Design: Phase 2b, randomised, observer-blinded, active- and placebo-controlled
Population: 366 acellular-primed children aged 6–17 in the UK, Australia and Costa Rica
Primary outcome: Fold rise in nasal secretory IgA at day 29
Effect: GMFR 3.8 (95% CI 3.1–4.7) BPZE1; 3.5 (2.9–4.3) BPZE1 plus Tdap

This phase 2b trial randomised 366 children aged 6 to 17 in the UK, Australia and Costa Rica, all primed with acellular pertussis vaccines, to intranasal BPZE1 with an intramuscular placebo, Tdap with a nasal placebo, or both.

BPZE1 raised nasal secretory IgA against whole-cell pertussis antigens about 3.5- to 3.8-fold by day 29, with or without Tdap. Giving BPZE1 alongside Tdap did not reduce serum antibody responses to pertussis, diphtheria or tetanus antigens. Solicited reactions were less frequent with BPZE1 alone than with Tdap, and there were no vaccine-related serious events.

Acellular vaccines protect against disease but do little to stop colonisation, which may explain pertussis resurgence in well-vaccinated populations. A vaccine producing mucosal immunity could block carriage and transmission. This trial shows immune response and safety only; protection against infection has not been tested in children.

Keep to the national pertussis schedule, including maternal Tdap in pregnancy, which protects young infants.
Recognise that acellular-vaccinated children can carry and transmit pertussis.
Consider pertussis in a child or adolescent with a cough lasting over two weeks, even if fully vaccinated.
Treat nasal IgA results as a marker of mucosal response, not proof of protection.

Why it matters

A vaccine that stops carriage, not just disease, is what pertussis control has lacked.

The statistics, in plain English

A geometric mean fold rise of 3.8 means nasal IgA roughly quadrupled on average. The trial was designed to show an immune response, not to count infections, so it cannot say how many cases the vaccine would prevent.