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Infections of the central nervous system (CNS) can be divided into 2 broad categories: those primarily involving the meninges (meningitis) and those primarily confined to the parenchyma (encephalitis). See the images of meningitis below.

Pneumococcal meningitis in a patient with alcoholism. Courtesy of the

CDC/Dr. Edwin P. Ewing, Jr. Acute bacterial meningitis. This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal


Acute bacterial meningitis. This axial T2-weighted

magnetic resonance image shows only mild ventriculomegaly. Acute bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows). Meningitis is a clinical syndrome characterized by inflammation of the meninges, 3 layers of membranes that enclose the brain and spinal cord. They consist of the following:
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Dura - A tough outer membrane Arachnoid - A lacy, weblike middle membrane Subarachnoid space - A delicate, fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cord

Risk factors for meningitis include the following:
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Age of 60 years or greater Age of 5 years or less Diabetes mellitus, renal or adrenal insufficiency, hypoparathyroidism, or cystic fibrosis Immunosuppression, which increases the risk of opportunistic infections and acute bacterial meningitis Human immunodeficiency virus (HIV) infection, which predisposes to bacterial meningitis caused by encapsulated organisms, primarily S pneumoniae, and opportunistic pathogens Crowding (eg, military recruits and college dorm residents), which increases the risk of outbreaks of meningococcal meningitis Splenectomy and sickle cell disease, which increase the risk of meningitis secondary to encapsulated organisms Alcoholism and cirrhosis Recent exposure to others with meningitis, with or without prophylaxis Contiguous infection (eg, sinusitis) Dural defect (eg, traumatic, surgical, congenital) Thalassemia major Intravenous (IV) drug abuse Bacterial endocarditis Ventriculoperitoneal shunt Malignancy (increased risk of Listeria species infection) Some cranial congenital deformities

as well as pleocytosis (an increased number of white blood cells) in the cerebrospinal fluid (CSF). and leptomeningitis.Clinically.) The specific infective agents that are involved in bacterial meningitis vary among different patient age groups. headache. sometimes referred to as pachymeningitis. (See Etiology and Clinical Presentation. The organisms usually enter the meninges through the bloodstream from other parts of the body.) Meningitis can also be divided into the following 3 general categories:    Pyogenic (bacterial) Granulomatous Lymphocytic The most common cause of meningeal inflammation is irritation caused by bacterial or viral infections. such as with fungal diseases and tuberculosis. meningitis manifests with meningeal symptoms (eg. meningitis may be concentrated at the base of the brain. under certain conditions. Nonetheless. the overall mortality rate from bacterial meningitis has decreased. but with the advent of antimicrobial therapy.) The emergence of resistant bacterial strains has prompted changes in antibiotic protocols in some countries. Depending on the duration of symptoms. (See Anatomy. nuchal rigidity.) Pyogenic (bacterial) meningitis consists of inflammation of the meninges and the underlying subarachnoid CSF. including the United States.[1] [2] The disease was uniformly fatal before the antimicrobial era. which is less common. If not treated. meningitis may be classified as acute or chronic. being approximately 25%. photophobia). (See Treatment and Management and Medication. (See Etiology. (See Epidemiology. and the inflammation may evolve into the following conditions (see the images below):    Ventriculitis Empyema Cerebritis . however.) Meningitis is anatomically divided into inflammation of the dura. neuronal cell protectants still hold only future promise as adjunctive therapy. which is more common and is defined as inflammation of the arachnoid tissue and subarachnoid space. Most cases of bacterial meningitis are localized over the dorsum of the brain. Apart from dexamethasone. it remains alarmingly high. bacterial meningitis may lead to lifelong debility or death.

Examples of common noninfectious causes include medications (eg. This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis). (See Etiology. This contrast-enhanced axial computed tomography scan shows leftsided parenchymal hypoattenuation in the middle cerebral artery territory. the syndrome may be called. any of the following:      Pneumococcal meningitis Haemophilus influenzae meningitis Staphylococcal meningitis Meningococcal meningitis Tuberculous meningitis . nonsteroidal anti-inflammatory drugs [NSAIDs]. Abscess formation Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. Numerous infectious and noninfectious causes of meningitis have been identified. for example. antibiotics) and carcinomatosis. with marked herniation and a prominent subdural empyema. Subdural empyema and arterial infarct in a patient with bacterial meningitis. and the absence of left mastoid air. Depending on the specific bacterial cause. an adjacent epidural empyema with marked dural enhancement (arrow).) Acute bacterial meningitis Acute bacterial meningitis denotes a bacterial cause of this syndrome. This is usually characterized by an acute onset of meningeal symptoms and neutrophilic pleocytosis. Meningitis can also be also classified more specifically according to its etiology.

with symptoms beginning several days prior. and parasitic agents. Go to Viral Meningitis for complete information on this topic. Depending on age and general condition. Meningitis caused by nonbacterial organisms Fungal and parasitic causes of meningitis are also termed according to their specific etiologic agent.Unlike subacute (1-7 d) or chronic (>7 d) meningitis. and so they require emergency care. herpes simplex virus [HSV] meningitis). acute meningitis (< 1 d) is almost always a bacterial infection caused by 1 of several organisms. enterovirus meningitis. When the cause of aseptic meningitis is discovered. Aseptic meningitis In many cases. after an extensive workup. fever. a cause for meningitis is not apparent after initial evaluation and is therefore classified as aseptic meningitis. such as cryptococcal meningitis. Patients with acute bacterial meningitis may decompensate very quickly. the disease can be reclassified according to its etiology. . and cerebrospinal pleocytosis that is usually prominently lymphocytic. and amebic meningoencephalitis. these gravely ill patients present acutely with signs and symptoms of meningeal inflammation and systemic infection of less than 24 hours' duration (and usually >12 hours’ duration). the condition can also be caused by bacterial. Approximately 75% of patients with bacterial meningitis present subacutely. Histoplasma meningitis. it can be reclassified as a form of acute viral meningitis (eg. However. These ill patients still require urgent ED diagnosis and care to prevent further decompensation. mycobacterial. see the following:     Meningococcal Meningitis Staphylococcal Meningitis Haemophilus Meningitis Tuberculous Meningitis Subacute bacterial meningitis Most bacterial meningitis is not acute. which have myriad infectious and noninfectious etiologies. For more information. ideally within 30 minutes of emergency department (ED) presentation. These patients characteristically have an acute onset of meningeal symptoms. Viral meningitis If. aseptic meningitis is found to have a viral etiology. a specific viral etiology is identified in 55-70% of cases of aseptic meningitis. If appropriate diagnostic methods are performed. including antimicrobial therapy. fungal.

