Ebert Dieter, Mangin Katrina L
Department of Zoology, ABRG, Oxford University, South Parks Road, Oxford, OX1 3PS, United Kingdom.
NERC Centre for Population Biology, Imperial College at Silwood Park, Ascot, Berks, SL5 7PY, United Kingdom.
Evolution. 1997 Dec;51(6):1828-1837. doi: 10.1111/j.1558-5646.1997.tb05106.x.
It is predicted that host exploitation should evolve to maximize parasite fitness and that virulence (= parasite-induced host mortality) evolves along with the rate of host exploitation. If the life expectancy of a parasite is short, it is expected to evolve a higher rate of host exploitation and therefore higher virulence because the penalty to the parasite for killing the host is reduced. We tested this hypothesis by keeping for 14 months the horizontally transmitted microsporidian parasite Glugoides intestinalis in mono-clonal host cultures (Daphnia magna) under conditions of high and low host background mortality. High host mortality, and thus parasite mortality, was achieved by replacing weekly 70-80% of all hosts in a culture with uninfected hosts from stock cultures (Replacement lines). In the low-mortality treatment no replacement took place. Contrary to our expectation, parasites from the Replacement lines evolved a lower within-host growth rate and virulence than parasites from the Nonreplacement lines. Across lines we found a strong positive correlation between within-host growth rate and virulence. We did further experiments to answer the question why our data did not support the predictions. Sporophorous vesicles (SVs, spore clusters) were smaller in doubly infected than in singly infected host-gut cells, indicating that competition within cells bears costs for the parasite. Due to our experimental protocol, the average life span of infections had been much higher in the Nonreplacement lines. Since the number of parasites inside a host increases with the time since infection, long-lasting infections led to high frequencies of multiply infected host-gut cells. Therefore, we speculated that within-cell competition was more severe in the Nonreplacement lines and may have led to selection for accelerated within-host growth. SVs in the Nonreplacement lines were indeed significantly larger. Our results point out that single-factor explanations for the evolution of virulence can lead to wrong predictions and that multiple infections are an important factor in virulence evolution.
据预测，宿主利用方式应朝着使寄生虫适应性最大化的方向进化，而毒力（即寄生虫引起的宿主死亡率）则随宿主利用速率一同进化。如果寄生虫的预期寿命较短，预计它会进化出更高的宿主利用速率，进而具有更高的毒力，因为杀死宿主对寄生虫造成的代价会降低。我们通过在高宿主背景死亡率和低宿主背景死亡率条件下，将水平传播的微孢子虫寄生虫肠道格鲁吉亚虫（Glugoides intestinalis）在单克隆宿主培养物（大型溞，Daphnia magna）中培养14个月，来检验这一假设。通过每周用来自原种培养物的未感染宿主替换培养物中70 - 80%的所有宿主（替换组），实现了高宿主死亡率，进而也实现了寄生虫死亡率。在低死亡率处理组中不进行替换操作。与我们的预期相反，替换组的寄生虫在宿主体内的生长速率和毒力比非替换组的寄生虫更低。在所有组中，我们发现宿主体内生长速率和毒力之间存在很强的正相关关系。我们进行了进一步的实验来回答为什么我们的数据不支持这些预测。在双重感染的宿主肠道细胞中，孢子囊泡（SVs，孢子簇）比单一感染的宿主肠道细胞中的更小，这表明细胞内的竞争对寄生虫来说是有代价的。由于我们的实验方案，非替换组感染的平均寿命要高得多。由于宿主体内寄生虫的数量会随着感染时间的增加而增加，长期感染导致多重感染的宿主肠道细胞频率很高。因此，我们推测非替换组中细胞内的竞争更为激烈，这可能导致了对宿主体内加速生长的选择。非替换组中的孢子囊泡确实显著更大。我们的结果指出，对毒力进化的单因素解释可能会导致错误的预测，而多重感染是毒力进化中的一个重要因素。
