Meningitis
Meningitis is an infection characterized by inflammation of the meninges (leptomeninges) that in 80% of cases is caused by viruses, in 15 to 20% by bacteria and in the rest of the cases it is due to poisoning, fungi, medicines and other diseases. It is a rare but potentially lethal condition that can injure the brain and lead to unconsciousness and damage to other organs.
Meningitis progresses very quickly, so early diagnosis and early treatment are important to prevent serious sequelae and avoid death.
Anyone can get meningitis, but the frequency of the disease is especially high in children and immunosuppressed people. The most frequent symptoms are headache, neck stiffness, fever, photophobia (abnormal intolerance to light) or phonophobia (intolerance to sounds), and disturbances of consciousness. Often, particularly in young children, only nonspecific symptoms such as irritability and drowsiness are present. The existence of a skin rash may indicate a particular form of meningitis, such as that associated with meningococcemia.
Classification
Meningitis can be classified in various ways based on its etiology, culture techniques, or clinical aspects. The classification can also be based on the evolutionary course of the process and in this case the disease will be categorized as acute (less than forty-eight hours), subacute (three to seven days of evolution) or chronic (more than four weeks). According to one author, this classification is not useful in medical practice and it is best to use the one that is most convenient for the therapeutic approach of patients. According to the classification based on etiology, meningitis can be divided into bacterial, tuberculous, aseptic, viral and related.
Organisms that cause bacterial meningitis include Neisseria meningitidis, Haemophilus influenzae, Streptococcus pneumoniae, group B streptococci, Listeria monocytogenes, gram-negative bacilli and others (Staphylococcus aureus and Staphylococcus epidermidis).
As for tuberculous meningitis and the like, the causative pathogens include Mycobacterium tuberculosis, Cryptococcus neoformans, other fungi, parasites, etc.
Lastly, aseptic or viral and related meningitis are due to viruses, Leptospira sp., Treponema pallidum , a partially treated bacterial meningitis, suppurative parameningeal foci and systemic diseases (eg, lymphoma, leukemia, and others).
Historical considerations
Some authors suggest that Hippocrates would have been aware of the existence of meningitis, and pre-Renaissance physicians, such as Avicenna, appear to have been aware of meningism.
The description of tuberculous meningitis, then called “cerebral dropsy”, is often attributed to an Edinburgh physician, Sir Robert Whytt, in a posthumous report that appeared in 1768, although the association with tuberculosis and the causative pathogen did not materialize until a century later.
Epidemic meningitis appears to be a relatively recent phenomenon. The first recorded major outbreak occurred in Geneva in 1805, and a paper on meningococcus also reports that in that year the physician Gaspard Vieusseux described the clinical picture of "epidemic meningitis" during an outbreak of meningitis that caused thirty-three deaths near Geneva, Switzerland. Shortly thereafter several other epidemics were described in Europe and the United States, and in 1840 the first report of an epidemic appeared. in Africa. In the 20th century African epidemics of meningitis became much more frequent, starting with a major one that ravaged Nigeria and Ghana in 1905-1908.
The first communication of a case of meningitis secondary to a bacterial infection was published by the Austrian bacteriologist Anton Weichselbaum, who in 1887 described meningococcus. In the first reports, mortality from meningitis was very high (over 90 percent).). Equine antiserum was produced in 1906, which was later improved by the American scientist Simon Flexner and significantly decreased mortality from meningococcal disease.
Between 1928 and 1945 there were numerous epidemics (Detroit 1928-1929, Milwaukee 1927-1929, Chile 1941-1943), with fatality rates reaching fifty percent. In the early 1930s the pathologist and German bacteriologist Gerhard Domagk discovered that the sulfonamide Prontosil protected laboratory mice against streptococci of the species Streptococcus pyogenes. Towards the end of that decade it was reported that the treatment of acute meningitis with sulfonamides had succeeded in reducing the fatality rate by fifteen percent. In addition, sulfonamides began to be used successfully to prevent the disease in contacts of people with meningitis. However, in less than five years the microorganism became resistant to that drug.In 1943 the Scottish physician Alexander Fleming reported the discovery of penicillin, for which he received the Nobel Prize. The efficacy of penicillin in the treatment of meningitis was first reported in 1944. However, it was soon found that neither sulfonamides nor penicillin were sufficient to control the problem in the population.
