eMedicine Specialties > Neurology > Neurological Infections

Meningococcal Meningitis

Francisco de Assis Aquino Gondim, MD, MSc, PhD, Professor Adjunto II, Departments of Physiology and Pharmacology, Neurology Residency Program Director, Faculdade de Medicina, Universidade Federal do Ceará, Brazil
Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience; Sidney E Croul, MD, Director of Neuropathology, Professor, Department of Pathology and Laboratory Medicine, Medical College of Pennsylvania Hahnemann University

Updated: Aug 11, 2009

Introduction

Background

Meningococcal meningitis (International Classification of Disease-9 [ICD-9] code: 036.0) has been recognized as a serious problem for almost 200 years. It was first identified definitely by Vieusseux in Geneva in 1805. The causative organism, Neisseria meningitidis, was isolated first in 1887.

Meningococcal disease still is associated with a high mortality rate and persistent neurological defects, particularly among infants and young children.

The first successful treatment of meningitis with intravenous and intrathecal penicillin was reported in 1944, and the first clinical trials using high doses of intravenous penicillin as monotherapy for the treatment of meningitis were reported in 1950. Since then, penicillin has remained the drug of choice for the treatment of meningococcal meningitis.¹

For related information, see eMedicine article Meningococcal Infections.

Pathophysiology

N meningitidis is a gram-negative, aerobic, encapsulated diplococcus that grows best on enriched media such as Mueller-Hinton or chocolate agar, at 37° and in an atmosphere of 5-10% carbon dioxide.

Meningococci comprise numerous serogroups that are based on the composition of their polysaccharide capsular antigens. They differ in their agglutination reactions to sera directed against polysaccharide antigens. At least 13 serogroups have been described: A, B, C, D, E, H, I, K, L, W-135, X, Y, and Z. Serogroups B and C have caused most cases of meningococcal meningitis in the United States since the end of World War II; before that, group A was more prevalent. More than 99% of meningococcal infections are caused by serogroups A, B, C, 29E, or W-135.

The natural habitat and reservoir for meningococci is the mucosal surfaces of the human nasopharynx and, to a lesser extent, the urogenital tract and anal canal. Approximately 5-10% of adults are asymptomatic nasopharyngeal carriers, but that number increases to as many as 60-80% of members of closed populations (eg, military recruits in camps).

The modes of infection include direct contact or respiratory droplets from the nose and throat of infected people. Meningococcal disease most likely occurs within a few days of acquisition of a new strain, before the development of specific serum antibodies.

The incubation period averages 3-4 days (range 1-10 days), which is the period of communicability. Bacteria can be found for 2-4 days in the nose and pharynx and for up to 24 hours after starting antibiotics. Treatment with penicillin may not eradicate the bacteria from the nasopharyngeal carriers.

After adherence to the nasopharyngeal mucosa, meningococci are transported to membrane-bound phagocytic vacuoles. Within 24 hours, they can be seen in the submucosa, close to vessels and local immune cells. In most cases, meningococcal colonization of mucosal surfaces leads to subclinical infection or mild symptoms. In approximately 10-20% of cases, N meningitidis enters the bloodstream. In the vascular compartment, they may be killed by bactericidal antibodies, complement, and phagocytic cells or may multiply, initiating the bacteremic phase. Organisms replicate rapidly.

Systemic disease appears with the development of meningococcemia and usually precedes meningitis by 24-48 hours. This can lead to systemic infection in the form of bacteremia, metastatic infection that commonly involves the meninges (see Media file 3), or severe systemic infection with circulatory collapse and disseminated intravascular coagulation (DIC). Meningococcemia leads to diffuse vascular injury, which is characterized by endothelial necrosis, intraluminal thrombosis, and perivascular hemorrhage.

Grossly purulent exudate is seen in the leptomeninges.

Meningococci that elaborate a capsule can lead to invasive disease. The capsule protects them from desiccation and from host immune mechanisms. Adhesins and endotoxins also enhance their pathogenic potential. Dysfunctional properdin (ie, component of the alternative pathway of complement), HIV infection, functional or anatomical asplenia, and congenital complement deficiencies also predispose individuals to meningococcal disease.

