Progression of Plasmodium berghei through Anopheles stephensi is density-dependent.
Progression of Plasmodium berghei through Anopheles stephensi is density-dependent.
复制标题
berghei疟原虫通过athepheles stephensi的进展是密度依赖的。
DOI：
10.1371/journal.ppat.0030195
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发表时间：
2007-12-28
期刊：
影响因子：
6.7
通讯作者：
Basanez, Maria-Gloria
中科院分区：
文献类型：
--
作者：
Sinden, Robert E.;Dawes, Emma J.;Alavi, Yasmene;Waldock, Joanna;Finney, Olivia;Mendoza, Jacqui;Butcher, Geoff A.;Andrews, Laura;Hill, Adrian V.;Gilbert, Sarah C.;Basanez, Maria-Gloria
据文献记载，疟原虫在其脊椎动物宿主中的密度调节诱导的生理反应;这反过来又调节寄生虫的存活和传播。蚊子体内的寄生虫密度是否调节这种重要病原体的存活和传播尚不清楚。许多研究已经描述了疟原虫在蚊子体内从一个生命阶段到下一个生命阶段的转化率，但很少有人认为这些转化率可能会随寄生虫密度而变化。在这里，我们建立感染与确定数量的啮齿类疟疾寄生虫伯氏疟原虫，以研究如何寄生虫密度在每个阶段的发展（配子体，动合子，卵囊和子孢子）的影响发展到随后的阶段斯氏按蚊，从而交付感染性子孢子的脊椎动物宿主。我们发现，每一个发展的过渡表现出很强的密度依赖性，随后的阶段在高密度饱和的数字。我们进一步表明，当以非常低的密度喂养动合子时，通过增加动合子数量（即，动合子-卵囊转化的效率遵循S形关系）。我们讨论了如何观察这个模型系统产生重要的假设疟疾生物学的理解，以及如何这些可能会指导合理的分析干预措施，对人类的疟疾寄生虫的传播，其不同的载体物种。疟疾是世界上最具破坏性的寄生虫病之一，由疟原虫属的原生动物寄生虫引起，并通过按蚊在哺乳动物宿主之间传播。在蚊子体内，寄生虫经历四个连续的发育转变，因为它从血粉通过蚊子的中肠上皮细胞到达唾液腺，当蚊子叮咬脊椎动物宿主时，寄生虫从唾液腺接种。这项研究表明，在实验室模型中，寄生虫输入密度在蚊子的每个发育阶段调节输出到随后的形式。统计模型拟合实验数据，以确定和描述最合适的功能关系。在所有情况下，两个连续的寄生虫阶段之间的关系可以在高寄生虫密度饱和，这表明在高寄生虫密度寄生虫数量可能必须大幅减少，以实现可观的减少寄生虫传播。这些结果可能有助于建立一个合理的基础，为新的研究物种的医学重要性，并进一步了解如何干预措施，旨在减少寄生虫生存的蚊子可能会影响传播。
It is well documented that the density of Plasmodium in its vertebrate host modulates the physiological response induced; this in turn regulates parasite survival and transmission. It is less clear that parasite density in the mosquito regulates survival and transmission of this important pathogen. Numerous studies have described conversion rates of Plasmodium from one life stage to the next within the mosquito, yet few have considered that these rates might vary with parasite density. Here we establish infections with defined numbers of the rodent malaria parasite Plasmodium berghei to examine how parasite density at each stage of development (gametocytes; ookinetes; oocysts and sporozoites) influences development to the ensuing stage in Anopheles stephensi, and thus the delivery of infectious sporozoites to the vertebrate host. We show that every developmental transition exhibits strong density dependence, with numbers of the ensuing stages saturating at high density. We further show that when fed ookinetes at very low densities, oocyst development is facilitated by increasing ookinete number (i.e., the efficiency of ookinete–oocyst transformation follows a sigmoid relationship). We discuss how observations on this model system generate important hypotheses for the understanding of malaria biology, and how these might guide the rational analysis of interventions against the transmission of the malaria parasites of humans by their diverse vector species. Malaria, one of the world's most devastating parasitic diseases, is caused by protozoan parasites of the genus Plasmodium and is transmitted between mammalian hosts by Anopheles mosquitoes. Within the mosquito, the parasite undergoes four sequential developmental transformations as it passes from the bloodmeal through the mosquito's midgut epithelium to the salivary glands, from where the parasite is inoculated when the mosquito bites the vertebrate host. This study demonstrates, in a laboratory model, that parasite input density at every developmental stage in the mosquito regulates output to the ensuing form. Statistical models were fitted to experimental data to identify and describe the most appropriate functional relationships. In all cases, the relationships between two consecutive parasite stages can saturate at high parasite densities, suggesting that at high parasite densities parasite numbers may have to be reduced substantially to effect an appreciable decrease in parasite transmission. These results may help establish a rational basis for new studies on species of medical importance and further our understanding of how interventions designed to reduce parasite survival within the mosquito might be expected to impact upon transmission.
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