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Clinical Manifestations and Molecular Characterization of Pertactin-deficient and Pertactin-producing Bordetella pertussis in Children, Philadelphia 2007 – 2014

  1. Sarah S. Long1
  1. 1Department of Pediatrics, Section of Infectious Diseases, St. Christopher's Hospital for Children and Drexel University College of Medicine, Philadelphia, Pennsylvania, USA
  2. 2Infectious Diseases & Vaccines, Janssen Research & Development, Raritan, New Jersey, USA
  3. 3Department of Pathology and Laboratory Medicine, St. Christopher's Hospital for Children and Drexel University College of Medicine, Philadelphia, Pennsylvania, USA
  1. Corresponding Author: Jennifer Vodzak, MD, St. Christopher's Hospital for Children, Section of Infectious Diseases, 160 East Erie Avenue, Philadelphia, PA 19134, Office Phone: 215-427-5201, Office Fax: 215-427-8389, Email: Jennifer.Vodzak{at}drexelmed.edu
  1. Alternate Corresponding Author: Sarah S. Long, MD, St. Christopher's Hospital for Children, Section of Infectious Diseases, 160 East Erie Avenue, Philadelphia, PA 19134, Office Phone: 215-427-5201, Office Fax: 215-427-8389, Email: Sarah.Long{at}drexelmed.edu, Cell Phone: 570-690-1397

Abstract

Background. B. 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 (January 2007 - March 2014) included Western blot analysis, pulse-field gel electrophoresis (PFGE), PCR and pertactin gene sequencing. Medical record review compared epidemiologic and clinical courses of pertactin-producing and pertactin-deficient B. pertussis infections.

Results. 60 of 72 B. pertussis isolates were viable for analysis. Cohort median age was 95 days, 90% received ≤1 dose of vaccine, 72% were hospitalized. Pertactin deficiency was first noted in 2008 and increased over time (68% overall prevalence). There were no statistically significant differences in presenting symptoms/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=0.04); no difference was noted in subgroup of infants <4 months. Molecular analyses identified 11 PFGE profiles (CDC002 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 clustered in time.

Conclusions. In this cohort of predominantly unimmunized infants, clinical disease was not different for infection with pertactin-deficient or pertactin-producing B. pertussis. Molecular analyses demonstrated remarkable PFGE strain diversity, with multiple mechanisms and molecular sites of pertactin inactivation.

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