AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

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 Image 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.

Invasive disease depends on host factors. Infants are protected from meningococcal disease for the first few months of life by transferred maternal antibodies and low rate of meningococcal acquisition. Subsequently, susceptibility peaks at age 6-12 months and decreases again after colonization of closely related nonpathogenic bacteria such as Neisseria lactamica that have surface antigens in common with virulent strains. Colonization with N meningitidis gradually replaces the nonpathogenic bacteria and induces antibodies to the infecting strain, thus reinforcing natural immunity. Invasive disease occurs if no protective bactericidal antibodies are mounted against the infecting strain.

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.

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%.
• 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.

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

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• 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.

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).

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

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

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab 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) may be used to complement standard laboratory procedures for the diagnosis of meningococcal meningitis. The IS-1106 PCR is a rapid and sensitive test for confirmation of the diagnosis; its sensitivity is not affected by prior antibiotic treatment. PCR of the nspA gene was also reported to be a fast diagnostic test.

Imaging Studies

• Perform a neuroimaging study (either MRI or CT scan) in all patients in whom meningitis is suspected. CT scan findings are usually normal.
• 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.

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

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

• Obtain CSF promptly, before any neuroimaging studies, unless the patient is in a coma or has papilledema, focal neurological deficits, or seizures.
• 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.
• 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

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

Drug Category: 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.)

Drug Name	Ceftriaxone (Rocephin)
Description	Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms.
Adult Dose	Treatment: 2 g IV q12h Chemoprophylaxis: 250 mg IM (single dose)
Pediatric Dose	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)
Contraindications	Documented hypersensitivity
Interactions	Probenecid may increase levels; ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Adjust dose in patients with renal impairment; caution in breastfeeding women

Drug Name	Rifampin (Rifadin, Rimactane)
Description	Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. For chemoprophylactic use only.
Adult Dose	600 mg PO for 2 d
Pediatric Dose	<1 month: 5 mg/kg PO q12h for 2 d >1 month: 10 mg/kg PO q12h for 2 d
Contraindications	Documented hypersensitivity
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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Name	Ciprofloxacin (Cipro)
Description	Single dose (500 mg) may be effective for eradication of meningococcal carriage in adults. For chemoprophylactic use only.
Adult Dose	500 mg PO qd
Pediatric Dose	<18 years: Not recommended; has caused cartilage damage in immature experimental animals
Contraindications	Documented hypersensitivity
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
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	With long-term use, may need periodic renal, hepatic, and hematologic evaluations; adjust dose in patients with impaired renal function

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.
• 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.
  • No effective vaccine exists to protect individuals from meningococcal meningitis caused by serogroup B.
  • 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.
  • 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.
  • 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 loss.
• 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

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal 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

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.
	View Full Size Image
Media type:  CT

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.
	View Full Size Image
Media type:  CT

