Abstract: Parasites exhibit remarkable diversity in their life history traits to adapt to the unique ecological challenges posed by their hosts. Within the genus Plasmodium, the life cycle of the malaria-causing species involves multiple rounds of replication, with a fraction of infected red blood cells being committed to producing specialized stages for onward transmission to vectors. The rate of proliferation is limited by the burst size or the average number of daughter cells to emerge from each infected red blood cell. As proliferation is crucial for establishing and maintaining the infection, parasites would be expected to evolve to the maximal burst size that does not prematurely end the infection by killing its host. In reality, observed burst sizes vary significantly across species and even among strains, suggesting that maximizing the burst size is not always the best strategy. More specifically, restricting within-host proliferation may be beneficial for the parasites though the exact mechanism is unclear.
Using a within-host model parameterized for the rodent malaria, Plasmodium chabaudi, we investigate how host mortality and resource limitation affect the optimal burst size. We focus on the acute phase which encompasses the first and typically largest wave of parasite abundance with most of the parasite's transmission success gained disproportionately in this phase. By calculating the cumulative transmission potential at the end of the acute phase, we find that the most transmissible strain does not maximize its burst size even if the value does not induce host mortality . Greater proliferation leads to the production of more sexual forms, but there are diminishing returns in transmission success. Moreover, the benefits of faster proliferation come at the cost of significantly shortening the period of high infectivity. Therefore, the optimal burst size emerges from the trade-off between the length of the acute phase and the production of the sexual forms. By identifying resource availability as a key mechanism limiting the burst size, we are better able to understand how parasite traits can influence the varying virulence we see in malaria infections.
