B ordetella pertussis, the causative agent of pertussis (whooping cough), continues to reemerge in countries that have high vaccine coverage, such as the United States, and has accelerated since the switch during the mid-1990s from whole-cell pertussis (wP) formulations comprising many partially characterized bacterial proteins to the less reactogenic 1-5 component acellular pertussis (aP) vaccines (1,2). These aP vaccines, including DTaP (diphtheria, tetanus, and aP for children) and Tdap (tetanus, diphtheria, and aP for adolescents and adults), protect against disease, but this protection wanes rapidly and does not prevent colonization or transmission of the pathogen (3-5). In this background of suboptimally performing aP vaccines, many countries have noted the emergence and expansion of strains specifi cally lacking pertactin (PRN), a membrane bound autotransporter, and 1 of up to 5 B. pertussis protein antigens included in the vaccines (6-11).