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Meningitis

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   CAPTION: Meningitis
   Classifications and external resources

     ICD- 10   G 00.- G 03.
     ICD- 9    320- 322
   DiseasesDB  22543
   MedlinePlus 000680
    eMedicine  med/2613  emerg/309 emerg/390

   Meningitis is inflammation of the meninges. Caused by bacteria, viral
   infections elsewhere in the body that has spread into the blood and
   into the cerebrospinal fluid (CSF). Other causes of meningitis such as
   fungal, protozoal, or certain non-infectious etiologies are much rarer.
   Meningitis should be distinguished from the condition encephalitis, the
   latter of which is the inflammation of the brain itself. Meningitis can
   affect anyone in any age group, from the newborn to the elderly,
   although the specific cause may be different. Typical signs and
   symptoms of meningitis include fever, headache, stiff neck,
   photophobia, or vomiting. The most common cause of meningitis is viral
   (which in some cases can be resolved within a few days with swift
   treatment), therefore anyone suspected of having meningitis should be
   evaluated promptly. Also, bacterial meningitis can be very serious and
   immediate treatment is necessary.

Pathophysiology

   Bacterial meningitis is usually caused by Streptococcus pneumoniae and
   Neisseria meningitidis. These organisms initially attach to the
   epithelial cells of the nasopharynx and are then transported via
   vacuoles into the bloodstream. They are able to avoid phagocytosis by
   neutrophils and complement-mediated bactericidal activity because of
   their polysaccharide capsule. They then reach the ventricles and
   directly infect the choroid plexus and gain access to the CSF. There,
   they are able to rapidly divide because of the absence of effective
   immune defenses since CSF contains relatively small amounts of white
   blood cells, complement proteins, and immunoglobulins. The scarcity of
   the latter two components renders opsonization of bacteria ineffective,
   leading to impaired phagocytosis by neutrophils. Eventually, the
   bacteria are lysed, with release of cell wall products into the
   subarachnoid space. These substances --- including lipopolysaccharide
   (LPS), teichoic acid, and peptidoglycan --- induce meningeal
   inflammation by stimulating cytokine release (such as TNF and IL-1) by
   CNS microglia, astrocytes, monocytes, endothelial cells, and
   leukocytes. In addition to meningeal inflammation, these cytokines are
   responsible for the fever, headache, and increased intracranial
   pressure present secondary to the formation of the purulent exudate and
   obstruction of CSF flow through the ventricular system as well as
   inhibiting resorption of CSF by the subarachnoid granulations. Because
   much of the symptoms of meningitis is due to the host inflammatory
   response rather than direct bacterial damage, this explains why
   symptoms may persist even after adequate antibiotic therapy.
   Interior view of a brain with meningitis caused by Haemophilus
   influenzae. Source: CDC
   Enlarge
   Interior view of a brain with meningitis caused by Haemophilus
   influenzae. Source: CDC

   Purulent (suppurative) leptomeningitis is a diffuse purulent
   inflammation. The leptomeninges (arachnoid and pia matter) contain
   purulent exudate (pus): leukocytes (neutrophils), fibrin, germs,
   proteins, and necrotic debris. Blood vessels in the subarachnoidian
   space and those intracerebral are congested and neutrophil margination
   is present.

Symptoms

   Symptoms of meningitis may progress either acutely, becoming fulminant
   within a few hours, or present subacutely over several days. The
   classical symptoms of meningitis are fever, headache, and nuchal
   rigidity ("neck stiffness") --- each presents in >90% of patients.
   Photophobia (intolerance to light), chills, nausea, or vomiting, may
   also occur. Seizures may occur in about 20 to 40% of patients. Other
   signs include Kernig's sign and Brudzinski's sign. Although commonly
   tested, the sensitivity and specificity of Kernig's and Brudzinski's
   tests are uncertain.
     * Nuchal rigidity is the pathognomonic sign of meningeal irritation
       and is present when the neck is resistant to passive flexion.
     * Kernig's sign is elicited when patient is lying supine, with both
       hips and knees flexed. Meningeal irritation is present if pain is
       elicited when the knees are passively extended.
     * Brudzinski's sign is elicited when the patient is lying supine,
       with both hips and knees flexed. Meningeal irritation is present if
       pain is elicited when the neck is passively flexed.

   An important clue in meningococcal meningitis is diffuse petechial rash
   present on the trunk, lower extremities, mucous membranes, conjunctiva,
   and occasionally on the palms and soles.