particularly when left untreated. in meningitis. This process. and the underlying parenchyma remains intact. However. obliterating CSF pathways (causing obstructive hydrocephalus). cytokine-induced disruptions in membrane transport. lactate. the pial barrier is broken. In less severe forms. and glucose in patients with this disease. cranial nerve VIII. in more severe forms of bacterial meningitis. protein. The pathophysiology of this complication is complex and may involve many proinflammatory molecules as well as mechanical elements. increasing numbers of inflammatory cells. white blood cells. as in hydrocephalus). the problem can worsen. worsening the symptoms of infection. cytotoxic edema (swelling of cellular elements of the brain through the release of toxic factors from the bacteria and neutrophils). pH. this protection is an advantage because the barrier prevents the body from attacking itself. damaging cranial nerves (eg. particularly to the basal cisterns. in turn. Exudates extend throughout the CSF. Intracranial pressure and cerebral brain fluid One complication of meningitis is the development of increased intracranial pressure (ICP). with resultant hearing loss).Chronic meningitis Chronic meningitis is a constellation of signs and symptoms of meningeal irritation associated with CSF pleocytosis that persists for longer than 4 weeks. and the underlying parenchyma is invaded by the inflammatory process. Thus. Normally. the pial barrier is not penetrated. bacterial meningitis may lead to widespread cortical destruction. Interstitial edema (secondary to obstruction of CSF flow. and vasogenic edema (increased . Replicating bacteria. and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis and account for the characteristic changes in CSF cell count. and inducing vasculitis and thrombophlebitis (causing local brain ischemia). they are somewhat isolated from the immune system and can spread.[3] Depending on the severity of bacterial meningitis. the barrier can become a problem. When the body tries to fight the infection. once bacteria or other organisms have found their way to the brain. and other infection-fighting particles to enter the meninges and brain. the inflammatory process may remain confined to the subarachnoid space. blood vessels become leaky and allow fluid. Pathophysiology The brain is naturally protected from the body's immune system by a barrier the meninges create between the bloodstream and the brain. causes brain swelling and can eventually result in decreasing blood flow to parts of the brain. However.

astrocytes. hypoglycorrhachia results from decreased glucose transport into the spinal fluid compartment. IL-1. peptidoglycan. astrocytes. Data indicate that this process is likely initiated by the ligation of the bacterial components (eg. In experimental models of meningitis. Eventually. lymphocytes. Cerebral edema The increased CSF viscosity resulting from the influx of plasma components into the subarachnoid space and diminished venous outflow lead to interstitial edema. endothelial cells. which contributes to increased lactate concentration and hypoglycorrhachia. The role of cytokines and secondary mediators in bacterial meningitis Key advances in understanding the pathophysiology of meningitis include insight into the pivotal roles of cytokines (eg. TNF-alpha is a glycoprotein derived from activated monocyte-macrophages. worsening cerebral edema. and may lead to stenosis of large and small vessels. TNF-alpha and IL-1 are most prominent among the cytokines that mediate this inflammatory cascade.) The proposed events involving these inflammation mediators in bacterial meningitis begin with the exposure of cells (eg. IL-1. such as the Toll-like receptors. Systemic hypotension (septic shock) also may impair CBF. and IL-8 are characteristic findings in patients with bacterial meningitis. and other cellular activation lead to cytotoxic edema. vasogenic. Without medical intervention.blood brain barrier permeability) are all thought to play a role in the development of increased ICP. IL-6. and increasing ICP proceeds unchecked. interleukin [IL]-1). chemokines (IL-8). Ongoing endothelial injury may result in vasospasm and thrombosis. transient neuronal dysfunction or permanent neuronal injury results. and the patient soon dies from systemic complications or from diffuse CNS ischemic injury. including those of IL-6. they appear early . microglia. Both molecules have been detected in the CSF of individuals with bacterial meningitis. lipopolysaccharide) to pattern-recognition receptors. is also produced primarily by activated mononuclear phagocytes and is responsible for the induction of fever during bacterial infections. (Cytokine levels. and meningeal macrophages) to bacterial products released during replication and death. if this uncontrolled process is not modulated by effective treatment. leukocytes. further compromising CBF. previously known as endogenous pyrogen. and microglial cells. Increased CSF concentrations of TNF-alpha. tumor necrosis factor-alpha [TNF-alpha]. In addition. TNF-alpha. and other proinflammatory molecules in the pathogenesis of pleocytosis and neuronal damage during occurrences of bacterial meningitis. have been found to be elevated in patients with aseptic meningitis. The ensuing cerebral edema (ie. Anaerobic metabolism ensues. neutrophils. and the products of bacterial degradation. cytotoxic. and interferon-gamma. this exposure incites the synthesis of cytokines and proinflammatory mediators. interstitial) significantly contributes to intracranial hypertension and a consequent decrease in cerebral blood flow. the cycle of decreasing cerebral brain fluid (CBF).

