Search

Host–parasite interactions are influenced by present and past eco‐evolutionary interactions and the local environment. An ecological community defines the potential host range of each parasite and the potential parasite diversity of each host species. Past and present processes translate potential to realised interaction niches of parasite and host species. Host–parasite interactions are antagonistic, which may slow the saturation of their interaction niches. Intervality, a property of bipartite networks, measures saturation of interaction niches. Intervality of a community increases as the interaction niches of species of one guild (e.g. hosts) become saturated for their interactions with another guild (e.g. parasites). Characteristics driving intervality in host and parasite communities are largely unknown, as well as the effect of environmental change on intervality of these communities. In our study, we assess if the characteristics 'phylogenetic relatedness' and 'overlap in ecological interactions' explain intervality of rodent host–helminth parasite communities. In addition, we contrast intervality of these communities from habitats that differ in their history of human‐driven modification. We performed the analyses for the interaction niches of both parasites and hosts, independently. Our results indicated that host and parasite communities were non‐interval or significantly less interval than expected by chance. Phylogenetic relatedness and overlap in ecological interactions did not explain the maximum values of intervality. We speculate that antagonistic coevolution in host–parasite communities may hinder communities to reach saturation, which would explain why it is difficult to find the characteristics that explain intervality of a community. Interestingly, intervality of the interaction niche of parasites (host range) increased with habitat modification (i.e. saturation increased), whereas intervality of the interaction niche of hosts (parasite diversity) decreased as habitat modification increased. These opposite trends suggest that interaction niches of parasites and hosts respond differently to habitat modification. [ABSTRACT FROM AUTHOR]

Nematodes belonging to the genus Oesophagostomum frequently infect wild chimpanzees (Pan troglodytes) across widely separated field sites. Nodular lesions (granulomas) containing Oesophagostomum are commonly seen in the abdomen of infected chimpanzees post‐mortem. At Taï National Park, Côte d'Ivoire, previous studies have identified larvae of a variety of Oesophagostomum spp. in wild chimpanzee stool, based on sequencing of larval DNA, and nodular lesions associated with Oesophagostomum, identified morphologically to the genus level but not sequenced. Here we present three recent cases of parasitic granulomas found post‐mortem in chimpanzees at Taï. We complement descriptions of gross pathology, histopathology and parasitology with PCR and sequencing of DNA isolated from the parasitic nodules and from adult worms found inside the nodules. In all three cases, we identify Oesophagostomum stephanostomum as the causative agent. The sequences from this study were identical to the only other published sequences from nodules in nonhuman primates—those from the wild chimpanzees of Gombe, Tanzania. Research highlights: Chimpanzees in Taï National Park (Côte d'Ivoire) commonly have a small number of abdominal parasitic nodules, observed post‐mortem.A variety of Oesophagostum spp. has been found in the stool of Taï chimps.The nodules are caused by Oesophagostomum stephanostomum, and the ITS‐2 sequence is identical to the only other sequence obtained from chimp nodules (in Gombe, Tanzania). [ABSTRACT FROM AUTHOR]

The impact of carnivore parvovirus infection on wild populations is not yet understood; disease signs are mainly developed in pups and assessing the health of litters in wild carnivores has big limitations. This study aims to shed light on the virus dynamics among wild carnivores thanks to the analysis of 213 samples collected between 1994 and 2013 in wild ecosystems from Spain. We determined the presence of carnivore parvovirus DNA by real‐time PCR and sequenced the vp2 gen from 22 positive samples to characterize the strains and to perform phylogenetic analysis. The presence of carnivore parvovirus DNA was confirmed in 18% of the samples, with a higher prevalence detected in wolves (Canis lupus signatus, 70%). Fourteen sequences belonging to nine wolves, three Eurasian badgers (Meles meles), a common genet (Genetta genetta) and a European wildcat (Felis silvestris) were classified as canine parvovirus 2c (CPV‐2c); five sequences from three wolves, a red fox (Vulpes vulpes) and a stone marten (Martes foina) as CPV‐2b; and three sequences from a badger, a genet and a stone marten as feline parvovirus (FPV). This was the first report of a wildcat infected with a canine strain. Sequences described in this study were identical or very close related to others previously found in domestic carnivores from distant countries, suggesting that cross‐species transmission takes place and that the parvovirus epidemiology in Spain, as elsewhere, could be influenced by global factors. [ABSTRACT FROM AUTHOR]

