Pertactin-negative B. pertussis strains: evidence for a possible selective advantage.

A recent increase in B. pertussis without the pertactin protein, an acellular vaccine immunogen, has been reported in the U.S. Determining whether pertactin-deficient (PRN-) B. pertussis is evading vaccine-induced immunity or altering the severity of illness is needed.


We retrospectively assessed for associations between pertactin production and both clinical presentation and vaccine history. Cases with isolates collected between May 2011 and February 2013 from 8 states were included. We calculated unadjusted and adjusted odds ratios (ORs) using multivariable logistic regression analysis.


Among 753 isolates, 640 (85%) were PRN-. The age distribution differed between cases caused by PRN- B. pertussis and cases caused by B. pertussis producing pertactin (PRN+) (p-value= 0.01). The proportion reporting individual pertussis symptoms was similar between the two groups, except a higher proportion of PRN+ case-patients reported apnea (p-value=0.005). 22 case-patients were hospitalized; 6% in the PRN+ group compared to 3% in the PRN- group (p-value=0.11). Cases having received at least one pertussis vaccine dose had a higher odds of having PRN- B. pertussis as compared to unvaccinated cases (adjusted OR=2.2; 95% CI= 1.3-4.0). When restricted to cases-patients at least 1 year of age and those age-appropriately vaccinated the adjusted OR increased to 2.7 (95% CI=1.2-6.1).


The significant association between vaccination and isolate pertactin produciton suggests the likelihood of having reported disease caused by PRN- compared to PRN+ strains is greater in vaccinated persons. Additional studies are needed to assess whether vaccine effectiveness is diminished against PRN- strains.

Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.


Authors:Martin SW1, Pawloski L1, Williams M1, Weening K2, DeBolt C3, Qin X4, Reynolds L5, Kenyon C6, Giambrone G7, Kudish K8, Miller L9, Selvage D10, Lee A1,Skoff TH1, Kamiya H1, Cassiday PK1, Tondella ML1, Clark TA1.

Journal:Clin Infect Dis. 2014