from other parts of the body. complement components) appear to be limited in this body compartment. such as IL-6. However. and platelet activation factor (PAF). appears to participate in the induction of increased blood-brain barrier permeability. are presumed to amplify this inflammatory event. Most meningeal pathogens are transmitted through the respiratory route. Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment. the precise roles of all these secondary mediators in meningeal inflammation remain unclear. a product of cyclo-oxygenase (COX). Once inside the CNS. immunoglobulins. local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. Organisms typically enter the meninges through the bloodstream. Many secondary mediators. the infectious agents likely survive because host defenses (eg. is believed to mediate the formation of thrombi and the activation of clotting factors within the vasculature. producing the profound neutrophilic pleocytosis characteristic of bacterial meningitis. neutrophils. Subsequently. The net result of the above processes is vascular endothelial injury and increased blood-brain barrier permeability. In patients without an identifiable source of infection. either synergistically or independently. as exemplified by the fact that Neisseria meningitidis (meningococcus) is carried nasopharyngeally and by the nasopharyngeal colonization with Streptococcus pneumoniae (pneumococcus). Many meningitis-causing bacteria are carried in the nose and throat. PGE2. prostaglandins (PGE2). presumably by damaging mucosal defenses. In response to the cytokines and chemotactic molecules. Bacterial seeding Bacterial seeding usually occurs by hematogenous spread. and neutrophil phagocytosis). nitric oxide. antibodies. This process of meningeal inflammation has been an area of . neutrophils migrate from the bloodstream and penetrate the damaged blood-brain barrier. with its myriad biologic activities. complementmediated bacterial killing. often without symptoms in the carrier. IL-8. Once inside the bloodstream. leading to the entry of many blood components into the subarachnoid space. hematogenous seeding into distant sites occurs. including the CNS. The specific pathophysiologic mechanisms by which the infectious agents gain access into the subarachnoid space remain unclear. In many patients.during the course of disease and have been detected within 30-45 minutes of intracisternal endotoxin inoculation. The presence and replication of infectious agents remain uncontrolled and incite a cascade of meningeal inflammation. The chemokine IL-8 mediates neutrophil chemoattractant responses induced by TNF-alpha and IL-1. this contributes to vasogenic edema and elevated CSF protein levels. Nitric oxide is a free radical molecule that can induce cytotoxicity when produced in high amounts. IL-6 induces acute-phase reactants in response to bacterial infection. the infectious agent must escape immune surveillance (eg. PAF.

extensive investigation in recent years that has led to a better understanding of meningitis pathophysiology. A retrograde neuronal (ie. and white blood cells allows the bacterial infection to flourish. or instrumentation. virus. Meningitis in the newborn is transmitted vertically from colonized pathogens in the maternal intestinal or genital tract or horizontally from nursery personnel or caregivers at home. local immunity. and subsequent seeding. which extends throughout the CSF. respiratory tract. Once in the CSF. infected contiguous structures invade via septic thrombi or osteomyelitic erosion. bacteremia. fungemia. parasitemia) and subsequent hematogenous seeding of the CNS. Rarely. phagocytes/macrophages). Etiology Initially. meningococcal. or genitourinary tract. syphilitic. Acute leptomeningitis results in congestion and hyperemia of the pia-arachnoid and distention of the subarachnoid space by the exudates. congenital malformations. olfactory and peripheral nerves) pathway (eg. the paucity of antibodies. This may be in the form of colonization or infection of the skin. and cranial nerves. an infectious agent colonizes or establishes a localized infection in the host. fungus. neurosurgery. The organism invades the submucosa by circumventing host defenses (eg. GI tract. meningeal seeding may also occur with a direct bacterial inoculate during trauma. basal cisterns. complement components. Inflammations are characterized by polymorphonuclear cell infiltration and extensive fibrinous exudation. otitis media. and the presence of toxic mediators in the CSF. cerebral edema. and parasite) gains access to the CNS and causes meningeal disease:   Invasion of the bloodstream (ie. direct inoculation during intracranial manipulation) Invasion of the bloodstream.and cytokine-mediated events that result in increased permeability of the bloodbrain barrier. Possible pathways for the migration of pathogens from the middle ear to the meninges include the following:  A systemic route in the bloodstream . is the most common mode of spread for most agents (eg. cerebral edema. Bacterial cell wall components initiate a cascade of complement. viremia. Local extension from contiguous extracerebral infection (eg. Naegleria fowleri. The following 3 major pathways exist by which an infectious agent (ie. cryptococcal. mastoiditis. Gnathostoma spinigerum) Direct contiguous spread (ie. and pneumococcal meningitis). otitis media. Bacterial seeding results in increased permeability of the blood-brain barrier. nasopharynx. physical barriers. or sinusitis) is a common cause. trauma. sinusitis. and the presence of toxic mediators in the CSF. bacterium.

Go to HIV-1 Associated CNS Conditions . or cranial osteomyelitis. Meningitis is the most serious acute manifestation of systemic infection with H influenzae. Pachymeningitis On the basis of the finding of abundant pus. S aureus. metronidazole. human herpesvirus-2 (HHV-2). and diphtheroids (rare). In patients who have had trauma or neurosurgery. IV immunoglobulin) and. posterior fossa) Temporal bone fractures The oval or round window membranes of the labyrinths In HIV-positive/AIDS patients. the most common microorganisms are S pneumoniae (if CSF leak is present). It can spread from one individual to another by airborne droplets or direct contact with secretions. skull fracture). draw a serum/CSF cryptococcal antigen and treat empirically as in adults older than 50 years (pending results of all blood and CSF tests) to cover the bacterial pathogens. coliforms. for which this patient population is most at risk . The source of the organisms is most often a skull defect (eg. HIV aseptic meningitis. Meningitis caused by Haemophilus influenzae H influenzae is a small. such as the following: . particularly S pneumoniae and L monocytogenes. gram-negative coccobacilli that is frequently found as part of the normal flora in the upper respiratory tract of humans. Manage by repeating LP if necessary to rule out partially treated bacterial meningitis. the most common microorganisms are Staphylococcus epidermidis. pachymeningitis most often results from a bacterial infection (usually due to staphylococcal or streptococcal organisms) that is localized to the dura. Staphylococcus aureus. lymphocytic choriomeningitis virus (LCM). the most common microorganisms are enteroviruses. Propionibacterium acnes. Mycobacterium tuberculosis. rarely. HIV. consider cryptococci. In patients with infected ventriculoperitoneal (atrial) shunt.Meningitis for complete information on this topic. coliforms. Other etiologies include drugs (NSAIDs. and P aeruginosa. If the pathogen is unknown after an ED workup. leptospirosis. The encapsulated type B strain of this bacterium is the form of H influenzae that most often causes meningitis. since early shunt removal is usually necessary for cure. and other viruses.   Along preformed tissue planes (eg. pleomorphic. an infection of the paranasal sinuses. The isolation of H influenzae in adults suggests the presence of an underlying medical disorder. Consult a neurosurgeon. and Listeria species. In patients with aseptic meningitis (CSF pleocytosis and normal CSF glucose. syphilis. negative bacteria on Gram stain).