Individuals acquire the infection if they are exposed to virulent bacteria and have no protective bactericidal antibodies. Smoking and concurrent viral infection of the upper respiratory tract diminish the integrity of the respiratory mucosa and increase the likelihood of invasive disease. Crowding living conditions also facilitate disease spread, since individuals from different areas have different strains of meningococci. The risk of invasive disease is higher in the first few days after exposure to a new strain.

Frequency

United States

Since 1960, the incidence has been stable, at approximately 0.9-1.5 cases per 100,000 people per year. Most cases occur during winter and early spring. In the United States, increased frequency of serogroups B and Y meningococci has been noted since 1990. The frequency of localized outbreaks has increased since 1991.^2,3

International

Serogroups A, B, and C are responsible for most cases of meningococcal disease throughout the world.

In Europe and the Americas, serogroup B is the predominant agent causing meningococcal disease, followed in frequency by serogroup C. Historically, serogroup A was the main cause of epidemic meningococcal disease globally, and serogroup A is still the predominant cause of meningococcal meningitis in Africa and Asia.

In the African "meningitis belt" (a region of savanna that extends from Ethiopia in the east to Senegal in the west), this disease frequently occurs in epidemics during the hot and dry weather (December to March).

The recent meningococcal meningitis pandemic, which began in 1996, has resulted so far in approximately 300,000 cases being reported to the World Health Organization (WHO).

Mortality/Morbidity

Morbidity and mortality rates from the disease remain high. Apart from epidemics, at least 1.2 million cases of bacterial meningitis are estimated to occur every year; 135,000 of them are fatal. Approximately 500,000 of these cases and 50,000 of the deaths are due to meningococci.

• Even when the disease is diagnosed early and adequate therapy is instituted, the case-fatality rate ranges from 5-10% and may exceed 40% in patients with meningococcal sepsis. In a review of 493 episodes of bacterial meningitis in adults, the overall case-fatality rate was 25%. In another study, patients with meningococcal meningitis had a case-fatality rate of 7.5%.⁴
• In developing countries, the mortality rate from bacterial meningitis is often higher (20-40%) than in developed countries.
• Among those who survive the meningococcal disease, 10-20% experience neurological sequelae.
• A 2008 published cohort study from Netherlands (the Meningitis Cohort Study) revealed a 7% mortality and unfavorable outcome in 12% of the cases.⁵

Race

In one study conducted in the United States, the incidence of meningococcal disease was slightly higher among African Americans (1.5 cases per 100,000 people) than whites (1.1 cases per 100,000 people).

Sex

In one study conducted in the United States, males accounted for 55% of total cases of meningococcal meningitis.

Age

Meningococcal meningitis most commonly affects individuals aged between 3 years and adolescence. It rarely occurs in individuals older than 50 years.

Clinical

History

• In a 2008 published cohort study from Netherlands (the Meningitis Cohort Study), only 70% of the patients had the classic triad of fever, neck stiffness, and change in mental status. If the presence of rash was added, 89% of the patients had 2 of the 4 features.⁵
• Meningococcal meningitis is characterized by acute onset of intense headache, fever, nausea, vomiting, photophobia, and stiff neck.
• Lethargy or drowsiness frequently is reported. Stupor or coma is less common. If coma is present, the prognosis is poor.
• Patients also may complain of skin rash, which usually points to disease progression.
• The clinical pattern of bacterial meningitis is quite different in young children: Bacterial meningitis usually presents as a subacute infection that progresses over several days.
  • Irritability is a common presenting feature, and headache and neck stiffness may not be present. Projectile vomiting may occur.
  • Seizures occur in 40% of children with meningitis, typically during the first few days. The majority of seizures have a focal onset.
  • In infants, the illness may have an insidious onset; stiff neck may be absent. In children, even when the combination of convulsive status epilepticus and fever is present, the classic signs and symptoms of acute bacterial meningitis may not be present.⁶

