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“Background Quisinostat purchase The globally occurring diarrhea-causing protozoan, Giardia intestinalis (syn. G. lamblia and G. duodenalis), makes up a species complex of eight different genotypes or assemblages, A-H
[1], where assemblages A and B can cause disease in humans [2]. Understanding of the epidemiology of the disease caused by G. intestinalis (giardiasis) has been hampered due to the genomic complexity of the parasite (cellular ploidy of 4 N-16 N in two nuclei) [3], along with the genetic heterogeneity that is present in assemblage B Giardia isolates [4–6]. The most commonly used genotyping loci; beta-giardin, glutamate dehydrogenase and triose- phosphate isomerase (bg, gdh and tpi, GS-1101 in vivo respectively) have low discriminatory power when applied to assemblage A Giardia. Assemblage A sub-assemblages may only be discriminated at a few positions, due to a high level of conservation in these genes in assemblage A isolates, however, three different sub-assemblages have been established at the current loci, namely AI, AII and AIII. In assemblage B on the contrary, high variability in the form of mixed base polymorphisms has been observed at these loci, which has impeded proper epidemiological analyses [7–11].