Review for "Host‐parasite dynamics in Chagas disease from systemic to hyper‐local scales"

Chagas' disease is caused by Trypanosoma cruzi, which is transmitted by reduviid bugs. The World Health Organization has estimated that about 16–18 million people in the Americas are infected, and that more than 100 million are at risk. In the present study we have used a murine model to analyse if particular T. cruzi strains (Tulahuen strain and SGO-Z12 isolate from a chronic patient) and/or re-infection may determine, during the indeterminate phase of experimental Chagas' disease, changes that could explain the different evolution of cardiac lesions. Re-infected mice reached higher parasitaemias than those infected for the first time. The survival in the indeterminate phase of mice infected with Tulahuen strain was 50.0%, while the SGO-Z12-infected group presented a significantly higher survival rate (77.1%; P<0.01). The SGO-Z12-re-infected group showed a survival rate (70.9%) significantly higher than that of the Tulahuen-re-infected group (37.0%; P<0.01). Electrocardiographic abnormalities were found in 66% of Tulahuen-infected mice, while in SGO-Z12-infected group such abnormalities were found in only 36% of animals (P<0.01). The two groups exhibited similar percentages of electrocardiographic dysfunction on re-infection, although intraventricular blocks were more frequent in Tulahuen-re-infected mice (P<0.01). Hearts from infected or re-infected mice with either parasite showed mononuclear infiltrates. The SGO-Z12-re-infected and Tulahuen-re-infected groups exhibited a significantly diminished affinity (P<0.05) and a significantly increased density (P<0.05) of cardiac β-adrenergic receptors compared with the infected and non-infected groups. The indeterminate phase of Chagas' disease is defined as a prolonged period that is clinically silent, but the present findings show that different T. cruzi strains and re-infection are able to alter the host–parasite equilibrium, and these factors may be responsible for inducing progressive cardiopathy.

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How host phenology impacts multi-season epidemic cycles

10.1101/2021.06.07.447391 ◽

2021 ◽

Author(s):

Hannelore MacDonald ◽

Dustin Brisson

Keyword(s):

Mathematical Model ◽

Population Dynamics ◽

Population Cycles ◽

Seasonal Activity ◽

Host Interactions ◽

Host Phenology ◽

Demographic Impact ◽

Host Parasite ◽

Parasite Populations ◽

Parasite Dynamics

Parasite-host interactions can result in periodic population dynamics when parasites over-exploit host populations. The timing of host seasonal activity, or host phenology, determines the frequency and demographic impact of parasite-host interactions which may govern if the parasite can sufficiently over-exploit their hosts to drive population cycles. We describe a mathematical model of a monocyclic, obligate-killer parasite system with seasonal host activity to investigate the consequences of host phenology on host-parasite dynamics. The results suggest that parasites can reach the densities necessary to destabilize host dynamics and drive cycling in only some phenological scenarios, such as environments with short seasons and synchronous host emergence. Further, only parasite lineages that are sufficiently adapted to phenological scenarios with short seasons and synchronous host emergence can achieve the densities necessary to over-exploit hosts and produce population cycles. Host-parasite cycles can also generate an eco-evolutionary feedback that slows parasite adaptation to the phenological environment as rare advantageous phenotypes are driven to extinction when introduced in phases of the cycle where host populations are small and parasite populations are large. The results demonstrate that seasonal environments can drive population cycling in a restricted set of phenological patterns and provides further evidence that the rate of adaptive evolution depends on underlying ecological dynamics.

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