Broad patterns in domestic vector-borne Trypanosoma cruzi transmission dynamics: synanthropic animals and vector control

Peterson, Jennifer K.; Bartsch, Sarah M.; Lee, Bruce Y.; Dobson, Andrew

doi:10.1186/s13071-015-1146-1

Cited by 32 publications

(27 citation statements)

References 50 publications

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“…Under such assumption (ν = 0), the expected level of T. cruzi virulence

α_{h}^{*}

would not depend on triatomine lifespan. However, significant effects of T. cruzi infection have been reported on the behaviour and/or life‐history of various triatomine species, which include T. infestans (Schaub, , ), R. prolixus (Elliot, Rodrigues, Lorenzo, Martins‐Filho, & Guarneri, ; Peterson, Bartsch, Lee, & Dobson, ), T. dimidiata (Ramirez‐Sierra et al., ), P. megistus (Lima et al., ) and Mepraia spinolai (Botto‐Mahan, ; Botto‐Mahan et al., ). This suggests that vectors could be considered as alternative hosts rather than a merely neutral compartment.…”

Section: Trypanosoma Cruzi Diversity and Virulence Evolutionmentioning

confidence: 99%

Evolutionary ecology of Chagas disease; what do we know and what do we need?

Flores-Ferrer

Marcou

Waleckx

et al. 2017

Evolutionary Applications

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The aetiological agent of Chagas disease, Trypanosoma cruzi, is a key human pathogen afflicting most populations of Latin America. This vectorborne parasite is transmitted by haematophageous triatomines, whose control by large‐scale insecticide spraying has been the main strategy to limit the impact of the disease for over 25 years. While those international initiatives have been successful in highly endemic areas, this systematic approach is now challenged by the emergence of insecticide resistance and by its low efficacy in controlling species that are only partially adapted to human habitat. In this contribution, we review evidences that Chagas disease control shall now be entering a second stage that will rely on a better understanding of triatomines adaptive potential, which requires promoting microevolutionary studies and –omic approaches. Concomitantly, we show that our knowledge of the determinants of the evolution of T. cruzi high diversity and low virulence remains too limiting to design evolution‐proof strategies, while such attributes may be part of the future of Chagas disease control after the 2020 WHO's target of regional elimination of intradomiciliary transmission has been reached. We should then aim at developing a theory of T. cruzi virulence evolution that we anticipate to provide an interesting enrichment of the general theory according to the specificities of transmission of this very generalist stercorarian trypanosome. We stress that many ecological data required to better understand selective pressures acting on vector and parasite populations are already available as they have been meticulously accumulated in the last century of field research. Although more specific information will surely be needed, an effective research strategy would be to integrate data into the conceptual and theoretical framework of evolutionary ecology and life‐history evolution that provide the quantitative backgrounds necessary to understand and possibly anticipate adaptive responses to public health interventions.

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“…Under such assumption (ν = 0), the expected level of T. cruzi virulence

α_{h}^{*}

Section: Trypanosoma Cruzi Diversity and Virulence Evolutionmentioning

confidence: 99%

Evolutionary ecology of Chagas disease; what do we know and what do we need?

Flores-Ferrer

Marcou

Waleckx

et al. 2017

Evolutionary Applications

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“…The variation in the rate of infection by T. cruzi in this study may be associated with the dominant vector in each region, since each triatomine genera has a preference to certain natural or artificial ecotypes 30,38 , which may make them more susceptible to infection. For example, Coutinho et al 30 observed that there is greater natural infection by T. cruzi in triatomines housed in wood piles, because these sites function as burrows of small animals, such as rodents and marsupials, that are wild reservoirs of T. cruzi.…”

Section: Discussionmentioning

confidence: 91%

Natural infection by Trypanosoma cruzi in triatomines and seropositivity for Chagas disease of dogs in rural areas of Rio Grande do Norte, Brazil

Freitas

Souza

Magalhães

et al. 2018

Rev. Soc. Bras. Med. Trop.

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“…The pathogenesis of chronic intestinal CD and the development of the megacolon are of great importance due to the high levels of morbidity and disability generated by the condition, the difficulties in therapeutic approaches, and especially considering the utmost priority given to control and elimination of CD according to the 2020 London Declaration [6]. Furthermore, a comprehensive understanding of the mechanistic neurodegenerative processes involved in enteric denervation and its consequences such as dilatation, dysmotility and intestinal smooth muscle hyperplasia remains elusive.…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence of denervation of myenteric ganglia [1][2][3][4][5] as a pathogenic mechanism of intestinal accompaniment. The best chance to avoid morbidity is the treatment of the disease at its early acute stages [6] and novel therapeutic approaches are dependent in better understanding of the complex pathogenesis of this disease.…”

Section: Introductionmentioning

confidence: 99%

Nitrergic Myenteric Neurons are Spared in Experimental Chagasic Megacolon

Ricci¹,

Campos²,

Cartelle³

et al. 2016

J Neuroinfect Dis

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Chagas disease is a chronic disorder caused by the Trypanosoma cruzi protozoan. The infection causes alterations to the enteric nervous system such as megaesophagus and megacolon. There is evidence of denervation of myenteric ganglia. The intense parasitism of acute phase affects neuronal integrity but contrasts with the absence of parasites and the discreet inflammatory process of chronic phase, indicating a progressive injury mechanism that needs to be better understood in the megacolons. The potential selectivity of enteric neurons classes affected by the progression of the disease is not yet clear. Nitrergic neurons which co-localize other neurotransmitters represent the most common inhibitory neuron of the ENS. Recently a chronic stage of the Chagas disease was reproduced experimentally in a suitable murine model of megacolon. Considering the limitation of studying human intestine and the controversy on the pattern of nNOS involvement in chagasic megacolon, we decided to assess the nitrergic neurons in the myenteric plexus of mice. We used antibodies against structural protein gene product 9.5 (PGP 9.5) and functional neuronal nitric oxide synthase (n-NOS) at the acute and chronic phase of the disease to quantify myenteric ganglionar neurons in the colon of infected and non-infected mice. We found a reduction in the ganglionar number of neurons detected by anti-protein gene product 9.5 antibodies in colon from mice at the chronic stage. However, the number of nitrergic neurons per ganglia remained unchanged along the acute to phase chronic of the disease. Our findings indicate a long-term preservation of nitregic neurons detrimental to other classes of enteric in our model of experimental Chagas disease. We propose that differential loss of enteric neurons is at least one of the structural substrate for the development of the longterm morphfunctional changes that lead to the megacolon.

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Broad patterns in domestic vector-borne Trypanosoma cruzi transmission dynamics: synanthropic animals and vector control

Cited by 32 publications

References 50 publications

Evolutionary ecology of Chagas disease; what do we know and what do we need?

Evolutionary ecology of Chagas disease; what do we know and what do we need?

Natural infection by Trypanosoma cruzi in triatomines and seropositivity for Chagas disease of dogs in rural areas of Rio Grande do Norte, Brazil

Nitrergic Myenteric Neurons are Spared in Experimental Chagasic Megacolon

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