Elliot Simon L, Rodrigues Juliana de O, Lorenzo Marcelo G, Martins-Filho Olindo A, Guarneri Alessandra A
Department of Entomology, Universidade Federal de Viçosa, Campus Universitário, Viçosa, Minas Gerais, Brazil.
Centro de Pesquisa René Rachou, Belo Horizonte, Minas Gerais, Brazil.
PLoS Negl Trop Dis. 2015 Mar 20;9(3):e0003646. doi: 10.1371/journal.pntd.0003646. eCollection 2015 Mar.
It 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.
人们通常认为寄生虫对其传播媒介没有致病性。然而，寄生虫通常会利用其传播媒介（例如在营养方面），所以这些传播媒介可被视为一种宿主形式。克氏锥虫是一种在美洲的哺乳动物和锥蝽中发现的原生动物，是导致影响人类和家畜的恰加斯病的病原体。虽然长期以来人们认为它对其传播媒介无致病性，但一些报告表明它会影响锥蝽的繁殖力。我们测试了感染是否会给锥蝽的适应性带来温度依赖性代价。我们将受感染的昆虫置于21至30°C的四个温度下，并同时在相同温度下体外测量克氏锥虫的生长情况。克氏锥虫感染导致昆虫蜕皮时间显著延迟（在温度加速蜕皮的背景效应下，无论感染状态如何）。克氏锥虫还降低了昆虫的存活率，但仅在24和27°C的中间温度下（在死亡率随温度升高而增加的背景下）。与此同时，克氏锥虫的体外生长随温度升高而增加。我们的结果证明了在这些条件下一种人类疾病的原生动物病原体对其昆虫传播媒介具有致病性。特别值得注意的是，在这些昆虫通常偏好的温度范围内，寄生虫引起的死亡率最高，这可能意味着寄生虫适应在这些温度下良好生存。因此我们提出，引发这种蜕皮延迟对寄生虫是适应性的，因为这将延迟锥蝽的下一次吸血，从而使寄生虫有时间发育并到达昆虫直肠，以便有可能传播给新的脊椎动物宿主。