such as pneumonia. either through choroid plexus seeding from bacteremia or through direct extension from sinusitis or otitis media. a gram-positive coccus. Austrian syndrome). S pneumoniae is a common colonizer of the human nasopharynx (5-10% of healthy adults and 20-40% of healthy children). In addition. Predisposing risks in adults include the following:     Diabetes mellitus Pregnancy Alcoholism Hepatic failure . Patients with the following conditions are at increased risk for S pneumoniae meningitis:           Hyposplenism Hypogammaglobulinemia Multiple myeloma Glucocorticoid treatment Defective complement (C1-C4) Diabetes mellitus Renal insufficiency Alcoholism Malnutrition Chronic liver disease Meningitis caused by Streptococcus agalactiae Streptococcus agalactiae (group B streptococci) is a gram-positive coccus that is isolated from the lower gastrointestinal tract. is the most common bacterial cause of meningitis. or endocarditis (ie. it is the most common bacterial agent in meningitis associated with basilar skull fracture and CSF leak.      Paranasal sinusitis Otitis media Alcoholism CSF leak following head trauma Functional or anatomic asplenia Hypogammaglobulinemia Go to Haemophilus Meningitis for complete information on this topic. which explains why it is the most common (70%) agent of neonatal meningitis. It also colonizes the female genital tract at a rate of 5-40%. Meningitis caused by Streptococcus pneumoniae S pneumoniae. It causes meningitis by escaping the local host defenses and phagocytic mechanisms. sinusitis. It may be associated with other foci of infection.

It initiates invasion by penetrating the airway epithelial surface. cheese. Outbreaks have been associated with consumption of contaminated coleslaw. household crowding. patients with acquired immunodeficiency syndrome [AIDS]) Individuals with chronic liver and renal disease Individuals with diabetes . it is the leading cause of bacterial meningitis in children and young adults. with a recovery rate of up to 70% from raw meat. Risk factors for Neisseria meningitis include the following:     Deficiencies in terminal complement components (eg. and alfalfa tablets. It is a common food contaminant. Meningitis caused by Neisseria meningitides N meningitides is a gram-negative diplococcus that is carried in the nasopharynx of otherwise healthy individuals. At-risk groups include the following:        Pregnant women Infants and children Elderly individuals (>60 y) Patients with alcoholism Adults who are immunosuppressed (eg. Most human cases appear to be food-borne. steroid use. no underlying disease is present. corticosteroid use.  Renal failure Corticosteroid treatment In 43% of adult cases. The precise mechanism by which this occurs is unclear. Most sporadic cases (95-97%) are caused by serogroups B. chronic medical illness. while the A and C strains are observed in epidemics (< 3% of cases). and meats. which has been reported for a clustering of cases Meningitis caused by Listeria monocytogenes Listeria monocytogenes is a small gram-positive bacillus that causes 8% of bacterial meningitis cases and is associated with one of the highest mortality rates (22%). accounting for 59% of cases. Currently. C5C9). C. vegetables. but recent viral or mycoplasmal infection has been reported to disrupt the epithelial surface and facilitate invasion by meningococcus. as is observed in college dormitories (college freshmen living in dormitories are at highest risk) and military facilities. and active or passive smoking Overcrowding. and Y. It is widespread in nature and has been isolated in the human stool of 5% of healthy adults. transplant recipients. membrane attack complex. milk. which increases attack rates but is associated with surprisingly lower mortality rates Properdin defects that increase the risk of invasive disease Antecedent viral infection. however.

However. Persons with iron-overload conditions (eg. E coli are a common agent of meningitis among neonates. hemochromatosis or transfusion-induced iron overload) Meningitis caused by gram-negative bacilli As a group. Meningitis caused by staphylococci is associated with the following risk factors:    Status post neurosurgery and post trauma Presence of CSF shunts Infective endocarditis and paraspinal infection Staphylococcus epidermidis is the most common cause of meningitis in patients with CNS (ie. fungi. a specific viral etiology is identified in 55-70% of cases of aseptic meningitis. partially treated bacterial meningitis accounts for a large number of meningitis cases with a negative microbiologic workup. Aerobic gram-negative bacilli include Escherichia coli. as a result of the translocation of gut microflora with the Strongyloides stercoralis larva during hyperinfection syndrome. Go to Staphylococcal Meningitis for complete information on this topic. and Salmonella species. Staphylococcus-associated meningitis Staphylococci species are gram-positive cocci that are part of the normal skin flora. Pseudomonas aeruginosa. . Other predisposing risk factors for meningitis associated with gram-negative bacilli include the following:      Neurosurgical procedures or intracranial manipulation Old age Immunosuppression High-grade gram-negative bacillary bacteremia Disseminated strongyloidiasis Disseminated strongyloidiasis has been reported as a classic cause of gram-negative bacillary bacteremia. As previously mentioned. Klebsiella pneumoniae. if appropriate diagnostic methods are performed. Serratia marcescens. ventriculoperitoneal) shunts. aseptic meningitis can also be caused by bacteria. Aseptic meningitis Aseptic meningitis is one of the most common infections of the meninges. and parasites (see the Table 1 “Infectious Agents Causing Aseptic Meningitis Syndrome. gram-negative bacilli can cause meningitis in certain groups of patients.” below). Importantly.

Infectious Agents Causing Aseptic Meningitis Syndrome (Open Table in a new window) Category Agent Bacteria Partially-treated bacterial meningitis L monocytogenes Brucella species Rickettsia rickettsii Ehrlichia species Mycoplasma pneumoniae Borrelia burgdorferi Treponema pallidum Leptospira species Mycobacterium tuberculosis Nocardia species Parasites N fowleri Acanthamoeba species Balamuthia species Angiostrongylus cantonensis G spinigerum Baylisascaris procyonis S stercoralis Taenia solium (cysticercosis) Fungi Cryptococcus neoformans . Table 1.Go to Aseptic Meningitis for complete information on this topic.

C immitis Blastomyces dermatitidis H capsulatum Candida species Aspergillus species Viruses Enterovirus Poliovirus Echovirus Coxsackievirus A Coxsackievirus B Enterovirus 68-71 Herpesvirus HSV-1 and HSV-2 Varicella-zoster virus EBV CMV HHV*-6 HHV-7 Paramyxovirus Mumps virus Measles virus Togavirus Rubella virus .

Flavivirus Japanese encephalitis virus St. The enteroviruses belong to the family Picornaviridae and are further classified as follows: . Louis encephalitis virus Bunyavirus California encephalitis virus La Crosse encephalitis virus Alphavirus Eastern equine encephalitis virus Western equine encephalitis virus Venezuelan encephalitis virus Reovirus Colorado tick fever virus Arenavirus LCM virus** Rhabdovirus Rabies virus Retrovirus HIV*** *Human herpes virus **Lymphocytic choriomeningitis ***Human immunodeficiency virus Enteroviruses account for 90% of cases of aseptic meningitis.

