Editorial commentary: pertussis is less severe in vaccinated than in unvaccinated patients.

After the introduction of vaccines against pertussis, there was a dramatic decrease of the disease, and the problem was considered to have been solved. But it was not. Recently, large outbreaks have occurred in the United States, in several European countries, and in Australia [1, 2]. It is evident that there are still many unresolved questions in pertussis, the first of which is that we do not know enough about the exact pathogenesis of this infection and the real appearance of Bordetella pertussis organisms in vivo. We also do not know much about the intracellular living of the bacteria and possible transition between the virulent and nonvirulent phenotypes in the mucosal environment in the lungs. Perhaps we should again pay more attention to the old questions of molecular mimicry [3]. The infection cascade is very complex, and immunity is multifactorial. During and after the development of the acellular vaccine, the main focus has been on the extracellular living of B. pertussis and humoral immunity. In pertussis, the function of Th1 and Th17 cells seems to be very important [4]. Surprisingly, even some 100 years after the discovery of B. pertussis, we do not even understand the exact mechanism behind the typical paroxysmal cough in whooping cough. Young infants are most vulnerable if they get B. pertussis infection. Historically, pertussis has been a serious killer, and recent outbreaks show that infants have a real risk of death and complications even today [1, 2]. One of the main problems is how to induce immunity against pertussis in young infants. The situation was so alarming in California in 2012 and in the United Kingdom that vaccinations against tetanus, diphtheria, and pertussis (Tdap) during pregnancy were introduced [5, 6]. How did we arrive at this situation? In the 1980s, there was much pressure to replace the reactogenic diphtheria, tetanus, and whole-cell pertussis (DTwP) vaccine with a more safe endotoxin-free vaccine. Now, many of the increased problems are considered to be caused by the acellular pertussis vaccines. Serological studies indicated that even before the switch to the acellular vaccines, pertussis was already common in adolescent and adult populations, which formed a reservoir of B. pertussis. More than 20 years ago, 2 serological studies indicated a high infectivity rate (83% in both) of pertussis in families [7, 8]. Serology also indicated that many infected individuals (earlier vaccinated) were totally asymptomatic. Thus, the wholecell vaccine prevented more disease than infection. In early 1990s, before the era of acellular vaccines and preschool boosters, it was found that during a local outbreak in a day-care center, among vaccinated children, pertussis polymerase chain reaction (PCR) positivity was less common in recently vaccinated children 1–3 years of age than in those 4–6 years of age [9]. Asymptomatic pertussis infection was more common in exposed preschool children than in schoolchildren during outbreaks. The older children more often had typical pertussis than the preschool children. This indicates that during a short period after the immunization, DTwP might have prevented infection; then, some years after immunization, there was a risk of asymptomatic PCRpositive infection and, later, when the major part of the immunity had waned, the symptomatic disease appeared. Now, in the era of the acellular pertussis vaccine, the study by Barlow et al in this issue of Clinical Infectious Diseases focuses on the question if vaccination status is associated with disease severity [10]. This surveillance study was based on 624 patients (aged 6 weeks–18 years) with pertussis in Oregon. Special attention was paid to obtain the vaccination status of the patients from Oregon’s Received 2 March 2014; accepted 4 March 2014; electronically published 14 March 2014. Correspondence: Jussi Mertsola, MD, PhD, Department of Paediatrics and Adolescent Medicine, Turku University Hospital, 20520 Turku, Finland ([email protected]). Clinical Infectious Diseases 2014;58(11):1530–2 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/cid/ciu161