bioRxivEcologyPreprint
Toxoplasma gondii and Trypanosoma lewisi infection in urban small mammals from Cotonou, Benin, with special emphasis on co-infection patterns
J. R. ETOUGBETCHE, G. HOUEMENOU, A. A. Missihoun, P. Gauthier, H.-J. Dossou, L. Galal, A. Dalecky, C. Diagne, G. Dobigny, A. MERCIER
Abstract
A growing number of studies has highlighted the importance of co-infections in eco-evolutionary processes underlying host-parasite interactions and the resulting epidemiology of zoonotic agents. Small mammals, and particularly rodents, are known to be important reservoirs of many zoonotic pathogens, such as Toxoplasma gondii and Trypanosoma lewisi that are responsible for toxoplasmosis and atypical trypanosomiasis in human, respectively. Laboratory experiments on rodent models have shown that primary infection with T. lewisi increases the host susceptibility to other co-infectious parasites, including T. gondii, following an alteration of the immune system. However, data on potential interactions between these parasites in wild small mammals remain scarce. In this study, we estimate the T. lewisi prevalence in 553 small mammals from four localities of Cotonou city, Benin. They were then combined with T. gondii data previously collected on the same individuals in order to investigate the influence of T. lewisi on T. gondii infection, and vice-versa, using cooccurrence tests and Generalized Linear Mixed Models. Despite quite high overall prevalence (32.5% and 15.2% for T. gondii and T. lewisi, respectively), we observed a clear and significant segregation between the two parasites. This may be explained by (i) differences in the species-specific susceptibility of small mammal host species to infection by these two parasites, with R. rattus and M. natalensis being the main reservoirs of T. lewisi while C. olivieri and M. m. domesticus are the main hosts for T. gondii; and/or by (ii) a possibly high mortality in co-infected animal in the wild. Although dedicated experimental studies are required to confirm this pattern, as they stand, our data fail to support that infection of small mammals by one of these two parasites favours widespread infection by the second one in nature.
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