Francisella tularensis is the causative agent of tularemia. Recent studies suggest that distinct clades of F. tularensis with specific geographical distribution are associated with different clinical presentations, ecological niches, and host species1. This study investigated naturally infected Swiss free-ranging European brown hares (Lepus europaeus).
Carcasses of hares were collected between February 2012 and May 2014. Multiple organs were tested by direct PCR and by culture. Isolates of F. tularensis were further genetically typed by canSNPs analysis and by MLVA and phenotypic and genotypic antibiotic resistance profiles were characterized. Moreover, histology and immunohistochemistry were performed.
Twenty-eight carcasses of hares out of 53 resulted positive for F. tularensis. Isolates were characterized as F. tularensis subsp. holarctica belonging to the lineage B.FTNF002-00 that is circulating in Western Europe and to the group B.13. Strains belonging to the group B. 13 were previously shown to be erythromycin resistant in association with mutations in the rrl and rplD genes2. Pathology investigation revealed that spleen, lung, liver, lymph nodes and trachea were more frequently involved but other organs, including adrenal glands, were also affected to variable extent. The features of the lesions were similar to those described in humans and in multiple animal species. However, the distribution was different from that described in hares infected with the B.13 group.
These results suggest that the group B.13, showing resistance to macrolides, is spread Western in Europe than previously described2. The pathology findings in the examined hares are consistent with B.FTNF002-00-associated lesions being different than those previously described to be associated with B.13 infection. This investigation also shows that European brown hares are a good model and a “sentinel” species to investigate F. tularensis infections since they are relatively easier to monitor than small rodents and they show several overlapping lesions with those known to develop in infected humans.