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Open Access Highly Accessed Research article

Population-level effects of clinical immunity to malaria

Lindsay T Keegan* and Jonathan Dushoff

Author Affiliations

Department of Biology, McMaster University, Hamilton, Ontario, Canada

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BMC Infectious Diseases 2013, 13:428  doi:10.1186/1471-2334-13-428

Published: 11 September 2013



Despite a resurgence in control efforts, malaria remains a serious public-health problem, causing millions of deaths each year. One factor that complicates malaria-control efforts is clinical immunity, the acquired immune response that protects individuals from symptoms despite the presence of parasites. Clinical immunity protects individuals against disease, but its effects at the population level are complex. It has been previously suggested that under certain circumstances, malaria is bistable: it can persist, if established, in areas where it would not be able to invade. This phenomenon has important implications for control: in areas where malaria is bistable, if malaria could be eliminated until immunity wanes, it would not be able to re-invade.


Here, we formulate an analytically tractable, dynamical model of malaria transmission to explore the possibility that clinical immunity can lead to bistable malaria dynamics. We summarize what is known and unknown about the parameters underlying this simple model, and solve the model to find a criterion that determines under which conditions we expect bistability to occur.


We show that bistability can only occur when clinically immune individuals are more “effective” at transmitting malaria than naïve individuals are. We show how this “effectiveness” includes susceptibility, ability to transmit, and duration of infectiousness. We also show that the amount of extra effectiveness necessary depends on the ratio between the duration of infectiousness and the time scale at which immunity is lost. Thus, if the duration of immunity is long, even a small amount of extra transmission effectiveness by clinically immune individuals could lead to bistability.


We demonstrate a simple, plausible mechanism by which clinical immunity may be causing bistability in human malaria transmission. We suggest that simple summary parameters – in particular, the relative transmission effectiveness of clinically immune individuals and the time scale at which clinical immunity is lost – are key to determining where and whether bistability is happening. We hope these findings will guide future efforts to measure transmission parameters and to guide malaria control efforts.