Physical

• Neurological signs include nuchal rigidity, lethargy, delirium, coma, or convulsions.
  • Most adult patients have an altered mental state, clinical signs of nuchal rigidity (eg, Kernig sign, Brudzinski sign), and fever.
  • Elderly patients are prone to have an altered mental state and a prolonged course with fever.
• Patients older than 30 years were noted to have petechiae (62%) less frequently than younger patients (81%).
• A more severe but less common form of meningococcal disease is meningococcal septicemia, which is characterized by rapid circulatory collapse and a hemorrhagic rash.
• The Waterhouse-Friderichsen syndrome may develop in 10-20% of children with meningococcal infection. This syndrome is characterized by large petechial hemorrhages in the skin and mucous membranes, fever, septic shock, and DIC.
• A petechial or purpuric rash usually is found on the trunk, legs, mucous membranes, and conjunctivae. Occasionally, it is on the palms and soles. The rash may progress to purpura fulminans, when it usually is associated with multiorgan failure (ie, Waterhouse-Friderichsen syndrome).

Differential Diagnoses

Other Problems to Be Considered

Rocky Mountain spotted fever⁷
Streptococcal meningitis
Listerial meningitis
Adrenal failure
Sepsis
Multiorgan failure

Workup

Laboratory Studies

• Laboratory examination of the cerebrospinal fluid (CSF) usually confirms the presence of meningitis. Typical CSF abnormalities in meningitis include the following:
  • Increased opening pressure (>180 mm water)
  • Pleocytosis of polymorphonuclear leukocytes (WBC counts between 10 and 10,000 cells/µL, predominantly neutrophils)
  • Decreased glucose concentration (<45 mg/dL)
  • Increased protein concentration (>45 mg/dL)
• Gram stain and culture of CSF identify the etiological organism, N meningitides. In bacterial meningitis, Gram stain is positive in 70-90% of untreated cases, and culture results are positive in as many as 80% of cases.
• More specialized laboratory tests, which may include culture of CSF and blood specimens, are needed for identification of N meningitidis and the serogroup of meningococci, as well as for determining its susceptibility to antibiotics.
• Polymerase chain reaction (PCR)⁸ may be used to complement standard laboratory procedures for the diagnosis of meningococcal meningitis.⁹ The IS1106 PCR is a rapid and sensitive test for confirmation of the diagnosis; its sensitivity is not affected by prior antibiotic treatment.¹⁰ PCR of the nspA gene was also reported to be a fast diagnostic test.¹¹

Imaging Studies

• Perform a neuroimaging study (either MRI or CT scan) prior to lumbar puncture in all patients in whom meningitis is suspected. CT scan findings are usually normal. However, imaging is an important cause of delay of therapy.
• MRI with contrast is preferred to CT scan because MRI better demonstrates meningeal lesions, cerebral edema, and cerebral ischemia. T1 may show obliterated cisterns. Contrast enhances the cisterns, and extension of enhancing subarachnoid exudate deep into the sulci may be seen in severe cases. Strokes can be seen with the development of vasculitis and cerebritis. CNS complications that can be visualized by MRI include hydrocephalus, aqueductal obstruction, ventriculitis (especially in neonates), choroid plexitis, subdural effusion, and empyema.
• Indications for performing CT scan prior to lumbar puncture include altered level of consciousness, papilledema, focal neurological deficits, and/or focal or generalized seizure activity.

Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead shows small intracerebral hemorrhage foci on the right temporal lobe, and the curved arrow shows the effect of increased intracranial pressure on the cerebellum.

Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique closed arrow). The black arrow head on the left shows soft tissue edema.

Other Tests

An electroencephalogram (EEG) study is sometimes useful to document irritable electrical patterns that may predispose the patient to seizures. Periodic complexes and periodic lateralizing epileptiform discharges (PLEDs) may be suggestive of encephalitis caused by herpes simplex virus.

Histologic Findings

During the first few days, the subarachnoid and ventricular exudate contains large numbers of neutrophils and necrotic debris. Intracellular and extracellular bacteria can be demonstrated. The exudate extends along the perivascular spaces into the cortex and cerebral cortex. Purulent material usually is observed in the choroid plexus. With time, the number of mononuclear leukocytes increases, and they predominate by the end of the first week. Fibroblasts also proliferate.

Inflammatory cells infiltrate leptomeningeal and cortical arteries and veins and accumulate in the intima. Thrombosis of small vessels leads to infarction. This pattern is common in autopsied cases.

