Little is known about how human disease vectors will modify their life history patterns and survival capacity as a result of climate change. One case is that of Chagas disease, which has triatomine bugs and Trypanosoma cruzi as vectors and parasite, respectively. This work aimed to determine: (i) the activity of the prophenoloxidase system (prophenoloxidase and phenoloxidase activity, two indicators of immune ability) in three intestine regions (anterior midgut, posterior midgutand rectum) of the triatomine bug Meccus pallidipennis under three temperature conditions (20 °C, 30 °C and 34 °C) against two T. cruzi strains [ITRI/MX/14/CHIL (Chilpancingo) and ITRI/MX/12/MOR (Morelos)], and (ii) whether vector survival varies under these three temperatures after infection by these T. cruzi strains. Our results indicate that prophenoloxidase activity was lower at higher temperatures, that the level of prophenoloxidase activity elicited by each strain was different (higher in Chilpancingo than in Morelos strains), and that prophenoloxidase activity was more intense in the anterior midgut than in the posterior midgut or rectum. Survival rates were lower in insects maintained at higher temperatures and infected by Chilpancingo strains. These results indicate that climate change could lead to lower prophenoloxidase activity and survival rates in triatomines when infected with different T. cruzi strains, which could reduce the vector capacity of M. pallidipennis.

Chagas disease is one of the most important tropical infections in the world and mainly affects poor people. The causative agent is the hemoflagellate protozoan Trypanosoma cruzi, which circulates among insect vectors and mammals throughout the Americas. A large body of research on Chagas disease has shown the complexity of this zoonosis, and controlling it remains a challenge for public health systems. Although knowledge of Chagas disease has advanced greatly, there are still many gaps, and it is necessary to continue generating basic and applied research to create more effective control strategies. The aim of this review is to provide up-to-date information on the components of Chagas disease and highlight current trends in research. We hope that this review will be a starting point for beginners and facilitate the search for more specific information.

Triatomine insects are vectors of Trypanosoma cruzi, the causal agent of Chagas disease. The insect-parasite interaction has been studied in relation to the transmission and prevalence of this disease. For most triatomines, however, several crucial aspects of the insect immune response are still unknown. For example, only for Rhodnius prolixus and Triatoma infestans has the activity of phenoloxidase (PO) and its zymogen prophenoloxidase (proPO) been reported in relation to the hemolymph and anterior midgut (AM). The aim of this study was to gain insight into the immune response to T. cruzi infection of an important triatomine in Mexico, Meccus pallidipennis. Parasites were quantified in the rectal contents of infected M. pallidipennis groups. We examined some key factors in disease transmission, including the systemic (hemolymph) and local (gut) immune response. Parasites were present in the rectal contents at 4 days post-infection (pi) and reached their maximum density on day 7 pi. At 7 and 9 days pi mainly metacyclic trypomastigotes occurred. Compared to the control, the infected insects exhibited diminished PO activity in the hemolymph on days 9, 16 and 20 pi, and in the AM only on day 9. Additionally, infected insects displayed lower proPO activity in the hemolymph on day 1, but greater activity in the AM on day 28. The parasite strain originating from M. pallidipennis rapidly colonized the rectum of nymphs of this triatomine and developed high numbers of metacyclic trypomastigotes. Neither the changes of concentrations of PO and proPO in the hemolymph nor in the AM correlated with the changes in the population of T. cruzi.

In Chagas disease, the mechanisms involved in cardiac damage are an active field of study. The factors underlying the evolution of lesions following infection by Trypanosoma cruzi and, in some cases, the persistence of its antigens and the host response, with the ensuing development of clinically observable cardiac damage, are analyzed in this review.

Background: Relatively little is known about how pathogens transmitted by vector insects are affected by changing temperatures analogous to those occurring in the present global warming scenario. One expectation is that, like their ectothermic vectors, an increase in temperature could reduce their fitness. Here, we have investigated the effect of high temperatures on the abundance ofTrypanosoma cruziparasites during infection in the vectorTriatoma pallidipennis.Methods: We exposedT. pallidipennisnymphs to two strains (Morelos and Chilpancingo) ofT. cruzi. Once infected, the fifth-instar bugs were distributed among three different temperature groups, i.e. 20, 30, and 34 °C, and the resulting parasites were counted when the bugs reached adulthood.Results: The number of parasites increased linearly with time at 20 °C and, to a lesser extent, at 30 °C, especially in the Chilpancingo compared to the Morelos strain. Conversely, at 34 °C, the number of parasites of both strains decreased significantly compared to the other two temperatures.Conclusions: These results suggest negative effects on the abundance ofT. cruziinT. pallidipennisat high temperatures. This is the first evidence of the effect of high temperatures on a pathogenic agent transmitted by an insect vector in the context of global warming. Further tests should be done to determine whether this pattern occurs with other triatomine species andT. cruzistrains.Graphical

Chagas disease is a complex zoonosis. Clinically, it presents in two distinct phases, acute and chronic. The ability of patients to respond to Trypanosoma cruzi infection depends on the balance between inflammatory and anti-inflammatory responses, in which cytokines play a key regulatory role. In this review, we discuss the role of cytokines in regulating the host response and as mediators of cardiac injury by inducing profibrotic alterations. The importance of characterizing cytokine profiles as biomarkers of the evolution of cardiac damage in T.-cruzi-infected individuals is also emphasized.