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"For parents, childhood vaccines are a source of reassurance -- protecting your child against disease naturally helps you sleep better at night -- but also anxiety about side effects and reactions.

With misinformation about vaccines and heal"...




N meningitidis causes both endemic and epidemic disease, principally meningitis and meningococcemia. As a result of the control of Haemophilus influenzae type b infections, N meningitidis has become the leading cause of bacterial meningitis in children and young adults in the United States (US), with an estimated 2,600 cases each year.5,6 The case-fatality rate is 13% for meningitis disease (defined as the isolation of N meningitidis from cerebrospinal fluid) and 11.5% for persons who have N meningitidis isolatedfrom blood,5,6 despite therapy with antimicrobial agents (eg, penicillin) to which US strains remain clinically sensitive.5

The incidence of meningococcal disease peaks in late winter to early spring. Based on multistate surveillance conducted during 1989 to 1991, serogroup B organisms accounted for 46% of all cases and serogroup C for 45%; serogroups W-135 and Y and strains that could not be serotyped accounted for most of the remaining cases.5,6 Recent data indicate that the proportion ofcases caused by serogroup Y strains is increasing.5 In 1995, among the 30 states reporting supplemental data on culture-confirmed cases of meningococcal disease, serogroup Y accounted for 21% of cases.7 Because of the success of H influenzae type b vaccinations, the median age of persons with bacterial meningitis increased from 15 months in 1986 to 25 years in 1995.8 The predominate organism causing meningitis in children 2 to 18 years of age is N meningitidis based on 1995 surveillance data.8 Serogroup A, which rarely causes disease in the US, is the most common cause of epidemics in Africa and Asia. A statewide serogroup B epidemic has been reported in the US.9 Within the US, a vaccine for serogroup B is not yet available.

Outbreaks of serogroup C meningococcal disease (SCMD) have been occurring more frequently in the US since the early 1990s, and the use of vaccine to control these outbreaks has increased.5 During 1980-1993, 21 outbreaks of SCMD were identified; eight of these occurred during 1992-1993.10 Each of these 21 outbreaks involved from three to 45 cases of SCMD, and most outbreaks had attack rates exceeding 10 cases per 100,000 population, which is approximately 20 times higher than rates of endemic SCMD.5 During 1981-1988, only 7,600 doses of meningococcal vaccine were used to control four outbreaks; whereas, from January 1992 through June 1993, 180,000 doses ofvaccine were used in response to eight outbreaks.5

Several discoveries impacted the future of meningococcal polysaccharide vaccines and demonstrated the significance of anti-capsular antibodies in protection.11 In the late 1930s, serogroup-specific antigens of meningococcal serogroups A and C were identified as polysaccharides.9 During the mid 1940s, investigators demonstrated that the protection of mice by anti-serogroup A meningococcal horse serum was directly related to its content of anti-polysaccharide antibodies.11 Meningococcal polysaccharide vaccines were first demonstrated to be immunogenic in humans by Gotschlich and his co-workers in the 1960s when immunization of US Army recruits with serogroup A and C polysaccharides induced protective antibodies.11 The investigators recorded a significantly reduced acquisition rate of serogroup C carriage among vaccinated recruits compared with unvaccinated individuals.11

Persons who have certain medical conditions are at increased risk for developing meningococcal infection. Meningococcal disease is particularly common among persons who have component deficiencies in the terminal common complement pathway (C3, C5-C9); many of these persons experience multiple episodes of infection.5Asplenic persons also may be at increased risk for acquiring meningococcal disease with particularly severe infections.5 Persons who have other diseases associated with immunosuppression (eg, human immunodeficiency virus [HIV] and Streptococcus pneumoniae) may be at higher risk for developing meningococcal disease and for disease caused by some other encapsulated bacteria.5 Evidence suggests that HIV-infected persons are not at substantially increased risk for epidemic serogroup A meningococcal disease;5 however, such patients may be at increased risk for sporadic meningococcal disease or disease caused by other meningococcal serogroups.5 Previously, military recruits had high rates of meningococcal disease, particularly serogroup C disease; however, since the initiation of routine vaccination of recruits with bivalent A/C meningococcal vaccine in 1971, the high rates of meningococcal disease caused by those serogroups have decreased substantially and cases occur infrequently.5

A retrospective, epidemiological study was conducted in Maryland to compare the incidence of invasive meningococcal infection in college students with that of the general population of the same age. For the years 1992 to 1997, the incidence of meningococcal infection in Maryland college students was similar to the incidence of the general Maryland population of the same age. However, college students residing on-campus appeared to be at higher risk than those residing offcampus.12

Vaccine efficacy. The immunogenicity and clinical efficacy of serogroups A and C meningococcal vaccines have been well established.5 The serogroup A polysaccharide induces antibody in some children as young as 3 months of age, although a response comparable with that among adults is not achieved until 4 or 5 years of age; the serogroup C component is poorly immunogenic in recipients who are less than 18 to 24 months of age.5 The serogroups A and C vaccines have demonstrated estimated clinical efficacies of 85% to 100% in older children and adults and are useful in controlling epidemics.5 Serogroups Y and W-135 polysaccharides are safe and immunogenic in adults and in children greater than 2 years of age.5 Although clinical protection has not been documented, vaccination with these polysaccharides induces bactericidal antibody. The antibody responses to each of the four polysaccharides in the quadrivalent vaccine are serogroup-specific and independent.5

