meningitidis is notifiable by name according to § 7 IfSG. The reporting requirement only applies to direct evidence from CSF, blood, hemorrhagic skin infiltrates or other normally sterile substrates. The laboratories etc. are obliged to report with regard to the detection of the pathogen ( § 8 IfSG).
In Austria are virus-related meningoencephalitis according to § 1 para. 1, point 2 Epidemics Act 1950 in case of illness and death notifiable . Doctors and laboratories, among others, are obliged to report this ( Section 3 Epidemics Act). According to the same norms, there are "invasive [e] bacterial diseases (meningitis or sepsis )" (e.g. due to meningococci , pneumococci , Haemophilus influenzae )
- S1 guidelines for community- acquired bacterial (purulent) meningoencephalitis of the German Society for Neurology (DGN). In: AWMF online (as of 2012)
- S1 guideline for viral meningoencephalitis of the German Society for Neurology (DGN). In: AWMF online (as of 2008)
- S1 guideline atypical pathogen-related meningoencephalitis of the German Society for Neurology (DGN). In: AWMF online (as of 2012)
- Kenneth L. Tyler: A history of bacterial meningitis. In: Stanley Finger, Francois Boller, Kenneth L. Tyler (Eds.): History of Neurology . Elsevier, Edinburgh 2010, ISBN 978-0-444-52009-8 , pp. 419-433.
- Manio von Maravic: Neurological Emergencies. In: Jörg Braun, Roland Preuss (Ed.): Clinic Guide Intensive Care Medicine. 9th edition. Elsevier, Munich 2016, ISBN 978-3-437-23763-8 , pp. 311–356, here: pp. 336–339 ( bacterial meningitis , viral meningitis ).
- Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , pp. 61-68 ( infections of the central nervous system: menigitis ).
- Karl Wurm, AM Walter: Infectious Diseases. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition, ibid. 1961, pp. 9-223, here: pp. 177-184.
- Link catalog on meningitis at curlie.org (formerly DMOZ )
- Website of the National Reference Center for Meningococci at the Institute for Hygiene and Microbiology at the University of Würzburg
- ↑ a b c d e f g L. Ginsberg: Difficult and recurrent meningitis . In: Journal of Neurology, Neurosurgery, and Psychiatry . 75 Suppl 1, March 2004, p. i16 – i21 , doi : 10.1136 / jnnp.2003.034272 , PMID 14978146 , PMC 1765649 (free full text).
- ↑ a b c d e f g h i j k l m n o p q X. Sáez-Llorens, George H. McCracken : Bacterial meningitis in children . In: The Lancet . tape 361 , no. 9375 , June 2003, p. 2139-2148 , doi : 10.1016 / S0140-6736 (03) 13693-8 , PMID 12826449 .
- ↑ 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 z A. R. Tunkel, BJ Hartman, SL Kaplan et al .: Practice guidelines for the management of bacterial meningitis . In: Clinical Infectious Diseases . tape 39 , no. 9 , November 2004, p. 1267-1284 , doi : 10.1086 / 425368 , PMID 15494903 .
- ↑ a b c d e f g h i D. van de Beek, J. de Gans, AR Tunkel, EF Wijdicks: Community-acquired bacterial meningitis in adults . In: The New England Journal of Medicine . tape 354 , no. 1 , January 2006, p. 44-53 , doi : 10.1056 / NEJMra052116 , PMID 16394301 .
- ^ Federal health reporting on notifiable diseases.
- ↑ a b c d e f J. Attia, R. Hatala, DJ Cook, JG Wong: The rational clinical examination. Does this adult patient have acute meningitis? In: JAMA . tape 282 , no. 2 , July 1999, p. 175-181 , doi : 10.1001 / jama.282.2.175 , PMID 10411200 .
- ↑ a b S1 guideline prophylaxis of newborn sepsis - early form - through streptococci of group B of the Society for Neonatology and Pediatric Intensive Care Medicine (GNPI), German Society for Gynecology and Obstetrics, German Society for Pediatric Infectious Diseases (DGPI), and German Society for Perinatal Medicine (DGPM). In: AWMF online (as of 7/2008)
- ^ Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , p. 61.
