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The Meningitis

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									Clinical Presentation:
Symptoms commonly associated with both microbe and viral meningitis
consist of acute onset of fever, headache, neck stiffness (meningismus),
photophobia, and confusion. Microbe meningitis brings about significant
morbidity (neurologic sequelae, particularly sensorineural hearing loss)
and mortality and thus requires immediate antibiotic treatment.With rare
exceptions, only supportive care with analgesics is essential for viral
meningitis. Because the clinical presentations of microbe and viral
meningitis might be indistinguishable, laboratory studies from the
cerebrospinal fluid are critical in differentiating these entities.
Cerebrospinal fluid leukocyte pleocytosis (white blood cells in the
cerebrospinal fluid) may be the hallmark of meningitis.Microbe meningitis
is generally characterized by neutrophilic pleocytosis (predominance of
polymorphonuclear neutrophils in the cerebrospinal fluid). Typical causes
of lymphocytic pleocytosis include viral infections (eg, enterovirus,
West Nile virus), fungal infections (eg, cryptococcus in HIV-infected
persons), and spirochetal infections (eg, neurosyphilis or Lyme
neuroborreliosis).Noninfectious brings about this kind of as cancer,
connective tissue diseases, and hypersensitivity reactions to drugs can
also trigger lymphocytic pleocytosis. The cerebrospinal fluid in
bacterial meningitis is usually characterized by marked elevations in
protein concentration, an very reduced glucose level, and, in the absence
of previous antibiotic treatment, a positive Gram stain for
bacteria.However, there is frequently substantial overlap between the
cerebrospinal fluid findings in bacterial and nonbacterial meningitis,
and differentiating these entities at presentation is really a
significant clinical challenge.Etiology:
The microbiology of microbe meningitis within the United States has
changed dramatically following the introduction from the Haemophilus
influenzae conjugate vaccine. The routine use of this vaccine in the
pediatric population has essentially eliminated H influenzae as a trigger
of meningitis, resulting in a shift in median age among sufferers with
microbe meningitis from 9 months to 25 years.Microbe agents causing
meningitis vary according to host age. In infants younger than 3 months,
E coli, Listeria, and group B streptococci are the most common brings
about of meningitis. For kids three months to 18 many years of age, S
pneumoniae and N meningitidis are the most common brings about, with H
influenzae a concern between nonimmunized kids.For adults aged 18-50 many
years, S pneumoniae and N meningitidis are the leading brings about of
meningitis, whereas the elderly are at chance for those pathogens as well
as for Listeria. Additional bacteria should be considered for
postneurosurgery sufferers (S aureus, P aeruginosa), sufferers with
ventricular shunts (S epidermidis, S aureus, gram-negative bacilli),
pregnant patients (Listeria), or neutropenic sufferers (gram-negative
bacilli, including P aeruginosa).Subacute or chronic meningitides may be
caused by M tuberculosis, fungi (eg, Coccidioides immitis, Cryptococcus
neoformans), and spirochetes such as Treponema pallidum (the bacterium
causing syphilis) or Borrelia burgdorferi (the bacterium causing Lyme
disease). The diagnosis of meningitis triggered by these organisms may be
delayed simply because many of these pathogens are difficult to culture
and need special serologic or molecular diagnostic
techniques.Pathogenesis:
The pathogenesis of bacterial meningitis involves a sequence of events in
which virulent microorganisms overcome the host defense mechanisms. Most
instances of bacterial meningitis begin with bacterial colonization of
the nasopharynx. An exception is Listeria, which enters the bloodstream
via ingestion of contaminated food.Pathogenic bacteria such as S
pneumoniae and N meningitidis secrete an IgA protease that inactivates
host antibody and facilitates mucosal attachment. Many of the causal
pathogens also possess surface characteristics that enhance mucosal
colonization. N meningitidis binds to nonciliated epithelial cells by
finger-like projections known as pili.Once the mucosal barrier is
breached, bacteria obtain access to the bloodstream, where they should
overcome host defense mechanisms to survive and invade the CNS. The
bacterial capsule, a feature typical to N meningitidis, H influenzae, and
S pneumoniae, is probably the most important virulence factor in this
regard.Host defenses counteract the protective effects of the
pneumococcal capsule by activating the alternative complement pathway,
resulting in C3b activation, opsonization, phagocytosis, and
intravascular clearance from the organism. This defense mechanism is
impaired in patients who have undergone splenectomy, and this kind of
patients are predisposed to the development of overwhelming bacteremia
and meningitis with encapsulated bacteria.Activation from the accentuate
system membrane attack complex is an essential host defense mechanism
against invasive disease by N meningitidis, and sufferers with
deficiencies from the late accentuate components (C5-9) are at elevated
chance for meningococcal meningitis.The mechanisms by which bacterial
pathogens obtain access to the CNS are largely unknown. Experimental
studies suggest that receptors for microbe pathogens are present on cells
within the choroid plexus, which might facilitate movement of these
pathogens to the subarachnoid space.Invasion from the spinal fluid by a
meningeal pathogen results in elevated permeability of the blood-brain
barrier, with leakage of albumin to the subarachnoid room, wherever local
host defense mechanisms are inadequate to control the infection.Usually,
complement elements are minimal or absent in the cerebrospinal fluid.
