The pla gene, encoding plasminogen activator, is not specific to Yersinia pestis

Hänsch, Stephanie; Cilli, Elisabetta; Catalano, Giulio; Gruppioni, Giorgio; Bianucci, Raffaella; Stenseth, Nils Chr.; Bramanti, Barbara; Pallen, Mark J.

doi:10.1186/s13104-015-1525-x

Cited by 29 publications

(20 citation statements)

References 9 publications

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“…The results found here supports other work which suggests that markers other than the pla gene should be included to help avoid false positive results when screening for Y. pestis , as has been stressed by Janse, Hamidjaja & Reusken (2013). This was recently confirmed by Hänsch et al, as they found evidence that the pla gene is present in some strains of Escherichia coli and Citrobacter koseri (Hänsch et al, 2015). It is not clear why the homologue was present in a larger percentage of R. rattus samples than in the other species tested; perhaps R. rattus carries more E. coli or C. koseri , but this is something that needs to be investigated further.…”

Section: Resultssupporting

confidence: 90%

Detection of aYersinia pestisgene homologue in rodent samples

Giles

Greenwood

Tsangaras

et al. 2016

PeerJ

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A homologue to a widely used genetic marker, pla, for Yersinia pestis has been identified in tissue samples of two species of rat (Rattus rattus and Rattus norvegicus) and of mice (Mus musculus and Apodemus sylvaticus) using a microarray based platform to screen for zoonotic pathogens of interest. Samples were from urban locations in the UK (Liverpool) and Canada (Vancouver). The results indicate the presence of an unknown bacterium that shares a homologue for the pla gene of Yersinia pestis, so caution should be taken when using this gene as a diagnostic marker.

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Section: Resultssupporting

confidence: 90%

Detection of aYersinia pestisgene homologue in rodent samples

Giles

Greenwood

Tsangaras

et al. 2016

PeerJ

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“…We also acknowledge that the prevalence of Y. pestis we reported may be underestimated due to limitations associated with suboptimal storage of fleas and could further be confounded by the variable number of individual fleas in diagnostic samples. Furthermore, the specificity observed for an assay targeting the pla gene must take into account homogeneity to other species (Hänsch et al 2015). In the absence of successful bacterial culture, it is recommended that alternative targets or methods confirm results utilizing a one target approach to avoid overestimation of prevalence.…”

Section: Discussionmentioning

confidence: 99%

Enzootic maintenance of sylvatic plague in Canada's threatened black‐tailed prairie dog ecosystem

et al. 2020

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Data paucity can seem to hinder science‐based approaches to the conservation of imperiled species. Yet, even individually limited datasets can improve understanding and management of complex ecological systems when carefully integrated. We demonstrate this approach to gain first insights on the transmission ecology of Yersinia pestis in Grasslands National Park (GNP), Canada, where both the bacterium and its rodent host, the nationally threatened black‐tailed prairie dog (BTPD, Cynomys ludovicianus), reach the northern limit of their distribution in North America. Primarily flea‐borne, Y. pestis causes sylvatic plague, a disease of exceptional relevance to both human health and wildlife conservation. We integrated data collected independently by multiple organizations in 2010–2017 across 17 BTPD colonies, where the species co‐occur with Richardson's ground squirrels (RGS, Urocitellus richardsonii). Available data included estimates of BTPD density and occupancy from visual counts and colony mapping; information on flea distribution, abundance, and prevalence of infection with Y. pestis from burrow swabbing, animal combing, and PCR assays; and the response of these variables to deltamethrin application on BTPD colony sections. Our analyses suggest that sylvatic plague in GNP is maintained at an enzootic level (i.e., chronic presence affecting a low proportion of individuals) with no evidence of widespread mortality, at least partially due to reduced flea activity after spring (percentage of prevalence in burrows: April–May = 11.69–33.89%; June–September: 1.75–3.19%), low prevalence of Y. pestis in flea samples (95% CI = 0.42–2.27%), and relatively low BTPD densities. Nonetheless, reducing flea prevalence through insecticide application had a positive effect on BTPD abundance, suggesting that enzootic plague is causing chronic mortality. Because flea prevalence on hosts was higher following drier years and higher on RGS than on BTPD (26.69% vs. 3.27%), insecticide application may be particularly important during dry periods and may need to take RGS and their movements into consideration. Differences between flea communities sampled by burrow swabbing and host combing suggest that plague surveillance should integrate both methods. Effects of projected climate change on vector life cycles, flea community composition, and host–parasite interactions warrant continued monitoring and an adaptive approach to species recovery actions and plague mitigation measures.