The introduction of Haemophilus vaccines at the end of the 20th century led to a significant reduction in cases of meningitis associated with this pathogen, and in 2002 it was reported that treatment with steroids improved the prognosis of patients with bacterial meningitis.
Epidemiology
Although meningitis is a notifiable disease in many countries, the exact incidence rate is unknown. In 2013, the disease was the cause of 303,000 deaths—fewer than the 464,000 it caused in 1990 —. Estimated deaths from meningitis in 2010 amounted to 420,000, not counting cases of cryptococcal meningitis.
In Western countries, bacterial meningitis affects about three people in a hundred thousand per year. Population studies have shown that viral meningitis is more common (affects 10.9 people per 100,000) and occurs more frequently in summer. In Brazil, the rate of bacterial meningitis is higher (affecting 45.8 people per 100,000 per year). Sub-Saharan Africa has been plagued by large epidemics of meningococcal meningitis for more than a century, leading to its called the "meningitis belt". Typically, epidemics occur in the dry season (December to June) and an epidemic wave lasts two to three years, with interruptions during the intervening rainy seasons. Medical care is scarce in this area and there are rates of attack of one hundred to eight hundred cases per hundred thousand, mostly caused by meningococci. The largest recorded epidemic in history devastated the entire region in the period 1996-1997 and caused more than two hundred and fifty thousand cases and twenty-five thousand deaths.
Meningococcal disease occurs in epidemics in places where many people live together for the first time, such as army barracks during mobilizations, college campuses, and the annual pilgrimage to Mecca (Hajj). The pattern of cycles epidemics in Africa is not well understood, but there are several factors thought to be associated with the development of epidemics in the meningitis belt; These include medical conditions (immune susceptibility of the population), demographic conditions (travel and displacement of large populations), socioeconomic conditions (overcrowding and poor living conditions), climatic conditions (droughts and dust storms), and concurrent infections (respiratory infections sharp).
There are significant differences in the local distribution of the different types of bacterial meningitis. For example, while Neisseria meningitidis serogroups B and C cause the majority of disease episodes in Europe, serogroup A is found in Asia and continues to dominate in Africa, where it is the cause of most large epidemics occur in the meningitis belt, accounting for about eighty to eighty-five percent of documented meningococcal meningitis cases.
Causes
As already mentioned, in typical cases meningitis is secondary to an infection by pathogenic microorganisms. In turn, most of these infections are due to viruses and, secondly, to bacteria, fungi and protozoa. In some cases, meningitis can be the consequence of non-infectious causes.
When in a patient with meningitis it is not possible to demonstrate a bacterial infection, we speak of aseptic meningitis, which is usually caused by a virus, but can also be secondary to a bacterial infection that has already been partially treated (so bacteria have disappeared from the meninges) or pathogens infecting a space adjacent to those structures (eg, in patients with sinusitis). Endocarditis (an infection of the heart valves in which small groups of bacteria spread through the bloodstream) can cause aseptic meningitis. There are also cases caused by spirochetes, such as Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (etiological agent of Lyme disease). There can be meningitis in cerebral malaria and there is also amebic meningitis, that is, meningitis caused by an infection by amoebas - such as Naegleria fowleri - contracted from freshwater sources.
The bacteria that cause meningitis vary depending on the age of the infected person. Thus, for example, in preterm infants and infants up to three months of age, the common etiologic agents are group B serotype III streptococci (which are normal inhabitants of the vagina and a main etiology during the first week of life). and bacteria that normally reside in the digestive tract, such as Escherichia coli (which carries the K1 antigen). Listeria monocytogenes (serotype b) is transmitted by the mother before birth and can cause meningitis in the newborn.
In older children the most common etiological agents are Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) in so much so that Haemophilus influenzae type B is more frequent in those under five years of age (in countries that do not have vaccines).
