Abstract
Contemporary patterns of land use and global climate change are modifying regional pools of parasite host species. The impact of host community changes on human disease risk, however, is difficult to assess due to a lack of information about zoonotic parasite host assemblages. We have used a recently developed method to infer parasite-host interactions for Chagas Disease (CD) from vector-host co-occurrence networks. Vector-host networks were constructed to analyze topological characteristics of the network and ecological traits of species’ nodes, which could provide information regarding parasite regional dispersal in Mexico. Twenty-eight triatomine species (vectors) and 396 mammal species (potential hosts) were included using a data-mining approach to develop models to infer most-likely interactions. The final network contained 1,576 links which were analyzed to calculate centrality, connectivity, and modularity. The model predicted links of independently registered Trypanosoma cruzi hosts, which correlated with the degree of parasite-vector co-occurrence. Wiring patterns differed according to node location, while edge density was greater in Neotropical as compared to Nearctic regions. Vectors with greatest public health importance (i.e., Triatoma dimidiata, T. barberi, T. pallidipennis, T. longipennis, etc), did not have stronger links with particular host species, although they had a greater frequency of significant links. In contrast, hosts classified as important based on network properties were synanthropic mammals. The latter were the most common parasite hosts and are likely bridge species between these communities, thereby integrating meta-community scenarios beneficial for long-range parasite dispersal. This was particularly true for rodents, >50% of species are synanthropic and more than 20% have been identified as T. cruzi hosts. In addition to predicting potential host species using the co-occurrence networks, they reveal regions with greater expected parasite mobility. The Neotropical region, which includes the Mexican south and southeast, and the Transvolcanic belt, had greatest potential active T. cruzi dispersal, as well as greatest edge density. This information could be directly applied for stratification of transmission risk and to design and analyze human-infected vector contact intervention efficacy.
Highlights
Many of the most important and yet neglected human infectious diseases, such as Chagas Disease (CD), Leishmaniasis, Onchocerciasis, and Schistosomiasis (Lozano et al, 2012; Murray et al, 2012), have etiologic agents that are transmitted among multiple vector and reservoir species (Taylor, Latham & Woolhouse, 2001; Heesterbeek et al, 2015)
The protozoan parasite Trypanosoma cruzi is responsible for human trypanosomiasis and Chagas Disease (CD)
Six species of the phyllosoma complex (Triatoma pallidipennis, Triatoma longipennis, Triatoma mazzottii, Triatoma picturata, Triatoma mexicana, and Triatoma gerstaeckeri), one of the protracta (Triatoma barberi), and two of the dimidiata complex (Triatoma dimidiata Pacific hg2, and T. dimidiata Gulf hg3), had their distributional ranges which coincided significantly with regions having a high number of mammal species
Summary
Many of the most important and yet neglected human infectious diseases, such as Chagas Disease (CD), Leishmaniasis, Onchocerciasis, and Schistosomiasis (Lozano et al, 2012; Murray et al, 2012), have etiologic agents that are transmitted among multiple vector and reservoir species (Taylor, Latham & Woolhouse, 2001; Heesterbeek et al, 2015). The Kinetplastid, Trypanosoma cruzi (Trypanosomatidae) is an obligate parasite that alternates between invertebrates (kissing bugs belonging to the family Reduviidae) and terrestrial mammals It has low species-host specificity along its geographic range in the American continent (Izeta-Alberdi et al, 2016), which may be explained by intrinsic factors related to sophisticated host defense response mechanisms (Freire-de-Lima et al, 2012; Caballero et al, 2015) and to extrinsic factors that ensure persistence and transmission in vector-host communities. With early evolution of the mechanism for T. cruzi host cell invasion (Caballero et al, 2015; Jackson et al, 2016), has deep phylogenetic roots, host-encounter filters are more labile and depend on community assemblages and host species’ population dynamics at local levels (Kribs-Zaleta, 2010)
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