The bacterium Treponema paraluisleporidarum causes syphilis in Lagomorphs. In a set of 1,095 samples from four species – European brown hare (Lepus europaeus), mountain hare (Lepus timidus), Corsican hare (Lepus corsicanus) and European rabbit (Oryctolagus cuniculus) – we genotyped the strains that infect wild lagomorphs. Samples originate from Sweden, the Netherlands, the United Kingdom, Germany, the Czech Republic and Italy. The phylogenetic analyses of two informative gene targets (tp0488 and tp0548) showed high genetic diversity among the lagomorph-infecting treponemes. More specifically, we found a high number of nucleotide variants and various short repeat units in the tp0548 locus which have not been described for human syphilis and primate yaws causing Treponema pallidum. While the functional aspect of these short repeat units remains subject to ongoing investigations, it likely enables the pathogen to better survive in its lagomorph host. Our data did not support any geographic clustering which is equally reflected in the host population genetics as shown by mitochondrial genome data corresponding to the sampled lagomorph populations. This is unexpected and in contrast with what has been shown for nonhuman primate infection with T. pallidum. In the future, the combination of multi-locus sequence typing and WGS from modern and ancient samples from a wide geographic range and multiple lagomorph species will contribute to a better understanding of the epidemiology and evolutionary path of lagomorph-infecting treponemes. In conclusion, our current study demonstrates a high genetic variation of the syphilis-causing pathogen in a higher number of positively PCR-tested European lagomorphs (n=496/1095).

Amongst newly developed approaches to analyse molecular data, phylodynamic models are receiving much attention because of their potential to reveal changes to viral populations over short periods. This knowledge can be very important for understanding disease impacts. However, their accuracy needs to be fully understood, especially in relation to wildlife disease epidemiology, where sampling and prior knowledge may be limited. The release of the rabbit haemorrhagic disease virus (RHDV) as biological control in naïve rabbit populations in Australia in 1996 provides a unique dataset with which to validate phylodynamic models. By comparing the results obtained for RHDV1 with our current understanding of the RHDV epidemiology in Australia, we evaluated the performances of these recently developed models. In line with our expectations, coalescent analyses detected a sharp increase in the virus trajectory in the first few months after the virus release, followed by a more gradual increase. The phylodynamic analyses with a birth-death tree prior generated effective reproductive number estimates (the average number of secondary infections per each infectious case, Re) larger than one for most of the epochs considered. However, the possible range of the initial Re included estimates lower than one despite the known rapid spread of RHDV1 in Australia. Furthermore, the analyses that took into account the geographical structuring failed to converge. We argue that the difficulties that we encountered most likely stem from the fact that the samples available from 1996 to 2014 were too sparse with respect to geographic and within outbreak coverage to adequately infer some of the model parameters. In general, while these Bayesian analyses proved to be greatly informative in some regards, we caution that their interpretation may not be straight forward and recommend further research in evaluating the robustness of these models to assumption violations and sensitivity to sampling regimes.

Wild animals are natural reservoir hosts for a variety of pathogens, and such is the case for deer (family Cervidae). Deer were introduced to Australia 150 years ago for farming and game, but wild deer populations have expanded considerably in recent years, posing increasing threats to biodiversity, agriculture and public health. There are few data currently available on pathogens that Australian wild deer carry or whether these organisms pose biosecurity threats to humans, wildlife, livestock or other domestic animals. To address this knowledge gap, we tested for the presence of seven parasitic genera in 243 blood samples collected from four wild deer species in eastern Australia. Blood samples were tested by PCR for the presence of Plasmodium, Trypanosoma, Babesia, Theileria, Toxoplasma, Sarcocystis and Neospora DNA. No amplification was obtained for either the 18S rRNA (or the cytochrome b gene in the case of Plasmodium) of the seven selected parasitic genera, suggesting that wild deer in eastern Australia currently pose little risk as vectors of these parasites to livestock and humans. This survey represents the first molecular study of its type in Australian deer and provides important baseline information about the health status of these animals.