As for adults, eighty percent of cases of bacterial meningitis are due to infections caused by Neisseria meningitidis and Streptococcus pneumoniae. The risk of infection by Listeria monocytogenes is highest in people over the age of fifty. Recent head trauma may cause bacteria present in the nasal passages to enter the meningeal space. Also, the presence of devices in the brain and meninges, such as a brain shunt, extraventricular drain, or Ommaya reservoir, increases the risk of meningitis. In such cases the likelihood of infection by staphylococci, Pseudomonas and other gram-negative bacteria is increased. These pathogens also cause meningitis in immunodeficient persons. In a small proportion of cases the development of an infection in the head and neck area (eg, otitis media or mastoiditis) can lead to meningitis. Patients with cochlear implants due to hearing loss are at increased risk of pneumococcal meningitis.
Pathogenesis (Route of Entry)
Bacteria reach the meninges in three ways, namely, by hematogenous route, directly through natural or artificial breaks, and by contiguity extension from a nearby suppurative focus.
The first form is the most frequent. The microorganisms that cause eighty percent of cases of meningitis, that is, N. meningitidis, S. pneumoniae and H. influenzae, are regular residents of the nasopharynx and oropharynx, where they normally do no harm. However, for unknown reasons, from time to time they pass into the blood and by this route reach the meninges and colonize them. As these microorganisms are encapsulated, it is possible that the encapsulation, with its antiphagocytic property, is related to some way with dissemination. In addition, the capsular polysaccharide would confer a certain meningeal tropism on the germs, perhaps due to the presence of surface receptors in the meninges, but this is speculation since none of this has been proven. Sometimes before the invasion of the bloodstream Viral infections of the upper respiratory tract occur, but their role as promoters of blood invasion is doubtful. The failure of some of the host's defense mechanisms against aggression explains the predisposition to certain infections. Thus, for example, sickle cell anemia, asplenia, congenital or acquired immunoglobulin deficiencies, and alcoholism predispose to S. pneumoniae. Microorganisms often reach the meninges from other points of origin, as in the case of S. pneumoniae, which can come from a pulmonary focus, from S. aureus, which can do so from endocarditis, and gram-negatives, whose points of origin can be the digestive tract and the genitourinary system.
The second way, as already mentioned, is the direct arrival of the pathogenic agents to the meninges through natural (myelomeningocele) or artificial (skull fractures, fissures of the ethmoid cribriform plate, surgical interventions)., ventriculoatrial shunts, or a lumbar puncture).
The third form is contiguity spread from a nearby suppurative focus, such as the paranasal sinuses, a suppurative mastoiditis, or the rupture of a brain abscess in the meninges. Some authors think that it is possible that microorganisms move from the nasopharynx to the meninges through the venules in a direct intracranial route.
The meninges are three membranes that, together with cerebrospinal fluid, enclose and protect the brain and spinal cord (ie, the central nervous system). The pia mater is a very delicate impermeable membrane that adheres firmly to the brain surface and is continuous throughout the lesser gyri. The arachnoid (so named because of its spider web-like appearance) is a loose sac on top of the pia mater. The subarachnoid space separates the arachnoid and pia mater and is filled with cerebrospinal fluid. The outermost, the dura mater, is a thick, tough membrane that attaches to both the arachnoid and the skull.
In bacterial meningitis, bacteria reach the meninges by one of two main routes, namely through the bloodstream or by direct contact between the meninges and the nasal cavity or skin. In most cases, meningitis is secondary to invasion of the bloodstream by microorganisms that reside on mucosal surfaces such as the nasal cavity. That invasion, in turn, is usually preceded by viral infections that break the normal barrier provided by mucosal surfaces. Once inside the bloodstream, the bacteria enter the subarachnoid space at sites where the blood-brain barrier is vulnerable, such as the choroid plexus. Meningitis occurs in 25 percent of newborns with group B strep bloodstream infections; this phenomenon is less common in adults. Direct contamination of cerebrospinal fluid can originate from indwelling devices, skull fractures, or infections of the nasopharynx or sinuses that have formed a tract with the subarachnoid space; sometimes it is possible to identify congenital defects of the dura mater.