- ^ BP Wei, RM Robins-Browne, RK Shepherd, GM Clark, SJ O'Leary: Can we prevent cochlear implant recipients from developing pneumococcal meningitis? In: Clin Infect Dis . tape 46 , no. 1 , January 2008, p. e1-e7 , doi : 10.1086 / 524083 , PMID 18171202 .
- ↑ a b M. Tebrügge, N. Curtis: Epidemiology, etiology, pathogenesis, and diagnosis of recurrent bacterial meningitis . In: Clinical Microbiology Reviews . tape 21 , no. 3 , July 2008, p. 519-537 , doi : 10.1128 / CMR.00009-08 , PMID 18625686 , PMC 2493086 (free full text).
- ↑ a b c G. Thwaites, TT Chau, NT Mai, F. Drobniewski, K. McAdam, J. Farrar: Tuberculous meningitis . In: Journal of Neurology, Neurosurgery, and Psychiatry . tape 68 , no. 3 , March 2000, p. 289-299 , doi : 10.1136 / jnnp.68.3.289 , PMID 10675209 , PMC 1736815 (free full text).
- ↑ Karl Wurm, AM Walter: Infectious Diseases. 1961, p. 181 f.
^ W. Böcker et al .: Pathology. Urban & FischerVerlag, 2008, ISBN 978-3-437-42382-6 , p. 286, books.google.de
Bankl H et al .: Workbook Pathology, Volumes 2-3. Facultas Verlag, 2000, ISBN 3-85076-536-9 , pp. 375 ff. + 501, books.google.de
- ↑ M. Douvoyiannis, N. Litman, DL Goldman: Neurologic manifestations associated with parvovirus B19 infection. In: Clin. Infect. Dis. (2009) 48 (12), pp. 1713-1723 PMID 19441978 .
- ↑ HW Doerr, WH Gerlich (ed.): Medical Virology. 2nd Edition. Stuttgart 2010, ISBN 978-3-13-113962-7 , pp. 206ff.
- ↑ V. Chotmongkol: Comparison of prednisolone plus albendazole with prednisolone alone for treatment of patients with eosinophilic meningitis. In: Am J Trop Med Hyg. 2009/81/3, p. 443ff. PMID 19706911
- ↑ C. Panackel et al .: Eosinophilic meningitis due to Angiostrongylus cantonensis. In: Ind J Med Microbio. 2006/24/3, pp. 220ff. PMID 16912445 .
- ^ PF Weller et al .: Eosinophilic meningitis. In: Semin Neurol. 1993/13/2, pp. 161-168, PMID 8356350
- ↑ MJ Schermoly et al .: Eosinophilia in coccidioidomycosis. In: Arch. Intern. Med. 1988/148/4, pp. 895-896, PMID 3355309
- ↑ Heinz-Walter Delank: Neurology. 5th, revised and supplemented edition. Enke, Stuttgart 1988, ISBN 3-432-89915-7 , p. 141 ( chronic lymphocytic meningitis ).
- ^ MC Chamberlain: Neoplastic meningitis . In: Journal of Clinical Oncology . tape 23 , no. May 15 , 2005, p. 3605-3613 , doi : 10.1200 / JCO.2005.01.131 , PMID 15908671 .
- ^ G. Moris, JC Garcia-Monco: The Challenge of Drug-Induced Aseptic Meningitis . In: Archives of Internal Medicine . tape 159 , no. 11 , June 1999, p. 1185-1194 , doi : 10.1001 / archinte.159.11.1185 , PMID 10371226 .
- ↑ Karl Wurm, AM Walter: Infectious Diseases. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition, ibid. 1961, pp. 9-223, here: pp. 177-180.
- ↑ SA Logan, E. MacMahon: Viral meningitis. In: BMJ. 2008 Jan 5; 336 (7634), pp. 36-40. PMID 18174598 .
