Pertussis incidence in Massachusetts declined throughout the 1950s and 1960s following increasing vaccine uptake. Since the mid-1970s, however, a pronounced rebound in incidence has been observed. The widely-accepted explanation for these patterns has focused on vaccine failure, especially modern acellular vaccines that have been in use since the mid-1990s. To assess the potential role played by changes in vaccinal immunity and the nature of age-specific pattern of contacts, we formulated different hypotheses regarding the mode of vaccine failure and fitted age-structured transmission models to incidence data. For this high-dimensional system, we used both deterministic (trajectory matching) and stochastic (maximum likelihood via iterated filtering) methods.
Results/Conclusions
The data identify waning of vaccine-derived immunity as the principal mechanism underlying loss of vaccinal immunity, irrespective of fitting methodology. Consistent with recent studies, we find infections in those previously vaccinated can be as transmissible but less visible than primary infections. Notably, the mean duration of vaccine protectiveness is long, leading to a high individual-level vaccine impact. Our model instead explains the resurgence of pertussis in Massachusetts as the end of the honeymoon: an inevitable long-term consequence of historically moderate vaccine coverage with an imperfect vaccine. Additionally, our fitted model identifies the 5-10 year-olds as the key epidemiological age group, with adults playing only a very minor role in contemporary pertussis transmission.