Did the failed acellular pertussis vaccine reduce rates of meningococcal disease in the US?

The acellular pertussis vaccine (APV) does not produce mucosal immunity. It therefore makes recipients susceptible to colonization by the Bordetella pertussis bacteria. Such colonized individuals transmit the bacteria⁠.

Meningococcal disease rates in the US have been declining since the late 1990s. Meningococcal vaccines introduced in the 1970s or 2005 obviously cannot explain this trend.

One possible explanation is the introduction of APV in 1991. Widespread B. pertussis colonization in the population occurred following APV introduction. With N. meningitidis and B. pertussis competing for the same nasopharyngeal (NP) real estate, a reduction in N. meningitidis colonization can be expected. The APV also resulted in IgE mediated sensitization against B. pertussis proteins⁠. The result can be local allergic reactions that perturb NP colonization (by any bacteria) upon exposure to B. pertussis. One can expect IgE mediated mast cell degranulation, histamine release, mucus production that result in perturbation of colonies. So N. meningitidis colonization of NP may have been impacted by competition with B. pertussis or perturbation due to IgE mediated immune reactions.

This may be one more unintended consequence (a rare positive one) of poorly understood vaccines, developed using trial and error. Of course, the APV more than made up for this benefit by contributing to life-threatening milk allergy, autism, asthma and numerous autoimmune disorders.