The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection, but can be largely attributed to the immune system's response to bacterial entry into the nervous system central. When the components of the bacterial cell membrane are identified by the brain's immune system cells (astrocytes and microglia), they respond by releasing large amounts of cytokines, hormone-like mediators that recruit other immune system cells and stimulate other tissues. to engage in a defensive response. The blood-brain barrier becomes more permeable, leading to "vasogenic" (swelling of the brain due to leakage of fluid from the blood vessels). The entry of large numbers of leukocytes into the CSF causes inflammation of the meninges and leads to "interstitial" (edema due to intercellular fluid). In addition, the very walls of the blood vessels become inflamed (cerebral vasculitis), which leads to decreased blood flow and a third type of edema, the so-called "cytotoxic" edema. All three forms of cerebral edema just mentioned lead to increased intracranial pressure; this increase, along with the drop in blood pressure that often accompanies acute infection, makes it difficult for blood to enter the brain, resulting in a starvation of oxygen to brain cells, which therefore undergo apoptosis (programmed cell death).
It is recognized that the administration of antibiotics initially may worsen the described process by increasing the amount of bacterial cell membrane products released as a result of killing the bacteria. To dampen the response of the immune system to this phenomenon, certain treatments are used, particularly the one based on the use of corticosteroids.
Pathology
Meningitis can be diagnosed post mortem. Autopsy findings usually consist of generalized swelling of the pia and arachnoid mater. Neutrophils have often migrated into the CSF and the base of the brain, along with the cranial nerves and spinal cord, may be surrounded by pus, as are the meningeal vessels.
In meningitis, inflammation can affect the pachymeninges or the leptomeninges. The most important are leptomeningitis. The etiological agents can be bacteria, fungi and viruses. Viral meningitis has a benign course and the inflammatory infiltrate they cause is dominated by lymphocytes after a short-lived leukocyte infiltration.
Macroscopic examination of autopsy material obtained from a patient who died of purulent meningitis reveals a swollen brain, engorged blood vessels, and the leptomeningeal space with purulent exudate, particularly on the convexity. When the exudate is not very abundant, it is found above all next to the vessels, along which it extends in the form of thin yellowish bands. The exudate also tends to accumulate in the cisterns and when abundant forms a continuous layer in the subarachnoid space. Typically, it is also found in the ventricular system. The exudate is mainly composed of polynuclear cells with variable amounts of fibrin. If it is not reabsorbed in the first week, in the second week lymphocytes and plasma cells will appear and in the third there will be granulation tissue.
In tuberculous meningitis, the inflammatory process develops characteristically in the meninges at the base of the brain and tends to also compromise the superficial brain tissue; it can be predominantly caseous or predominantly productive. In the first case the exudate is pale greenish yellowish in color and greasy in appearance, sometimes somewhat glassy. Very often there is involvement of the vessels; a productive endarteritis or thrombosis occurs in the arteries, which can lead to heart attacks. Ependymitis is also common. As in other tuberculosis isolated from organs, tuberculous meningitis can be the starting point of generalized miliary tuberculosis.
In the autopsy of patients who have died from bacterial meningitis, a purulent exudate is observed that covers the cerebral cortex and is more abundant in the sulci, at the base of the brain, and in the spinal cord; there is also cerebral edema, polymorphonuclear leukocyte infiltrate in the leptomeninges, and dilation and thrombosis of the capillaries, venules, and major vessels.
The purulent exudate from the meninges is discharged into the CSF and through the subarachnoid space it spreads throughout the central nervous system to later accumulate in the basal cisterns and inside the cerebral sulci. The outer subarachnoid membrane contains inflammation very effectively, but in 15% of children with bacterial meningitis, subdural effusions form, usually sterile, and sometimes become infected and develop into subdural empyemas.
The pia mater also acts as an efficient barrier that prevents infection of the cerebral and underlying gray matter. Meningeal inflammation affects the structures that traverse the subarachnoid space, such as veins, arteries, and cranial nerves, so that thrombophlebitis of the cortical veins with venous stasis and cerebral infarction can occur. The small arteries of the pia mater are also damaged, with formation of aneurysms and, again, stroke. For topographic reasons, the most damaged cranial nerves are III and VI.
