Kinetics of the Antibody Response to Tetanus-Diphtheria-Acellular Pertussis Vaccine in Women of Childbearing Age and Postpartum Women

Abstract

Because adolescents and adults act as a primary source of pertussis infection for infants, vaccination of mothers immediately postpartum is a potential strategy to reduce transmission (cocoon strategy). For this to be effective, high levels of antibodies must be achieved rapidly after vaccination. We sought to determine whether the antibody response to tetanus-diphtheria-acellular pertussis vaccine (Tdap) is sufficiently rapid to support the cocoon strategy. Two sequential studies were performed. The first was a nonrandomized, open study of a 5-pertussis-component Tdap vaccine (tetanus toxoid, diphtheria toxoid, pertussis toxoid [PT], filamentous hemagglutinin [FHA], fimbriae types 2 and 3 [FIM], and pertactin [PRN]) given to women of childbearing age; the second was a randomized, open study of Tdap or no vaccine in postpartum women. Serum levels of immunoglobin (Ig) G and IgA against pertussis antigens, serum levels of IgG against diphtheria and tetanus, and breast milk levels of IgA against pertussis antigens were measured at various times after vaccination. In both studies, the antibody response was relatively rapid, with serum IgG and IgA levels beginning to increase noticeably by days 5-7 and approaching peak levels by day 14. Greater than 68% and 84.4% of IgG and IgA responders, respectively, achieved ≥ 90% of their maximum titer by day 14. The diphtheria and tetanus antibody kinetics followed a similar time course. Breast milk levels of IgA against PT, FHA, and FIM were first detectable at day 7, peaked by day 10, and then slowly decreased through day 28. Antibodies against PRN showed a similar response, although the peak occurred at day 14. There were no significant antibody responses in the control group. Although the antibody response to a dose of Tdap in healthy nonpregnant women of child-bearing age and postpartum women occurs by day 14 and is suggestive of an anamnestic immune response, it may not be sufficiently rapid to protect infants in the first weeks of life.