Soil transmitted nematodes, including Strongyloides, cause one of the most prevalent Neglected Tropical Diseases. Here we compare the genomes of four Strongyloides spp., including the human pathogen S. stercoralis, and their close relatives that are facultatively parasitic (Parastrongyloides trichosuri) and free-living (Rhabditophanes sp). A significant paralogous expansion of key gene families – astacin-like and SCP/TAPS coding gene families – is associated with the evolution of parasitism in this clade. Exploiting the unique Strongyloides life cycle we compare the transcriptome of its parasitic and free-living stages and find that these same genes are upregulated in the parasitic stages, underscoring their role in nematode parasitism.

A disproportionate burden of helminthiases in human populations occurs in marginalised, low-income, and resource-constrained regions of the world, with over 1 billion people in developing areas of sub-Saharan Africa, Asia, and the Americas infected with one or more helminth species. The morbidity caused by such infections imposes a substantial burden of disease, contributing to a vicious circle of infection, poverty, decreased productivity, and inadequate socioeconomic development. Furthermore, helminth infection accentuates the morbidity of malaria and HIV/AIDS, and impairs vaccine efficacy. Polyparasitism is the norm in these populations, and infections tend to be persistent. Hence, there is a great need to reduce morbidity caused by helminth infections. However, major deficiencies exist in diagnostics and interventions, including vector control, drugs, and vaccines. Overcoming these deficiencies is hampered by major gaps in knowledge of helminth biology and transmission dynamics, platforms from which to help develop such tools. The Disease Reference Group on Helminths Infections (DRG4), established in 2009 by the Special Programme for Research and Training in Tropical Diseases (TDR), was given the mandate to review helminthiases research and identify research priorities and gaps. In this review, we provide an overview of the forces driving the persistence of helminthiases as a public health problem despite the many control initiatives that have been put in place; identify the main obstacles that impede progress towards their control and elimination; and discuss recent advances, opportunities, and challenges for the understanding of the biology, epidemiology, and control of these infections. The helminth infections that will be discussed include: onchocerciasis, lymphatic filariasis, soil-transmitted helminthiases, schistosomiasis, food-borne trematodiases, and taeniasis/cysticercosis.

An abnormal-leaf soybean [Glycine max (L.) Merr.] plant was observed in an F 4:8 line at Urbana, Illinois, in the summer of 1992. Petiolules of the plant were shorter than normal and leaflet margins curled uniformly upward forming a cuppedshaped leaf. All progeny of the single plant exhibited leaf cupping. Laboratory analysis showed an absence of soybean mosaic and tobacco ringspot virus in the plants. Seeds from the progeny were bulked and designated line LN89-3502TP. Further observation of LN89-3502TP revealed dense pubescence on the short petiolule plants. The objective of this study was to determine the inheritance of the short petiolule trait of LN89-3502TP. In F 2 populations derived from LN89-3502TP crossed with normal leaf-type cultivars, three petiolule phenotypes (short, intermediate, and normal) segregated in a 1:2:1 ratio. The 1:2:1 ratio was confirmed in the F 2:3 families. These ratios indicate the short petiolule trait is controlled by a single gene showing incomplete dominance that we designated lc. Genetically controlled abnormalities of soybean petioles and leaves have been documented. Kilen (1983) published the inheritance of a short petiole-type soybean conditioned by a single recessive gene, lps. Rode and Bernard (1975a,b) concluded two leaf mutants, wavy and bullate, are each controlled by two recessive genes, lw 1 , lw 2 and lb 1 , lb 2 , respectively. Tharp et al. (1994) determined that a sinuate leaf type was conditioned by two recessive genes. In the summer of 1992, an abnormal-leaf plant, not resembling any previously documented plant type, was observed at Urbana, Illinois, in an F 4:8 line derived from the cross Hobbit 87 (Cooper et al. 1991) ϫ Asgrow 3205. Petiolules, which connect the leaflets to the petiole, were shorter than normal and the leaflet margins curled uniformly upward forming a cup-shaped leaf. All progeny of the single plant exhibited the short petiolule trait and leaf cupping. Also, dense pubescence was observed on all plants. Seeds from the progeny were bulked and designated LN89-3502TP. Leaf cupping is apparent on the first trifoliolate and every subsequent leaf until maturity. An enzyme-linked immunosorbent assay (ELISA) test (Hancock and Evan 1992) performed in the laboratory of Dr. Glen Hartman, USDA Plant Pathologist at the University of Illinois, showed an absence of soybean mosaic or tobacco ringspot virus. The absence of virus and the uniformity of the phenotype suggested that short petiolules and leaf cupping are under genetic control. The objective of this study was to determine the inheritance of the short-petiolule trait of LN89-3502TP.

Preventive chemotherapy has long been practiced against nematode parasites of livestock, leading to widespread drug resistance, and is increasingly being adopted for eradication of human parasitic nematodes even though it is similarly likely to lead to drug resistance. Given that the genetic architecture of resistance is poorly understood for any nematode, we have analyzed multidrug resistant Teladorsagia circumcincta, a major parasite of sheep, as a model for analysis of resistance selection. We introgressed a field-derived multiresistant genotype into a partially inbred susceptible genetic background (through repeated backcrossing and drug selection) and performed genome-wide scans in the backcross progeny and drug-selected F2 populations to identify the major genes responsible for the multidrug resistance. We identified variation linking candidate resistance genes to each drug class. Putative mechanisms included target site polymorphism, changes in likely regulatory regions and copy number variation in efflux transporters. This work elucidates the genetic architecture of multiple anthelmintic resistance in a parasitic nematode for the first time and establishes a framework for future studies of anthelmintic resistance in nematode parasites of humans.

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