Ventriculitis, which as already mentioned is constant in meningitis, rarely evolves into ventricular empyema. In contrast, CSF obstruction by adhesions within the ventricular system and subarachnoid space is somewhat more common and can lead to obstructive hydrocephalus. Communicating hydrocephalus is rare. In some very acute cases—almost all of them due to meningococcal meningitis—cerebral edema predominates with the possibility of cerebellar or temporal lobe herniation and danger of sudden death due to brainstem and spinal cord compression.
Clinical picture
Meningitis is an important cause of fever in children and newborns, who in addition to that main symptom very soon develop chills, mental status changes, nausea and vomiting, abnormal sensitivity to light (photophobia), headache severe pain and a stiff neck (meningismus). In some cases there is also agitation, bulging fontanelles, decreased level of consciousness, anorexia or irritability (in children), rapid breathing, and an unusual posture with the head and neck arched back. As both types of meningitis present the same symptoms, in the presence of high fever and any of the other clinical manifestations, a doctor should be consulted as soon as possible.
According to another author, the disease typically begins abruptly with fever, severe headache, nausea and vomiting, back and neck pain, and general weakness. It is common to find a decreased level of consciousness and seizures. Rarely, initial symptoms consist of abdominal pain, delirium, or an acute confusional syndrome. Physical examination reveals a stiff neck and positive Kernig and Brudzinski signs; these classic symptoms of the meningeal syndrome are sometimes absent, both in the very young and in the elderly or if there is a degree of severe obtundation.
In addition to the classic meningeal syndrome, there are certain clinical characteristics that correspond to the various etiological forms. Thus, for example, in meningococcal meningitis, sometimes with a fulminant evolution, hemorrhagic skin lesions can be observed and, on occasions, circulatory failure. Although the presence of petechiae, purpuric syndrome, or ecchymosis in a patient with acute meningitis is almost synonymous with meningococcal meningitis—which guides immediate treatment—it must be remembered that, although very occasionally, S. pneumoniae and H. influenzae cause similar lesions.
Sometimes viral meningitis, especially those caused by Echovirus 9, are associated with purpuric lesions resembling those associated with Neisseria meningitidis. Pneumococcal meningitis should be suspected in patients with pulmonary infections, acute or chronic otitis media, purulent conjunctivitis, CSF rhinorrhea secondary to developmental abnormalities or trauma, sickle cell disease, alcoholism, or splenectomy.
H. influenzae often causes meningitis in young children with ear or upper respiratory tract infections. Finally, there are bacterial meningitis that are associated with more atypical clinical pictures. Thus, for example, the presence of meningitis in a patient with furunculosis or a recent neurosurgical procedure suggests a staphylococcal meningeal infection. Invasion of the meninges by Enterobacteriaceae, Listeria, Acinetobacter (ex Mima-Herellea) and Pseudomonas is seen favored by the presence of a brain abscess, diseases associated with immune deficiency, or cranial bone defects. Focal neurological deficits are rare and are seen more frequently in patients with H. influenzae and pneumococcal meningitis. In the latter, cranial nerve injuries are also common.
According to the CDC, the classic symptoms of bacterial meningitis appear suddenly or over a few days, but typically develop within three to seven days post-exposure.
In newborns and infants, the classic symptoms of meningitis such as fever, headache, and neck stiffness may be absent or difficult to identify. Infants may be inactive, irritable, vomiting, or anorexic. In newborns, other signs of meningitis that may be seen are bulging fontanelles or abnormal reflexes. Late symptoms of bacterial meningitis can be very severe (eg, seizures and coma).
Diagnosis
| Type of meningitis | Glucorraquia | Proteinoraquia | Cells |
|---|---|---|---|
| Acute Bacterial | Low | High | Polymorphonuclear (PMN), often (+34)300/mm3 |
| Acute vial | Normal | Normal or high | Mononuclear, ≥300/mm3 |
| Tuberculosa | Low | High | Mononuclear and PMN, ≥300/mm3 |
| Fungal | Low | High | ≥300/mm3 |
| Maligna | Low | High | Generally mononuclear |
Meningitis may be suspected based on symptoms, but it is diagnosed with a medical procedure called a lumbar puncture, which involves inserting a special needle into the spinal column to remove a sample of the cerebrospinal fluid that surrounds the brain and the spinal cord.
