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The source of Darwin’s illness has been a contentious issue in the literature for almost 70 years. Different causal factors have been invoked to account for his symptoms, including Chagas disease. The Chagas hypothesis is based upon Darwin’s diary, in which he narrates his experience with kissing bugs, the main vector of the protozoan Trypanosoma cruzi, the etiological agent of Chagas disease. In this contribution, we examine the consistency of the “Chagas disease hypothesis” in the light of current ecological and epidemiological knowledge of the disease in Chile. According to his diary and letters, during his overland trips, Darwin slept in rural houses and outdoors for 128 days in a “hyperendemic” area for Chagas disease, more than exposing him to kissing bugs. This observation conveys a likely additional source of infection than previously considered, which might reinforce the idea that Chagas disease contributed to Darwin’s manifest physical deterioration.

Trypanosoma cruzi, the protozoan causative of Chagas disease, is primarily transmitted through blood-sucking insects and infects mammalian and some reptilian hosts. In Chile, insects of the Mepraia genus are key vectors of T. cruzi in its wild transmission cycle. High prevalence and mixed infection of T. cruzi lineages have been reported in a Mepraia population on Santa María Island in the Atacama Desert. However, no small mammals have been reported. The island’s vertebrate community is dominated by the lizard Microlophus atacamensis and marine and scavenger birds. This study aimed to research blood samples of M. atacamensis for the presence of T. cruzi DNA (kDNA and satDNA) using conventional PCR (cPCR) and quantitative real-time PCR (qPCR) and estimate parasitemia. Our findings reveal that 39.4% of 33 individuals were positive with both cPCR and qPCR, while when assessing infection with either technique, it rises up to 81.8%. These findings confirm that M. atacamensis is a host of T. cruzi, suggesting its potential role as a key reservoir in the island’s transmission cycle. This study provides new insights into the life cycle of T. cruzi in the coastal Atacama Desert, highlighting the importance of reptiles in the epidemiology of this parasite.

We assessed 4 lizard species in Chile for Trypanosoma cruzi, the causative agent of Chagas disease, and 1 species for its ability to transmit the protozoan to uninfected kissing bugs. All lizard species were infected, and the tested species was capable of transmitting the protozoan, highlighting their role as T. cruzi reservoirs.

Studies of host-parasite relationships largely benefit from adopting a multifactorial approach, including the complexity of multi-host systems and habitat features in their analyses. Some host species concentrate most infection and contribute disproportionately to parasite and vector population maintenance, and habitat feature variation creates important heterogeneity in host composition, influencing infection risk and the fate of disease dynamics. Here, we examine how the availability of specific groups of hosts and habitat features relate to vector abundance and infection risk in 18 vector populations along the Mediterranean-type ecosystem of South America, where the kissing bug Mepraia spinolai is the main wild vector of the parasite Trypanosoma cruzi , the etiological agent of Chagas disease. For each population, data on vectors, vertebrate host availability, vegetation, precipitation, and temperature were collected and analyzed. Vector abundance was positively related to temperature, total vegetation, and European rabbit availability. Infection risk was positively related to temperature, bromeliad cover, and reptile availability; and negatively to the total domestic mammal availability. The invasive rabbit is suggested as a key species involved in the vector population maintenance. Interestingly, lizard species –a group completely neglected as a potential reservoir–, temperature, and bromeliads were relevant factors accounting for infection risk variation across populations.

Background Mepraia gajardoi and Mepraia spinolai are endemic triatomine vector species of Trypanosoma cruzi , a parasite that causes Chagas disease. These vectors inhabit arid, semiarid and Mediterranean areas of Chile. Mepraia gajardoi occurs from 18° to 25°S, and M. spinolai from 26° to 34°S. Even though both species are involved in T. cruzi transmission in the Pacific side of the Southern Cone of South America, no study has modelled their distributions at a regional scale. Therefore, the aim of this study is to estimate the potential geographical distribution of M. spinolai and M. gajardoi under current and future climate scenarios. Methods We used the Maxent algorithm to model the ecological niche of M. spinolai and M. gajardoi , estimating their potential distributions from current climate information and projecting their distributions to future climatic conditions under representative concentration pathways (RCP) 2.6, 4.5, 6.0 and 8.5 scenarios. Future predictions of suitability were constructed considering both higher and lower public health risk situations. Results The current potential distributions of both species were broader than their known ranges. For both species, climate change projections for 2070 in RCP 2.6, 4.5, 6.0 and 8.5 scenarios showed different results depending on the methodology used. The higher risk situation showed new suitable areas, but the lower risk situation modelled a net reduction in the future potential distribution areas of M. spinolai and M. gajardoi . Conclusions The suitable areas for both species may be greater than currently known, generating new challenges in terms of vector control and prevention. Under future climate conditions, these species could modify their potential geographical range. Preventive measures to avoid accidental human vectorial transmission by wild vectors of T. cruzi become critical considering the uncertainty of future suitable areas projected in this study.