- ↑ DN Irani: Aseptic meningitis and viral myelitis. In: Neurol Clin. 2008 Aug; 26 (3), pp. 635-655, vii-viii. PMID 18657719
- ↑ L. Kupila, T. Vuorinen, R. Vainionpää, V. Hukkanen, RJ Marttila, P. Kotilainen: Etiology of aseptic meningitis and encephalitis in an adult population. In: Neurology . 2006 Jan 10; 66 (1), pp. 75-80. PMID 16401850 .
- ^ HA Rotbart: Viral meningitis. In: Semin Neurol. 2000; 20 (3), pp. 277-292. PMID 11051293 .
- ↑ AG Michos, VP Syriopoulou, C. Hadjichristodoulou, GL Daikos, E. Lagona, P. Douridas, G. mostrou, M. Theodoridou: Aseptic meningitis in children: analysis of 506 cases. In: PLOS ONE . 2007 Aug 1; 2 (7), p. E674. PMID 17668054 .
- ↑ cdc.gov
- ↑ R. Kumar: Aseptic meningitis: diagnosis and management. In: Indian J Pediatr. 2005 Jan; 72 (1), pp. 57-63. PMID 15684450
- ↑ DN Irani: Aseptic meningitis and viral myelitis. In: Neurol Clin. 2008 Aug; 26 (3), pp. 635-655, vii-viii. PMID 18657719 .
- ↑ R. Shahien, V. Vieksler, A. Bowirrat: amoxicillin-induced aseptic meningoencephalitis. In: Int J Gen Med. 2010 Jul 21; 3, pp. 157-162. PMID 20689687 .
- ↑ G. Moris, JC Garcia-Monco: The challenge of drug-induced aseptic meningitis. In: Arch Intern Med. 1999 Jun 14; 159 (11), pp. 1185-1194. Review. PMID 10371226 .
- ^ H. Peltola, PS Kulkarni, SV Kapre, M. Paunio, SS Jadhav, RM Dhere: Mumps outbreaks in Canada and the United States: time for new thinking on mumps vaccines. In: Clin Infect Dis. 2007 Aug 15; 45 (4), pp. 459-466. Epub 2007 Jul 10. PMID 17638194 .
- ^ MC Chamberlain: Neoplastic meningitis. In: Oncologist. 2008 Sep; 13 (9), pp. 967-977. Epub 2008 Sep 5th Review. PMID 18776058
- ^ RL Zheng, H. Lv, W. Zhang, MX Yu, Y. Yuan: Rheumatoid leptomeningitis: a case report and literature review. In: Beijing Da Xue Xue Bao. 2006 Jun 18; 38 (3), pp. 324-325. PMID 16778982 .
- ^ RA Avery, G. Frank, JJ Glutting, SC Eppes: Prediction of Lyme meningitis in children from a Lyme disease-endemic region: a logistic-regression model using history, physical, and laboratory findings. In: Pediatrics . 2006 Jan; 117 (1), pp. E1 – e7. PMID 16396843 .
- ↑ J. Perevoscikovs, A. Brila, L. Firstova, T. Komarova, I. Lucenko, J. Osmjana, L. Savrasova, I. Singarjova, J. Storozenko, N. Voloscuka, N. Zamjatina: Ongoing outbreak of aseptic meningitis in South-Eastern Latvia, June - August 2010. In: Eurosurveillance . 2010 Aug 12; 15 (32). pii, p. 19639. PMID 20738995 .
- ↑ D. van de Beek, J. de Gans, L. Spanjaard, M. Weisfelt, JB Reitsma, M. Vermeulen: Clinical features and prognostic factors in adults with bacterial meningitis . In: The New England Journal of Medicine . tape 351 , no. October 18 , 2004, p. 1849-1859 , doi : 10.1056 / NEJMoa040845 , PMID 15509818 .