With few exceptions, there are insufficient differences between the clinical and laboratory findings associated with acute viral meningitis to permit an etiologic diagnosis, and distinguishing these disorders from a number of nonviral diseases can be difficult. However, it is important to differentiate acute viral meningitis, for which there is no specific treatment in immunocompetent individuals (except for herpes meningitis), from meningitis associated with treatable etiologies.
The main causes of aseptic meningitis are enteroviruses, and diagnosis continues to focus on confirming infection with these viruses or ruling out bacterial infection. Bacterial meningitis cannot be differentiated from aseptic meningitis on the basis of clinical features alone. The differential diagnosis of viral meningitis, which is very broad, is based on clinical presentation and CSF examination results including lymphocyte-predominant pleocytosis of less than 500 cells/µL, a normal glucose concentration, normal or slightly elevated protein level, and negative bacterial antigen detection tests. The CSF profile in drug-induced aseptic meningitis, including neutrophilic pleocytosis (one of the typical features of bacterial meningitis). which can convert CSF into true pus), does not allow differentiation of this disorder from infectious meningitis.
If implemented correctly, CSF nucleic acid tests are more sensitive than cultures for the diagnosis of enterovirus infections and can reduce cost and unnecessary treatment. Other findings, including the detection of low levels of tumor necrosis factor and lactic acid, add further validity to the diagnosis of aseptic rather than bacterial meningitis.
Differential diagnosis
There are several specialized tests that can be used to distinguish between different types of meningitis. A latex agglutination test may be positive in meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and group B streptococci; its routine use is not recommended because it rarely leads to changes in treatment, but it can be used if other tests are not diagnostic. The Limulus lysate test may be positive in meningitis caused by Gram-negative bacteria, but is of limited use unless other tests have been ineffective. Polymerase chain reaction (PCR, from polymerase chain reaction) is a technique used to amplify DNA residues bacterial in order to establish whether the DNA present in the CSF is bacterial or viral; it is a highly sensitive and specific test because only minute amounts of DNA of the infectious agent need to be tracked. It allows the identification of bacteria in bacterial meningitis and can help distinguish the different causes of viral meningitis (enterovirus, herpes simplex virus type 2 and mumps virus in patients not vaccinated against them). Serology (identification of antibodies against the virus) may be useful in viral meningitis. If tuberculous meningitis is suspected, the specimen is processed for Ziehl-Neelsen staining, which has low sensitivity, and culture for Mycobacterium tuberculosis, which it takes a long time to process. PCR is being used more and more. The diagnosis of cryptococcal meningitis can be established inexpensively by India ink staining of CSF, but tests to detect Cryptococcal antigen in blood or CSF are more sensitive, especially in people with AIDS.
Patients with meningitis who receive partial treatment and present with meningeal symptoms after receiving antibiotics (such as for suspected sinusitis) present a diagnostic and therapeutic challenge. In such cases, CSF findings may resemble those of viral meningitis, but antibiotic therapy may need to be continued until there is definitive positive evidence of a viral cause (eg, a PCR positive for enterovirus).
Treatment
Treatment must be immediate and include the administration of antibiotics in the case of bacterial meningitis or antivirals if the etiology is viral. In some cases, to prevent the sequelae of inflammation, the administration of corticosteroids such as dexamethasone is indicated, which tend to improve neurological evolution.
According to a Cuban work already mentioned, among the general measures for the treatment of patients with meningitis are the supportive measures necessary in any severe acute infection. Intensive care unit assistance may be essential in the first few hours to maintain adequate respiratory and hemodynamic functions, monitor fluid administration, control fever and seizures, and identify potential fluid and electrolyte or coagulation disorders and treat if necessary. they show up.