Meningeal inflammation leads to increased, but still reduced,
concentrations of complement, inadequate for opsonization, phagocytosis,
and removal of encapsulated meningeal pathogens. Immunoglobulin
concentrations are also reduced in the cerebrospinal fluid, with an
average blood to cerebrospinal fluid IgG ratio of 800:1.Although the
absolute quantity of immunoglobulin within the cerebrospinal fluid
increases with infection, the ratio of immunoglobulin within the
cerebrospinal fluid relative to that in the serum remains low. The
ability of meningeal pathogens to induce a marked subarachnoid space
inflammatory response contributes to many from the pathophysiologic
consequences of bacterial meningitis.Although the microbe capsule is
largely responsible for intravascular and cerebrospinal fluid survival
from the pathogens, the subcapsular surface elements (ie, the cell wall
and lipopolysaccharide) of bacteria are more essential determinants of
meningeal inflammation. The major mediators of the inflammatory process
are thought to be IL-1, IL-6, matrix metalloproteinases, and tumor
necrosis aspect (TNF).Within 1-3 hours after intracisternal inoculation
of purified lipopolysaccharide in an animal model, there's a brisk
release of TNF and IL-1 to the cerebrospinal fluid, preceding the
improvement of inflammation. Indeed, direct inoculation of TNF and IL-1
to the cerebrospinal fluid produces an inflammatory cascade identical to
that seen with experimental bacterial infection.Cytokine and proteolytic
enzyme release leads to loss of membrane integrity, with resultant
cellular swelling. The improvement of cerebral edema contributes to an
increase in intracranial pressure, potentially resulting in life-
threatening cerebral herniation. Vasogenic cerebral edema is principally
caused by the increase in blood-brain barrier permeability.Cytotoxic
cerebral edema results from swelling from the cellular elements from the
brain simply because of toxic factors from bacteria or neutrophils.
Interstitial cerebral edema reflects obstruction of flow of cerebrospinal
fluid, as in hydrocephalus. The literature suggests that oxygen free
radicals and nitric oxide might also be important mediators in cerebral
edema.Other complications of meningitis consist of cerebral vasculitis
with alterations in cerebral blood flow. The vasculitis leads to
narrowing or thrombosis of cerebral blood vessels, resulting in ischemia
and feasible brain infarction. Understanding the pathophysiology of
bacterial meningitis has therapeutic implications.Even though
bactericidal antibiotic treatment is critical for adequate treatment,
rapid bacterial killing releases inflammatory bacterial fragments,
potentially exacerbating inflammation and abnormalities of the cerebral
microvasculature. In animal models, antibiotic treatment has been shown
to cause rapid bacteriolysis and release of microbe endotoxin, resulting
in increased cerebrospinal fluid inflammation and cerebral edema.The
importance of the immune response in triggering cerebral edema has led
researchers to study the role of adjuvant anti-inflammatory medications
for bacterial meningitis. The use of corticosteroids has been shown to
decrease the chance of sensorineural hearing loss between kids with H
influenzae meningitis and mortality among adults with pneumococcal
meningitis, and these agents are routinely given at the time of initial
antibiotic therapy.Clinical Manifestations:
Between sufferers who produce community-acquired bacterial meningitis, an
antecedent upper respiratory tract infection is typical. Sufferers having
a history of head injury or neurosurgery, especially those having a
persistent cerebrospinal fluid leak, are at particularly high risk for
meningitis.Manifestations of meningitis in infants may be hard to
recognize and interpret; consequently, the physician should be alert
towards the possibility of meningitis in the evaluation of any febrile
neonate. Most sufferers with meningitis have a rapid onset of fever,
headache, lethargy, and confusion.Fewer than half complain of neck
stiffness, but nuchal rigidity is noted on physical examination in 30-
70%. Other clues seen in a variable proportion of instances include
altered mental status, nausea or vomiting, photophobia, Kernig's sign
(resistance to passive extension from the flexed leg with the patient
lying supine), and Brudzinski's sign (involuntary flexion of the hip and
knee when the examiner passively flexes the patient's neck).More than
half of patients with meningococcemia produce a characteristic petechial
or purpuric rash, predominantly on the extremities. Although a change in
mental status (lethargy, confusion) is typical in bacterial meningitis,
up to one third of patients present with normal mentation. From 10% to
30% of sufferers have cranial nerve dysfunction, focal neurologic signs,
or seizures.Coma, papilledema, and Cushing's triad (bradycardia,
respiratory depression, and hypertension) are ominous signs of impending
herniation (brain displacement through the foramen magnum with brain stem
compression), heralding imminent death.Any patient suspected of having
meningitis demands emergent lumbar puncture for Gram stain and culture
from the cerebrospinal fluid, followed immediately by the administration
of antibiotics and corticosteroids. Alternatively, if a focal neurologic
process (eg, brain abscess) is suspected, antibiotics should be initiated
immediately, followed by brain imaging (computed tomography or magnetic
resonance imaging) and lumbar puncture performed only if there is no
radiologic contraindication.

								
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