HSV-1 has also been implicated as a cause. The nonpolio enteroviruses (NPEV) account for approximately 90% of cases of viral meningitis in which a specific pathogen can be identified. Varicella-zoster virus (VZV). DNA-containing enveloped viruses. and encephalitis. and CMV are causes of meningitis in immunocompromised hosts. Most of the cases of California encephalitis are probably caused by mosquitoborne La Crosse encephalitis virus. St. it is most commonly associated with primary genital infection and is less likely during recurrences.     Poliovirus (3 serotypes) Coxsackievirus A (23 serotypes) Coxsackievirus B (6 serotypes) Echovirus (31 serotypes) Newly recognized enterovirus serotypes 68-71 The virus is usually spread by fecal-oral or respiratory routes. Louis encephalitis virus (a flavivirus). Although Mollaret syndrome. Epstein-Barr virus (EBV. HSV-1 is a cause of encephalitis. while HSV-2 more commonly causes meningitis. infection occurs during summer and fall in temperate climates and year-round in tropical regions. and California encephalitis virus (bunyavirus group. including La Crosse encephalitis virus). aseptic meningitis syndrome. a recurrent.5-3% of cases of aseptic meningitis. with the exception of HHV-8 or Kaposi sarcoma–associated virus. California encephalitis is a common childhood disease of the CNS that is caused by a virus in the genus Bunyavirus. especially patients with acquired immunodeficiency syndrome (AIDS) and transplant recipients. Louis encephalitis virus is a mosquito-borne flavivirus that may cause a febrile syndrome. . is more frequently associated with HSV-2. The Herpesviridae family consists of large. and all have been implicated in meningitis syndromes. or HHV-5) may manifest as meningitis during the mononucleosis syndrome. The most common arthropod-borne viruses are St. Eight members are known to cause human infections. but benign. or HHV-3. Colorado tick fever virus. HHV-6 and HHV-7 have been reported to cause meningitis in transplant recipients. Other members of the flavivirus group that may cause aseptic meningitis include tick-borne encephalitis virus and Japanese encephalitis virus. Echovirus 30 was reported as the cause of an epidemic in Japan in 1991 and also as the cause of 20% of cases of aseptic meningitis reported to the Centers for Disease Control and Prevention (CDC) in 1991. or HHV-4) and cytomegalovirus (CMV. HSV accounts for 0. aseptic meningitis syndrome.

Table 2. 6. Chronic meningitis The agents responsible for chronic meningitis are listed in Table 2 “Causes of Chronic Meningitis. Always suspect HIV as a cause of aseptic meningitis in a patient with risk factors such as intravenous drug use and in individuals who practice high-risk sexual behaviors. RNA-containing viruses in which rodents are the animal reservoir.LCM virus is a member of the arenaviruses. The infection is usually acquired through a respiratory route. occurring in 30% of all patients with mumps.” below. Go to Aseptic Meningitis for complete information on this topic. Following exposure. The modes of transmission include aerosols and direct contact with rodents. and 32. a family of single-stranded. followed by a nonspecific febrile illness and an acute onset of aseptic meningitis. Causes of Chronic Meningitis (Open Table in a new window) Category Agent Bacteria M tuberculosis B burgdorferi T pallidum Brucella species Francisella tularensis Nocardia species . and 12) has been associated with cases of meningoencephalitis. arthritis. 7. and alopecia. This may be associated with orchitis. Outbreaks have also been traced to infected laboratory mice and hamsters. myocarditis. This usually is part of the mononucleosis-like acute seroconversion phenomenon. The mumps virus is the most common cause of aseptic meningitis in unimmunized populations. 12. Chronic meningoencephalitis has been reported with serotypes 7. Adenovirus (serotypes 1. Aseptic meningitis syndrome may be the presenting symptom in a patient with acute HIV infection. an incubation period of approximately 5-10 days ensues.

and laboratory workers dealing with these animals are also at risk. sheep. Transmission to humans occurs following direct or indirect exposure to infected animals (eg. Always consider tuberculous meningitis in the differential diagnoses of patients with aseptic meningitis or chronic meningitis syndromes. It is spread through airborne droplet nuclei. B suis. M tuberculosis is an acid-fast bacillus that causes a broad range of clinical illnesses that can affect virtually any organ of the body. Involvement of . B melitensis. cattle). Direct infection of the CNS occurs in fewer than 5% of cases. goat. abattoir workers. and B canis. Veterinarians. and it infects one third of the world's population.Actinomyces species Fungi C neoformans C immitis B dermatitidis H capsulatum Candida albicans Aspergillus species Sporothrix schenckii Parasites Acanthamoeba species N fowleri Angiostrongylus cantonensis G spinigerum B procyonis Schistosoma species S stercoralis Echinococcus granulosus Brucella species are small gram-negative coccobacilli that cause zoonoses as a result of infection with B abortus. intake of unpasteurized milk products). cattle) or their products (eg. goat. with most patients presenting with acute or chronic meningitis. Persons at risk include individuals who had contact with infected animals (eg. sheep.