Background Triatomines are blood-sucking insects capable of transmitting Trypanosoma cruzi , the parasite that causes Chagas disease in humans. Vectorial transmission entails an infected triatomine feeding on a vertebrate host, release of triatomine infective dejections, and host infection by the entry of parasites through mucous membranes, skin abrasions, or the biting site; therefore, transmission to humans is related to the triatomine–human contact. In this cross-sectional study, we evaluated whether humans were detected in the diet of three sylvatic triatomine species ( Mepraia parapatrica , Mepraia spinolai , and Triatoma infestans ) present in the semiarid–Mediterranean ecosystem of Chile. Methods We used triatomines collected from 32 sites across 1100 km, with an overall T. cruzi infection frequency of 47.1% ( N  = 4287 total specimens) by conventional PCR or qPCR. First, we amplified the vertebrate cytochrome b gene ( cytb ) from all DNA samples obtained from triatomine intestinal contents. Then, we sequenced cytb -positive PCR products in pools of 10–20 triatomines each, grouped by site. The filtered sequences were grouped into amplicon sequence variants (ASVs) with a minimum abundance of 100 reads. ASVs were identified by selecting the best BLASTn match against the NCBI nucleotide database. Results Overall, 16 mammal (including human), 14 bird, and seven reptile species were identified in the diet of sylvatic triatomines. Humans were part of the diet of all analyzed triatomine species, and it was detected in 19 sites representing 12.19% of the sequences. Conclusions Sylvatic triatomine species from Chile feed on a variety of vertebrate species; many of them are detected here for the first time in their diet. Our results highlight that the sylvatic triatomine–human contact is noteworthy. Education must be enforced for local inhabitants, workers, and tourists arriving in endemic areas to avoid or minimize the risk of exposure to Chagas disease vectors. Graphical Abstract

We describe the geographical variation of corolla and nectar guide size in seven populations of Mimulus luteus (Phrymaceae) in central Chile, and examine whether flower phenotypes associate with taxonomic composition and flower visit patterns of pollinators across populations. Flowers showed higher variation in nectar guide size than corolla size. Mean corolla size increased with the proportion of bees and decreased with the proportion of lepidopterans in the pollinator assemblages. Nectar guide size increased with the proportion of hummingbirds in the pollinator assemblages. When the frequency of flower visits rather than taxonomic composition was considered, the results revealed similar patterns. Because these traits previously have been described as targets of bee- and hummingbird-mediated selection in M. luteus, our results have implications for understanding the processes that determine flower diversification in Chilean Mimulus. Although we cannot rule out ecological sorting as an explanation for the geographical association between pollinators and flower phenotypes, changes in the prevalence and importance of bees and hummingbirds across populations appear to account, at least in part, for the flower phenotypic variation across populations. The extent to which insect and hummingbird pollination in M. luteus produces pollinator-mediated divergence among populations needs to be examined in future studies.

