Multiple evolutionary origins of Trypanosoma evansi in Kenya

Trypanosoma evansi is the parasite causing surra, a form of trypanosomiasis in camels and other livestock, and a serious economic burden in Kenya and many other parts of the world. Trypanosoma evansi transmission can be sustained mechanically by tabanid and Stomoxys biting flies, whereas the closely related African trypanosomes T. brucei brucei and T. b. rhodesiense require cyclical development in tsetse flies (genus Glossina) for transmission. In this study, we investigated the evolutionary origins of T. evansi. We used 15 polymorphic microsatellites to quantify levels and patterns of genetic diversity among 41 T. evansi isolates and 66 isolates of T. b. brucei (n = 51) and T. b. rhodesiense (n = 15), including many from Kenya, a region where T. evansi may have evolved from T. brucei. We found that T. evansi strains belong to at least two distinct T. brucei genetic units and contain genetic diversity that is similar to that in T. brucei strains. Results indicated that the 41 T. evansi isolates originated from multiple T. brucei strains from different genetic backgrounds, implying independent origins of T. evansi from T. brucei strains. This surprising finding further suggested that the acquisition of the ability of T. evansi to be transmitted mechanically, and thus the ability to escape the obligate link with the African tsetse fly vector, has occurred repeatedly. These findings, if confirmed, have epidemiological implications, as T. brucei strains from different genetic backgrounds can become either causative agents of a dangerous, cosmopolitan livestock disease or of a lethal human disease, like for T. b. rhodesiense

Data from: Multiple evolutionary origins of Trypanosoma evansi in Kenya

Trypanosoma evansi is the parasite causing surra, a form of trypanosomiasis in camels and other livestock, and a serious economic burden in Kenya and many other parts of the world. Trypanosoma evansi transmission can be sustained mechanically by tabanid and Stomoxys biting flies, whereas the closely related African trypanosomes T. brucei brucei and T. b. rhodesiense require cyclical development in tsetse flies (genus Glossina) for transmission. In this study, we investigated the evolutionary origins of T. evansi. We used 15 polymorphic microsatellites to quantify levels and patterns of genetic diversity among 41 T. evansi isolates and 66 isolates of T. b. brucei (n = 51) and T. b. rhodesiense (n = 15), including many from Kenya, a region where T. evansi may have evolved from T. brucei. We found that T. evansi strains belong to at least two distinct T. brucei genetic units and contain genetic diversity that is similar to that in T. brucei strains. Results indicated that the 41 T. evansi isolates originated from multiple T. brucei strains from different genetic backgrounds, implying independent origins of T. evansi from T. brucei strains. This surprising finding further suggested that the acquisition of the ability of T. evansi to be transmitted mechanically, and thus the ability to escape the obligate link with the African tsetse fly vector, has occurred repeatedly. These findings, if confirmed, have epidemiological implications, as T. brucei strains from different genetic backgrounds can become either causative agents of a dangerous, cosmopolitan livestock disease or of a lethal human disease, like for T. b. rhodesiense

Evaluation of the genetic differentiation between isolates of <i>Trypanosoma brucei brucei</i> and <i>T</i>. <i>b</i>. <i>rhodesiense</i> (Tb) and <i>T</i>. <i>evansi</i> (Tev) genetic clusters using principal components analysis (PCA) of microsatellite data.

<p>PCA was performed in R using the package “adegenet” [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.ref086" target="_blank">86</a>]. Points representing individual genotypes are marked by color of their STRUCTURE assignment following the key and connected by a line to the centroid of an ellipse, which circumscribes a region encompassing 95% of the variance observed within each subgroup identified. Black arrows point out the Tev isolates.</p

Kamidi et al. 2017 genotypes_GENEPOP

GENEPOP format. Populations according to STRUCTURE results K=7 as described in Kamidi et al. 2017

Sample details and PCR assay results of <i>T</i>. <i>evansi</i> genotyped for this study showing sample ID, isolate source and reference in footnote, kinetoplast DNA (kDNA) type, PCR assay results (ITS1 + indicates pathogenic African trypanosome, SRA–indicates not <i>T</i>. <i>b</i>. <i>rhodesiense</i>, RoTat 1.2 + indicates the serological diagnostic antigen variant, A281del + indicates deletion of a GTC (Ala) triplet in F_OF₁-ATPase subunit γ unique to <i>T</i>. <i>evansi</i> isolates of kDNA type A, n/a indicates failure of the positive PCR control), host of isolation, the locality of origin and year of isolation.

<p>See also <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.s006" target="_blank">S1 Table</a> for isolates genotyped in previous studies.</p

Genetic diversity found within each STRUCTURE-based [51] genetic clusters considering (A) all isolates, (B) <i>T</i>. <i>brucei</i> (Tb) isolates only, and (C) <i>T</i>. <i>evansi</i> (Tev) isolates only.

<p>Sample size within the cluster (N), allelic richness (A_R) calculated in <i>FSTAT v1</i>.<i>2</i> [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.ref054" target="_blank">54</a>], and observed heterozygosity (H_O), expected heterozygosity under Hardy-Weinberg expectations (H_E), and the inbreeding coefficient (F_IS) calculated in the R package <i>HIERFSTAT v0</i>.<i>4–10</i> [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.ref055" target="_blank">55</a>]. Allelic richness could not be calculated in clusters made up of less than 4 individuals (marked n/a). </p

Multiple evolutionary origins of <i>Trypanosoma evansi</i> in Kenya - Fig 2

<p>Plot of assignment scores of all isolates using STRUCTURE v2.3.4 [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.ref051" target="_blank">51</a>] with K = 7 of <b>(A)</b> all isolates, and <b>(B)</b> the close up of <i>Trypanosoma evansi</i> isolates (Tev) with labels added showing isolate ID and kDNA type in parentheses (based on literature, where available, or predicted from the A281del PCR assay). Each vertical bar represents an isolate’s probability of assignment to one of seven genetic clusters "a" through "g" shown in orange, purple, blue, green, yellow, grey and red, as presented in the legend to the right. <i>T</i>. <i>brucei brucei</i> is indicated with a diamond, <i>T</i>. <i>b</i>. <i>rhodesiense</i> is indicated with a bullet point, and <i>T</i>. <i>evansi</i> is indicated by a plus "+" if RoTat 1.2 positive and minus "-" if RoTat 1.2 negative. The high virulence isolate is marked with a double asterix "**", and the low virulence isolate is marked by a single asterix "*". Note that Tev isolates in panel B are ordered according to <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.t001" target="_blank">Table 1</a> and not strictly according to cluster assignment.</p

Map of Africa showing in black location of Kenya (https://commons.wikimedia/wiki/Atlas_of_the_world).

<p>The insert to the right shows the location of the <i>Trypanosoma evansi</i> (Tev) and <i>T</i>. <i>brucei brucei</i> (Tbb) isolates genotyped for this study (small black circles). Sample details are listed in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0005895#pntd.0005895.t001" target="_blank">Table 1</a>.</p

Fourth Report on Chicken Genes and Chromosomes 2022

International audienc