Optimal pattern of replication and transmission for parasites with two stages in their life cycle (Q1897486): Difference between revisions

Microparasites, which often infect their host in low numbers, must replicate extensively within their host so that they can reach a density that is high enough to ensure their transmission. However, replication of parasites within their hosts, and thus transmission between hosts, are constrained by the increased mortality of the host at high parasite densities. This association between parasite transmission and host mortality has been made explicit in mathematical models of parasite transmission where the most commonly used measure of a parasite's fitness, the basic reproductive number, is in the simplest case proportional to the number of (infectious) parasites produced and to the lifespan of the infected host. We discuss possible evolutionary reasons that may lead to observed variability in the within-host dynamics of parasites with distinct stages for both replication and transmission. To do so, we assume that parasites have evolved their pattern of production of the two stages to maximise the number of parasites transmitted to a new host. That this number is maximised by an intermediate level of investment into transmission stages seems clear: On the one hand, high or early investment into transmission will decrease the density of the replication stage and thus will limit future production of the transmission stage before the parasite is cleared by the host's immune response. On the other hand, low or late investment into transmission will result in high parasite densities, increasing the chances that the host dies before the parasite can be transmitted. In order to examine quantitatively the subtle interplay between the needs of the parasite, the survival of the host, and the effectiveness of the immunological defences, we have constructed a mathematical model of the population densities of the replication and transmission stages of the parasite within its host. We use this model to calculate the pattern of production of the two stages that allows maximal transmission of the parasite and in particular to consider the effect of the host's immune system on this pattern. We consider the cases (1) where investment into transmission stages is predetermined and thus constant during the course of infection and (2) where parasites can vary their investment in transmission during the course of infection.