Complications

   An increased intracranial pressure is a known and a potentially fatal
   complication of bacterial meningitis. The main sign of an increased
   intracranial pressure is an altered states of consciousness, which may
   vary from lethargy to confusion to coma. More than 90% of cases will
   present with CSF opening pressure > 180 mmHg and some with > 400 mmHg.
   Other signs of increased ICP in addition to headache and vomiting
   include papilledema, sixth cranial nerve palsies, decerebrate
   posturing, and Cushing's reflex ( tachycardia, hypotension, and
   Cheyne-Stokes respiration). The most fatal complication of ICP is brain
   herniation, which may present in 1 to 8% of cases.

Associated features

   Arthritis (bacterial infection of joints) occurs in around 7% of all
   cases of bacterial meningitis and 12% of cases of meningococcal
   meningitis.

Diagnosis

   Although diagnosis of meningitis as well as its specific etiology is
   important, laboratory testing takes time. Because bacterial meningitis
   is such an urgent issue, treatment is usually instituted before a
   definite diagnosis is made.
     * When a patient is suspected of meningitis, blood culture should be
       drawn and empiric antibiotics started immediately.
     * Diagnosis of meningitis can then be carried out with examination of
       CSF with a lumbar puncture (LP). However, if the patient has had
       recent head trauma, is immunocompromised, have known malignant or
       CNS neoplasm, or have focal neurologic deficits such as papilledema
       or altered consciousness, a CT or MRI should be performed prior to
       the LP in order to avoid a potentially fatal brain herniation
       during the procedure.
     * Otherwise, the CT or MRI should be performed after the LP, with MRI
       preferred over CT due to its superiority in demonstrating areas of
       cerebral edema, ischemia, and meningeal enhancement.

   Antibiotics started within 4 hours of lumbar puncture will not
   significantly affect lab results. The opening pressure is noted during
   the LP and the CSF fluid sent for examination of white blood cell, red
   blood cell, glucose, protein, Gram stain, culture, and possibly latex
   agglutination test, limulus lysates, or PCR for bacterial DNA.

CSF analysis in bacterial meningitis

     * Opening pressure: > 180 mmH2O
     * White blood cell: 10-10,000/uL with neutrophil predominance
     * Glucose: < 40 mg/dL
     * CSF glucose to serum glucose ratio: < 0.4
     * Protein: > 4.5 mg/dL
     * Gram stain: positive in >60%
     * Culture: positive in >80%
     * Latex agglutination: may be positive in meningitis due to
       Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus
       influenzae, Escherichia coli, Group B Streptococci
     * Limulus lysates: positive in Gram-negative meningitis

   CSF cultures are usually positive in 30 to 70% of patients with viral
   meningitis and those with negative cultures will usually have a
   positive CSF PCR test.

Treatment

   Bacterial meningitis is a medical emergency and has a high mortality
   rate if untreated. All suspected cases, however mild, need emergency
   medical attention. Empiric antibiotics must be started immediately,
   even before the results of the lumbar puncture and CSF analysis are
   known.

   The choice of antibiotic depends on local advice. In most of the
   developed world, the most common organisms involved are Streptococcus
   pneumoniae and Neisseria meningitidis: first line treatment in the UK
   is a third-generation cephalosporin (such as ceftriaxone or
   cefotaxime). In those under 3 years of age, over 50 years of age, or
   immunocompromised, ampicillin should be added to cover Listeria
   monocytogenes. In the U.S. and other countries with high levels of
   penicillin resistance, the first line choice of antibiotics is
   vancomycin and a carbapenem (such as meropenem). In sub-Saharan Africa,
   oily chloramphenicol or ceftriaxone are often used because only a
   single dose is needed in most cases.

   Staphylococci and gram-negative bacilli are common infective agents in
   patients who have just had a neurosurgical procedure. Again, the choice
   of antibiotic depends on local patterns of infection: cefotaxime and
   ceftriaxone remain good choices in many situations, but ceftazidime is
   used when Pseudomonas aeruginosa is a problem, and intraventricular
   vancomycin is used for those patients with intraventricular shunts
   because of high rates of staphylococcal infection. In patients with
   intracerebral prothetic material (metal plates, electrodes or implants,
   etc.) then sometimes chloramphenicol is the only antibiotic that will
   adequately cover infection by Staphylococcus aureus (cephalosporins and
   carbapenems are inadequate under these circumstances).