- ↑ KE Thomas, R. Hasbun, J. Jekel, VJ Quagliarello: The diagnostic accuracy of Kernig's sign, Brudzinski's sign, and nuchal rigidity in adults with suspected meningitis . In: Clinical Infectious Diseases . tape 35 , no. 1 , July 2002, p. 46-52 , doi : 10.1086 / 340979 , PMID 12060874 .
- ↑ a b c U. Theilen, L. Wilson, G. Wilson, JO Beattie, S. Qureshi, D. Simpson: Management of invasive meningococcal disease in children and young people: Summary of SIGN guidelines . In: BMJ (Clinical research ed.) . tape 336 , no. 7657 , June 2008, p. 1367-1370 , doi : 10.1136 / bmj.a129 , PMID 18556318 , PMC 2427067 (free full text). Full guideline page ( memento of the original from July 19, 2011 in the Internet Archive ) Info: The archive link was automatically inserted and not yet checked. Please check the original and archive link according to the instructions and then remove this notice.
- ↑ a b c d e f g S. A. Logan, E. MacMahon: Viral meningitis . In: BMJ (Clinical research ed.) . tape 336 , no. 7634 , January 2008, p. 36-40 , doi : 10.1136 / bmj.39409.673657.AE , PMID 18174598 , PMC 2174764 (free full text).
- ↑ a b c d X. Sáez-Llorens, GH McCracken: Bacterial meningitis in children. In: Lancet. 2003, vol. 361/9375, pp. 2139-2148 PMID 12826449
- ^ J. Varon, K. Chen, GL Sternbach: Rupert Waterhouse and Carl Friderichsen: adrenal apoplexy. In: J Emerg Med. 1998, vol. 16/4, pp. 643-647. PMID 9696186
- ↑ a b c d D. van de Beek, J. de Gans, AR Tunkel, EF Wijdicks: Community-acquired bacterial meningitis in adults. In: The New England Journal of Medicine . vol. 354/1, pp. 44-53, 2006, PMID 16394301
- ↑ AR Tunkel, BJ Hartman, SL Kaplan, et al .: Practice guidelines for the management of bacterial meningitis. In: Clinical Infectious Diseases, vol. 39/9, pp. 1267-1284, 2004, PMID 15494903
- ↑ D. Philippon, F. Bergeron, P. Ferron, R. Bussières: Cochlear implantation in postmeningitic deafness. In: Otol Neurotol. 2010 Jan; 31 (1), pp. 83-87. PMID 20050267
- ↑ P. Merkus, RH Free, EA Mylanus, R. Stokroos, M. Metselaar, E. van Spronsen, W. Grolman, JH Frijns: Dutch Cochlear Implant Group (CI-ON) consensus protocol on postmeningitis hearing evaluation and treatment. In: Otol Neurotol. 2010 Oct; 31 (8), pp. 1281-1286. PMID 20814346
- ^ Drew Provan, Andrew Krentz: Oxford Handbook of Clinical and Laboratory Investigation . Oxford University Press, Oxford 2005, ISBN 0-19-856663-8 .
- ↑ a b c d e f g h i j A. Chaudhuri et al .: EFNS guideline on the management of community-acquired bacterial meningitis: report of an EFNS Task Force on acute bacterial meningitis in older children and adults. In: European Journal of Neurolology. 2008 15/7, pp. 649-659, PMID 18582342 .
- ↑ a b c d S. E. Straus et al .: How do I perform a lumbar puncture and analyze the results to diagnose bacterial meningitis? In: JAMA (Journal of the American Medical Association). 2006 296/16, pp. 2012-2022, PMID 17062865 .