Parasite hybrid zones resulting from host secondary contact have never been described in nature although parasite hybridization is well known and secondary contact should affect them similarly to free‐living organisms. When host populations are isolated, diverge and recontact, intimate parasites (host specific, direct life cycle) carried during isolation will also meet and so may form parasite hybrid zones. If so, we hypothesize these should be narrower than the host's hybrid zone as shorter parasite generation time allows potentially higher divergence. We investigate multilocus genetics of two parasites across the European house mouse hybrid zone. We find each host taxon harbours its own parasite taxa. These also hybridize: Parasite hybrid zones are significantly narrower than the host's. Here, we show a host hybrid zone is a suture zone for a subset of its parasite community and highlight the potential of such systems as windows on the evolutionary processes of host–parasite interactions and recombinant pathogen emergence. [ABSTRACT FROM AUTHOR]

Abstract: Changes in species distributions open novel parasite transmission routes at the human–wildlife interface, yet the strength of biotic and biogeographical factors that prevent or facilitate parasite host shifting are not well understood. We investigated global patterns of helminth parasite (Nematoda, Cestoda, Trematoda) sharing between mammalian wildlife species and domestic mammal hosts (including humans) using >24,000 unique country‐level records of host–parasite associations. We used hierarchical modelling and species trait data to determine possible drivers of the level of parasite sharing between wildlife species and either humans or domestic animal hosts. We found the diet of wildlife species to be a strong predictor of levels of helminth parasite sharing with humans and domestic animals, followed by a moderate effect of zoogeographical region and minor effects of species’ habitat and climatic niches. Combining model predictions with the distribution and ecological profile data of wildlife species, we projected global risk maps that uncovered strikingly similar patterns of wildlife parasite sharing across geographical areas for the different domestic host species (including humans). These similarities are largely explained by the fact that widespread parasites are commonly recorded infecting several domestic species. If the dietary profile and position in the trophic chain of a wildlife species largely drives its level of helminth parasite sharing with humans/domestic animals, future range shifts of host species that result in novel trophic interactions may likely increase parasite host shifting and have important ramifications for human and animal health. [ABSTRACT FROM AUTHOR]

Phylogenetic relationships, evolutionary history and systematics of tapeworms of the family Catenotaeniidae were studied using nucleotide sequences of the partial 28S nuclear rDNA (ca. 1,500 bp) and mitochondrial 12S–16S DNA (ca. 820 bp) genes. The tapeworm material consists of 29 species, including type species of the genera Catenotaenia Janicki, 1904, Catenotaenioides Haukisalmi, Hardman and Henttonen, 2010, Pseudocatenotaenia Tenora, Mas‐Coma, Murai and Feliu, 1980, Skrjabinotaenia Akhumyan, 1946, Meggittina Lynsdale, 1953, and Hemicatenotaenia Tenora, 1977. The basal phylogenetic structure of the Catenotaeniidae remains unresolved, but it is shown that most of the catenotaeniids in Eurasia and Africa comprise a large clade represented by species of Catenotaenia, Catenotaenioides, Skrjabinotaenia and Meggittina, parasitizing murid, cricetid, nesomyid and sciurid rodents. The results suggest that the divergence and early radiation of this clade have occurred in murid rodents (represented by Apodemus spp. and Mus musculus in the present material) in western Eurasia, followed by colonization of Africa, most likely independently of the colonization of their murid hosts between these continents. There is very little evidence of cophylogeny between hosts and parasites, suggesting that host transfers have played a major role in the divergence of catenotaeniids. In Africa, catenotaeniids have radiated in other murid and nesomyid rodents, and later colonized Madagascar and recolonized Eurasia. The results also show that the subfamily Skrjabinotaeniinae (including Skrjabinotaenia and Meggittina) is monophyletic, but the Catenotaeniinae (including Catenotaenia, Catenotaenioides, Pseudocatenotaenia and Hemicatenotaenia) is clearly non‐monophyletic. In addition, the genera Catenotaenia and Skrjabinotaenia were both found to be non‐monophyletic. Based on the phylogenetic and morphological evidence, several taxonomical changes, mainly new combinations, are proposed. Overall, the present results suggest that the family Catenotaeniidae is in need of major systematic revision. [ABSTRACT FROM AUTHOR]

