J Clin Microbiol. 2014 Jul 16. pii: JCM.01189-14. [Epub ahead of print]
Molecular Epidemiology of Pertussis Epidemic - Washington State, 2012.
Bowden KE1, Williams MM1, Cassiday PK1, Milton A1, Pawloski L1, Harrison M1, Martin SW1, Meyer S1, Qin X2, DeBolt C3, Tasslimi A3, Syed N4, Sorrell R4,Tran M4, Hiatt B4, Tondella ML1.
Although pertussis disease is vaccine-preventable, Washington State experienced a substantial rise in pertussis incidence beginning in 2011. By June 2012, the reported cases reached 2,520 (37.5 cases per 100,000 residents), a 1,300% increase compared with the same period in 2011. We assessed the molecular epidemiology of this statewide epidemic using 240 isolates collected from case-patients reported from 19 of 39 Washington counties during 2012-2013. Typing methods included pulsed-field gel electrophoresis (PFGE), multilocus variable number tandem repeat analysis (MLVA), multilocus sequence typing (MLST), and pertactin gene (prn) mutational analysis. Using the scheme PFGE-MLVA-MLST-prn mutations-Prn deficiency, the 240 isolates comprised 65 distinct typing profiles. Thirty-one PFGE types were found, with the most common types, CDC013 (n=51), CDC237 (n=44), and CDC002 (n=42), accounting for 57% of them. Eleven MLVA types were observed, mainly comprising type 27 (n=183; 76%). Seven MLST types were identified, with the majority of the isolates typing as prn2-ptxP3-ptxA1-fim3-1 (n=157; 65%). Four different prn mutations accounted for the 76% of isolates exhibiting pertactin-deficiency. PFGE provided the highest discriminatory power (D=0.87) and was found to be a more powerful typing method than MLVA and MLST combined (D=0.67). This study provides evidence for the continued predominance of MLVA 27 and prn2-ptxP3-ptxA1, along with the reemergence of the fim3-1 allele. Our results indicate that the B. pertussis population causing this epidemic was diverse, with a few molecular types predominating. PFGE, MLVA, and MLST profiles were consistent with predominate types circulating in the US and other countries. For prn, several mutations were present in multiple molecular types.
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