Journal articles: 'Biomphalaria; Schistosoma mansoni; Host-parasite'

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Théron, A., and C. Coustau. "Are Biomphalaria snails resistant to Schistosoma mansoni?" Journal of Helminthology 79, no. 3 (September 2005): 187–91. http://dx.doi.org/10.1079/joh2005299.

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AbstractAmong Biomphalaria glabrata/Schistosoma mansoni snail–trematode combinations, it appears that some parasites succeed whilst others fail to infect snails. Snails that become infected are termed susceptible hosts. Those which are not infected are traditionally determined as ‘resistant’. Here the concept of B. glabrata resistance to S. mansoni is re-examined in the light of additional observations. It is suggested that, in B. glabrata/S. mansoni, compatibility is tested independently for each individual miracidium and host, and that the success or failure of an infection does not depend on the snail susceptibility/resistance status, but on the ‘matched’ or ‘mismatched’ status of the host and parasite phenotypes.

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Portet, Anaïs, Eve Toulza, Ana Lokmer, Camille Huot, David Duval, Richard Galinier, and Benjamin Gourbal. "Experimental Infection of the Biomphalaria glabrata Vector Snail by Schistosoma mansoni Parasites Drives Snail Microbiota Dysbiosis." Microorganisms 9, no. 5 (May 18, 2021): 1084. http://dx.doi.org/10.3390/microorganisms9051084.

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Host-parasite interaction can result in a strong alteration of the host-associated microbiota. This dysbiosis can affect the fitness of the host; can modify pathogen interaction and the outcome of diseases. Biomphalaria glabrata is the snail intermediate host of the trematode Schistosoma mansoni, the agent of human schistosomiasis, causing hundreds of thousands of deaths every year. Here, we present the first study of the snail bacterial microbiota in response to Schistosoma infection. We examined the interplay between B. glabrata, S. mansoni and host microbiota. Snails were infected and the microbiota composition was analysed by 16S rDNA amplicon sequencing approach. We demonstrated that the microbial composition of water did not affect the microbiota composition. Then, we characterised the Biomphalaria bacterial microbiota at the individual scale in both naive and infected snails. Sympatric and allopatric strains of parasites were used for infections and re-infections to analyse the modification or dysbiosis of snail microbiota in different host-parasite co-evolutionary contexts. Concomitantly, using RNAseq, we investigated the link between bacterial microbiota dysbiosis and snail anti-microbial peptide immune response. This work paves the way for a better understanding of snail/schistosome interaction and should have critical consequences in terms of snail control strategies for fighting schistosomiasis disease in the field.

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MORGAN, J. A. T., R. J. DEJONG, S. D. SNYDER, G. M. MKOJI, and E. S. LOKER. "Schistosoma mansoni and Biomphalaria: past history and future trends." Parasitology 123, no. 7 (November 2001): 211–28. http://dx.doi.org/10.1017/s0031182001007703.

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Schistosoma mansoni is one of the most abundant infectious agents of humankind. Its widespread distribution is permitted by the broad geographic range of susceptible species of the freshwater snail genus Biomphalaria that serve as obligatory hosts for its larval stages. Molecular phylogenetic studies suggest that Schistosoma originated in Asia, and that a pulmonate-transmitted progenitor colonized Africa and gave rise to both terminal-spined and lateral-spined egg species groups, the latter containing S. mansoni. Schistosoma mansoni likely appeared only after the trans-Atlantic dispersal of Biomphalaria from the Neotropics to Africa, an event that, based on the present African fossil record, occurred only 2–5 million years ago. This parasite became abundant in tropical Africa and then entered the New World with the slave trade. It prospered in the Neotropics because a remarkably susceptible and productive host, B. glabrata, was widely distributed there. Indeed, a snail similar to B. glabrata may have given rise to the African species of Biomphalaria. Schistosoma mansoni has since spread into other Neotropical Biomphalaria species and mammalian hosts. The distribution of S. mansoni is in a state of flux. In Egypt, S. mansoni has nearly completely replaced S. haematobium in the Nile Delta, and has spread to other regions of the country. A susceptible host snail, B. straminea, has been introduced into Asia and there is evidence of S. mansoni transmission in Nepal. Dam and barrage construction has lead to an epidemic of S. mansoni in Senegal, and the parasite continues its spread in Brazil. Because of competition with introduced aquatic species and environmental changes, B. glabrata and consequently S. mansoni have become less abundant on the Caribbean islands. Control of S. mansoni using praziquantel and oxamniquine has reduced global prevalence but control is difficult to sustain, and S. mansoni can develop tolerance/resistance to praziquantel, raising concerns about its future efficacy. Because of legitimate environmental concerns, snail control is unlikely to be an option in future control efforts. Global warming will impact the distribution of Biomphalaria and S. mansoni, but the magnitude and nature of the effects are poorly understood.

