Strongyloidiasis is a much-neglected soil born helminthiasis caused by the nematode Strongyloides stercoralis. Human derived S. stercoralis can be maintained in dogs in the laboratory and this parasite has been reported to also occur in dogs in the wild. Some authors have considered strongyloidiasis a zoonotic disease while others have argued that the two hosts carry host specialized populations of S. stercoralis and that dogs play a minor role, if any, as a reservoir for zoonotic S. stercoralis infections of humans. We isolated S. stercoralis from humans and their dogs in rural villages in northern Cambodia, a region with a high incidence of strongyloidiasis, and compared the worms derived from these two host species using nuclear and mitochondrial DNA sequence polymorphisms. We found that in dogs there exist two populations of S. stercoralis, which are clearly separated from each other genetically based on the nuclear 18S rDNA, the mitochondrial cox1 locus and whole genome sequence. One population, to which the majority of the worms belong, appears to be restricted to dogs. The other population is indistinguishable from the population of S. stercoralis isolated from humans. Consistent with earlier studies, we found multiple sequence variants of the hypervariable region I of the 18 S rDNA in S. stercoralis from humans. However, comparison of mitochondrial sequences and whole genome analysis suggest that these different 18S variants do not represent multiple genetically isolated subpopulations among the worms isolated from humans. We also investigated the mode of reproduction of the free-living generations of laboratory and wild isolates of S. stercoralis. Contrary to earlier literature on S. stercoralis but similar to other species of Strongyloides, we found clear evidence of sexual reproduction. Overall, our results show that dogs carry two populations, possibly different species of Strongyloides. One population appears to be dog specific but the other one is shared with humans. This argues for the strong potential of dogs as reservoirs for zoonotic transmission of S. stercoralis to humans and suggests that in order to reduce the exposure of humans to infective S. stercoralis larvae, dogs should be treated for the infection along with their owners. Infections of humans with the nematode Strongyloides stercoralis can persist for a very long time, due to the capacity of this pathogen to undergo an autoinfective life cycle and re-infect the same host over and over again. Clinical manifestation, known as human stongyloidiasis, may be fatal and can arise many years and generations of worms after the initial infection occurred. Although Strongyloides stercoralis has been known as the causative agent of strongyloidiasis for a very long time, some key questions about its biology and epidemiology remain open. Here we address two of them. Firstly, it has long been known that dogs can serve as experimental hosts for S. stercoralis but it is a matter of debate whether Strongyloides spp. found in dogs in the wild are human pathogenic S. stercoralis, and whether dogs therefore are a source of zoonotic transmission of this parasite. Here we show that dogs carry two genetically different populations of Strongyloides spp. one of which is shared with humans. This demonstrates that dogs represent a possible reservoir for zoonotic strongyloidiasis. Secondly, the all female, parthenogenetic parasitic generations may alternate with single facultative free-living generations, which consist of both females and males. In spite of the presence of both sexes, it had been postulated that males do not contribute genetic material to the progeny and that sperm are merely required to trigger parthenogenetic embryonic development. Here we show that the free-living adults of S. stercoralis reproduce sexually.

Background: In the androdioecious nematodeCaenorhabditis elegansvirtually all progeny produced by hermaphrodite self-fertilization is hermaphrodite while 50% of the progeny that results from cross-fertilization by a male is male. In the standard laboratory wild type strain N2 males disappear rapidly from populations. This is not the case in some other wild type isolates ofC. elegans, among them the Hawaiian strain CB4856.Results: We determined the kinetics of the loss of males over time for multiple population sizes and wild isolates and found significant differences. We performed systematic inter- and intra-strain crosses with N2 and CB4856 and show that the males and the hermaphrodites contribute to the difference in male maintenance between these two strains. In particular, CB4856 males obtained a higher number of successful copulations than N2 males and sired correspondingly more cross-progeny. On the other hand, N2 hermaphrodites produced a higher number of self-progeny, both when singly mated and when not mated.Conclusion: These two differences have the potential to explain the observed variation in male persistence, since they should lead to a predominance of self-progeny (and thus hermaphrodites) in N2 and, at the same time, a high proportion of cross-progeny (and thus the presence of males as well as hermaphrodites) in CB4856.

SUMMARY: Nematodes of the genusStrongyloidesparasitize the small intestines of vertebrates. In addition to a parasitic life-cycle, which is generally considered to be parthenogenetic,Strongyloidescan also have a facultative, free-living generation involving male and female worms. The purpose of the present article was to review the literature on the modes of reproduction, the routes of development in the two generations ofStrongyloides, discuss the controversial opinions in the literature regarding these aspects and point to new opportunities for addressing key questions in relation to the biology of reproduction of members of the genus employing genetic and genomic tools.

Background: In the hermaphrodite of the nematode Caenorhabditis elegans, the first germ cells differentiate as sperm. Later the germ line switches to the production of oocytes. This process requires the activity of a genetic regulatory network that includes among others the fem, fog and mog genes. The function of some of these genes is germline specific while others also act in somatic tissues. DEAD box proteins have been shown to be involved in the control of gene expression at different steps such as transcription and pre-mRNA processing. Results: We show that the Caenorhabditis elegans gene mel-46 (maternal effect lethal) encodes a DEAD box protein that is related to the mammalian DDX20/Gemin3/DP103 genes. mel-46 is expressed throughout development and mutations in mel-46 display defects at multiple developmental stages. Here we focus on the role of mel-46 in the hermaphrodite germ line. mel-46(yt5) mutant hermaphrodites are partially penetrant sterile and fully penetrant maternal effect lethal. The germ line of mutants shows variable defects in oogenesis. Further, mel-46(yt5) suppresses the complete feminization caused by mutations in fog-2 and fem-3, two genes that are at the top and the center, respectively, of the genetic germline sex determining cascade, but not fog-1 that is at the bottom of this cascade. Conclusion: The C. elegans gene mel-46 encodes a DEAD box protein that is required maternally for early embryogenesis and zygotically for postembryonic development. In the germ line, it is required for proper oogenesis. Although it interacts genetically with genes of the germline sex determination machinery its primary function appears to be in oocyte differentiation rather than sex determination.