Persistence of Group C Anticapsular Antibodies Two to Three Years After Immunization with an Investigational Quadrivalent Neisseria Meningitidis-diphtheria Toxoid Conjugate Vaccine

Overview

Journal Pediatr Infect Dis J

Specialty Pediatrics

Date 2005 Feb 11

PMID 15702041

Citations 11

Authors

Dan M Granoff

Amy Morgan

Jo Anne Welsch

Affiliations

Soon will be listed here.

Abstract

Background: An investigational quadrivalent (A, C, Y and W-135) meningococcal conjugate (MC-4) vaccine was reported to be more immunogenic in 2-year-olds than the currently licensed meningococcal polysaccharide vaccine, but persistence of serum antibody beyond 6 months after conjugate vaccination is unknown.

Objective: Determine persistence and the immunologic basis of protective activity of group C anticapsular antibodies in sera obtained 2-3 years after MC-4 vaccination.

Design: Group C antibody concentrations, bactericidal activity and passive protective activity were measured in sera from 48 children, ages 4-5 years, who had been immunized 2-3 years earlier with an MC-4 vaccine and from 47 children who had not been previously vaccinated.

Results: Serum antibody concentrations were higher in the vaccinated than the unvaccinated children (geometric means, 0.30 and 0.09 mug/mL, respectively, P < 0.0001). Bactericidal titers > or =1/4 (considered protective) were infrequent in both vaccinated and unvaccinated children (14.6 and 6.4%, respectively, P = 0.3). Passive protective activity against bacteremia in the infant rat model was more frequent in sera from vaccinated (37.5%) than sera from unvaccinated children (12.5%, P < 0.02). The proportion of sera with passive protective activity increased with increasing anticapsular antibody concentrations (P < 0.0001).

Interpretation: Serum group C antibody concentrations remained elevated for 2-3 years after MC-4 vaccination, and passive protective activity was more frequent in vaccinated than unvaccinated children. However, serum antibody concentrations in many vaccinated children were no longer sufficient to activate complement-mediated bacteriolysis in vitro or to confer passive protection against experimental group C disease.

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