Media file 3:  Grossly purulent exudate is seen in the leptomeninges.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Ahlawat S, Kumar R, Roy P, et al. Meningococcal meningitis outbreak control strategies. J Commun Dis. Dec 2000;32(4):264-74. [Medline].
• Andersen J, Backer V, Voldsgaard P, et al. Acute meningococcal meningitis: analysis of features of the disease according to the age of 255 patients. Copenhagen Meningitis Study Group. J Infect. May 1997;34(3):227-35. [Medline].
• Bhatt KM, Bhatt SM, Mirza NB. Meningococcal meningitis. East Afr Med J. Jan 1996;73(1):35-9. [Medline].
• Blazer S, Berant M, Alon U. Bacterial meningitis. Effect of antibiotic treatment on cerebrospinal fluid. Am J Clin Pathol. Sep 1983;80(3):386-7. [Medline].
• Caugant DA, Høiby EA, Magnus P, et al. Asymptomatic carriage of Neisseria meningitidis in a randomly sampled population. J Clin Microbiol. Feb 1994;32(2):323-30. [Medline].
• Chin RF, Neville BG, Scott RC. Meningitis is a common cause of convulsive status epilepticus with fever. Arch Dis Child. Jan 2005;90(1):66-9. [Medline].
• Coll MT, Uriz MS, Pineda V, et al. Meningococcal meningitis with 'normal' cerebrospinal fluid. J Infect. Nov 1994;29(3):289-94. [Medline].
• Cuevas LE, Hart CA. Chemoprophylaxis of bacterial meningitis. J Antimicrob Chemother. Feb 1993;31 Suppl B:79-91. [Medline].
• Durand ML, Calderwood SB, Weber DJm, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med. Jan 7 1993;328(1):21-8. [Medline].
• Edwards MS, Baker CJ. Complications and sequelae of meningococcal infections in children. J Pediatr. Oct 1981;99(4):540-5. [Medline].
• Feske SK. Coma and confusional states: emergency diagnosis and management. Neurol Clin. May 1998;16(2):237-56. [Medline].
• Galimand M, Gerbaud G, Guibourdenche M, et al. High-level chloramphenicol resistance in Neisseria meningitidis. N Engl J Med. Sep 24 1998;339(13):868-74. [Medline].
• Gjini AB, Stuart JM, Cartwright K, et al. Quality of in-hospital care for adults with acute bacterial meningitis: a national retrospective survey. QJM. Nov 2006;99(11):761-9.
• Greenfield S, Sheehe PR, Feldman HA. Meningococcal carriage in a population of "normal" families. J Infect Dis. Jan 1971;123(1):67-73. [Medline].
• Greenwood BM, Bradley AK, Wall RA. Meningococcal disease and season in sub-Saharan Africa. Lancet. Oct 12 1985;2(8459):829-30. [Medline].
• Hart CA, Cuevas LE, Marzouk O, et al. Management of bacterial meningitis. J Antimicrob Chemother. Jul 1993;32 Suppl A:49-59. [Medline].
• Helmick CG, Bernard KW, D'Angelo LJ. Rocky Mountain spotted fever: clinical, laboratory, and epidemiological features of 262 cases. J Infect Dis. Oct 1984;150(4):480-8. [Medline].
• Hodgson A, Smith T, Gagneux S, et al. Risk factors for meningococcal meningitis in northern Ghana. Trans R Soc Trop Med Hyg. Sep-Oct 2001;95(5):477-80. [Medline].
• Hui L, Tokeshi J. Dexamethasone use in adult meningococcal meningitis. Hawaii Med J. Jul 2000;59(7):308-9. [Medline].
• Jackson LA, Schuchat A, Reeves MW, Wenger JD. Serogroup C meningococcal outbreaks in the United States. An emerging threat. JAMA. Feb 1 1995;273(5):383-9. [Medline].
• Jong EC. Travel immunizations. Med Clin North Am. Jul 1999;83(4):903-22, vi. [Medline].
• Kanegaye JT, Soliemanzadeh P, Bradley JS. Lumbar puncture in pediatric bacterial meningitis: defining the time interval for recovery of cerebrospinal fluid pathogens after parenteral antibiotic pretreatment. Pediatrics. Nov 2001;108(5):1169-74. [Medline].
• Kirsch EA, Barton RP, Kitchen L, Giroir BP. Pathophysiology, treatment and outcome of meningococcemia: a review and recent experience. Pediatr Infect Dis J. Nov 1996;15(11):967-78; quiz 979. [Medline].
• Kotilainen P, Jalava J, Meurman O, et al. Diagnosis of meningococcal meningitis by broad-range bacterial PCR with cerebrospinal fluid. J Clin Microbiol. Aug 1998;36(8):2205-9. [Medline].
• Kutz JW, Simon LM, Chennupati SK, et al. Clinical predictors for hearing loss in children with bacterial meningitis. Arch Otolaryngol Head Neck Surg. Sep 2006;132(9):941-5. [Medline].
