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Clinical Manifestations and Molecular Characterization of Pertactin-Deficient and Pertactin-Producing Bordetella pertussis in Children, Philadelphia 2007-2014
Journal article   Open access   Peer reviewed

Clinical Manifestations and Molecular Characterization of Pertactin-Deficient and Pertactin-Producing Bordetella pertussis in Children, Philadelphia 2007-2014

Jennifer Vodzak, Anne Marie Queenan, Emily Souder, Alan T Evangelista and Sarah S Long
Clinical infectious diseases, v 64(1)
01 Jan 2017
DOI: https://doi.org/10.1093/cid/ciw632
PMID: 27624959
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1093/cid/ciw632View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

Adolescent Bacterial Outer Membrane Proteins - biosynthesis Bacterial Outer Membrane Proteins - genetics Bordetella pertussis - classification Bordetella pertussis - genetics Bordetella pertussis - isolation & purification Child Child, Preschool Comorbidity Electrophoresis, Gel, Pulsed-Field Female Humans Infant Infant, Newborn Male Molecular Diagnostic Techniques Polymerase Chain Reaction Prevalence Sequence Analysis, DNA Symptom Assessment Virulence Factors, Bordetella - biosynthesis Virulence Factors, Bordetella - genetics Whooping Cough - diagnosis Whooping Cough - epidemiology Whooping Cough - microbiology
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.  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.  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.  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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12 citations in Web of Science
17 citations in Scopus

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UN Sustainable Development Goals (SDGs)

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#3 Good Health and Well-Being

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Collaboration types
Industry collaboration
Domestic collaboration
Web of Science research areas
Immunology
Infectious Diseases
Microbiology
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