Adaptive Loss of the pYV Virulence Plasmid During a Yersinia pseudotuberculosis Epizootic in Seba's Short-Tailed Bats
Yersinia pseudotuberculosis is an important zoonotic pathogen that frequently causes epizootics in wildlife and zoo populations, yet the evolutionary dynamics of its virulence determinants during outbreaks are poorly understood. In 2020, a prolonged epizootic of Y. pseudotuberculosis in Seba's short-tailed bats (Carollia perspicillata) in a zoological collection resulted in high mortality within a colony affected by hemosiderosis, an iron-overload condition. A combination of phenotypic and genomic analyses was used to characterise Y. pseudotuberculosis isolates recovered during this event and to compare them with geographically linked isolates from sporadic infections in other hosts. Growth assays under varying iron conditions showed that epizootic isolates, particularly those from the early outbreak, exhibited higher growth rates than sporadic isolates in iron-replete media. PCR screening and whole-genome sequencing demonstrated that all epizootic isolates belonged to a single sequence type (ST-43) and shared a conserved repertoire of iron-acquisition genes with sporadic isolates, indicating that the outbreak was not driven by a high density of iron-uptake systems.  Virulence profiling showed early epizootic isolates carried the pYV virulence plasmid, encoding the type III secretion system and associated Yop effectors, whereas later isolates had lost pYV. This plasmid loss correlated with reduced virulence and impaired proliferation in a Galleria mellonella infection model, indicating attenuation of the outbreak lineage. We propose that progressive pYV loss represents an instance of adaptive gene loss, reflecting a trade off in which maintenance within the bat host population is favoured over acute virulence. More broadly, our findings highlight the dynamic nature of virulence plasmids in Yersinia and illustrate how pathoadaptive gene loss can be just as critical to microbial survival as gene acquisition.
Yersinia pseudotuberculosis is an important zoonotic pathogen that frequently causes epizootics in wildlife and zoo populations, yet the evolutionary dynamics of its virulence determinants during outbreaks are poorly understood. In 2020, a prolonged epizootic of Y. pseudotuberculosis in Seba's short-tailed bats (Carollia perspicillata) in a zoological collection resulted in high mortality within a colony affected by hemosiderosis, an iron-overload condition. A combination of phenotypic and genomic analyses was used to characterise Y. pseudotuberculosis isolates recovered during this event and to compare them with geographically linked isolates from sporadic infections in other hosts. Growth assays under varying iron conditions showed that epizootic isolates, particularly those from the early outbreak, exhibited higher growth rates than sporadic isolates in iron-replete media. PCR screening and whole-genome sequencing demonstrated that all epizootic isolates belonged to a single sequence type (ST-43) and shared a conserved repertoire of iron-acquisition genes with sporadic isolates, indicating that the outbreak was not driven by a high density of iron-uptake systems.  Virulence profiling showed early epizootic isolates carried the pYV virulence plasmid, encoding the type III secretion system and associated Yop effectors, whereas later isolates had lost pYV. This plasmid loss correlated with reduced virulence and impaired proliferation in a Galleria mellonella infection model, indicating attenuation of the outbreak lineage. We propose that progressive pYV loss represents an instance of adaptive gene loss, reflecting a trade off in which maintenance within the bat host population is favoured over acute virulence. More broadly, our findings highlight the dynamic nature of virulence plasmids in Yersinia and illustrate how pathoadaptive gene loss can be just as critical to microbial survival as gene acquisition.
University of Surrey