Forecast
Meningitis can be associated with serious long-term consequences, such as deafness, epilepsy, hydrocephalus, or cognitive impairment, especially in patients for whom treatment has been delayed. Certain vaccines can prevent some bacterial infections that cause meningitis.
Untreated bacterial meningitis is almost always fatal. In contrast, viral meningitis tends to self-limit and is rarely fatal. With treatment, mortality (the risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause. When the disease affects newborns, twenty to thirty percent of them may die from an episode of bacterial meningitis. That risk is much lower in older children, in whom the mortality rate is around 2 percent, but rises again to around 19 to 37 percent in adults. Risk prediction The rate of death is based on several factors other than age, such as the pathogen and the time it takes for it to be cleared from the CSF, the severity of generalized illness, a decreased level of consciousness or an abnormally low white blood cell count in the CSF. Meningitis caused by H. influenzae and meningococci have a better prognosis than infection secondary to group B streptococci, coliforms, and S. pneumoniae. In adults, meningococcal meningitis is also associated with lower mortality (3 to 7 percent) than that associated with pneumococcal disease.
In children, damage to the nervous system can lead to disabilities including sensorineural hearing loss, epilepsy, learning and behavioral problems, and decreased intelligence. These sequelae occur in about fifteen percent of survivors. Some hearing loss may be reversible. Among adults sixty-six percent of all cases remain without disability. The main problems are deafness (in fourteen percent of affected patients) and cognitive impairment (in ten percent).
Aseptic meningitis is usually a benign disease with low morbidity and mortality rates, except in newborns. In most patients recovery is complete five to fourteen days after the onset of symptoms. However, in some cases the fatigue, dizziness and asthenia (feeling of previous and sustained tiredness that precedes the performance of the physical act) persist for months.
In children, tuberculous meningitis continues to be associated with a significant risk of death (19 percent of cases) even with treatment, and a significant proportion of those who survive have permanent neurological problems. In just over a third of all cases the children survive without problems.
Prevention
Prevention comprises two aspects, namely chemoprophylaxis of contacts and passive immunization of people at risk. The goal of chemoprophylaxis, which is used for the prevention of secondary cases of Neisseria meningitidis and Haemophilus influenzae meningitis, is to eradicate bacteria from the nasopharynx of contacts. The drug of choice is oral rifampicin, which in the case of meningococcus in children is administered at a dose of 10 mg/kg every twelve hours for two days and in the case of H. influenzae is applied at a dose of 20 mg/kg once daily for four days. In adults, prophylaxis is similar, with a maximum of 600 mg at each administration.
There are useful vaccines for the prevention of meningitis caused by serotype B of H. influenzae. In some countries, widespread immunization with these vaccines appears to have resulted in a significant decrease in incidence.
In Cuba, the meningococcal vaccine against groups B and C was developed, which is indicated for children and adults who live in closed communities, boarding schools, nurseries, military camps, populated areas or high-risk communities. The vaccination scheme it consists of two 0.5 mL doses administered six to eight weeks apart. The second dose is essential to achieve protection. This scheme is valid from three months of age.
According to the CDC, the most effective way to protect children and adults from certain types of bacterial meningitis is to complete the recommended vaccination schedule. Vaccines are available against all three types of bacteria that can cause meningitis, namely Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (pneumococcus) and Haemophilus influenzae type b (Hib).
Antibiotics are a recommended option for the prophylaxis of close contacts of people with meningococcal meningitis. In addition, their administration may be recommended for the whole family if one of its members develops a severe infection by Haemophilus influenzae type b and there is a high-risk person in the home. In these cases, the goal of chemoprophylaxis is to reduce the risk of spreading the infection to that person in whom the disease would be more severe and the doctor will say if there is a person at high risk in the home and if it is necessary to use antibiotics.
Maintaining healthy habits like not smoking and avoiding cigarette smoke, getting plenty of rest, and not coming into close contact with people who are sick can also help. Such preventative measures are especially important for young children, the elderly, and individuals with weakened immune systems, who are most at risk of severe disease.