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WALKER, A. J., and D. ROLLINSON. "Specific tyrosine phosphorylation induced in Schistosoma mansoni miracidia by haemolymph from schistosome susceptible, but not resistant, Biomphalaria glabrata." Parasitology 135, no. 3 (December 6, 2007): 337–45. http://dx.doi.org/10.1017/s0031182007003964.

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SUMMARYMolecular interplay during snail-schistosome interactions is poorly understood and there is much to discover concerning the effect of snail host molecules on molecular processes in schistosomes. Using the Biomphalaria glabrata – Schistosoma mansoni host-parasite system, the effects of exposure to haemolymph, derived from schistosome-resistant and susceptible snail strains, on protein tyrosine phosphorylation in miracidia have been investigated. Western blotting revealed several tyrosine phosphorylated proteins in this larval stage. Exposure of miracidia to haemolymph from susceptible snails for 60 min resulted in a striking, 5-fold, increase in the tyrosine phosphorylation of a 56 kDa (p56) S. mansoni protein. In contrast, haemolymph from resistant snails had little effect on protein tyrosine phosphorylation levels in miracidia. Confocal microscopy revealed that tyrosine phosphorylation was predominantly associated with proteins present in the tegument. Finally, treatment of miracidia with the tyrosine kinase inhibitor genistein significantly impaired their development into primary sporocysts. The results open avenues for research that focus on the potential importance of phospho-p56 to the outcome of schistosome infection in snails, and the significance of protein tyrosine kinase-mediated signalling events to the transformation of S. mansoni larvae.

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KALBE, M., B. HABERL, J. HERTEL, and W. HAAS. "Heredity of specific host-finding behaviour in Schistosoma mansoni miracidia." Parasitology 128, no. 6 (May 13, 2004): 635–43. http://dx.doi.org/10.1017/s0031182004005037.

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Two strains of Schistosoma mansoni were used to investigate the hereditary basis of species-specific host recognition by analysing behavioural responses of miracidia to snail-conditioned water. An Egyptian strain of S. mansoni, capable of distinguishing its host snail Biomphalaria alexandrina from other snails was cycled repeatedly through Biomphalaria glabrata, the intermediate host of a Brazilian strain known to respond even to non-susceptible snails with high intensity. After 5 cycles in the non-natural host, miracidia of the Egyptian strain still retained their preference for the original host snail. In a second experiment, host-finding behaviour of hybrids between these two parasite strains was studied. In the F1 generation, hybrids of both parental combinations showed the same low degree of specificity as the pure-bred Brazilian strain. Approximately one quarter of F2 hybrids proved to be as discriminatory as the Egyptian strain, confirming dominant Mendelian inheritance of non-specificity in schistosome miracidial host-finding behaviour. Moreover, hybrids seem to have lost the ability to develop in B. alexandrina, possibly suggesting a link between host recognition and host compatibility. The heredity of this behavioural trait is of evolutionary and epidemiological significance, since a shift to low host-finding specificity might have been a prerequisite for S. mansoni to acquire new host snails after being introduced to South America by the slave trade.

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LEWIS, F. A., C. N. PATTERSON, M. KNIGHT, and C. S. RICHARDS. "The relationship between Schistosoma mansoni and Biomphalaria glabrata: genetic and molecular approaches." Parasitology 123, no. 7 (November 2001): 169–79. http://dx.doi.org/10.1017/s0031182001007831.

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Biomphalaria glabrata is a major intermediate host for the helminth parasite Schistosoma mansoni. Beginning in the mid-20th century, studies were carried out with this snail species to identify the immunological and genetic components that might be involved in controlling schistosome development. A number of genetically well-defined snail stocks were derived as a direct result of these studies and have since played major roles in helping investigators to identify important cellular and humoral components in the snail/schistosome relationship. This review will explore the historical development of these stocks and describe some of the major advances in several areas of medical malacology that have been made possible by their use.

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PRUGNOLLE, F., T. DE MEEÛS, J. P. POINTIER, P. DURAND, A. ROGNON, and A. THÉRON. "Geographical variations in infectivity and susceptibility in the host-parasite system Schistosoma mansoni/Biomphalaria glabrata: no evidence for local adaptation." Parasitology 133, no. 3 (May 24, 2006): 313–19. http://dx.doi.org/10.1017/s0031182006000412.