bones and joints. Other modes of transmission include direct contact with an active lesion. The onset may be acute. the Middle East. Dissemination may occur in certain individuals (including individuals with underlying immune deficiency [eg. from HIV or pharmaceutical agents] and extremes of age) and may involve the skin. and other immunosuppressants). Hodgkin disease. T pallidum is a slender. a dimorphic fungus. It is usually found in soil. and blood transfusion (rare). but the incidence of non-albicans candidal infections (eg. tourists and local populations) and those with immune deficiency (ie. Involvement of the CNS occurs in fewer than 5% of cases. Inhalation of the conidia establishes a pulmonary infection. The most common species is C albicans. The 4 serotypes are designated A through D. is not well defined. and sarcoidosis. passage through the placenta. with no known T-cell defect). those who use steroids. Most cases of C neoformans have occurred among individuals with AIDS and among organ transplant recipients. however. A large number of cases occur in healthy hosts (eg. B dermatitidis is a dimorphic fungus that has been reported to be endemic in North America (eg. cyclosporine. especially among patients with AIDS. including species with antifungal resistance (eg. and the female genital tract. is the agent of Lyme disease. genitourinary tract. approximately 50-80% of cases occur in immunocompromised hosts. It has been found in high concentrations in aged pigeon droppings and pigeon nesting places.the CNS with tuberculous meningitis is usually caused by rupture of a tubercle into the subarachnoid space. C glabrata). At particular risk are individuals with defects of T-cell–mediated immunity (eg. It has also been isolated from parts of Central America. the gastrointestinal tract. H capsulatum is one of the dimorphic fungi that exist in mycelial and yeast forms. B burgdorferi. Soil that is rich in decaying matter and environments around riverbanks and waterways have been demonstrated to harbor the fungus during outbreaks and are thought to be risk factors for acquiring the infection. The natural habitat of B dermatitidis. . C tropicalis) is increasing. yeast like fungus that is ubiquitous. It has also been reported in patients with idiopathic CD-4 lymphopenia. organ transplantation). dimorphic fungus that exists in mycelial and yeast (spherule) forms. Persons at risk for coccidioidal meningitis include individuals exposed to the endemic regions (eg. C immitis is a soil-based. C neoformans is an encapsulated. Mississippi and Ohio River basins). with the A serotype causing most human infections. South America. and the CNS. AIDS. the most common vectorborne disease in the United States. C krusei. tightly coiled spirochete that is usually acquired by sexual contact. Candida species are ubiquitous in nature. and India. a tick-borne spirochete. They are normal commensals in humans and are found in the skin.

headache. with meningeal sporotrichosis (a rare complication) being the worst complication of S schenckii infections. Infection with free-living amebas is an infrequent but often life-threatening human illness. photophobia. such as placement of ventricular shunts. usually land snails. even in immunocompetent individuals. Duration of illness is weeks to few months. N fowleri is the only recognized human pathogenic species of Naegleria. and crabs. AIDS is also considered a predisposing risk factor. and soil. inadequately chlorinated water and sources associated with poor decontamination techniques). can cause eosinophilic meningitis (pleocytosis with >10% eosinophils) in humans. The first form is an acute onset of high fever. Additional causes of meningitis . Human infections occur following accidental ingestion of food products contaminated with raccoon feces. Its eggs hatch and the larval stages are expelled in the feces. The adult parasite resides in the lungs of rats. B procyonis is an ascarid parasite that is prevalent in the raccoon populations in the United States and rarely causes human eosinophilic meningoencephalitis. The second form. Acanthamoeba and Balamuthia cause granulomatous amebic encephalitis. A cantonensis. Because it is acquired through the nasal area. and it is the agent of primary amebic meningoencephalitis (PAM). ponds. tap water. rivers. It is associated with a poor outcome. is an insidious onset of low-grade fever. Infection occurs when swimming or playing in the contaminated water sources (eg. Humans acquire the infection by ingesting raw mollusks. pools. Death occurs in 3 days in patients who are not treated. plants.Involvement of the CNS usually follows hematogenous dissemination. PAM occurs in 2 forms. and change in mental status. The most important predisposing risk for acquiring disseminated candidal infection appears to be iatrogenic in nature (eg. Go to Staphylococcal Meningitis for complete information on this topic. headache. which is a subacute opportunistic infection that spreads hematogenously from the primary site of infection (skin or lungs) to the CNS and causes an encephalitis syndrome. involvement of the olfactory nerves may manifest as abnormal smell sensation. use of broad-spectrum antibiotics and indwelling devices such as urinary and vascular catheters). The N fowleri amebas invade the CNS through the nasal mucosa and cribriform plate. freshwater prawns. Extracutaneous manifestations may occur. may cause eosinophilic meningoencephalitis. the subacute or chronic form. The parasite has been isolated in lakes. AIDS is a reported underlying risk factor in many described cases. G spinigerum. Humans acquire the infection following ingestion of undercooked infected fish and poultry. and plant products. S schenckii is an endemic dimorphic fungus that is often isolated from soil. occurring within a week following exposure. Infection may also follow neurosurgical procedures. and focal neurologic signs. similar to bacterial meningitis. a gastrointestinal parasite of wild and domestic dogs and cats. the rat lungworm. The larvae develop in the intermediate host.

and other developing areas. . Chad. An incidence rate that is 10-fold higher than that in developed countries has been reported. Epidemiology of bacterial meningitis With almost 8000 cases and 2000 deaths occurring annually. Meningococcal meningitis is endemic in parts of Africa. but N meningitidis causes approximately 4 cases per 100. and Mali.9 to 1.000 children aged 1-23 months. comminuted skull fracture.25-1 case per 1000 live births. especially in the region of the frontal ethmoid sinuses. however. and osteomyelitic erosion. Epidemiology The incidence of meningitis varies with the specific etiologic agent. In the United States. Direct implantation of bacteria into the meninges occurs less frequently and is a complication of head and neck surgery. Periodic epidemics occur in the so-called sub-Saharan "meningitis belt. Nigeria. India. Meningitis affects people of all races.5 cases per 1000 premature births. Patients with any of these conditions are at risk for bacterial meningitis. The incidence is presumed to be higher in developing countries because of less access to preventive services. In 1996. An increased incidence of HIV infection worldwide resulted in a correspondingly increased frequency of meningitis caused by encapsulated organisms (primarily S pneumoniae).Congenital malformation of the stapedial footplate has also been implicated in the development of meningitis.6-4 cases per 100.5 cases per 100. Approximately 30% of newborns with clinical sepsis have associated bacterial meningitis.5 cases per 100. HIB. the biggest wave of meningococcal meningitis outbreaks ever recorded arose in West Africa.000 cases and 25. In parts of Africa. the overall incidence of bacterial meningitis declined from 1.1% for daycare contacts.15 case per 1000 full-term births and 2." as well as among religious pilgrims traveling to Saudi Arabia for the Hajj. Previously. widespread epidemics of meningococcal meningitis occur regularly.000 between 1998 and 2003. penetrating head injury. Since the late 20th century. black people have a higher reported rate of meningitis than white people and Hispanic people. as well as in conjunction with a nation’s medical resources.000 population. The incidence of neonatal bacterial meningitis is 0. Burkina Faso. the incidence is 0.[5] This was partially due to the widespread use of the HIB vaccination. such as vaccination. In addition. the epidemiology of bacterial meningitis has been substantially changed by multiple developments. N meningitidis. The attack rate per year in the United States is reportedly 0. The rate of meningitis caused by S pneumoniae is 6.000 children aged 1-23 months. An estimated 250. The frequency of H influenzae type B (HIB) disease has been markedly reduced.000 deaths occurred in Niger. bacterial meningitis continues to be a significant source of morbidity and mortality. Skull fractures can tear the dura and cause a CSF fistula.[4] Even so. The risk of secondary meningitis is 1% for family contacts and 0. and S pneumoniae accounted for more than 80% of cases of bacterial meningitis.

