Successful parasitism of vector snail Biomphalaria glabrata by the human blood fluke (trematode) Schistosoma mansoni: A 2009 assessment

Abstract

Schistosomiasis, caused by infections by human blood flukes (Trematoda), continues to disrupt the lives of over 200,000,000 people in over 70 countries, inflicting misery and precluding the individuals’ otherwise reasonable expectations of productive lives. Infection requires contact with freshwater in which infected snails (the intermediate hosts of schistosomes) have released cercariae larvae. Habitats suitable for the host snails continue to expand as a consequence of water resource development. No vaccine is available, and the emergence and spread of resistance to the single licensed schistosomicide drug would be devastating. Since human infections would cease if parasite infections in snails were prevented, efforts are being made to discover requirements of intra-molluscan development of these parasites. Wherever blood flukes occur, naturally resistant conspecific snails are present. To understand the mechanisms used by parasites to ensure their survival in immunocompetent hosts, one must comprehend the internal defense mechanisms that are available to the host. For one intermediate host snail (Biomphalaria glabrata) and trematodes for which it serves as vector, molecular genetic and proteomic surveys for genes and proteins influencing the outcomes on infections are yielding lists of candidates. A comparative approach drawing on data from studies in divergent species provides a robust basis for hypothesis generation to drive decisions as to which candidates merit detailed further investigation. For example, reactive oxygen and nitrogen species are known mediators or effectors in battles between infectious agents and their hosts. An approach targeting genes involved in relevant pathways has been fruitful in the Schistosoma mansoni-B. glabrata parasitism, leading to discovery of a functionally relevant gene set (encoding enzymes responsible for the leukocyte respiratory burst) that associates significantly with host resistance phenotype. This review summarizes advances in the understanding of strategies used by both this trematode parasite and its molluscan host to ensure their survival.

Control of infection of Biomphalaria alexandrina (Ehrenberg, 1831) with Schistosoma mansoni Sambon, 1907 using Eucalyptus camaldulensis

“…Schistosoma mansoni Sambon, 1907 depends on snails of the genus Biomphalaria Preston, 1910 as its intermediate host. Within Biomphalaria, the parasite develops from miracidia, the snails' infective larvae, to cercariae, the human infective stage (MeuleMan 1971, MoRGan et al 2001, bayne 2009). Up to date, no effective vaccine has been found against schistosomiasis and the disease control depends entirely on praziquantel.…”

Larval excretory-secretory products from the parasite Schistosoma mansoni modulate HSP70 protein expression in defence cells of its snail host, Biomphalaria glabrata

“…Once S. mansoni eggs are released in faeces of the infected human host, a free-living miracidium hatches from each egg and infects a susceptible snail host. Inside the snail, the parasite transforms into a mother and subsequently daughter sporocysts which release cercariae capable of infecting the definitive host (reviewed in Bayne 2009). As the parasite transforms from a miracidium into a mother sporocyst, it releases ciliary epidermal plates and a variety of molecules from its surface and excretes a range of molecules from its excretory pore, these being jointly referred to as excretory-secretory products (ESPs; Lodes and Yoshino 1989); the protein fraction, comprising larval transformation proteins has recently been analysed by proteomics (Wu et al 2009).…”

“…These strains are therefore invaluable for studying snail-schistosome interactions in the context of parasite survival. Larval stage ESPs are thought to assist the survival of developing sporocysts in a susceptible snail host by interacting with haemocytes via cell surface receptors and modulating the activities of cell signalling pathways, such as the extracellular signal-regulated kinase (ERK) pathway that regulates cellular responses including cell spreading, NO and hydrogen peroxide production (Bayne 2009;Humphries and Yoshino 2008;Johnston and Yoshino 1996;Johnston and Yoshino 2001;Walker 2006;Zahoor et al 2008;Zahoor et al 2009). In the present study, we report for the first time that intracellular HSP70 protein levels in haemocytes from schistosome-susceptible and schistosomeresistant snails are reduced following exposure to S. mansoni larval ESPs.…”

Role for a somatically diversified lectin in resistance of an invertebrate to parasite infection

“…pronounced during the early stages of infection (20): The parasite attempts to suppress the snail immune response (21) or to disguise itself from it (22), thereby allowing the parasite to establish. For its part, the snail host mounts humoral and cellular responses to encapsulate and kill the parasite (20,23,24). In some snaildigenean combinations, the snail is resistant to infection and the immune components responsible have been a frequent topic of study (23), in part because of the ramifications for interrupting transmission of schistosomes to humans.…”

“…For its part, the snail host mounts humoral and cellular responses to encapsulate and kill the parasite (20,23,24). In some snaildigenean combinations, the snail is resistant to infection and the immune components responsible have been a frequent topic of study (23), in part because of the ramifications for interrupting transmission of schistosomes to humans. Below we provide evidence to implicate FREP3 in resistance of snails to trematode infection, confirm that it is diversified among hemocytes, and that specific knockdown of FREP3 using siRNAs can increase the susceptibility of snails to digenean infection.…”