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We investigated local adaptation in the spatially structured natural Biomphalaria glabrata/Schistosoma mansoni host-parasite system in the marshy forest focus of Guadeloupe using cross-transplantation experiments. We demonstrated strong and highly significant variations in susceptibility/infectivity of host and parasite populations, respectively, but found no evidence of local adaptation neither for S. mansoni nor for B. glabrata. Environmental as well as genetic factors are discussed to explain susceptibility/infectivity variations between both host and parasite populations. The absence of local adaptation is discussed in relation to the metapopulation dynamics of both host and parasite, in particular their relative rates of dispersal at the scale under scrutiny. Our study constitutes the first cross-transplantation experiment concerning this host-parasite system of which both hosts and parasites came directly from the wild, excluding laboratory generations and experimental host passages.

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Simões, L. F., L. D. B. Bastos, E. A. F. Camargo, M. F. Neves, A. X. Linhares, L. A. Magalhães, and E. M. Zanotti-Magalhães. "Host-parasite relationship between Biomphalaria amazonica (Paraense, 1966) and Schistosoma mansoni (Sambon, 1907)." Brazilian Journal of Biology 77, no. 2 (September 26, 2016): 340–46. http://dx.doi.org/10.1590/1519-6984.14415.

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Abstract Biomphalaria amazonica is a planorbid species considered a potential host of Schistosoma mansoni. It is widely distributed in the Neotropical zone, particularly in the North and Centre-West of Brazil and in the North of Bolivia. The aim of the present study was to determine the host-parasite relationship between B. amazonica and S. mansoni (BH and SJ strains). Specimens of B. amazonica and their snail-conditioned water were examined in terms of their ability to attract miracidia. The infectivity of the mollusks was determined by exposing them to 20 miracidia of both strains. Sporocyst development and amebocyte reactions were studied after each mollusk specimen was exposed to 100 miracidia. Although no cercariae were eliminated, specimens of B. amazonica proved capable of attracting 77% of the miracidia they were exposed to. Viable sporocysts with no amebocyte reaction were found 96 hours after the exposure to miracidia. These results indicate the susceptibility of B. amazonica to the BH and SJ strains of S. mansoni, and therefore demonstrate the importance of this planorbid species as a potential vector of the trematode in the areas where it occurs.

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Azevedo, Carine M., Claudia Cunha Borges, and Zilton A. Andrade. "Behavior of Schistosoma mansoni-induced histopathological lesions in Biomphalaria glabrata submitted to ionizing radiation." Revista da Sociedade Brasileira de Medicina Tropical 37, no. 3 (June 2004): 218–21. http://dx.doi.org/10.1590/s0037-86822004000300005.

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Present report demonstrates that repeated radiation of Schistosoma mansoni-infected Biomphalaria glabrata, totaling 15,000 rads, caused a sudden, albeit transient, suppression of cercarial shedding. Initially, sporocysts practically disappeared from the snail tissues. The more resistant developing cercariae presented nuclear clumping and vacuolation, before undergoing lysis. No host tissue reaction was evident at any time. Thirty-four days after the last irradiation, the snails resumed cercarial elimination. By that time numerous sporocysts and developing cercariae were detected, disseminated throughout snail tissues in a pattern similar to that of a highly malignant neoplasm, with no signs of host cellular reactions, which on the other hand were present in non-irradiated infected controls. The region of the ovo-testis was apparently destroyed after radiation, but returned to its normal appearance around 40 days after the last radiation. Ionizing radiation affected both host and parasite in S. mansoni-infected Biomphalaria glabrata, but the resulting impressive changes were soon reversed.

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Paraense, W. Lobato, and Lygia R. Corrêa. "Further experiments on susceptibility of Biomphalaria amazonica to Schistosoma mansoni." Memórias do Instituto Oswaldo Cruz 80, no. 3 (September 1985): 259–62. http://dx.doi.org/10.1590/s0074-02761985000300001.

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A sample of Biomphalaria amazonica from Porto Velho, Rondônia state, was exposed to miracidia of Schistosoma mansoni (SJ2 strain) from São José dos Campos, São Paulo state (five miracidia per snail). Water freshly taken from the snails' breeding place was used to make sure that its quality was compatible with hatching of miracidia and their penetration into the snails. The resulting infection rate was 3.5%, as against 45% in B. tenagophila controls. In comparison with the controls, B. amazonica, besides a lower infection rate, showed a longer prepatent period and a lower cercarial production. These characteristics seem to indicate that it is a poor host of S. mansoni, like B. straminea, but it should be considered that, this notwithstanding, the latter is admittedly a good vector of the parasite in hyperendemic areas of northeastern Brazil. These results point to the possibility of introduction of schistosomiasis mansoni into the western Amazonian region, where B. amazonica is widespread.