- ↑ a b c d e R. S. Heyderman et al .: Early management of suspected bacterial meningitis and meningococcal septicaemia in adults. In: The Journal of infection. 2003/46/2, pp. 75-77, PMID 12634067 - Guideline Early management of suspected meningitis and meningococcal septicaemia in immunocompetent adults. the British Infection Society & UK Meningitis Research Trust, 2004, pdf ( Memento of March 27, 2009 in the Internet Archive )
- ↑ Ali Yikilmaz, George A. Taylor: Sonographic findings in bacterial meningitis in neonates and young infants. In: Pediatric Radiology. 38 (2008), pp. 129-137, doi: 10.1007 / s00247-007-0538-6
- ^ I. Maconochie, H. Baumer, ME Stewart: Fluid therapy for acute bacterial meningitis . In: Cochrane Database Syst Rev . No. 1 , 2008, p. CD004786 , doi : 10.1002 / 14651858.CD004786.pub3 , PMID 18254060 .
- ^ PF Weller, LX Liu: Eosinophilic meningitis . In: Semin Neurol . tape 13 , no. 2 , June 1993, p. 161-168 , PMID 8356350 .
- ^ Herbert Renz-Polster , Steffen Krautzig: Basic textbook internal medicine . 4th edition. Elsevier / Urban & Fischer, 2008, ISBN 978-3-437-41053-6 , pp. 1185 .
- ^ A b T. Bicanic, TS Harrison: Cryptococcal meningitis . In: British Medical Bulletin . tape 72 , 2004, p. 99-118 , doi : 10.1093 / bmb / ldh043 , PMID 15838017 ( oxfordjournals.org ).
- ↑ MS Saag, RJ Graybill, RA Larsen et al .: Practice guidelines for the management of cryptococcal disease. Infectious Diseases Society of America . In: Clin. Infect. Dis. tape 30 , no. 4 , April 2000, pp. 710-718 , doi : 10.1086 / 313757 , PMID 10770733 .
- Jump up ↑ D. Sloan, S. Dlamini, N. Paul, M. Dedicoat: Treatment of acute cryptococcal meningitis in HIV infected adults, with an emphasis on resource-limited settings . In: Cochrane Database Syst Rev . No. 4 , 2008, p. CD005647 , doi : 10.1002 / 14651858.CD005647.pub2 , PMID 18843697 .
- ↑ A. David et al .: Oxford Textbook of Medicine Volume One. Oxford Press, 2003, ISBN 0-19-852787-X , pp. 1115-1129.
- ^ A b c d e f S. Segal, AJ Pollard: Vaccines against bacterial meningitis . In: British Medical Bulletin . tape 72 , 2004, p. 65-81 , doi : 10.1093 / bmb / ldh041 , PMID 15802609 .
- ↑ a b H. Peltola: Worldwide Haemophilus influenzae type b disease at the beginning of the 21st century: global analysis of the disease burden 25 years after the use of the polysaccharide vaccine and a decade after the advent of conjugates. In: Clinical microbiology reviews. Volume 13, Number 2, April 2000, pp. 302-317, ISSN 0893-8512 . PMID 10756001 . PMC 100154 (free full text). (Review).
- ^ LH Harrison: Prospects for vaccine prevention of meningococcal infection. In: Clinical microbiology reviews. Volume 19, Number 1, January 2006, pp. 142-164, ISSN 0893-8512 . doi: 10.1128 / CMR.19.1.142-164.2006 . PMID 16418528 . PMC 1360272 (free full text). (Review).
- ↑ a b A. Wilder-Smith: Meningococcal vaccine in travelers . In: Current Opinion in Infectious Diseases . tape 20 , no. 5 , October 2007, p. 454-460 , doi : 10.1097 / QCO.0b013e3282a64700 , PMID 17762777 .
- ↑ a b Ärzteblatt from January 19, 2012: Vaccine against meningitis B effective ( memento of the original from January 24, 2012 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice.
- ↑ T. Vesikari, S. Esposito, R. Prymula, E. Ypma, A. Kleinschmidt, D. Toneatto, A. Kimura, P. Dull: Use of an investigational multicomponent meningococcal serogroup B vaccine (4CMenB) in a clinical trial in 3630 infants. In: Archives of Disease in Childhood . 96, 2011, pp. A3-A3, doi: 10.1136 / adc.2011.212563.6 .
