Frédéric Thomas

Differential Mortality of Two Closely Related Host Species Induced by One Parasite

Understanding the importance of parasites in affecting the biodiversity of host species in ecosystems is a central aim of conservation biology. Recent advances in ecology have suggested that differential parasite susceptibilities between taxonomically related host species may be a determinant of animal community structure. Although conceptually appealing, such an hypothesis suffers from a lack of field evidence. Here, we report that the populations of two congeneric and sympatric host species (Gammarus insensibilis and G. aequicauda), infected by the same parasite (Microphallus Papillorobustus), exhibit a strongly contrasted pattern of parasite-induced mortality.

Parasites and ecosystem engineering : what roles could they play?

In recent years, there has been a growing interest in understanding the ecological importance of ecosystem engineers. In this paper we argue that parasites, through the phenotypic alterations they induce in their hosts, are likely to be involved in engineering processes for at least two reasons. First, when ecosystem engineers are themselves infected, phenotypic alterations induced by parasites can interfere with host traits involved in the engineering processes. Secondly, parasites themselves can be ecosystem engineers since the phenotypic alterations of hosts directly modify the habitat of all the species inhabiting free-living organisms. This new research area at the interface between ecology and parasitology should improve our understanding of the ecological consequences of phenotypic alterations induced by parasites in ecosystems.

Assortative pairing in Gammarus insensibilis (Amphipoda) infected by a trematode parasite

We have investigated the influence of Microphallus papillorobustus (Trematoda) on the reproductive biology and mating patterns of its intermediate host Gammarus insensibilis (Amphipoda). Infected Gammarus species show altered behaviour which renders them more susceptible to predation by Charadriiform birds, the parasites definitive hosts. In a natural population of G. insensibilis, mean parasite intensity was higher for unpaired individuals than for paired individuals. Fecundity was reduced in infected amphipods. Size-assortative pairing was significant, although infected males were found with smaller females compared to uninfected males of the same size. There was also a positive assortative pairing by parasitic prevalence. Vertical segregation between infected and uninfected individuals, male-male competition for access to uninfected females, and female choice may explain assortative mating for prevalence. This study provides the first empirical evidence that parasites can have a direct effect on patterns of mating in gammarids.

Parasitism and Ecology of Wetlands: A Review

Recent advances in ecology have suggested that parasites, through the spectrum of their effects, could act as key species in ecosystems. Wetlands are productive ecosystems within which parasitism is diversified. There already exists evidence for direct and indirect effects of parasites on their host species. The influence of parasites on the population ecology of hosts includes survival, castration, sexual selection, predation, and spatial distribution. Parasites can also affect the evolution of host biological diversity (i.e., genetic structure and interspecific competition) and trophic interactions between prey and predators. The key role parasites might play in the ecology of coastal waters and wetlands should be considered in conservation programs applied to such ecosystems.

Natural resistance to cancers: a Darwinian hypothesis to explain Peto's paradox.

BackgroundPetos paradox stipulates that there is no association between body mass (a surrogate of number of cells and longevity) and cancer prevalence in wildlife species. Resolving this paradox is a very promising research direction to understand mechanisms of cancer resistance. As of present, research has been focused on the consequences of these evolutionary pressures rather than of their causes.DiscussionHere, we argue that evolution through natural selection may have shaped mechanisms of cancer resistance in wildlife species and that this can result in a threshold in body mass above which oncogenic and tumor suppressive mechanisms should be increasingly purified and positively selected, respectively.SummaryWe conclude that assessing wildlife species in their natural ecosystems, especially through theoretical modeling, is the most promising way to understand how evolutionary processes can favor one or the other pathway. This will provide important insights into mechanisms of cancer resistance.

