Abstract
BackgroundMalaria programmes estimate changes in prevalence to evaluate their efficacy. In this study, parasite genetic data was used to explore how the demography of the parasite population can inform about the processes driving variation in prevalence. In particular, how changes in treatment and population movement have affected malaria prevalence in an area with seasonal malaria.MethodsSamples of Plasmodium falciparum collected over 8 years from a population in Turbo, Colombia were genotyped at nine microsatellite loci and three drug-resistance loci. These data were analysed using several population genetic methods to detect changes in parasite genetic diversity and population structure. In addition, a coalescent-based method was used to estimate substitution rates at the microsatellite loci.ResultsThe estimated mean microsatellite substitution rates varied between 5.35 × 10−3 and 3.77 × 10−2 substitutions/locus/month. Cluster analysis identified six distinct parasite clusters, five of which persisted for the full duration of the study. However, the frequencies of the clusters varied significantly between years, consistent with a small effective population size.ConclusionsMalaria control programmes can detect re-introductions and changes in transmission using rapidly evolving microsatellite loci. In this population, the steadily decreasing diversity and the relatively constant effective population size suggest that an increase in malaria prevalence from 2004 to 2007 was primarily driven by local rather than imported cases.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-015-0887-9) contains supplementary material, which is available to authorized users.
Highlights
Malaria programmes estimate changes in prevalence to evaluate their efficacy
During the 1970s and 1980s, malaria incidence increased in South America due to the disorganized development of cities and the emergence of drug resistance in Plasmodium falciparum [1, 2]
Plasmodium isolates A total of 257 P. falciparum blood samples collected on filter paper between 2002 and 2009 from surveillance studies carried out in Turbo (Antioquia department, Colombia) were genotyped: 94 samples were collected between October 2002 and July 2003, 80 from January 2004 to December 2005, 47 between April and October 2007, and 36 between March 2008 and July 2009
Summary
Plasmodium isolates A total of 257 P. falciparum blood samples collected on filter paper between 2002 and 2009 from surveillance studies carried out in Turbo (Antioquia department, Colombia) were genotyped: 94 samples were collected between October 2002 and July 2003, 80 from January 2004 to December 2005, 47 between April and October 2007, and 36 between March 2008 and July 2009. The samples were genotyped by direct sequencing to evaluate mutations at Pfcrt (codons 72–76), Pfdhfr (codons 50, 51, 59, 108, and 164) and Pfdhps (codons 436, 437, 540, 581, and 613) which have been associated with chloroquine, pyrimethamine, and sulfadoxine resistance, respectively. Samples from single infections as determined by neutral microsatellite loci were sequenced. The tip dates (sampling dates) were recorded in months and the coalescent constant population size model was used with a strict molecular clock and a standard uniform prior on the mean substitution rate. The best supported substitution model and the corresponding substitution rate were used in an Extended Bayesian Skyline Plot (EBSP) to estimate the parasite effective population size (Ne) through time, assuming a generation time for malaria infections of a month. Convergence of the Markov chains was assessed by monitoring both the trace plots and effective sample sizes
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