Treatment

Medical Care

Meningococcal disease is potentially fatal and always should be viewed as a medical emergency. Admission to a hospital is necessary. To prevent serious neurological morbidity and death, prompt institution of antibiotic therapy is essential when the diagnosis of bacterial meningitis is suspected.

• Institute antimicrobial therapy as soon as possible after the lumbar puncture is performed.
• If imaging studies are indicated before lumbar puncture, draw blood for culture and begin administration of empiric antibiotics. Administration of empiric antibiotics is unlikely to decrease diagnostic sensitivity if CSF is tested for bacterial antigens early in the course of the illness.
• Long delays may occur in the emergency department before initiation of antibiotics in patients with suspected bacterial meningitis. In general, these delays appear to be physician generated and, to a great extent, potentially avoidable.¹²
• In children and adults, the recommended initial empiric therapy consists of third-generation cephalosporins, but the addition of ampicillin is required in patients in whom a Listeria species pathogen is suspected (eg, patients older than 50 years, neonates). Once the organism is identified, the antibiotic regimen can be changed appropriately.
• A recent study has suggested that at least in children, CSF sterilization may occur more rapidly after initiation of parenteral antibiotics than previously suggested, with complete sterilization of meningococcus within 2 hours and the beginning of sterilization of pneumococcus by 4 hours.

Surgical Care

Surgical interventions may be necessary for the management of complications such as subdural effusions, empyema, and hydrocephalus.

Medication

At presentation, meningitis due to N meningitidis may be impossible to differentiate from other types of meningitis. Thus, empirical treatment with an antibiotic with effective CNS penetration should be based on age and underlying disease status, since delay in treatment is associated with adverse clinical outcome.

Standard empirical therapy varies according to age, as follows:

• In infants younger than 4 weeks, it consists of ampicillin plus cefotaxime or an aminoglycoside.
• Infants aged 4-12 weeks should be treated with ampicillin plus a third-generation cephalosporin.
• In children aged 12 weeks to 18 years, a third-generation cephalosporin or ampicillin plus chloramphenicol is an appropriate combination.
• Adults aged 18-50 years and individuals with basilar skull fracture should be treated with a third-generation cephalosporin, while individuals older than 50 years should be treated with ampicillin plus a third-generation cephalosporin.

Once the accurate diagnosis of meningococcal meningitis is established, appropriate changes can be made. Currently, penicillin is the drug of choice for the treatment of meningococcal meningitis and septicemia. Unresponsiveness to penicillin has not been observed in the United States. Routine testing for susceptibility of meningococcal isolates is not necessary, unless the patient does not exhibit appropriate clinical response.

Therapy should be changed to ceftriaxone (or cefotaxime) if the isolate is resistant to penicillin.

The use of dexamethasone in the management of bacterial meningitis in adults remains controversial. It may be used in children, especially in those with meningitis caused by Haemophilus influenzae. In adults with suspected bacterial meningitis, especially in high-risk cases, the adjunctive use of dexamethasone may be beneficial.

Person-to-person transmission can be interrupted by chemoprophylaxis, which eradicates the asymptomatic nasopharyngeal carrier state. Rifampin, quinolones, and ceftriaxone are the antimicrobials used to eradicate meningococci from the nasopharynx.

Antibiotics

Penicillin is the drug of choice for the treatment of meningococcal meningitis and septicemia. Chemoprophylactic antimicrobials most commonly used to eradicate meningococci include rifampin, quinolones (eg, ciprofloxacin), and sulfonamides. (Also included in this category are ceftriaxone, minocycline, and spiramycin.)

Penicillin G (Pfizerpen)

Patients in whom meningococcal disease is suspected should receive a high dose of this drug, which interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Dosing

Adult

4 million U initially through intermittent IV q4h

Pediatric

250,000 U/kg/d IV in divided doses

Interactions

Probenecid can increase effectiveness

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with impaired renal function

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms.

Dosing

Adult

Treatment: 2 g IV q12h
Chemoprophylaxis: 250 mg IM (single dose)

Pediatric

Treatment: 50 mg/kg IV q12h; not to exceed 4 g/d
Chemoprophylaxis
<15 years: 125 mg IM (single dose)
>15 years: 250 mg IM (single dose)

Interactions

Probenecid may increase levels; ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients with renal impairment; caution in breastfeeding women

Rifampin (Rifadin, Rimactane)

Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. For chemoprophylactic use only.