Specific treatments

   Once the results of the CSF analysis are known along with the
   Gram-stain and culture, empiric therapy may be switched to therapy
   targeted to the specific causative organisms. Because
   antibiotic-resistance is a prevalent problem, information from drug
   susceptibility testing should also be gathered.
     * Neisseria meningitidis can usually be treated with a 7-day course
       of IV antibiotics:
          + Penicillin-sensitive -- penicillin G or ampicillin
          + Penicillin-resistant -- ceftriaxone or cefotaxime
          + Prophylaxis for close contacts (contact with oral secretions)
            -- rifampin 600 mg bid for 2 days (adults) or 10 mg/kg bid
            (children). Rifampin is not recommended in pregnancy and as
            such, these patients should be treated with single doses of
            ciprofloxacin, azithromycin, or ceftriaxone
     * Streptococcus pneumoniae can usually be treated with a 2-week
       course of IV antibiotics:
          + Penicillin-sensitive -- penicillin G
          + Penicillin-intermediate -- ceftriaxone or cefotaxime
          + Penicillin-resistant -- ceftriaxone or cefotaxime + vancomycin
     * Listeria monocytogenes is treated with a 3-week course of IV
       ampicillin + gentamicin.
     * Gram negative bacilli -- ceftriaxone or cefotaxime
     * Pseudomonas aeruginosa -- ceftazidime
     * Staphylococcus aureus
          + Methicillin-sensitive -- nafcillin
          + Methicillin-resistant -- vancomycin
     * Streptococcus agalactiae -- penicillin G or ampicillin
     * Haemophilus influenzae -- ceftriaxone or cefotaxime

Viral meningitis

   Unlike bacteria, viruses cannot be killed by antibiotics. Patients with
   very mild viral meningitis may only have to spend a few hours in
   hospital, while those who have a more serious infection may be
   hospitalised for many more days for supportive care. Patients with mild
   cases, which often cause only flu-like symptoms, may be treated with
   fluids, bed rest (preferably in a quiet, dark room), and analgesics for
   pain and fever. The physician may prescribe anticonvulsants such as
   phenytoin to prevent seizures and corticosteroids to reduce brain
   inflammation. If inflammation is severe, pain medicine and sedatives
   may be prescribed to make the patient more comfortable. This type of
   meningitis is, however, during its early stages highly contagious, so
   patients must be kept isolated for at least several days.

Increased intracranial pressure

   Treatment of increased intracranial pressure include elevation of head
   to 30 to 45 degrees, intubation and hyperventilation, and mannitol.

Vaccination

   Vaccinations against Haemophilus influenzae (Hib) have decreased early
   childhood meningitis significantly.

   Vaccines against type A and C Neisseria meningitidis, the kind that
   causes most disease in preschool children and teenagers in the United
   States, have also been around for a while. Type A is also prevalent in
   sub-Sahara Africa and W135 outbreaks have affected those on the Hajj
   pilgrimage to Mecca.

   A vaccine called MeNZB for a specific strain of type B Neisseria
   meningitidis prevalent in New Zealand has completed trials and is being
   given to many people in the country under the age of 20. There is also
   a vaccine, MenBVac, for the specific strain of type B meningoccocal
   disease prevalent in Norway, and another specific vaccine for the
   strain prevalent in Cuba.

   Pneumovax against Streptococcus pneumoniae is recommended for all those
   > 65 years. Now, all children should receive vaccination against
   Streptococcus pneumoniae starting at 6 weeks - 2 months according to
   American Association of Pediatrics (AAP) recommendations.

History

   The symptoms of meningitis were recorded in the Middle Ages along with
   those of tuberculosis and the Black Plague, but it was first accurately
   identified by the Swiss Vieusseux (a scientific-literary association),
   during an outbreak in Geneva, Switzerland in 1805. In the 19th Century
   meningitis was a scourge of the Japanese Imperial family, playing the
   largest role in the horrendous pre-maturity death rate the family
   endured. In the mid-1800s, only the Emperor Komei and two of his
   siblings reached maturity out of fifteen total children surviving
   birth. Komei's son, the Emperor Meiji, was one of two survivors out of
   Komei's six children, including an elder brother of Meiji who would
   have taken the throne had he lived to maturity. Five of Meiji's fifteen
   children survived, including only his third son, the Taisho Emperor,
   who was feeble-minded, perhaps as a result of having contracted
   meningitis himself. By Emperor Hirohito's generation the family was
   receiving modern medical attention. As the focal point of tradition in
   Japan, during the Tokugawa Shogunate the family was denied modern
   "Dutch" medical treatment then in use among the upper caste; despite
   extensive modernization during the Meiji Restoration the Emperor
   insisted on traditional medical care for his children. The inbreeding
   produced among the very few families considered worthy of marriage into
   the imperial line, most of whom were descendents from that same line
   and therefore none too distant cousins of one another, also played an
   important role.

The African Meningitis Belt

   The "Meningitis Belt" is an area in sub-Saharan Africa which stretches
   from Senegal in the west to Ethiopia in the east in which large
   epidemics of meningococcal meningitis occur. It contains an estimated
   total population of 300 million people. The largest epidemic outbreak
   was in 1996, when over 250,000 cases occurred and 25,000 people died as
   a consequence of the disease.

   Retrieved from " http://en.wikipedia.org/wiki/Meningitis"
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