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“…The validation of ancient genomes with relatively low coverage as presented here is challenging since the DNA extracted from archaeological remains results in metagenomic data and the differentiation between target organism DNA and environmental background can be difficult. The identification of Y. pestis DNA based on PCR targeting the pla locus on the pPCP1 plasmid has theoretically been shown to be problematic (36), leading to discussions about false positive results (16). However, assignment to Y. pestis based on reads retrieved from shotgun sequencing and mapping to a reference genome also can be challenging in case of extremely low genomic coverage (3, 4).…”

Section: Discussionmentioning

confidence: 99%

AncientYersinia pestisgenomes from across Western Europe reveal early diversification during the First Pandemic (541–750)

Keller

Spyrou²,

Scheib

et al. 2018

Preprint

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The first historically documented pandemic caused byYersinia pestisstarted as the Justinianic Plague in 541 within the Roman Empire and continued as the so-called First Pandemic until 750. Although palaeogenomic studies have previously identified the causative agent asY. pestis, little is known about the bacterium’s spread, diversity and genetic history over the course of the pandemic.To elucidate the microevolution of the bacterium during this time period, we screened human remains from 20 sites in Austria, Britain, Germany, France and Spain forY. pestisDNA and reconstructed six new genomes. We present a novel methodological approach assessing SNPs in ancient bacterial genomes, facilitating qualitative analyses of low coverage genomes from a metagenomic background. Phylogenetic analysis reveals the existence of previously undocumentedY. pestisdiversity during the 6th–7thcenturies, and provides evidence for the presence of multiple distinctY. pestisstrains in Europe. We offer genetic evidence for the presence of the Justinianic Plague in the British Isles, previously only hypothesized from ambiguous documentary accounts, as well as southern France and Spain, and that southern Germany seems to have been affected by at least two distinctY. pestisstrains. Four of the reported strains form a polytomy similar to others seen across theY. pestisphylogeny, associated with the Second and Third Pandemics. We identified a deletion of a 45 kb genomic region in the most recent First Pandemic strain affecting two virulence factors, intriguingly overlapping with a deletion found in 17th–18th-century genomes of the Second Pandemic.Significance StatementThe first historically reported pandemic attributed toYersinia pestisstarted with the Justinianic Plague (541–544) and continued for around 200 years as the so-called First Pandemic. To date, only oneY. pestisstrain from this pandemic has been reconstructed using ancient DNA. In this study, we present six new genomes from Britain, France, Germany and Spain, demonstrating the geographic range of plague during the First pandemic and showing microdiversity in the Early Medieval Period. Moreover, we detect similar genome decay during the First and Second Pandemic (17thto 18thcentury) that includes the same two virulence factors, thus providing an example of potential convergent evolution ofY. pestisduring large scale epidemics.

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The pla gene, encoding plasminogen activator, is not specific to Yersinia pestis

Abstract: Here we present evidence to show that the pla gene, previously thought to be specific to Yersinia pestis, occurs in some strains of Citrobacter koseri and Escherichia coli. This means that detection of this gene on its own can no longer be taken as evidence of detection of Y. pestis.

Cited by 29 publications

References 9 publications

Detection of aYersinia pestisgene homologue in rodent samples

Detection of aYersinia pestisgene homologue in rodent samples

Enzootic maintenance of sylvatic plague in Canada's threatened black‐tailed prairie dog ecosystem

AncientYersinia pestisgenomes from across Western Europe reveal early diversification during the First Pandemic (541–750)

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