Antimicrobial resistance in wildlife

1. The spread of antimicrobial resistance is of major concern for human health and leads to growing economic costs. While it is increasingly hypothesized that wildlife could play an important role in antimicrobial-resistant bacteria dynamics, empirical data remain scarce. 2. The present work builds on a systematic review of the available data in order to highlight the main information we have and to suggest research pathways that should be followed if we aim to fill the gaps in our current knowledge. 3. To achieve this goal, we address four questions: (i) Which resistant bacteria are the most frequently observed in wildlife? (ii) How are resistant bacteria exchanged between wildlife and the other hosts involved? (iii) In which habitats are those resistant bacteria found? (iv) Are resistances associated with certain ecological traits of the host? 4. Synthesis and applications. We highlight the strong link existing between the impact of human activities on natural habitats and the carriage of antimicrobial-resistant bacteria by wildlife. Furthermore, we underline that omnivorous, anthropophilic and carnivorous species are at high risk of being carriers and potentially spreaders of antimicrobial-resistant bacteria. Identifying among those groups key sentinel species may be of particular interest to implement ecosystem contamination surveillance. Finally, we discuss possible exchange routes for antimicrobial-resistant bacteria between humans and wildlife. Considering that water is of major importance in those exchanges, a critical way to control antimicrobial resistance spread may be to limit aquatic environment contamination by antimicrobial-resistant bacteria and antibiotics.

Preventive evolutionary medicine of cancers.

Evolutionary theory predicts that once an individual reaches an age of sufficiently low Darwinian fitness, (s)he will have reduced chances of keeping cancerous lesions in check. While we clearly need to better understand the emergence of precursor states and early malignancies as well as their mitigation by the microenvironment and tissue architecture, we argue that lifestyle changes and preventive therapies based in an evolutionary framework, applied to identified high‐risk populations before incipient neoplasms become clinically detectable and chemoresistant lineages emerge, are currently the most reliable way to control or eliminate early tumours. Specifically, the relatively low levels of (epi)genetic heterogeneity characteristic of many if not most incipient lesions will mean a relatively limited set of possible adaptive traits and associated costs compared to more advanced cancers, and thus a more complete and predictable understanding of treatment options and outcomes. We propose a conceptual model for preventive treatments and discuss the many associated challenges.

The influence of intensity of infection by a trematode parasite on the reproductive biology of Gammarus insensibilis (Amphipoda)

Following the behavioural alterations induced by the trematode Microphallus papillorobustus Rankin 1940 (Trematoda, Microphallidae) on its second intermediate host, the amphipod Gammmarus insensibilis, infected individuals are likely to mate among themselves. We investigated the influence of parasite intensity on the reproductive biology of infected hosts. In the mating system of amphipods, males compete severely for access to females and large males have greater ability to obtain large and more fecund females. We showed that the null hypothesis of random pair formation according to parasite intensity could not be rejected. In addition, infected males obtained females of the expected size according to their own sizes, whatever their parasite intensities. However, in both males and females, the parasite intensity increased the intermoult duration. Because size and reproductive success are strongly correlated in amphipods, we discuss the influence of this process on host fitness.

Parasites as to host evolutionary prints: Insights into host evolution from parasitological data

Abstract The close relationships which link parasitic organisms to their hosts have led to the use of parasites as biological tags. Most studies on this topic refer to parasites as host ecological tags. Recent development of molecular methods which give access to the genomic structures of populations have provided new information on the evolutionary biology of parasites. In this paper, we have attempted to review whether parasites can be considered as “host evolutionary prints”, and focus our discussion on host biodiversity and biogeography.

Parasites, age and the Hamilton-Zuk hypothesis : inferential fallacy ?

Hamilton and Zuks hypothesis suggests that male showiness allows females to assess males ability to resist parasites. In this hypothesis the full expression of secondary sexual traits and parasite load are respectively assumed to mainly depend on individual vigour and genetic resistance. Here, we propose that a negative correlation between brightness and parasite load can incorrectly suggest a causal relationship between parasitism and mating success. Parasitism can negatively covary with host age in certain circumstances of host mortality induced by parasite accumulation, while both male brightness and female preferences positively covary with age. Thus some properties of host-parasites associations, coupled with host reproductive behaviour can provide fortuitous support for the Hamilton-Zuk hypothesis.