  Many models of within-host malaria infection dynamics have been formulated
since the pioneering work of Anderson et al. in 1989. Biologically, the goal of
these models is to understand what governs the severity of infections, the
patterns of infectiousness, and the variation thereof across individual hosts.
Mathematically, these models are based on dynamical systems, with standard
approaches ranging from Kcompartments ordinary differential equations (ODEs) to
delay differential equations (DDEs), in order to capture the relatively
constant duration of replication and bursting once a parasite infects a host
red blood cell. Using malariatherapy data, which offers fine-scale resolution
on the dynamics of infection across a number of individual hosts, we compare
the fit of one of these standard approaches (K-compartments ODEs) with a
partial differential equations (PDEs) model, which explicitly tracks the "age"
of an infected cell. We find that the PDE model outperforms the Kcompartments
ODEs, particularly early on in infections, where ODEs wildly overestimate
parasite densities. Further, the PDE model highlights a strong qualitative
connection between the density of transmissible parasite stages (i.e.,
gametocytes) and the density of host-damaging (and asexually-replicating)
parasite stages, which is difficult to capture by the K-compartments ODEs
model. This finding provides a simple tool for predicting which hosts are most
infectious to mosquitoes-vectors of Plasmodium parasites-which is a crucial
component of global efforts to control and eliminate malaria.
