RESUMO
WHO promotes the implementation of a comprehensive strategy to control and eliminate schistosomiasis through preventive chemotherapy, snail control, clean water supply, improved sanitation, behaviour change interventions, and environmental management. The transmission of schistosomiasis involves infected definitive hosts (humans or animals) excreting eggs that hatch (miracidia), which infect freshwater snail vectors (also referred to as intermediate snail hosts) living in marshlands, ponds, lakes, rivers, or irrigation canals. Infective larvae (cercariae) develop within the snail, which, when released, may infect humans and/or animals in contact with the water. Snail control aims to interrupt the transmission cycle of the disease by removing the vector snails and, by so doing, indirectly improves the impact of the preventive chemotherapy by reducing reinfection. Snail control was, for many years, the only strategy for the prevention of schistosomiasis before preventive chemotherapy became the primary intervention. Snails can be controlled through various methods: environmental control, biological control, and chemical control. The chemical control of snails has proven to be the most effective method to interrupt the transmission of schistosomiasis. The current review aims to describe the vector snails of human schistosomiasis, present the chemicals and strategies for the control of snails, the challenges with the implementation, and the future needs. Snail control can play a key role in reducing schistosomiasis transmission and, thus, complements other interventions for disease control. There is a need to develop new molluscicide products or new formulations and methods of applications for existing molluscicides that would target snail vectors more specifically.
RESUMO
Do mutations required for adaptation occur de novo, or are they segregating within populations as standing genetic variation? This question is key to understanding adaptive change in nature, and has important practical consequences for the evolution of drug resistance. We provide evidence that alleles conferring resistance to oxamniquine (OXA), an antischistosomal drug, are widespread in natural parasite populations under minimal drug pressure and predate OXA deployment. OXA has been used since the 1970s to treat Schistosoma mansoni infections in the New World where S. mansoni established during the slave trade. Recessive loss-of-function mutations within a parasite sulfotransferase (SmSULT-OR) underlie resistance, and several verified resistance mutations, including a deletion (p.E142del), have been identified in the New World. Here we investigate sequence variation in SmSULT-OR in S. mansoni from the Old World, where OXA has seen minimal usage. We sequenced exomes of 204 S. mansoni parasites from West Africa, East Africa and the Middle East, and scored variants in SmSULT-OR and flanking regions. We identified 39 non-synonymous SNPs, 4 deletions, 1 duplication and 1 premature stop codon in the SmSULT-OR coding sequence, including one confirmed resistance deletion (p.E142del). We expressed recombinant proteins and used an in vitro OXA activation assay to functionally validate the OXA-resistance phenotype for four predicted OXA-resistance mutations. Three aspects of the data are of particular interest: (i) segregating OXA-resistance alleles are widespread in Old World populations (4.29-14.91% frequency), despite minimal OXA usage, (ii) two OXA-resistance mutations (p.W120R, p.N171IfsX28) are particularly common (>5%) in East African and Middle-Eastern populations, (iii) the p.E142del allele has identical flanking SNPs in both West Africa and Puerto Rico, suggesting that parasites bearing this allele colonized the New World during the slave trade and therefore predate OXA deployment. We conclude that standing variation for OXA resistance is widespread in S. mansoni.
