Meza Sheila Karina Lüders, Kaneshima Edilson Nobuyoshi, Silva Sueli de Oliveira, Gabriel Maristela, de Araújo Silvana Marques, Gomes Mônica Lúcia, Monteiro Wuelton Marcelo, Barbosa Maria das Graças Vale, Toledo Max Jean de Ornelas
Post-Graduate Program in Health Sciences, State University of Maringá (UEM), Paraná, Brazil; Center for Medical and Pharmaceutical Sciences, State University of Western Paraná, Paraná, Brazil.
Department of Basic Health Sciences, UEM, Paraná, Brazil.
Exp Parasitol. 2014 Nov;146:34-42. doi: 10.1016/j.exppara.2014.08.014. Epub 2014 Oct 5.
The geographical heterogeneity of Chagas disease (ChD) is mainly caused by genetic variability of the etiological agent Trypanosoma cruzi. Our hypothesis was that the pathogenicity for mice may vary with the genetic lineage (or Discrete Typing Unit - DTU) of the parasite. To test this hypothesis, parasitological and histopathological evaluations were performed in mice inoculated with strains belonging to the DTU T. cruzi IV (TcIV) from the State of Amazonas (northern Brazil), or the DTU T. cruzi II (TcII) from the State of Paraná (southern Brazil). Groups of 10 Swiss mice were inoculated with eight strains of TcIV obtained from acute cases (7) from two outbreaks of orally acquired ChD, and from the triatomine Rhodnius robustus (1) from Amazonas; and three strains of TcII obtained from chronic patients in Paraná. We evaluated the pre-patent period, patent period, maximum peak of parasitemia, day of maximum peak of parasitemia, area under the parasitemia curve, inflammatory process, and tissue parasitism in the acute phase. TcIV was less virulent than TcII, and showed significantly (p < 0.005) lower parasitemia levels. Although the levels of tissue parasitism did not differ statistically, mice infected with TcIV displayed significantly (p < 0.001) fewer inflammatory processes than mice infected with TcII. This supported the working hypothesis, since TcIV from Amazonas was less pathogenic than TcII from Paraná; and agreed with the lower severity of human cases of ChD in the Amazon region.
恰加斯病(ChD)的地理异质性主要由病原体克氏锥虫的基因变异性引起。我们的假设是,该寄生虫对小鼠的致病性可能随其基因谱系(或离散分型单元 - DTU)而变化。为了验证这一假设,我们对接种了来自巴西北部亚马逊州的DTU克氏锥虫IV型(TcIV)菌株或来自巴西南部巴拉那州的DTU克氏锥虫II型(TcII)菌株的小鼠进行了寄生虫学和组织病理学评估。将10只瑞士小鼠分为几组,分别接种从两起经口感染的恰加斯病急性病例(7株)以及从亚马逊州的强壮红猎蝽(1株)中获得的8株TcIV;还有从巴拉那州慢性患者中获得的3株TcII。我们评估了急性期的潜伏期、发病期、寄生虫血症的最大峰值、寄生虫血症最大峰值出现的天数、寄生虫血症曲线下面积、炎症过程以及组织寄生情况。TcIV的毒力低于TcII,且寄生虫血症水平显著更低(p < 0.005)。尽管组织寄生水平在统计学上没有差异,但感染TcIV的小鼠所表现出的炎症过程明显少于感染TcII的小鼠(p < 0.001)。这支持了我们的工作假设,因为来自亚马逊州的TcIV的致病性低于来自巴拉那州的TcII;并且与亚马逊地区恰加斯病人类病例的较低严重程度相符。