dc.creatorElliot, Simon L.
dc.creatorRodrigues, Juliana de O.
dc.creatorLorenzo, Marcelo G.
dc.creatorMartins-Filho, Olindo A.
dc.creatorGuarneri, Alessandra A.
dc.date2018-05-29T17:00:18Z
dc.date2018-05-29T17:00:18Z
dc.date2015-03-20
dc.date.accessioned2023-09-27T20:46:21Z
dc.date.available2023-09-27T20:46:21Z
dc.identifier1935-2735
dc.identifierhttps://doi.org/10.1371/journal.pntd.0003646
dc.identifierhttp://www.locus.ufv.br/handle/123456789/19870
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8947590
dc.descriptionIt is often assumed that parasites are not virulent to their vectors. Nevertheless, parasites commonly exploit their vectors (nutritionally for example) so these can be considered a form of host. Trypanosoma cruzi, a protozoan found in mammals and triatomine bugs in the Americas, is the etiological agent of Chagas disease that affects man and domestic animals. While it has long been considered avirulent to its vectors, a few reports have indicated that it can affect triatomine fecundity. We tested whether infection imposed a temperature-dependent cost on triatomine fitness. We held infected insects at four temperatures between 21 and 30°C and measured T. cruzi growth in vitro at the same temperatures in parallel. Trypanosoma cruzi infection caused a considerable delay in the time the insects took to moult (against a background effect of temperature accelerating moult irrespective of infection status). Trypanosoma cruzi also reduced the insects’ survival, but only at the intermediate temperatures of 24 and 27°C (against a background of increased mortality with increasing temperatures). Meanwhile, in vitro growth of T. cruzi increased with temperature. Our results demonstrate virulence of a protozoan agent of human disease to its insect vector under these conditions. It is of particular note that parasite-induced mortality was greatest over the range of temperatures normally preferred by these insects, probably implying adaptation of the parasite to perform well at these temperatures. Therefore we propose that triggering this delay in moulting is adaptive for the parasites, as it will delay the next bloodmeal taken by the bug, thus allowing the parasites time to develop and reach the insect rectum in order to make transmission to a new vertebrate host possible.
dc.formatpdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherPLOS Neglected Tropical Diseases
dc.relationVolume 9, Issue 3, e0003646, March 2015
dc.rightsOpen Access
dc.subjectTrypanosoma cruzi
dc.subjectEtiological Agent of Chagas Disease
dc.subjectTriatomine Vector Rhodnius prolixus
dc.titleTrypanosoma cruzi, etiological agent of Chagas disease, is virulent to its triatomine vector Rhodnius prolixus in a temperature-dependent manner
dc.typeArtigo


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