in contrast to 20. . patients younger than 5 years or older than 60 years are at increased risk for bacterial meningitis. Of patients with bacterial meningitis.000 cases among children in 1987. Changing Epidemiology of Acute Bacterial Meningitis in the United States* (Open Table in a new window) Bacteria 1978-1981 1986 1995 19982007 6.7-7. the incidence of meningitis declined by 31%. The median age for persons with bacterial meningitis was 25 years in 1998. independent of other factors. nearly eliminating it in many developed countries where routine HIB vaccination is used. This shift has reportedly been less dramatic in developing countries. while in 1986.8 cases per 100. The routine screening of group B streptococcus in pregnant women may have also reduced the incidence of meningitis due to S agalactiae. it was 15 months. During a 1998-2007 survey. the peak incidence is in infants aged 3-8 months.which decreased the incidence of HIB meningitis by more than 90% (see Table 3 “Changing Epidemiology of Acute Bacterial Meningitis in the United States. The introduction of vaccines against S pneumoniae has substantially reduced the incidence of pneumococcal meningitis in children. Because the frequency of bacterial meningitis in children has declined.[6] A total of 255 cases of invasive H influenzae disease among children younger than 5 years were reported to the CDC in 1998.000 adults. and the mean annual incidence has been reported as 3. In addition. Newborns are at highest risk for acute bacterial meningitis. has reduced the incidence of meningitis in recent years. After the first month of life.4% 13. These efforts. the condition is becoming more of a disease of adults. together with the use of the HiB vaccine.7% 3. where the use of the HIB vaccine is not as widespread.2 cases per 100. 61% had no previous or present accompanying diseases that may have predisposed them to meningitis.1% 58% H influenzae 48% 45% 7% Listeria monocytogenes 2% 3% 8% N meningitidis 20% 14% 25% S agalactiae 3% 6% 12% S pneumoniae 13% 18% 47% *Nosocomial meningitis is not included. Annual incidences are 1. Routine vaccination against meningococcus with the use of serogroup C meningococcal conjugate vaccine may also reduce the incidence of N meningitidis infections.[7] Excluding meningococcal meningitis. despite the above-mentioned shift in median age for persons with the disease. statistics show an increased incidence in persons aged 60 years and older.000 adults. Table 3. These data include only the 5 major meningeal pathogens.9% 18.” below).

000 population. Table 4. the male-to-female ratio is 3:1.) The attack rate for bacterial meningitis is reportedly 3.000 population.Depending on their age. E coli K1 and S agalactiae meningitis are common among the neonatal group. compared with 2.) In neonates. (The development of neonatal meningitis is related to labor delivery.3 male cases per 100. immaturity. and L monocytogenes meningitis is common among neonates and elderly individuals. The Most Common Bacterial Pathogens Based on Age and Predisposing Risks (Open Table in a new window) Risk and/or Predisposing Factor Age 0-4 weeks Bacterial Pathogen Streptococcus agalactiae (group B streptococci) E coli K1 Listeria monocytogenes Age 4-12 weeks S agalactiae E coli H influenzae S pneumoniae N meningitidis Age 3 months to 18 years N meningitidis S pneumoniae H influenzae Age 18-50 years S pneumoniae N meningitidis .6 female cases per 100. (In meningitis caused by the mumps virus. The epidemiology of bacterial meningitis continues to evolve as preventive strategies are implemented. males and females are affected equally.” below). individuals are also predisposed to other etiologic agents (see Table 4 “The Most Common Bacterial Pathogens Based on Age and Predisposing Risks. and environment. it results from colonized pathogens in the maternal intestinal or genital tract.

including P aeruginosa Basilar skull fracture S pneumoniae H influenzae Group A streptococci CSF shunts Coagulase-negative staphylococci S aureus Aerobic gram-negative bacilli Propionibacterium acnes Epidemiology of specific bacterial pathogens of acute meningitis H influenzae meningitis primarily affects infants younger than 2 years. including neurosurgery Staphylococcus aureus Coagulase-negative staphylococci Aerobic gram-negative bacilli.H influenzae Age older than 50 years S pneumoniae N meningitidis L monocytogenes Aerobic gram-negative bacilli Immunocompromised state S pneumoniae N meningitidis L monocytogenes Aerobic gram-negative bacilli Intracranial manipulation. .

S pneumoniae is associated with one of the highest mortality rates among the bacterial agents that cause meningitis (19-26%). South America. H capsulatum has been reported from many areas of the world. It has also been found in rats outside this region. the last epidemic of St. Louis encephalitis virus usually occurs during the summer and early fall. the Middle East. Louis encephalitis was in Florida in 1990. The enteroviruses are distributed worldwide. Go to Haemophilus Meningitis for complete information on this topic. Infections with the St. . Aseptic meningitis occurs in individuals of all ages. Aseptic meningitis tends to occur 3 times more frequently in males than in females. primarily affecting individuals older than age 60 years. Puerto Rico.9 cases per 100. No racial differences are reported. with the highest attack rates in children who are younger than 1 year. A cantonensis is common in Southeast Asia and the Pacific Islands. most human cases occur among young adults during autumn.000 person-years. Twenty-four cases were reported to the CDC in 1998. Epidemiology of aseptic meningitis Viruses are the major cause of aseptic meningitis syndrome. with most cases originating from Louisiana. Infection with the La Crosse encephalitis virus also usually occurs during the summer and early fall. and India. although it is more common in children. Mississippi and Ohio River basins).S agalactiae has also been reported in adults. with the Mississippi and Ohio River valleys being the most endemic regions in North America. B dermatitidis is reportedly endemic in North America (eg. Infections with the LCM virus occur worldwide. with symptoms being typical of acute aseptic meningitis. an illness that is reported to occur with an incidence rate of 10. Most enterovirus infections occur in individuals who are younger than age 15 years. It has also been isolated from parts of Central America. The overall case-fatality rate in adults is 34%. and Louisiana. and the infection rates vary depending on the season of the year and a population’s age and socioeconomic status. In the United States. especially during summer. presumably introduced by ship-borne rats from endemic areas. with symptoms again being typical of acute aseptic meningitis. particularly in regions of Africa.

