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  • Title: Clinical Manifestations and Molecular Characterization of Pertactin-Deficient and Pertactin-Producing Bordetella pertussis in Children, Philadelphia 2007-2014.
    Author: Vodzak J, Queenan AM, Souder E, Evangelista AT, Long SS.
    Journal: Clin Infect Dis; 2017 Jan 01; 64(1):60-66. PubMed ID: 27624959.
    Abstract:
    BACKGROUND:  Bordetella pertussis strains lacking expression of pertactin, a bacterial adhesin and vaccine target, are emerging. There are limited data on disease manifestations of mutant strains in children. We sought to compare clinical manifestations of pertactin-deficient and pertactin-producing B. pertussis infection in infants and describe corresponding molecular characteristics. METHODS:  Molecular characterization of archived B. pertussis isolates (collected January 2007 to March 2014) included Western blot analysis, pulsed-field gel electrophoresis (PFGE), polymerase chain reaction, and pertactin gene sequencing. Medical record review compared epidemiologic and clinical courses of pertactin-producing and pertactin-deficient B. pertussis infections. RESULTS:  Sixty of 72 B. pertussis isolates were viable for analysis. Within the cohort of infants, the median age was 95 days, 90% received ≤1 dose of vaccine, and 72% were hospitalized. Pertactin deficiency was first noted in 2008, and its prevalence increased over time (68% overall prevalence). There were no statistically significant differences in presenting symptoms or signs, hospitalization, intensive care, respiratory support, or laboratory results related to pertactin expression. Illness length was shorter in pertactin-deficient group (mean difference, 3.2 days; P = .04); no difference was noted in the subgroup of infants <4 months old. Molecular analyses identified 11 PFGE profiles (Centers for Disease Control and Prevention profile No. 002 predominant, 47%). In 41 pertactin-deficient strains, sequencing identified 2 stop codon and 3 IS481 locations disrupting the prn gene. Mutations and nucleotide positions were not unique to PFGE type, nor were they clustered in time. CONCLUSIONS:  In this cohort of predominantly unimmunized infants, clinical disease did not differ between infection with pertactin-deficient and those with pertactin-producing B. pertussis. Molecular analyses demonstrated remarkable PFGE strain diversity, with multiple mechanisms and molecular sites of pertactin inactivation.
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