Chagas disease is caused by Trypanosoma cruzi and transmitted by the triatomine Mepraia spinolai in the southwest of South America. Here, we examined the T . cruzi -infection dynamics of field-caught M . spinolai after laboratory feeding, with a follow-up procedure on bug populations collected in winter and spring of 2017 and 2018. Bugs were analyzed twice to evaluate T . cruzi- infection by PCR assays of urine/fecal samples, the first evaluation right after collection and the second 40 days after the first feeding. We detected bugs with: the first sample positive and second negative (+/-), the first sample negative and second positive (-/+), and with both samples positive or negative (+/+; -/-). Bugs that resulted positive on both occasions were the most frequent, with the exception of those collected in winter 2018. Infection rate in spring was higher than winter only in 2018. Early and late stage nymphs presented similar T . cruzi -infection rates except for winter 2017; therefore, all nymphs may contribute to T . cruzi -transmission to humans. Assessment of infection using two samples represents a realistic way to determine the infection a triatomine can harbor. The underlying mechanism may be that some bugs do not excrete parasites unless they are fed and maintained for some time under environmentally controlled conditions before releasing T . cruzi , which persists in the vector hindgut. We suggest that T . cruzi -infection dynamics regarding the three types of positive-PCR results detected by follow-up represent: residual T . cruzi in the rectal lumen (+/-), colonization of parasites attached to the rectal wall (-/+), and presence of both kinds of flagellates in the hindgut of triatomines (+/+). We suggest residual T . cruzi -infections are released after feeding, and result 60–90 days after infection persisting in the rectal lumen after a fasting event, a phenomenon that might vary between contrasting seasons and years.

Trypanosoma cruzi is a protozoan parasite that is transmitted by triatomine vectors to mammals. It is classified in six discrete typing units (DTUs). In Chile, domestic vectorial transmission has been interrupted; however, the parasite is maintained in non-domestic foci. The aim of this study was to describe T. cruzi infection and DTU composition in mammals and triatomines from several non-domestic populations of North-Central Chile and to evaluate their spatio-temporal variations. A total of 710 small mammals and 1140 triatomines captured in six localities during two study periods (summer/winter) of the same year were analyzed by conventional PCR to detect kDNA of T. cruzi. Positive samples were DNA blotted and hybridized with specific probes for detection of DTUs TcI, TcII, TcV, and TcVI. Infection status was modeled, and cluster analysis was performed in each locality. We detected 30.1% of overall infection in small mammals and 34.1% in triatomines, with higher rates in synanthropic mammals and in M. spinolai. We identified infecting DTUs in 45 mammals and 110 triatomines, present more commonly as single infections; the most frequent DTU detected was TcI. Differences in infection rates among species, localities and study periods were detected in small mammals, and between triatomine species; temporally, infection presented opposite patterns between mammals and triatomines. Infection clustering was frequent in vectors, and one locality exhibited half of the 21 clusters found. We determined T. cruzi infection in natural host and vector populations simultaneously in a spatially widespread manner during two study periods. All captured species presented T. cruzi infection, showing spatial and temporal variations. Trypanosoma cruzi distribution can be clustered in space and time. These clusters may represent different spatial and temporal risks of transmission.

The influence of parasites on host reproduction has been widely studied in natural and experimental conditions. Most studies, however, have evaluated the parasite impact on female hosts only, neglecting the contribution of males for host reproduction. This omission is unfortunate as sex‐dependent infection may have important implications for host–parasite associations. Here, we evaluate for the first time the independent and nonindependent effects of gender infection on host reproductive success using the kissing bug Mepraia spinolai and the protozoan Trypanosoma cruzi as model system. We set up four crossing treatments including the following: (1) both genders infected, (2) both genders uninfected, (3) males infected—females uninfected, and (4) males uninfected—females infected, using fecundity measures as response variables. Interactive effects of infection between sexes were prevalent. Uninfected females produced more and heavier eggs when crossed with uninfected than infected males. Uninfected males, in turn, sired more eggs and nymphs when crossed with uninfected than infected females. Unexpectedly, infected males sired more nymphs when crossed with infected than uninfected females. These results can be explained by the effect of parasitism on host body size. As infection reduced size in both genders, infection on one sex only creates body size mismatches and mating constraints that are not present in pairs with the same infection status. Our results indicate the fitness impact of parasitism was contingent on the infection status of genders and mediated by body size. As the fecundity impact of parasitism cannot be estimated independently for each gender, inferences based only on female host infection run the risk of providing biased estimates of parasite‐mediated impact on host reproduction. Most studies have evaluated the parasite impact on female hosts only, neglecting the contribution of males for host reproduction. This omission is unfortunate as sex‐dependent infection may have important implications for host–parasite associations. We evaluate the independent and nonindependent effects of gender infection on host reproductive success using a insect–protozoan model system. Interactive effects of infection between sexes were prevalent. These results can be explained by the effect of parasitism on host body size. As infection reduced size in both genders, infection on one sex only creates body size mismatches and mating constraints that are not present in pairs with the same infection status.