• Leedom JM, Underman AE. Epidemiology of central nervous system infections. Neuroimaging Clin N Am. May 2000;10(2):297-308. [Medline].
• Memish ZA. Meningococcal disease and travel. Clin Infect Dis. Jan 1 2002;34(1):84-90. [Medline].
• Ni H, Knight AI, Cartwright K, et al. Polymerase chain reaction for diagnosis of meningococcal meningitis. Lancet. Dec 12 1992;340(8833):1432-4. [Medline].
• Pardo F, Juncal R, Rajo C, Perez del Molino ML. [Usefulness of polymerase chain reaction (PCR) in the diagnosis of meningococcal meningitis]. Enferm Infecc Microbiol Clin. Feb 1999;17(2):74-7. [Medline].
• Prevention and control of meningococcal disease. Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. Jun 30 2000;49(RR-7):1-10. [Medline].
• Pruitt AA. Infections of the nervous system. Neurol Clin. May 1998;16(2):419-47. [Medline].
• Quagliarello V, Scheld WM. Bacterial meningitis: pathogenesis, pathophysiology, and progress. N Engl J Med. Sep 17 1992;327(12):864-72. [Medline].
• Quagliarello VJ, Scheld WM. Treatment of bacterial meningitis. N Engl J Med. Mar 6 1997;336(10):708-16. [Medline].
• Roos KL. Acute bacterial meningitis. Semin Neurol. 2000;20(3):293-306. [Medline].
• Rosenberg DH, Arling PA. Penicillin in the treatment of meningitis. JAMA. 1944;125:1011-1017.
• Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease. N Engl J Med. May 3 2001;344(18):1378-88. [Medline].
• Rosenstein NE, Perkins BA, Stephens DS, et al. The changing epidemiology of meningococcal disease in the United States, 1992-1996. J Infect Dis. Dec 1999;180(6):1894-901. [Medline].
• Schuchat A, Robinson K, Wenger JD, et al. Bacterial meningitis in the United States in 1995. Active Surveillance Team. N Engl J Med. Oct 2 1997;337(14):970-6. [Medline].
• Schwartz B, Al-Tobaiqi A, Al-Ruwais A, et al. Comparative efficacy of ceftriaxone and rifampicin in eradicating pharyngeal carriage of group A Neisseria meningitidis. Lancet. Jun 4 1988;1(8597):1239-42. [Medline].
• Snape MD, Pollard AJ. Meningococcal polysaccharide-protein conjugate vaccines. Lancet Infect Dis. Jan 2005;5(1):21-30. [Medline].
• Stephens DS, Hajjeh RA, Baughman WS, et al. Sporadic meningococcal disease in adults: results of a 5-year population-based study. Ann Intern Med. Dec 15 1995;123(12):937-40. [Medline].
• Stephens DS. Neisseria meningitidis. Infect Control. Jan 1985;6(1):37-40. [Medline].
• Straus SE, Thorpe KE, Holroyd-Leduc J. How do I perform a lumbar puncture and analyze the results to diagnose bacterial meningitis?. JAMA. Oct 25 2006;296(16):2012-22. [Medline].
• Suri M, Kabra M, Singh S, et al. Group B meningococcal meningitis in India. Scand J Infect Dis. 1994;26(6):771-3. [Medline].
• Talan DA, Guterman JJ, Overturf GD, et al. Analysis of emergency department management of suspected bacterial meningitis. Ann Emerg Med. Aug 1989;18(8):856-62. [Medline].
• Tikhomirov E, Santamaria M, Esteves K. Meningococcal disease: public health burden and control. World Health Stat Q. 1997;50(3-4):170-7. [Medline].
• Tunkel AR, Wispelwey B, Scheld WM. Bacterial meningitis: recent advances in pathophysiology and treatment. Ann Intern Med. Apr 15 1990;112(8):610-23. [Medline].
• Tzeng YL, Stephens DS. Epidemiology and pathogenesis of Neisseria meningitidis. Microbes Infect. May 2000;2(6):687-700. [Medline].
• Van Scoy RE, Wilkowske CJ. Prophylactic use of antimicrobial agents in adult patients. Mayo Clin Proc. Mar 1992;67(3):288-92. [Medline].
• Wang VJ, Malley R, Fleisher GR, et al. Antibiotic treatment of children with unsuspected meningococcal disease. Arch Pediatr Adolesc Med. Jun 2000;154(6):556-60. [Medline].
• de Filippis I, do Nascimento CR, Clementino MB, et al. Rapid detection of Neisseria meningitidis in cerebrospinal fluid by one-step polymerase chain reaction of the nspA gene. Diagn Microbiol Infect Dis. Feb 2005;51(2):85-90. [Medline].

Article Last Updated: Jan 10, 2007