[8] Cerebral infarction and edema are predictors of poor outcome. mortality. within the north and south 40° latitudes (ie.5 cases per 100. with most cases coming from the tropical regions of the Americas. Epidemiology of chronic meningitis Brucella -associated chronic meningitis has a worldwide distribution and is common in the Middle East. A seizure during an episode of meningitis also is a risk factor for mortality or neurologic sequelae.000 population. In the United States following the control of bovine infections. Serotypes B and C of C neoformans have been restricted mostly to tropical and subtropical regions. and Central and South America). India. Mexico.000 population. and prognosis depend on the pathogen. China. Wisconsin. B burgdorferi is a tick-borne spirochete that occurs in the temperate regions of North America (eg.G spinigerum is common in Southeast Asia. Mexico. and serotype B has been isolated from eucalyptus trees. the estimated case rates among endemic countries ranged from 62-411 cases per 100. Morbidity. M tuberculosis is worldwide in distribution. Morbidity and mortality for bacterial and viral meningitis Bacterial meningitis causes long-term sequelae and results in significant mortality beyond the neonatal period. as are the signs of disseminated intravascular coagulopathy and endotoxic shock. parts of California and Oregon). Prolonged or difficult-to-control seizures are predictors of complications. Go to Aseptic Meningitis for complete information on this topic. and the severity of acute illness. parts of the southwest United States. Bacterial meningitis can be extremely serious. C neoformans has a worldwide distribution. S schenckii has been reported worldwide. the patient's age and condition. The presence of low-level pleocytosis (< 20 cells) in patients with bacterial meningitis suggests a poorer outcome. Europe. . incidence decreased to less than 0. Patients with meningitis who present with an impaired level of consciousness are at increased risk for developing neurologic sequelae or dying. and humans are its only reservoir. and Central and South America. The distribution of C immitis is limited to the endemic regions of the Western Hemisphere. northeast United States. Minnesota. In 1997. and Asia. and only 79 cases were reported to the CDC in 1998. and Japan but has been reported sporadically worldwide.

coma. The reported mortality rates for specific bacterial organisms are as follows:   S pneumoniae meningitis . agammaglobulinemia). 10% in children) and morbidity (15%) in meningitis. Patients usually have subtle CNS changes. In patients with deficient humoral immunity (eg. even with immediate medical treatment. Among bacterial pathogens. with significant long-term sequelae in survivors.Advanced bacterial meningitis can lead to brain damage. and 1 in 7 survivors is left with a severe handicap. and gram-negative bacilli has a higher case-fatality rate compared with meningitis caused by other bacterial agents. enterovirus meningitis may have a fatal outcome. patient age. and hospital course. Bacterial meningitis is fatal in 1 in 10 cases. L monocytogenes. Mortality is 50-90% and morbidity is even higher if severe neurologic impairment is evident at the time of presentation (or with extremely rapid onset of illness).19-26% H influenzae meningitis . Serious complications include the following:              Hearing loss Cortical blindness Other cranial nerve dysfunction Paralysis Muscular hypertonia Ataxia Multiple seizures Mental motor retardation Focal paralysis Ataxia Subdural effusions Hydrocephalus Cerebral atrophy Mortality rates for bacterial meningitis are highest in the first year of life. Despite effective antimicrobial and supportive therapy. and increase again in old age. presenting features.3-6% . The prognosis of meningitis caused by opportunistic pathogens depends on the underlying immune function of the host. pneumococcal bacteria cause the highest rates of mortality (20-30% in adults. long-term fluconazole for suppression in patients with HIV-associated cryptococcal meningitis). Many patients who survive the disease require lifelong suppressive therapy (eg. and death. Meningitis caused by S pneumoniae. Long-term sequelae are seen in as many as 30% of survivors and vary with etiologic agent. such as deafness or brain injury. decrease in midlife. mortality rates among neonates remain high.

These tests can also help your doctor look for infection in other areas of the body that may be associated with meningitis. however. Spinal tap (lumbar puncture). chest or sinuses may reveal swelling or inflammation. < 2 y. Patients with viral meningitis usually have a good prognosis for recovery. you may need additional tests.15-29% Patients with meningococcal meningitis have a better prognosis than do those with pneumococcal meningitis. This may provide results about your meningitis in as little as four hours and help to determine proper treatment. agammaglobulinemia). If your doctor suspects meningitis. During the exam. >60 y) and those with significant comorbidities and underlying immunodeficiencTests and diagnosis By Mayo Clinic staff Your family doctor or pediatrician can diagnose meningitis based on a medical history. your doctor may check for signs of infection around the head. The definitive diagnosis of meningitis is often made by analyzing a sample of your cerebrospinal fluid (CSF). The prognosis is worse for patients at the extremes of age (ie. which is collected during a procedure known as a spinal tap. a physical exam and certain diagnostic tests. with a mortality rate of 20-30%. Blood drawn from a vein is sent to a laboratory and placed in a special dish to see if it grows microorganisms. In people with meningitis. In patients with deficient humoral immunity (eg. X-rays and computerized tomography (CT) scans of the head. with a mortality rate of 4-5%. The mortality rate for viral meningitis (without encephalitis) is less than 1%. particularly bacteria. If you have chronic meningitis caused by cancer or an inflammatory illness. he or she may order a DNA-based test known as a polymerase chain reaction (PCR) amplification to check for the presence of viral causes of meningitis. then examined under a microscope for bacteria.3-13% L monocytogenes meningitis . the CSF fluid often shows a low sugar (glucose) level along with an increased white blood cell count and increased protein. throat and the skin along the spine. y. You or your child may undergo the following diagnostic tests:    Blood cultures. CSF analysis may also help your doctor identify the exact bacterium that's causing the illness. enterovirus meningitis may have a fatal outcome. It can take up to a week to get these test results. Imaging. . A sample may also be placed on a slide to which stains are added (Gram's stain). patients with meningococcemia have a poor prognosis.  N meningitidis meningitis . ears.

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