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PLoS Negl Trop Dis. 2015 Feb 19;9(2):e0003353. doi: 10.1371/journal.pntd.0003353. eCollection 2015 Feb.

Genetic diversity and population structure of Trypanosoma brucei in Uganda: implications for the epidemiology of sleeping sickness and Nagana.

Author information

1
Faculty of Science, Gulu University, Gulu, Uganda.
2
Department of Ecology and Evolutionary Biology, Yale University, New Haven, Connecticut, United States of America.
3
Trypanosomiasis Research Centre, Kenya Agricultural Research Institute, Kikuyu, Kenya.
4
National Agricultural Research Organisation, National Livestock Resources Research Institute, Tororo, Uganda.
5
Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, Connecticut, United States of America.
6
School of Biological Sciences, Makerere University, Kampala, Uganda.
7
School of Biological Sciences, University of Bristol, Bristol, United Kingdom.
8
Department of Ecology and Evolutionary Biology, Yale University, New Haven, Connecticut, United States of America; Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, Connecticut, United States of America.

Abstract

BACKGROUND:

While Human African Trypanosomiasis (HAT) is in decline on the continent of Africa, the disease still remains a major health problem in Uganda. There are recurrent sporadic outbreaks in the traditionally endemic areas in south-east Uganda, and continued spread to new unaffected areas in central Uganda. We evaluated the evolutionary dynamics underpinning the origin of new foci and the impact of host species on parasite genetic diversity in Uganda. We genotyped 269 Trypanosoma brucei isolates collected from different regions in Uganda and southwestern Kenya at 17 microsatellite loci, and checked for the presence of the SRA gene that confers human infectivity to T. b. rhodesiense.

RESULTS:

Both Bayesian clustering methods and Discriminant Analysis of Principal Components partition Trypanosoma brucei isolates obtained from Uganda and southwestern Kenya into three distinct genetic clusters. Clusters 1 and 3 include isolates from central and southern Uganda, while cluster 2 contains mostly isolates from southwestern Kenya. These three clusters are not sorted by subspecies designation (T. b. brucei vs T. b. rhodesiense), host or date of collection. The analyses also show evidence of genetic admixture among the three genetic clusters and long-range dispersal, suggesting recent and possibly on-going gene flow between them.

CONCLUSIONS:

Our results show that the expansion of the disease to the new foci in central Uganda occurred from the northward spread of T. b. rhodesiense (Tbr). They also confirm the emergence of the human infective strains (Tbr) from non-infective T. b. brucei (Tbb) strains of different genetic backgrounds, and the importance of cattle as Tbr reservoir, as confounders that shape the epidemiology of sleeping sickness in the region.

PMID:
25695634
PMCID:
PMC4335064
DOI:
10.1371/journal.pntd.0003353
[Indexed for MEDLINE]
Free PMC Article
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