Abstract
In Austria, vaccination coverage against Bordetella pertussis infections during infancy is estimated at around 90%. Within the last years, however, the number of pertussis cases has increased steadily, not only in children but also in adolescents and adults, indicating both insufficient herd immunity and vaccine coverage. Waning immunity in the host and/or adaptation of the bacterium to the immunised hosts could contribute to the observed re-emergence of pertussis. In this study we therefore addressed the genetic variability in B. pertussis strains from several Austrian cities. Between the years 2002 and 2008, 110 samples were collected from Vienna (n = 32), Linz (n = 63) and Graz (n = 15) by nasopharyngeal swabs. DNA was extracted from the swabs, and bacterial sequence polymorphisms were examined by MLVA (multiple-locus variable number of tandem repeat analysis) (n = 77), by PCR amplification and conventional Sanger sequencing of the polymorphic regions of the prn (pertactin) gene (n = 110), and by amplification refractory mutation system quantitative PCR (ARMS-qPCR) (n = 110) to directly address polymorphisms in the genes encoding two pertussis toxin subunits (ptxA and ptxB), a fimbrial adhesin (fimD), tracheal colonisation factor (tcfA), and the virulence sensor protein (bvgS). Finally, the ptxP promoter region was screened by ARMS-qPCR for the presence of the ptxP3 allele, which has been associated with elevated production of pertussis toxin. The MLVA analysis revealed the highest level of polymorphisms with an absence of MLVA Type 29, which is found outside Austria. Only Prn subtypes Prn1/7, Prn2 and Prn3 were found with a predominance of the non-vaccine type Prn2. The analysis of the ptxA, ptxB, fimD, tcfA and bvgS polymorphisms showed a genotype mixed between the vaccine strain Tohama I and a clinical isolate from 2006 (L517). The major part of the samples (93%) displayed the ptxP3 allele. The consequences for the vaccination strategy are discussed.
Highlights
Bordetella pertussis, the causative agent of whooping cough, is still responsible for significant morbidity and mortality in many countries of the world
The first part, collected from 2002 to 2006 (n = 77) was characterised by multiple-locus variable-number tandem repeat analysis (MLVA) typing [17], and all samples (n = 110) were examined by sequencing of the prn gene polymorphic region-1 [21], and ARMS-qPCR [30] of target single nucleotide polymorphisms (SNPs) in the genes coding for pertussis toxin, fimbrial adhesin, tracheal colonisation factor, the virulence sensor protein [20], and the pertussis toxin promoter region ptxP [22]
MLVA typing shows significant genotypic diversity of B. pertussis strains in Austria
Summary
Bordetella pertussis, the causative agent of whooping cough, is still responsible for significant morbidity and mortality in many countries of the world. ACVs contain the detoxified pertussis toxin (Ptx), filamentous hemagglutinin (FHA), pertactin (Prn) and fimbriae (Fim) in various combinations. A recent review from the Cochrane Acute Respiratory Infections Group [2] summed up six efficacy trials with a total of 46,283 participants. Multicomponent ACVs (n 3 components) had an efficacy between 84% and 85% in preventing typical whooping cough. The examined one- or two-component ACVs prevented only between 59% and 75% of typical whooping cough, a new Danish monocomponent ACV, containing only Ptx toxoid, was recently shown to achieve excellent 93% efficacy against severe pertussis requiring hospitalisation [3]. The Cochrane Group assessed 52 safety trials with a total of 136,541 participants to show that the ACVs lead to significantly fewer local and systemic adverse reactions than the WCVs [2]
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