scholarly journals Was Chagas disease responsible for Darwin’s illness? The overlooked eco-epidemiological context in Chile

2021 ◽  
Vol 94 (1) ◽  
Author(s):  
Carezza Botto-Mahan ◽  
Rodrigo Medel

AbstractThe 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.

Author(s):  
Michael Z. Levy

The forces that lead to the emergence of Trypanosoma cruzi, the etiologic agent of Chagas disease, are often distinct from those that maintain its transmission, and these are distinct again from those that allow the parasite to persist over decades. Just as kindling, logs, and coals all play discrete roles in the growth of a fire, a myriad of mammalian hosts contribute differently to epidemics of Trypanosoma. cruzi. Chagas disease affects millions of people in the Americas, and, through migration, thousands more on other continents. The agent of the disease, Trypanosoma cruzi, is a slender, highly-motile, unicellular parasite. T. cruzi does not migrate to the salivary glands of its insect vector–the blood-sucking triatomine insects–as many other vector-borne parasites do.


2003 ◽  
Vol 47 (6) ◽  
pp. 2047-2050 ◽  
Author(s):  
Julio A. Urbina ◽  
Juan Luis Concepcion ◽  
Andrea Montalvetti ◽  
Juan B. Rodriguez ◽  
Roberto Docampo

ABSTRACT We investigated the molecular basis of the activity of 4-phenoxyphenoxyethyl thiocyanate (WC-9) against Trypanosoma cruzi, the etiological agent of Chagas’ disease. We found that growth inhibition of T. cruzi epimastigotes induced by this compound was associated with a reduction in the content of the parasite's endogenous sterols due to a specific blockade of their de novo synthesis at the level of squalene synthase.


2015 ◽  
Vol 9 (3) ◽  
pp. e0003646 ◽  
Author(s):  
Simon L. Elliot ◽  
Juliana de O. Rodrigues ◽  
Marcelo G. Lorenzo ◽  
Olindo A. Martins-Filho ◽  
Alessandra A. Guarneri

2013 ◽  
Vol 142 (1) ◽  
pp. 156-162 ◽  
Author(s):  
Z. DÍAZ-BELLO ◽  
M. C. THOMAS ◽  
M. C. LÓPEZ ◽  
R. ZAVALA-JASPE ◽  
O. NOYA ◽  
...  

SUMMARYTrypanosoma cruzi I, a discrete typing unit (DTU) found in human infections in Venezuela and other countries of the northern region of South America and in Central America, has been recently classified into five intra-DTU genotypes (Ia, Ib, Ic, Id, Ie) based on sequence polymorphisms found in the spliced leader intergenic region. In this paper we report the genotype identification of T. cruzi human isolates from one outbreak of acute orally acquired Chagas disease that occurred in a non-endemic region of Venezuela and from T. cruzi triatomine and rat isolates captured at a guava juice preparation site which was identified as the presumptive source of infection. The genotyping of all these isolates as TcId supports the view of a common source of infection in this oral Chagas disease outbreak through the ingestion of guava juice. Implications for clinical manifestations and dynamics of transmission cycles are discussed.


2019 ◽  
Vol 26 (36) ◽  
pp. 6519-6543 ◽  
Author(s):  
Adriana Egui ◽  
Paola Lasso ◽  
Elena Pérez-Antón ◽  
M. Carmen Thomas ◽  
Manuel Carlos López

Chagas disease courses with different clinical phases and has a variable clinical presentation and progression. The acute infection phase mostly exhibits a non-specific symptomatology. In the absence of treatment, the acute phase is followed by a chronic phase, which is initially asymptomatic. This chronic asymptomatic phase of the disease is characterized by a fragile balance between the host’s immune response and the parasite replication. The loss of this balance is crucial for the progression of the sickness. The virulence and tropism of the T. cruzi infecting strain together to the inflammation processes in the cardiac tissue are the main factors for the establishment and severity of the cardiomyopathy. The efficacy of treatment in chronic Chagas disease patients is controversial. However, several studies carried out in chronic patients demonstrated that antiparasitic treatment reduces parasite load in the bloodstream and leads to an improvement in the immune response against the Trypanosoma cruzi parasite. The present review is mainly focused on the cellular patterns associated to the clinical status and the evolution of the disease in chronic patients, as well as the effectiveness of the treatment related to T. cruzi infection control. Therefore, an emphasis is placed on the dynamics of specific-antigens T cell subpopulations, their memory and activation phenotypes, their functionality and their contribution to pathogenesis or disease control, as well as their association with risk of congenital transmission of the parasite.


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