Dosing

Adult

600 mg PO for 2 d

Pediatric

<1 month: 5 mg/kg PO q12h for 2 d
>1 month: 10 mg/kg PO q12h for 2 d

Interactions

Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, cyclosporine, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; enalapril may increase blood pressure; isoniazid may result in higher chances of hepatotoxicity than with either agent alone

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic disease, as drug may cause further hepatic damage; serious thrombocytopenia may occur, which is reversible if therapy discontinued; if treatment continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur

Ciprofloxacin (Cipro)

Single dose (500 mg) may be effective for eradication of meningococcal carriage in adults. For chemoprophylactic use only.

Dosing

Adult

500 mg PO qd

Pediatric

<18 years: Not recommended; has caused cartilage damage in immature experimental animals

Interactions

Reduces therapeutic effects of phenytoin; antacids, iron salts, and zinc salts may reduce serum levels; may increase toxicity of theophylline, cyclosporine, and digoxin; may increase effects of anticoagulants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

With long-term use, may need periodic renal, hepatic, and hematologic evaluations; adjust dose in patients with impaired renal function

Follow-up

Further Inpatient Care

• Complete appropriate antimicrobial therapy course.
• Observe the patient for any complications or neurological sequelae.

Further Outpatient Care

• Advise any household contacts and close respiratory contacts that chemoprophylaxis agents are available to eliminate the carrier state and prevent the spread of infection.¹³
• Observe patients for any late complication or neurological sequelae.

Deterrence/Prevention

• Can be achieved by either immunoprophylaxis or chemoprophylaxis
• Immunoprophylaxis
  • Vaccination is used for close contacts of patients with meningococcal disease due to A, C, Y, or W135 serogroups to prevent secondary cases.¹⁴
  • No effective vaccine exists to protect individuals from meningococcal meningitis caused by serogroup B.¹⁵
  • Epidemics usually spread rapidly to a peak within weeks but may last for several months in the absence of vaccination.
  • Mass immunization of selected communities using polyvalent A and C polysaccharide vaccine is a useful control measure.
• Chemoprophylaxis
  • In general, chemoprophylaxis is not recommended during epidemics because of multiple sources of exposure and prolonged risk of exposure. Logistic problems and high cost also make this an impractical alternative.¹⁶
  • Chemoprophylaxis can be considered for people in close contact with patients in the endemic situation. It is not an effective means of interrupting transmission during an epidemic. Ciprofloxacin 500 mg in a single dose is probably the easiest option in adults. Children could receive either a single IM injection of ceftriaxone or 4 oral doses of rifampin over 2 days, according to body weight.
  • Antimicrobials commonly used for chemoprophylaxis are rifampin, ciprofloxacin, ceftriaxone, minocycline, and spiramycin.
  • When oral rifampin (4 doses in 2 d) was compared with a single IM dose of ceftriaxone for prophylaxis, follow-up cultures indicated that ceftriaxone was significantly more effective. Ceftriaxone may provide an effective alternative to rifampin for prophylaxis for people in close contact with patients with meningococcal meningitis.¹⁷
  • Sometimes, an alternative to chemoprophylaxis may be protective chemotherapy that can prevent the development of meningitis in individuals incubating the disease.

Complications

• Early complications of bacterial meningitis include seizures, raised intracranial pressure, cerebral venous thrombosis, sagittal sinus thrombosis, and hydrocephalus. The risk of cerebral herniation from acute meningitis is about 6-8%.
• In fulminant meningococcemia, severe DIC may develop, leading to hemorrhagic diathesis with bleeding into the lungs, urinary tract, and gastrointestinal tract. Ischemic complications of DIC also are common.
• Infrequent suppurative complications include septic arthritis, purulent pericarditis, endophthalmitis, and pneumonia. Of survivors, 10% developed allergic complications manifested as cutaneous vasculitis or arthritis.
• Late complications may include communicating hydrocephalus (which can present with gait difficulty, mental status changes, and incontinence) and hearing loss¹⁸ .
• In one study, 27% of survivors experienced one or more suppurative, allergic, or neurological complications, including hearing loss, cutaneous vasculitis, and arthritis.
• Hearing loss, noted in 9% of children, occurred significantly more often in patients with marked leukocytosis or leukopenia or with CSF leukocytosis greater than 10 X 10⁹/L.

