Where chloroquine still works: the genetic make-up and susceptibility of Plasmodium vivax to chloroquine plus primaquine in Bhutan

Table 2 Genetic diversity and structure in the Plasmodium vivax population

Infection origin	% Polyclonal infections	MOI, mean, median (range)	H _E, mean ± SE (range)	LD in all isolates^a, I _A ^S	LD in unique MLGs^b, I _A ^S
Autochthonous	38 % (5/13)	1.46, 1 (1–3)	0.87 ± 0.01(0.78–0.91)	0.495 **	0.179**
Imported	7 % (1/15)	1.07, 1 (1–2)	0.90 ± 0.02 (0.81–0.98)	−0.029^NS	−0.029^NS
All	21.4 % (6/28)	1.25, 1 (1–3)	0.91 ± 0.01 (0.85–0.97)	0.158 **	0.024**

Circles depict the 12 sentinel sites at which enrolment was conducted over the full duration of the study (old Site). Squares depict the additional 23 sites from which enrolment was started 8 months into the study (new Site)
H _E expected heterozygosity, LD linkage disequilibrium, I _A ^S index of association
NS not significant (p > 0.05)
^aOnly samples with no missing data at all nine loci are included in the analyses (infections from 13 autochthonous and 13 imported cases)
^bUnique set of multi-locus genotypes (11 autochthonous and 13 imported cases)
* 0.01 < p ≤ 0.05
** p ≤ 0.01

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