- Jump up ↑ ME Santolaya, ML O'Ryan, MT Valenzuela, V. Prado, R. Vergara, A. Muñoz, D. Toneatto, G. Graña, H. Wang, R. Clemens, PM Dull: Immunogenicity and tolerability of a multicomponent meningococcal serogroup B (4CMenB) vaccine in healthy adolescents in Chile: a phase 2b / 3 randomized, observer-blind, placebo-controlled study. In: Lancet. Volume 379, Number 9816, February 2012, pp. 617-624, ISSN 1474-547X . doi: 10.1016 / S0140-6736 (11) 61713-3 . PMID 22260988 .
- ↑ Clinical and Vaccine Immunology 2011; 18, pp. 483-486.
- ↑ First meningococcal B vaccine approved . In: Pharmaceutical newspaper . January 23, 2013.
- ↑ a b M. Weisfelt, J. de Gans, T. van der Poll, D. van de Beek: Pneumococcal meningitis in adults: new approaches to management and prevention . In: Lancet Neurol . tape 5 , no. 4 , April 2006, p. 332-342 , doi : 10.1016 / S1474-4422 (06) 70409-4 , PMID 16545750 .
- ↑ A. Fraser, A. Gafter-Gvili, M. Paul, L. Leibovici: Antibiotics for preventing meningococcal infections . In: Cochrane Database of Systematic Reviews (Online) . No. 4 , 2006, p. CD004785 , doi : 10.1002 / 14651858.CD004785.pub3 , PMID 17054214 .
- ↑ K. Prasad, MB Singh: Corticosteroids for managing tuberculous meningitis . In: Cochrane Database of Systematic Reviews (Online) . No. 1 , 2008, p. CD002244 , doi : 10.1002 / 14651858.CD002244.pub3 , PMID 18254003 .
- ↑ AM Assiri, FA Alasmari, VA Zimmerman, LM Baddour, PJ Erwin, IM Tleyjeh: Corticosteroid administration and outcome of adolescents and adults with acute bacterial meningitis: a meta-analysis . In: Mayo Clin. Proc. tape 84 , no. 5 , May 2009, p. 403-409 , doi : 10.4065 / 84.5.403 , PMID 19411436 , PMC 2676122 (free full text).
- ↑ J. de Gans, D. van de Beek: Dexamethasone in adults with bacterial meningitis . In: The New England Journal of Medicine . tape 347 , no. 20 , November 2002, p. 1549-1556 , doi : 10.1056 / NEJMoa021334 , PMID 12432041 .
- ↑ D. van de Beek, J. de Gans, P. McIntyre, K. Prasad: Corticosteroids for acute bacterial meningitis . In: Cochrane Database of Systematic Reviews (Online) . No. 1 , 2007, p. CD004405 , doi : 10.1002 / 14651858.CD004405.pub2 , PMID 17253505 .
- ^ PB McIntyre, CS Berkey, SM King et al .: Dexamethasone as adjunctive therapy in bacterial meningitis. A meta-analysis of randomized clinical trials since 1988 . In: JAMA . tape 278 , no. September 11 , 1997, pp. 925-931 , doi : 10.1001 / jama.278.11.925 , PMID 9302246 .
- ↑ Meningitis and Encephalitis Fact Sheet. National Institute of Neurological Disorders and Stroke (NINDS), December 11, 2007, accessed April 27, 2009 .
- ↑ M. Gottfredsson, JR Perfect: Fungal meningitis . In: Seminars in Neurology . tape 20 , no. 3 , 2000, pp. 307-322 , doi : 10.1055 / s-2000-9394 , PMID 11051295 .
- ↑ C. Roed, L. Omland, P. Skinhoj, KJ Rothman, H. Sorensen, N. Obel: Educational Achievement and Economic Self-sufficiency in Adults After Childhood Bacterial Meningitis. In: JAMA. 2013; 309 (16), pp. 1714-1721. doi: 10.1001 / jama.2013.3792 .