Efficacy of serogroup A meningococcal vaccines was demonstrated in the 1970s in Africa and Finland, Egyptian school children aged 6 to 15 years showed 90% or greater protection during the first year after immunization with two different molecular sizes of serogroup A polysaccharide.11 The higher molecular weight vaccine provided protection for at least three years.11 In Finland, a randomized controlled mass immunization trial with serogroup A vaccine was conducted in response to a serogroup A epidemic. Results indicated 90 to 100% protection for three years.11 In Rwanda, vaccination with bivalent A/C polysaccharide vaccine was performed in response to a serogroup A epidemic. A complete cessation of meningococcal disease was observed within two weeks of vaccination, yet the serogroup A carrier rate remained unchanged.11

Efficacy of serogroup C meningococcal vaccines was demonstrated in a field trial involving 20,000 troops in the US Army. Results suggested 90% efficacy under epidemic conditions which existed in basic training centers.13 In Brazil, young children were vaccinated with serogroup C polysaccharide in response to a serogroup C epidemic. Results indicated that the vaccine was not effective in children under 24 months of age and only 52% effective in children aged 24 to 36 months.11 However, studies suggested that the vaccine used in this trial was less immunogenic than other batches of similar vaccine that were used in US children; also, it was shown that the molecular size of the vaccine was smaller than the serogroup C polysaccharide in the present vaccine.13 Thus, it is quite probable that the current serogroup C polysaccharide vaccine is more effective.11

A study performed using 4 lots of Menomune (meningococcal polysaccharide vaccine) - A/C/Y/W-135 vaccine in 150 adults showed at least a 4-fold increase in bactericidal antibodies to all groups in greater than 90 percent of the subjects.14,15

A study was conducted in 73 children 2 to 12 years of age. Post-immunization sera were not obtained on four children; seroconversion rates were calculated on 69 paired samples. Seroconversion rates as measured by bactericidal antibody were: Group A - 72%, Group C - 58%, Group Y - 90% and Group W-135 - 82%. Seroconversion rates as measured by a 2-fold rise in antibody titers based on Solid Phase Radioimmunoassay were: Group A - 99%, Group C - 99%, Group Y - 97% and Group W-135 - 89%.16

Duration of efficacy. Measurable levels of antibodies against the group A and C polysaccharides decrease markedly during the first 3 years following a single dose of vaccine.5 This decrease in antibody occurs more rapidly in infants and young children than in adults. Similarly, although vaccine-induced clinical protection probably persists in schoolchildren and adults for at least 3 years, the efficacy of the group A vaccine in young children may decrease markedly with the passage of time. In a 3-year study, efficacy declined from greater than 90% to less than 10% among children who were less than 4 years of age at the time of vaccination, whereas among children who were greater than or equal to 4 years of age when vaccinated, efficacy was 67% 3 years later.5,17 In a New Zealand study, children 2 to 13 years of age received a single dose of monovalent group A vaccine, 26% of children 3 to 23 months of age in this study received two doses of the vaccine, given approximately 3 months apart. After 2-1/2 years of active surveillance (1987 to 1989) there were no cases of invasive group A disease in children vaccinated at 2 years of age and older.18


5.Recommendation of the Advisory Committee on Immunization Practices (ACIP). Control and prevention of meningococcal disease and control and prevention of serogroup C meningococcal disease: evaluation and management of suspected outbreaks. MMWR 46: No. RR-5, 1997

6.CDC. Laboratory-based surveillance for meningococcal disease in selected areas - United States, 1989-1991. MMWR 42: No. SS-2, 1993

7.CDC. Serogroup Y Meningococcal Disease - Illinois, Connecticut, and Selected Areas, United States, 1989-1996. MMWR 46: Vol. 45, 1010-1013, 1996

8.Schuchat A, et al. Bacterial Meningitis in the United States in 1995. N Engl J Med 337: 970-976, 1997

9.CDC. Serogroup B meningococcal disease - Oregon 1994. MMWR 44: 121-124, 1995

10. Jackson LA, et al. Serogroup C meningococcal outbreaks in the United States: an emerging threat. JAMA 273: 383-389, 1995

11. Frasch CE. Meningococcal vaccines; past, present and future. Ed. K. Cartwright. John Wiley and Sons Ltd, 1995

12. Harrison LH, et al. Risk ofmeningococcal infection in college students. JAMA 281: 1906-1910, 1999

13. Lepow ML. Meningococcal vaccines, in Vaccines, ed. SA Plotkin and EA Mortimer. WB Saunders Co., 1994

14. Hankins WA, et al. Clinical and serological evaluation of a Meningococcal Polysaccharide Vaccine Groups A, C, Y and W-135. Proc Soc Exper Biol Med 169: 54-57, 1982

15. Lepow ML, et al. Reactogenicity and immunogenicity of a quadrivalent combined meningococcal polysaccharide vaccine in children. J Infect Dis 154: 1033-1036, 1986

16. Data on file at Sanofi Pasteur Inc.

17. Reingold AL, et al. Age-specific differences in duration of clinical protection after vaccination with meningococcal polysaccharide A vaccine. Lancet. No. 8447: 114-118, 1985

18. Lennon D, et al. Successful intervention in a Group A meningococcal outbreak in Auckland, New Zealand. Pediatr Infect Dis J 11: 617-623, 1992

Last reviewed on RxList: 9/18/2008
This monograph has been modified to include the generic and brand name in many instances.


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