Host-parasite interaction studies across hybrid zones often focus on host genetic variation, treating parasites as homogeneous. 'Intimately' associated hosts and parasites might be expected to show similar patterns of genetic structure. In the literature, factors such as no intermediate host and no free-living stage have been proposed as 'intimacy' factors likely constraining parasites to closely follow the evolutionary history of their hosts. To test whether the whipworm, Trichuris muris, is intimately associated with its house mouse host, we studied its population genetics across the European house mouse hybrid zone ( HMHZ) which has a strong central barrier to gene flow between mouse taxa. T. muris has a direct life cycle and nonmobile free stage: if these traits constrain the parasite to an intimate association with its host we expect a geographic break in the parasite genetic structure across the HMHZ. We genotyped 205 worms from 56 localities across the HMHZ and additionally T. muris collected from sympatric woodmice ( Apodemus spp.) and allopatric murine species, using mt- COX1, ITS1-5.8S- ITS2 rDNA and 10 microsatellites. We show four haplogroups of mt- COX1 and three clear ITS1-5.8S- ITS2 clades in the HMHZ suggesting a complex demographic/phylogeographic history. Microsatellites show strong structure between groups of localities. However, no marker type shows a break across the HMHZ. Whipworms from Apodemus in the HMHZ cluster, and share mitochondrial haplotypes, with those from house mice. We conclude Trichuris should not be regarded as an 'intimate' parasite of the house mouse: while its life history might suggest intimacy, passage through alternate hosts is sufficiently common to erase signal of genetic structure associated with any particular host taxon. [ABSTRACT FROM AUTHOR]

We summarize the current knowledge on parasitism-related invasion processes of the globally invasive Rattus lineages, originating from Asia, and how these invasions have impacted the local epidemiology of rodent-borne diseases. Parasites play an important role in the invasion processes and successes of their hosts through multiple biological mechanisms such as 'parasite release,' 'immunocompetence advantage,' 'biotic resistance' and 'novel weapon.' Parasites may also greatly increase the impact of invasions by spillover of parasites and other pathogens, introduced with invasive hosts, into new hosts, potentially leading to novel emerging diseases. Another potential impact is the ability of the invader to amplify local parasites by spillback. In both cases, local fauna and humans may be exposed to new health risks, which may decrease biodiversity and potentially cause increases in human morbidity and mortality. Here we review the current knowledge on these processes and propose some research priorities. [ABSTRACT FROM AUTHOR]

While the effects of deforestation and habitat fragmentation on parasite prevalence or richness are well investigated, host-parasite networks are still understudied despite their importance in understanding the mechanisms of these major disturbances. Because fragmentation may negatively impact species occupancy, abundance and co-occurrence, we predict a link between spatiotemporal changes in habitat and the architecture of host-parasite networks., For this, we used an extensive data set on 16 rodent species and 29 helminth species from seven localities of South-East Asia. We analysed the effects of rapid deforestation on connectance and modularity of helminth-parasite networks. We estimated both the degree of fragmentation and the rate of deforestation through the development of land uses and their changes through the last 20 to 30 years in order to take into account the dynamics of habitat fragmentation in our statistical analyses., We found that rapid fragmentation does not affect helminth species richness per se but impacts host-parasite interactions as the rodent-helminth network becomes less connected and more modular., Our results suggest that parasite sharing among host species may become more difficult to maintain with the increase of habitat disturbance. [ABSTRACT FROM AUTHOR]

Aim Geographic spread and range expansion of species into novel environments may merge originally separated species assemblages, yet the possible drivers of geographic heterogeneity in host-parasite associations remain poorly understood. Here, we examine global patterns in the parasite assemblages of two rat species and explore the role of parasite acquisition from local pools of host species. Location Global. Methods We compiled a global data set of helminth parasites (n = 241 species) from two rat species (Rattus rattus species complex, R. norvegicus) and, concomitantly, from all other mammal species known to be infected by the same parasites. We used an inverse Bayesian modelling approach to explicitly link species-level to community-level infestation probabilities at different geographic scales and alleviate the shortcoming of sampling bias. Results Patterns of species richness and turnover of parasites in the two focal rat species revealed clear biogeographic structure with lowest species richness and most distinct assemblages in Madagascar and highest species richness and least distinct assemblages in the Palaearctic region. Parasite species richness and turnover across regions were correlated for the two focal hosts, although they were associated with distinct assemblages within regions. Infection probability of a focal host with any given parasite was clearly related to infection probability of the local species pool of wildlife hosts with that same parasite. Infection probability of other mammal species infected with these parasite species, in turn, decreased with their taxonomic distance to the genus Rattus. Main conclusions Our study demonstrates the importance of spillover of parasites from local wildlife hosts to invasive rats on global patterns of host-parasite associations. Considering both changes in local pools of host species and the global distributions of parasite and pathogen diversity in consistent model frameworks may therefore advance the forecasting of species-level infestation patterns and the possible risk of disease emergence from local to global scale. [ABSTRACT FROM AUTHOR]