Abstract
Previous work suggests that Brazilian Plasmodium falciparum has limited genetic diversity and a history of bottlenecks, multiple reintroductions due to human migration, and clonal expansions. We hypothesized that Brazilian P. falciparum would exhibit clonal structure. We examined isolates collected across two decades from Amapá, Rondônia, and Pará state (n = 190). By examining more microsatellites markers on more chromosomes than previous studies, we hoped to define the extent of low diversity, linkage disequilibrium, bottlenecks, population structure, and parasite migration within Brazil. We used retrospective genotyping of samples from the 1980s and 1990s to explore the population genetics of SP resistant dhfr and dhps alleles. We tested an existing hypothesis that the triple mutant dhfr mutations 50R/51I/108N and 51I/108N/164L developed in southern Amazon from a single origin of common or similar parasites. We found that Brazilian P. falciparum had limited genetic diversity and isolation by distance was rejected, which suggests it underwent bottlenecks followed by migration between sites. Unlike Peru, there appeared to be gene flow across the Brazilian Amazon basin. We were unable to divide parasite populations by clonal lineages and pairwise FST were common. Most parasite diversity was found within sites in the Brazilian Amazon, according to AMOVA. Our results challenge the hypothesis that triple mutant alleles arose from a single lineage in the Southern Amazon. SP resistance, at both the double and triple mutant stages, developed twice and potentially in different regions of the Brazilian Amazon. We would have required samples from before the 1980s to describe how SP resistance spread across the basin or describe the complex internal migration of Brazilian parasites after the colonization efforts of past decades. The Brazilian Amazon basin may have sufficient internal migration for drug resistance reported in any particular region to rapidly spread to other parts of basin under similar drug pressure.
Highlights
Malaria has been reported in Brazil since the 1500s when Plasmodium falciparum spread along the coast with the sugarcane industry
We previously showed that Peruvian P. falciparum populations were highly clonal [27] and here we used the same tools to examine Brazilian P. falciparum
The hypothesis that Brazilian P. falciparum has undergone bottlenecks followed by migration between sites is supported by its limited genetic diversity and the rejection of isolation by distance
Summary
Malaria has been reported in Brazil since the 1500s when Plasmodium falciparum spread along the coast with the sugarcane industry. Migration patterns driven by later industry (gold panning, diamond mining, rubber tapping, agriculture, cattle ranching, etc) and colonization propagated malaria epidemics and the principal vector, Anopheles darlingi into the interior [1,2,3]. By the early 1940s, there were six million malaria cases per year in Brazil, which was a seventh of the population [4]. After the introduction of DDT and chloroquine treatment, there were only 28,557 P. falciparum cases in 1970 among 92.3 million people and 73% of cases were reported in the Amazon region [4,5,6,7,8]. By 1990, 99% of malaria in Brazil occurred in states around the Amazon basin: Acre, Amapa, Amazonas, Maranhao, Mato Grosso, Para, Rondonia, Roraima and Tocantins [6]
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