Meningitis in the literature
In his personal history of bacteria, an author recalls that in 1914 the German writer Hermann Hesse masterfully described the meningeal cry, convulsions, and opisthotonos in his novel Rosshalde: “In There was no room in her ears for more than the echo of the horrifying, desperate scream, stuck in her conscience like a knife in a wound. He rushed onto the bed. In it lay Pierre, deathly pale, his mouth horribly twisted, his gaunt limbs arched in a violent spasm, and his eyes petrified in a gesture of irrational fear. He suddenly uttered another cry, even more savage and mournful than the last, and, rising on head and feet, she lifted his body and arched it onto the bed with such force that the very frame of it trembled…”.
Another description of this symptom can be read in an anthology of Spanish short stories: "At that moment a harsh, shrill cry was heard, launched by Valentín and that left both of them suspended in terror. It was the meningeal cry, similar to the cry of a peacock. That strange encephalic symptom had started that morning and revealed the very serious and terrifying course of the poor mathematician boy's illness...".
The Uruguayan writer Horacio Quiroga describes in one of his short stories (Meningitis and its Shadow) the prodromal symptoms of a woman with the disease: “Four or five nights before, when concluding a receipt in In her own house, María Elvira had felt unwell — a matter of a bath that was too cold that afternoon, according to her mother's opinion. The truth is that she had spent the night fatigued, and with a bad headache. The next morning, greater breakdown, fever; and at night, a meningitis, with all the courtship of her. The delirium, above all, frank and prolonged to ask for more. Concomitantly, a distressing anxiety, impossible to calm. The psychological projections of the delirium, so to speak, have risen and revolved since the first night around a single issue, a single one, but one that absorbs her entire life. It is an obsession, continued Ayestarain, a simple obsession at 42 °C. His eyes are constantly fixed on the door, but he doesn't call anyone. Her nervous state suffers from that mute anxiety that is killing her, and since yesterday we have been thinking with my colleagues about calming that down... She can't go on like this. And do you know —she concluded— whom she names when she is overwhelmed by torpor?
Quiroga once again refers to meningitis and, fundamentally, to its sequelae in another story, La gallina degollada, in which he narrates: “All day, sitting in the patio, on a bench were the four idiot children of the Mazzini-Ferraz couple. They had their tongues between their lips, their eyes stupid, and they turned their heads with their mouths open.[…] The oldest was twelve years old and the youngest was eight. There was a complete lack of any motherly care in all her dirty, helpless appearance. Those four idiots, however, had once been the charm of their parents. […] when the [first] child arrived, fourteen months after their marriage, they believed their happiness had been fulfilled. The creature grew beautiful and radiant, until it was a year and a half old. But in the twentieth month he was shaken one night by terrible convulsions, and the next morning he no longer knew his parents. After a few days the paralyzed limbs recovered movement; but the intelligence, the soul, even the instinct, were completely gone; he had remained profoundly stupid, slimy, dangling, dead forever on his mother's knees. [...] Naturally, the couple put all their love in the hope of another child. This one was born, and his health and limpid laughter reignited the extinguished future. But at eighteen months the seizures of the firstborn were repeated, and the next day the second son woke up idiot. […] Out of the new disaster came new flames of aching love, a mad longing to redeem once and for all the holiness of his tenderness. Twins ensued, and point by point the process of the two older ones was repeated. […] The parents reproached each other: […] I have had healthy parents, you hear?, healthy! My father did not die of delirium! I would have had children like everyone else's! Those are your sons, the four yours! said the woman and Mazzini, the father, exploded in turn: "Consumption viper! That's what I told you, what I want to tell you! Ask him, ask the doctor who is most to blame for your children's meningitis: my father or your chopped lung, viper!?"
In a work that explores the relationship between medicine and literature, the description of the condition of a five-year-old boy with meningitis taken from the novel Doktor Faustus by Thomas Mann is reproduced: “The small […] he held his head in his hands and uttered shrill cries of pain that were a real torture for all who had to hear them and sometimes lasted as long as breathing allowed. He extended his arms to those around him and exclaimed: 'Help! Help! Headache, headache!’ From time to time he would roll his eyes, clench his arms against his body, and the spasm, hideous to look at, though perhaps no longer painful, contracted his little limbs.”
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