10 research outputs found
Plasticity and genetic variation in traits underpinning asexual replication of the rodent malaria parasite, Plasmodium chabaudi
Adaptive plasticity in the gametocyte conversion rate of malaria parasites
<div><p>Sexually reproducing parasites, such as malaria parasites, experience a trade-off between the allocation of resources to asexual replication and the production of sexual forms. Allocation by malaria parasites to sexual forms (the conversion rate) is variable but the evolutionary drivers of this plasticity are poorly understood. We use evolutionary theory for life histories to combine a mathematical model and experiments to reveal that parasites adjust conversion rate according to the dynamics of asexual densities in the blood of the host. Our model predicts the direction of change in conversion rates that returns the greatest fitness after perturbation of asexual densities by different doses of antimalarial drugs. The loss of a high proportion of asexuals is predicted to elicit increased conversion (terminal investment), while smaller losses are managed by reducing conversion (reproductive restraint) to facilitate within-host survival and future transmission. This non-linear pattern of allocation is consistent with adaptive reproductive strategies observed in multicellular organisms. We then empirically estimate conversion rates of the rodent malaria parasite <i>Plasmodium chabaudi</i> in response to the killing of asexual stages by different doses of antimalarial drugs and forecast the short-term fitness consequences of these responses. Our data reveal the predicted non-linear pattern, and this is further supported by analyses of previous experiments that perturb asexual stage densities using drugs or within-host competition, across multiple parasite genotypes. Whilst conversion rates, across all datasets, are most strongly influenced by changes in asexual density, parasites also modulate conversion according to the availability of red blood cell resources. In summary, increasing conversion maximises short-term transmission and reducing conversion facilitates in-host survival and thus, future transmission. Understanding patterns of parasite allocation to reproduction matters because within-host replication is responsible for disease symptoms and between-host transmission determines disease spread.</p></div
An Epidemiological Model of the Effects of Insecticide-Treated Bed Nets on Malaria Transmission.
Insecticide-treated bed nets (ITNs) have become a central tool for malaria control because they provide personal and community-wide protection through their repellent and insecticidal properties. Here we propose a model that allows to assess the relative importance of those two effects in different epidemiological contexts and we show that these two levels of protection may oppose each other. On the one hand, repellency offers personal protection to the users of ITNs. The repellent action, however, is a two-edged sword, for it diverts infectious mosquitoes to non-users, thereby increasing their risk. Furthermore, with increasing ITN coverage, the personal protection effect of repellency decreases as mosquitoes are forced to perform multiple feeding attempts even on ITN users. On the other hand, the insecticidal property, which offers community-wide protection by killing mosquitoes, requires that mosquitoes contact the insecticide on the ITN and is thus counteracted by the repellency. Our model confirms that ITNs are an effective intervention method by reducing total malaria prevalence in the population, but that there is a conflict between personal protection, offered by repellency, and community-wide protection, which relies on the ITN's insecticidal properties. Crucially, the model suggests that weak repellency allows disease elimination at lower ITN coverage levels
The effects of repellency and probability of surviving the exposure to the insecticide on malaria prevalence.
<p>The epidemiological equilibrium prevalence is shown for low ITN coverage (<i>Ï•</i> = 0.2) and high ITN coverage (<i>Ï•</i> = 0.7). Other parameters are given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0144173#pone.0144173.t001" target="_blank">Table 1</a>.</p
Host searching cycle of a mosquito.
<p>A mosquito bites indoors with probability <i>ϵ</i> (for night-active and highly anthropophilic mosquitoes, this happens mainly at night) and takes a bite outdoors with probability 1 − <i>ϵ</i>. A mosquito then bites humans with a probability <i>Q</i>. If biting indoors, it will enter a house where a person sleeps under a bed net with a probability <i>ϕ</i> (the ITN coverage) or a house with an unprotected person with a probability 1 − <i>ϕ</i>. If the person is protected, the mosquito is repelled by the insecticide (or mechanically blocked by the net) with a probability <i>r</i>; if it is not repelled, it takes its bite and escapes with probability <i>s</i> or it is killed by the insecticide on the net with probability (1 − <i>s</i>). If a mosquito is repelled by a bed net, it leaves the house and continues to search for a host. There is a mortality cost <i>μ</i><sub><i>r</i></sub> associated with each repellency event. We assume that a mosquito will always land a successful bite on unprotected people and and on animals, whereas the feeding success on protected people depends on <i>r</i> and <i>s</i>. The host search happens once per mosquito gonotrophic cycle, i.e. once every three days (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0144173#pone.0144173.t001" target="_blank">Table 1</a>).</p
The effect of bed net coverage (<i>Ï•</i>) and repellency (<i>r</i>) on malaria prevalence.
<p>Panel (a) shows a situation with highly anthropophilic mosquitoes (<i>Q</i> = 0.95; panel (b) with zoophilic mosquitoes (<i>Q</i> = 0.3). Other parameters are given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0144173#pone.0144173.t001" target="_blank">Table 1</a>.</p
The effect of repellency on malaria prevalence at the epidemiological equilibrium.
<p>Unprotected people are represented by the dashed line, protected people by the dotted line, and the population as a whole by the solid line. In panel (a) coverage is <i>Ï•</i> = 0.2, in panel (b) <i>Ï•</i> = 0.7. Other parameters are given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0144173#pone.0144173.t001" target="_blank">Table 1</a>.</p
Adaptive plasticity in the gametocyte conversion rate of malaria parasites
Malaria parasites in the host replicate asexually and, during each replication cycle, some asexuals transform into sexual stages that enable between-host transmission. It is not understood why the rate of conversion to sexual stages varies during infections despite its importance for the severity and spread of the disease. We combined a mathematical model and experiments to show that parasites adjust conversion rates depending on changes in their in-host population size. When population sizes plummet, between-host transmission is prioritised. However, smaller losses in number elicit reproductive restraint, which facilitates in-host survival and future transmission. We show that increased and decreased conversion in response to a range of in-host environments are actually part of one continuum: a sophisticated reproductive strategy similar to that of multicellular organisms.Schneider, Petra; Greischar, Megan A; Birget, Philip L G; Repton, Charlotte; Mideo, Nicole; Reece, Sarah E. (2018). Adaptive plasticity in the gametocyte conversion rate of malaria parasites, [dataset]. University of Edinburgh. https://doi.org/10.7488/ds/2460