- ^ MP Richardson, A. Reid, MJ Tarlow, PT Rudd: Hearing loss during bacterial meningitis . In: Archives of Disease in Childhood . tape 76 , no. 2 , February 1997, p. 134-138 , doi : 10.1136 / adc.76.2.134 , PMID 9068303 , PMC 1717058 (free full text).
- ↑ Mortality and Burden of Disease Estimates for WHO Member States in 2002. (xls; 3.0 MB) In: World Health Organization. 2002, accessed January 12, 2011 .
- ↑ a b World Health Organization: Control of epidemic meningococcal disease, practical guidelines, 2nd edition, WHO / EMC / BA / 98 . tape 3 , 1998, p. 1-83 ( who.int [PDF]).
- ^ B. Greenwood: Manson Lecture. Meningococcal meningitis in Africa . In: Trans. R. Soc. Trop. Med. Hyg. Band 93 , no. 4 , 1999, p. 341-353 , PMID 10674069 .
- ^ WHO: Detecting meningococcal meningitis epidemics in highly-endemic African countries . In: Weekly Epidemiological Record . tape 78 , no. 33 , 2003, p. 294-296 , PMID 14509123 ( who.int [PDF]).
- ^ Meningococcal Disease: situation in the African Meningitis Belt. WHO, accessed March 29, 2009 .
- ↑ a b Kenneth L. Tyler: A history of bacterial meningitis. In: S. Finger, F. Boller, KL Tyler (Eds.): History of Neurology . Elsevier, 2010, ISBN 978-0-444-52009-8 , p. 417.
- ^ A b Arthur Earl Walker, Edward R. Laws, George B. Udvarhelyi: The Genesis of Neuroscience . Thieme, 1998, ISBN 1-879284-62-6 , Infections and inflammatory involvement of the CNS, p. 219-221 .
- ↑ Kenneth L. Tyler: A history of bacterial meningitis. In: S. Finger, F. Boller, KL Tyler (Eds.): History of Neurology . Elsevier, 2010, ISBN 978-0-444-52009-8 , p. 418.
- ^ Whytt R: Observations on the Dropsy in the Brain . J. Balfour, Edinburgh 1768.
- ↑ a b c B. Greenwood: 100 years of epidemic meningitis in West Africa - has anything changed? In: Tropical Medicine & International health: TM & IH . tape 11 , no. 6 , June 2006, p. 773-780 , doi : 10.1111 / j.1365-3156.2006.01639.x , PMID 16771997 .
- ^ G. Vieusseux: Memoire sur la maladie qui regnéà Geneve au printemps de 1805 . In: Journal de Médecine, de Chirurgie et de Pharmacologie (Bruxelles) . tape 11 , 1806, pp. 50-53 .
- ↑ A. Weichselbaum: About the etiology of acute cerebro-spinal meningitis . In: Progress of Medicine . tape 5 , 1887, p. 573-583 .
- ^ S. Flexner: The results of the serum treatment in thirteen hundred cases of epidemic meningitis . In: J Exp Med . tape 17 , 1913, pp. 553-576 , doi : 10.1084 / Jem.17.5.553 .
- ↑ a b M. N. Swartz: Bacterial meningitis - a view of the past 90 years . In: The New England Journal of Medicine . tape 351 , no. October 18 , 2004, p. 1826-1828 , doi : 10.1056 / NEJMp048246 , PMID 15509815 .
- ↑ DH Rosenberg, PA Arling: Penicillin in the treatment of meningitis . In: JAMA . tape 125 , 1944, pp. 1011-1017 . reproduced in DH Rosenberg, PA Arling: Penicillin in the treatment of meningitis . In: JAMA . tape 251 , no. April 14 , 1984, pp. 1870-1876 , doi : 10.1001 / jama.251.14.1870 , PMID 6366279 .
- ^ Illnesses subject to notification in Austria by the Federal Ministry for Social Affairs, Health, Care and Consumer Protection, as of January 2020 (PDF, 4 pages, tabular representation)