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