Malaria population dynamics with superinfection: Critical transitions and responses to forcing

Background/Question/Methods

Malaria transmission dynamics do not easily conform to the standard Susceptible-Infected-Recovered (SIR) structure because of the multiple levels of host immunity associated with antigenic diversity of the parasite; vector mediated transmission adds a further layer of complexity.  A variety of compartmental structures have attempted  to better represent the acquisition of immunity with repeated infection, the multiplicity of infection due to parasite diversity (superinfection), and the existence of chronic, asymptomatic individuals that stiil contribute to transmission.  However, we still do not sufficiently understand the dynamical implications of these immunological subtleties, from the perspective of how malaria dynamics respond to seasonal and interannual cycles in transmission intensity, as well as long term trends, in climate or control.  For example, it has been argued that immunity can play an important role in the interannual variability of the disease in highland regions and lead to cycles that are only weakly correlated to climate variability. 

Results/Conclusions

Here we show that models that incorporate superinfection and more complex representations of immunity can exhibit dynamics that differ from earlier expectations based on the dynamics of simpler SIR models.   Responses to long-term change in the force of infection can be discontinuous, involving the existence of alternative steady states and hysteresis.  Nonlinear responses to seasonal and interannual forcing do occur, as expected, for intermediate transmission rates, in between epidemic and highly endemic regimes, but the importance of this region can be limited and is strongly dependent on the specific parameters of the vector.  These findings emphasize gaps in our understanding of malaria population dynamics that are especially relevant to changes in transmission intensity as the result of both control and climate.  We discuss these implications for other infectious diseases whose transmission dynamics are intimately coupled to climate variation.