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التهاب السحايا Meningitis

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  • التهاب السحايا Meningitis

    Meningitis


    Meningitis is an inflammation of the pia-arachnoid meninges. It can be caused by growth of bacteria, fungi, or parasites within the subarachnoid space or by the growth of bacteria or viruses within the meningeal or ependymal cells. Meningitis is a diffuse infection caused by a variety of different agents (Fig. 96-3).

    Etiology

    Approximately 20,000 cases of bacterial meningitis occur in the United States each year. Seventy percent of these are in children younger than 10 years old. Infants are particularly susceptible because of their predisposition to bacterial infection, possible lower integrity of barriers, and immature defense mechanisms. In neonates younger than 28 days old, meningitis is usually due to enteric bacilli (especially Escherichia coli), group B streptococci, or Listeria. Neonatal meningitis represents fewer than 10 percent of cases of meningitis, but more than 50 percent of meningitis deaths. In the postnatal period, Haemophilus influenzae is the most common cause of bacterial meningitis, but this infection is largely limited to childhood. Significant reductions in some countries are occurring due to use of capsular polysaccharide-protein conjugate vaccines during infancy. Adult bacterial meningitis is predominantly due to Neisseria meningitidis and Streptococcus pneumoniae, except in cases where there had been a penetrating wound to the skull, surgery, or immunosuppression in the host. Neisseria meningitidis causes epidemic disease, all other forms of pyogenic meningitis are sporadic. Tuberculosis and fungi usually cause subacute meningitis. Cryptococcus neoformans often causes meningitis in immunosuppressed patients, but can cause indolent meningitis in immunocompetent individuals. Coccidioides immitis and, rarely, other fungi also cause subacute meningitis.

    Viral meningitis occurs more frequently than bacterial meningitis, with over 50,000 cases each year in the United States. The disease is benign and tends to be seasonal. Enteroviruses (echoviruses and coxsackieviruses) cause disease, primarily in the late summer and early fall; mumps virus spreads predominantly in the spring; and lymphocytic choriomeningitis virus is more common in winter, since this virus is acquired from mice, which move indoors during cold weather and increase human exposure.

    Pathogenesis

    Most bacteria and viruses invade the CNS from the blood (Table 96-1), and the risk of CNS invasion has been shown to be related to the magnitude and duration of the bacteremia or viremia. Particles in the blood, including bacteria or viruses, are normally cleared by the reticuloendothelial system, and speed of removal is proportional to size. The bacteria that maintain a bacteremia (and incidentally cause meningitis) are largely those which elaborate capsid polysaccharides that increase their resistance to phagocytosis. Intracellular bacteria and a variety of viruses elude clearance by growing within blood cells. Enteroviruses and some arthropod-borne viruses (arboviruses) are cleared less effectively from serum because of their small size. Some viruses enter the CNS by infecting endothelial cells or choroid plexus epithelium. Indeed, in mumps virus meningitis, choroid plexus cells containing viral nucleocapsids are frequently found within the CSF.

    Clinical Manifestations

    The primary clinical manifestations of meningitis are headache, fever, and nuchal rigidity (stiffness of the neck on passive forward flexion due to stretching of the inflamed meninges). Flexion of the neck may also cause reflex flexion of the legs (Brudzinski sign), and meningeal irritation may limit extension of the leg when flexed at the knee (Kernig sign). Meningeal inflammation may also cause some degree of obtundation (reduced consciousness), and seizures are common in children. If bacterial meningitis is not promptly treated, purulent material collects around the base of the brain, which may cause cranial nerve palsies and obstruct the flow of CSF, resulting in hydrocephalus. Vasculitis develops, with infarction of the brain and multifocal neurological deficits. Untreated bacterial meningitis is a uniformly fatal disease. Viral meningitis, on the other hand, is benign and self-limited.

    Systemic clinical signs sometimes suggest the agent (e.g., the rash or herpangina of enterovirus infections, the parotitis of mumps, or the multiple petechiae of meningococcemia). Examination of the CSF provides the most important diagnostic information (Table 96-2). Acute bacterial infections evoke a polymorphonuclear cell response in the CSF and profound reductions of CSF sugar content. Bacteria can usually be seen on smears of the CSF and can be cultured if antibiotics have not been given. Subacute tuberculous or fungal meningitis is more difficult to diagnose. The inflammatory response is usually composed of mononuclear cells, and the reduction of CSF sugar evolves slowly. Organisms are difficult to see on direct smears, although cryptococci may be identified by mixing India ink with the CSF to outline the capsule of the organism and differentiate it from mononuclear inflammatory cells. In general, viruses produce a modest mononuclear cell response, and although the CSF protein may be elevated, CSF sugar is normal or only mildly depressed. Viruses, such as enteroviruses and mumps virus, can be grown from the CSF, but this requires special viral cultures. A rapid diagnosis may be achieved by demonstrating antigen of various bacterial and fungal agents or the presence of IgM against specific viral agents.

    Treatment

    Early diagnosis of bacterial and fungal meningitis and treatment with appropriate antimicrobial agents are crucial. The mortality rate due to untreated disease approaches 100 percent. Even with treatment, the death rate of individuals with acute bacterial meningitis remains approximately 15%; it is as high as 30% for pneumococcal meningitis. Sequelae are frequent in survivors. This mortality and morbidity have remained relatively unchanged since the introduction of antibiotics. Further reduction of death and disability rests primarily on the physician's early suspicion, diagnosis, and treatment of the disease. Viral meningitis requires only symptomatic treatment since the disease is self-limited; the prime management problem is to rule out nonviral, treatable illnesses that can mimic acute viral meningitis (partially treatable bacterial meningitis, tuberculous or fungal meningitis, syphilis, Lyme disease, etc.).
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