Background: Vaccination during group A meningococcal epidemics is reported to decrease the number of new cases of disease. However, implementing mass vaccination is often delayed, and little information is available on whether immunity increases in a population vaccinated during an epidemic when exposure to the epidemic strain is common.
Methods: A convenience sample of 134 previously unimmunized persons, ages 3–49 years, were immunized with a meningococcal polysaccharide vaccine. Their serum group A antibody responses were compared with those of 26 adults immunized in California with no known group A exposure.
Results: Before immunization, serum anticapsular antibody concentrations were 10-fold higher in Sudanese adults and 4-fold higher in Sudanese, ages 3–17 years, than in North American adults (geometric means, 29 and 13 μg/ml, respectively, versus 3 μg/ml, P < 0.001). Seventy-five percent of the Sudanese had serum bactericidal titers that correlate with protection (≥1/128). Nearly all Sudanese with low bactericidal titers before vaccination developed protective bactericidal antibody responses after vaccination, and the magnitude of the anticapsular antibody responses of the Sudanese was similar to that of the immunized North Americans.
Interpretation: The high titers of naturally acquired antibody in the Sudanese may reflect widespread exposure to the epidemic strain and underscore difficulties of instituting immunization before exposure occurs. Also epidemics in sub-Saharan Africans may not abate even if 75% of the population is immune to disease as long as the organism is transmitted widely among both immune and susceptible persons.
From the *Children’s Hospital Oakland Research Institute, Oakland CA; and †National Health Laboratory, Ministry of Health, Khartoum, Sudan
Supported by grant V23-370-2 from the World Health Organization and grants AI 45642 and AI46464 from the National Institutes of Allergy and Infectious Disease, National Institutes of Health. The vaccine trial in the North American adults was performed in the Pediatric Clinical Research Center of Children’s Hospital and Research Center at Oakland and was supported by grant M01-RR01271 from the National Center for Research Resources, National Institutes of Health.
Accepted for publication April 7, 2004.
Reprints not available.