Alexander G Theofiles1, Scott A Cunningham2, Nicholas Chia3, Patricio R Jeraldo4, Daniel J Quest5, Jayawant N Mandrekar6, Robin Patel7. 1. Department of Medicine, Mayo Clinic, Rochester, MN. 2. Division of Clinical Microbiology, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN. 3. Department of Surgery, Mayo Clinic, Rochester, MN; Center for Individualized Medicine, Mayo Clinic, Rochester, MN. 4. Department of Surgery, Mayo Clinic, Rochester, MN; Institute for Genome Biology, University of Illinois at Urbana-Champaign, Urbana. 5. Center for Individualized Medicine, Mayo Clinic, Rochester, MN. 6. Department of Health Sciences Research, Mayo Clinic, Rochester, MN. 7. Division of Clinical Microbiology, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN; Division of Infectious Diseases, Mayo Clinic, Rochester, MN. Electronic address: patel.robin@mayo.edu.
Abstract
OBJECTIVE: To describe clinical and laboratory findings from the 2012 southeastern Minnesota pertussis outbreak. PATIENTS AND METHODS: Patients were selected for 2 parts of the study. In the first part, nasopharyngeal swabs from a convenience sample of 265 unique patients were used for both the clinician-requested polymerase chain reaction (PCR) test and culture. B pertussis isolates were tested for macrolide susceptibility and typed using whole genome sequencing and pulsed-field gel electrophoresis. Pertactin gene sequences were analyzed to identify pertactin-deficient B pertussis. In the second part, all patients seen at Mayo Clinic in Rochester, Minnesota, who had PCR results positive for Bordetella pertussis or Bordetella parapertussis between January 1, 2012, and December 31, 2012, were analyzed for patient demographic features and vaccination records. RESULTS: One hundred sixty patients had results positive for B pertussis, and 21 patients had results positive for B parapertussis. Among the 265 swabs cultured, B pertussis was detected by both culture and PCR in 11. One swab was positive for B pertussis by culture alone, and 13 were positive by PCR alone. Polymerase chain reaction detected B pertussis more frequently than did culture (P=.001). No macrolide resistance was detected. All 12 isolates tested had an altered pertactin gene, including 9 with a signal sequence deletion, 2 with insertion sequence disruptions, and 1 with a premature stop codon. Nine and 3 isolates were pertactin types prn1 and prn2, respectively. Whole genome sequencing and pulsed-field gel electrophoresis detected the presence of multiple B pertussis strains. The mean age of patients with pertussis was younger than that of those without pertussis (15.6 and 25.5 years, respectively; P=.002). Compared with those whose test results were negative for B pertussis, fewer patients with positive results had received whole-cell pertussis vaccine (P=.02). In the subgroup who had received acellular vaccine exclusively, the time since the most recent pertussis vaccination in those with results positive for B pertussis was longer than that in those with negative results (1363 vs 1010 days; P=.004). CONCLUSION: The 2012 pertussis outbreak in southeastern Minnesota included multiple strains of B pertussis, all putatively lacking pertactin. Our findings may indicate decreased efficacy of (and waning immunity from) acellular vaccines as contributors to the outbreak.
OBJECTIVE: To describe clinical and laboratory findings from the 2012 southeastern Minnesota pertussis outbreak. PATIENTS AND METHODS: Patients were selected for 2 parts of the study. In the first part, nasopharyngeal swabs from a convenience sample of 265 unique patients were used for both the clinician-requested polymerase chain reaction (PCR) test and culture. B pertussis isolates were tested for macrolide susceptibility and typed using whole genome sequencing and pulsed-field gel electrophoresis. Pertactin gene sequences were analyzed to identify pertactin-deficient B pertussis. In the second part, all patients seen at Mayo Clinic in Rochester, Minnesota, who had PCR results positive for Bordetella pertussis or Bordetella parapertussis between January 1, 2012, and December 31, 2012, were analyzed for patient demographic features and vaccination records. RESULTS: One hundred sixty patients had results positive for B pertussis, and 21 patients had results positive for B parapertussis. Among the 265 swabs cultured, B pertussis was detected by both culture and PCR in 11. One swab was positive for B pertussis by culture alone, and 13 were positive by PCR alone. Polymerase chain reaction detected B pertussis more frequently than did culture (P=.001). No macrolide resistance was detected. All 12 isolates tested had an altered pertactin gene, including 9 with a signal sequence deletion, 2 with insertion sequence disruptions, and 1 with a premature stop codon. Nine and 3 isolates were pertactin types prn1 and prn2, respectively. Whole genome sequencing and pulsed-field gel electrophoresis detected the presence of multiple B pertussis strains. The mean age of patients with pertussis was younger than that of those without pertussis (15.6 and 25.5 years, respectively; P=.002). Compared with those whose test results were negative for B pertussis, fewer patients with positive results had received whole-cell pertussis vaccine (P=.02). In the subgroup who had received acellular vaccine exclusively, the time since the most recent pertussis vaccination in those with results positive for B pertussis was longer than that in those with negative results (1363 vs 1010 days; P=.004). CONCLUSION: The 2012 pertussis outbreak in southeastern Minnesota included multiple strains of B pertussis, all putatively lacking pertactin. Our findings may indicate decreased efficacy of (and waning immunity from) acellular vaccines as contributors to the outbreak.
Authors: Katherine E Bowden; Margaret M Williams; Pamela K Cassiday; Andrea Milton; Lucia Pawloski; Marsenia Harrison; Stacey W Martin; Sarah Meyer; Xuan Qin; Chas DeBolt; Azadeh Tasslimi; Nusrat Syed; Ronald Sorrell; Mike Tran; Brian Hiatt; Maria Lucia Tondella Journal: J Clin Microbiol Date: 2014-07-16 Impact factor: 5.948
Authors: J M Bartkus; B A Juni; K Ehresmann; C A Miller; G N Sanden; P K Cassiday; M Saubolle; B Lee; J Long; A R Harrison; J M Besser Journal: J Clin Microbiol Date: 2003-03 Impact factor: 5.948
Authors: Lynne M Sloan; Marlene K Hopkins; P Shawn Mitchell; Emily A Vetter; Jon E Rosenblatt; W Scott Harmsen; Franklin R Cockerill; Robin Patel Journal: J Clin Microbiol Date: 2002-01 Impact factor: 5.948
Authors: Shashank Dalvi; Prasad S Kulkarni; M A Phadke; S S More; Sanjay K Lalwani; Dipty Jain; Mamta Manglani; B S Garg; Mohan K Doibale; C T Deshmukh Journal: Hum Vaccin Immunother Date: 2015 Impact factor: 3.452
Authors: Ruth Koepke; Michael L Bartholomew; Jens C Eickhoff; Roman A Ayele; Diane Rodd; Joan Kuennen; Jean Rosekrans; David M Warshauer; James H Conway; Jeffrey P Davis Journal: Clin Infect Dis Date: 2015-06-25 Impact factor: 9.079