Prognosis

• The prognosis for meningococcal meningitis is fair if the patient does not have focal neurological deficits and is not stuporous or comatose. The prognosis of meningococcal disease is poor when the infection has a septicemic component. Most patients with meningococcal meningitis recover completely if appropriate antibiotic therapy is instituted promptly.
• Thrombocytopenia, a lowered coagulation index, moderate anemia (hemoglobin <11 g/dL), an obtunded mental state, and history of convulsions were reported to be poor prognostic factors. In one study, only anemia was correlated independently with fatality; the results suggested that anemia should be considered an important prognostic marker in the acute phase of meningococcal meningitis.

Patient Education

For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education articles Meningitis in Adults and Meningitis in Children.

Miscellaneous

Medicolegal Pitfalls

• To prevent death, prompt institution of antibiotic therapy is essential when the diagnosis of bacterial meningitis is suspected.
• Failure to make the early diagnosis of meningococcal disease and failure to provide prompt treatment are common reasons for malpractice claims.
• In early stages, meningococcal meningitis may be misdiagnosed as a viral infection and the patient may be discharged from an emergency department.
• The petechial rash may be difficult to recognize in dark-skinned patients.

Special Concerns

• The Advisory Committee on Immunization Practices (ACIP) modified its guidelines after 2 studies by the Centers for Disease Control and Prevention (CDC), which were performed in 1998, identified the slightly higher risk among college freshman dormitory residents. Vaccination should be provided or made easily available to freshmen who wish to reduce their risk of disease.
• Travelers who are planning to visit areas affected by meningococcal outbreaks are advised vaccination.
• Oily chloramphenicol may be the drug of choice in areas with limited health facilities because a single dose of the long-acting form has been shown to be effective.
• More information on meningococcal disease may be found at the CDC Web site.

Multimedia

Media file 1: Head CT demonstrates enlargement of the temporal horns indicating increased intracranial pressure (horizontal open large arrow). The closed arrowhead shows small intracerebral hemorrhage foci on the right temporal lobe, and the curved arrow shows the effect of increased intracranial pressure on the cerebellum.

Media file 2: Head CT shows small intracerebral hemorrhage foci (vertical closed arrow). Basal ganglia can also not be visualized because of diffuse edema (oblique closed arrow). The black arrow head on the left shows soft tissue edema.

Media file 3: Grossly purulent exudate is seen in the leptomeninges.

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Keywords

Neisseria meningitidis, N meningitidis, meningococcal disease, meningococci, meningococcal infections, Neisseria lactamica, N lactamica, bacterial meningitis, Waterhouse-Friderichsen syndrome, meningococcal septicemia

Contributor Information and Disclosures

Author

Francisco de Assis Aquino Gondim, MD, MSc, PhD, Professor Adjunto II, Departments of Physiology and Pharmacology, Neurology Residency Program Director, Faculdade de Medicina, Universidade Federal do Ceará, Brazil
Francisco de Assis Aquino Gondim, MD, MSc, PhD is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society
Disclosure: Boehringer-Ingelheim Honoraria Speaking and teaching

Coauthor(s)

Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine
Disclosure: Nothing to disclose.

Sidney E Croul, MD, Director of Neuropathology, Professor, Department of Pathology and Laboratory Medicine, Medical College of Pennsylvania Hahnemann University
Sidney E Croul, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuropathologists, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Norman C Reynolds Jr, MD, Neurologist, Veterans Affairs Medical Center of Milwaukee; Professor Medical College of Wisconsin (retired)
Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

Related guidelines

Management of invasive meningococcal disease in children and young people. A national clinical guideline.

EFNS guideline on the management of community-acquired bacterial meningitis: report of an EFNS Task Force on acute bacterial meningitis in older children and adults.

Prevention and control of meningococcal disease. Recommendations of the Advisory Committee on Immunization Practices (ACIP). (Addendum 1) Recommendations for all persons aged 11--18 years; (Addendum 2) Recommendations for children aged 2--10 years at increased risk for invasive meningococcal disease.

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