Carvalho Leonardo J de Moura, Alves Francisco Acácio, de Oliveira Salma Gomes, do Valle Rodrigo del Rio, Fernandes Andréa A Morais, Muniz José A Pereira Carneiro, Daniel-Ribeiro Claudio T
Laboratório de Pesquisas em Malária, Departamento de Imunologia, Instituto Oswaldo Cruz, Fiocruz, Rio de Janeiro, RJ, Brasil.
Mem Inst Oswaldo Cruz. 2003 Jul;98(5):679-86. doi: 10.1590/s0074-02762003000500016. Epub 2003 Sep 8.
Severe anemia is the earliest and a frequently fatal complication of Plasmodium falciparum infection. Here we describe Aotus infulatus as a primate model suitable to study this malaria complication. Both non-splenectomized and splenectomized monkeys receiving different inocula of P. falciparum FVO strain presented large (> 50%) decreases in hematocrit values during infection. Non-splenectomized animals were able to control parasite growth (parasitemia did not exceed 4%), but they had to be treated because of severe anemia. Three of 4 splenectomized monkeys did not control parasitemia and were treated, but developed severe anemia after treatment when presenting a negative blood film. Destruction of parasitized red blood cells alone cannot account for the degree of anemia. Non-splenectomized monkeys repeatedly infected with homologous parasites became rapidly and progressively resistant to reinfection and to the development of severe anemia. The data presented here point to A. infulatus as a suitable model for studying the pathogenesis of severe malarial infection.
严重贫血是恶性疟原虫感染最早出现且常导致死亡的并发症。在此，我们描述了一种适合研究这种疟疾并发症的灵长类动物模型——缨冠夜猴。接受不同剂量恶性疟原虫FVO株接种的未切除脾脏和切除脾脏的猴子在感染期间血细胞比容值均大幅下降（>50%）。未切除脾脏的动物能够控制寄生虫生长（寄生虫血症不超过4%），但由于严重贫血不得不接受治疗。4只切除脾脏的猴子中有3只无法控制寄生虫血症并接受了治疗，但在治疗后血涂片呈阴性时出现了严重贫血。仅寄生红细胞的破坏无法解释贫血的程度。反复感染同源寄生虫的未切除脾脏的猴子对再次感染和严重贫血的发展迅速产生并逐渐增强抵抗力。此处呈现的数据表明缨冠夜猴是研究严重疟疾感染发病机制的合适模型。
