Neisseria meningitidis


Infection usually manifests in one of three syndromes: either meningitis or meningitis with meningococcemia or meningococcemia without meningitis.

Is the organism responsible for most cases of bacterial meningitis in adolescents and at risk populations (military trainees, dormitory residents).

It is a major cause of severe disease in infants and children.

Colonizes the nasopharynx in approximately 10% of healthy persons, and less frequently, also colonizes  other mucosal sites, such as the cervix urethra and rectum.

Increasingly recognized as being sexually transmissible with associated urethritis in heterosexual men and invasive meningococcal disease in men having sex with men.

Causes severe sepsis meningococcemia.

Meningococcus is pathogenic only in humans.

Even with treatment 10-15 of every 100 people who have meningococcal meningitis die as a result.

It can cause permanent disabilities that include loss of limbs, deafness, or brain damage.

Estimated 1.2 million cases of invasive meningococcal disease and 135,000 deaths worldwide annually.

Expose her to M. meningitidis is common in the general population, leading to asymptomatic pharyngeal carriage, which may be transient or long term.

Age influences carriage rate, within increasing carriage prevalence from 15 years to a peak at approximately 19 years, probably due to increases in numbers and closeness of social contact and behavior.

Meningococcal disease is a rare outcome of infection.

Can occur at any age, but people who are at risk if they live in places with many new people, like a college dormitory with military barracks.

People without a spleen and those with an impaired immune system are at higher risk.

Overwhelming meningococcal disease can develop very quickly and is associated with a mortality rate greater than 20%.

Transported by respiratory droplets and this organism can be a normal constituent of the oropharyngeal flora.

Infants and adolescents are especially affected by meningococcal disease.

Presentation can vary and be confused with many other disease processes.

Meningitis indistinguishable from that caused by streptococcus and hemophilus influenza.

Chronic meningococcemia can be present as an acute arthritis or dermatitis which is seen most often in individuals with terminal complement deficiency.

History requires exposures, travel and immunization status.

Presence of tachycardia, hypotension, and prolonged capillary fill are ominous signs.

Clinical findings include impaired mentation and meningeal signs, macular papular rash and petechiae.

Neisseria meningitidis, a Gram-negative diplococcus organism, releases endotoxin when it lyses. 

Endotoxin activates the Hageman factor, clotting factor XII, which causes disseminated intravascular coagulation (DIC). 


The DIC is what appears as a rash on the affected individual.

Diagnosis based on isolation of meningococci from sterile body fluids.

Colonizes the nasopharynx asymptomatically in up to 40% of adults.

There are 12 different meningococcal capsular groups recognized.

Only six polysaccharide capsule groups surrounding the bacterium are associated with invasive disease: A, B, C, W-135, X, and Y

(Stephens DS).

Group B disease predominates in many high income countries.

The meningococcus bacteria can live in the nose and throat of some healthy people, known as carriers.

Meningococcus can spread from person-to person through saliva and respiratory secretions, and the spread requires close and prolonged contacts such as kissing, coughing, or sharing cups.

Meningococcal disease is not spread through the air.

Group A is responsible for large epidemics in Africa.

Groups B and C are responsible for disease in industrialized and newly industrialized countries.

Gram staining and latex agglutination can identify type of infection.

Outer surface of the meningococcus involved in evading complement.

Polysaccharide capsule containing sialic acid found in all meningococcal groups except A, protects against complement mediated bacterial killing. opsonization and phagocytosis (Stephens DS).

Protection from infection depends on innate immunity, particularly from the complement system, and humoral antibody response.

Patients with impaired complement system are at increased risk of infection (Schneider MC).

A serum bactericidal antibody (SBA) assay is available to measure the presence of specific antibodies to N. meningitidis that activate complement.

The SBA assay correlates immunologic protection from infection, and low levels indicate high risk among infants 6-24 months and is highest among infants below 6 months because they lack maternal serum bactericidal antibody (Cohn A).

A CSF antigen test can be obtained for N meningitidis.

Pretreatment with antibiotics before culture decreases probability of a positive culture.

Polymerase chain reaction tests can be useful in patients already on antibiotics.

Antibiotic treatment should begin before culture identification.

Patients with suspected infection require immediate hospitalization and the initiation of appropriate antibiotics including penicillin G, ceftriaxone and cefotaxime.

Case fatality rate is 10-14 percent and survivors can experience brain damage, hearing loss, limb impairment and learning disabilities.

Ceftriaxone can eradicate the carriage of the organism.

Agents used to control the carrier state include ceftriaxone, rifampin and ciprofloxacin.

Chemoprophylaxis recommended for household contacts and anyone with direct exposure to the index patient’s secretions within 7 days of onset of symptoms.

Individuals traveling on airplanes and who sat next to the patient during flights of 8 hours or more should receive chemoprophylaxis.

Chloramphenicol remains an alternative for penicillin allergic patients.

Benefits of corticosteroid are inconclusive.

Presently no broadly effective vaccine against N. Meningitidis group B, the predominant isolate.

Several vaccines are available to prevent meningococcal infection.

The conjugate meningococcal vaccine covers four of the most common serogroups that can cause meningococcal meningitis A, C, W, and Y.

The conjugate meningococcal vaccine is recommended for children age 11-12 years, with the booster dose around age 16.

The vaccine is required for students entering college in most states.

The conjugate vaccine does not cover all strains of Meningococci that cause meningitis, including serogroup B.

Two new vaccines are now available for serogroup B meningococcal disease and can be given to teens and young adults between 16 and 23 years.

Conjugate polysaccharide vaccines can use mucosal respiratory responses that interfere with the acquisition of carriage of several meningococcal capsule groups.

The use of Menninger cargo capsular polysaccharide-proteasome conjugate vaccines has led to a major successes in the prevention of invasive meningococcal disease.

Conjugate polysaccharide vaccines can induce mucosal respiratory responses that interfere with the acquisition of carriage up several meningococcal capsular groups-Group C and group W, however the same canNOT assumed for meningococcal B vaccines.

The meningococcal group B vaccine 4CMenB is a recombinant protein-based vaccine.

Complete vaccination with 4CMenB is effective in preventing invasive disease by serogroup B and non-serogroup B meningococcal  in children younger than five years of age.

Leave a Reply

Your email address will not be published. Required fields are marked *