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JONES, C. S., A. E. LOCKYER, D. ROLLINSON, and L. R. NOBLE. "Molecular approaches in the study of Biomphalaria glabrata – Schistosoma mansoni interactions: linkage analysis and gene expression profiling." Parasitology 123, no. 7 (November 2001): 181–96. http://dx.doi.org/10.1017/s0031182001008174.

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Gene mapping and the generation of linkage groups are fundamental to an understanding of the organization and relationships of genes and marker sequences, providing a framework with which to investigate their association with traits of interest. The abundance of techniques available for generating polymorphic molecular markers, and recent advances in high throughput screening, have allowed the extension of map analysis to the tropical freshwater snail Biomphalaria glabrata, an important intermediate host for Schistosoma mansoni. Direct comparison of gene expression by differential display screening, without prior identification of candidate genes, can be combined with mapping to quantify the involvement of specific sequences in the schistosome resistance response, and other important host–parasite interactions. Here we discuss the application of current and emergent technologies to gene characterization and linkage analysis in snail–schistosome interactions. Preliminary results from the analysis of comparative gene expression in resistant and susceptible snails are also presented.

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DAVIES, C. M., E. FAIRBROTHER, and J. P. WEBSTER. "Mixed strain schistosome infections of snails and the evolution of parasite virulence." Parasitology 124, no. 1 (January 2002): 31–38. http://dx.doi.org/10.1017/s0031182001008873.

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Mathematical models often propose that within-host competition between parasites can be a major factor in the evolution of increased parasite virulence. Kin selection predicts that as the coefficient of relatedness between infecting parasites decreases, the benefits of competition to individual genotypes increases. Thus where parasites can adjust their behaviour in response to current conditions, higher virulence is predicted in multiple genotype infections. There is limited experimental data, however, regarding the effects of mixed strain infections on host and parasite fitness. We investigated, for a snail–schistosome system, whether a conditional increase in replication rates occurred in mixed genotype infections and resulted in increased virulence. Four groups of Biomphalaria glabrata snails were exposed to 1 or 2 laboratory strains of Schistosoma mansoni. Mixed genotype infections were observed to be more virulent than single genotype infections, in terms of reductions in host reproductive success and survival. Parasite reproductive rate was also increased in mixed strain groups. Reduced host reproductive success was suggested to be directly due to the genetic heterogeneity of the parasitic infections resulting in increased host defence costs. Reduced host survival was consistent with an adaptive conditional parasite response.

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SIRE, C., J. LANGAND, V. BARRAL, and A. THÉRON. "Parasite (Schistosoma mansoni) and host (Biomphalaria glabrata) genetic diversity: population structure in a fragmented landscape." Parasitology 122, no. 5 (May 2001): 545–54. http://dx.doi.org/10.1017/s0031182001007727.

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Random amplified polymorphic DNA (RAPD) markers were used to quantify genetic diversity within and between 5 populations ofSchistosoma mansoniwithin its definitive host (Rattus rattus) and the 5 corresponding populations of the snail intermediate host (Biomphalaria glabrata) from a limited endemic area of murine schistosomiasis on the island of Guadeloupe. Analysis of molecular variance (AMOVA) and canonical correspondence analysis (CCA) were used to test the significance of genetic differentiation between populations. Both methods gave similar results. Of total gene diversity, 15.1% (AMOVA) and 18.8% (CCA) was partitioned between localities forS. mansoniwith an absence of association between genetic and geographical distances. Geographical localities accounted for 20.5% (CCA) of the total diversity forB. glabratapopulations. The genetic distances between pairs of parasite populations were not correlated with the genetic distances between the corresponding pairs of snail host populations. Such strong patterns of local differentiation of both parasite and snail populations are consistent with predictions based on metapopulation dynamics and may have implications on host–parasite susceptibility relationship through local adaptation processes.

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Bayne, C. J., E. S. Loker, and Mary A. Yui. "Interactions between the plasma proteins of Biomphalaria glabrata (Gastropoda) and the sporocyst tegument of Schistosoma mansoni (Trematoda)." Parasitology 92, no. 3 (June 1986): 653–64. http://dx.doi.org/10.1017/s0031182000065513.

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SUMMARYThe tegumental surface of Schistosoma mansoni sporocysts is the site of both nutritive and immunological interactions with haemolymph cells and plasma of Biomphalaria glabrata, the schistosome intermediate host. Within minutes of being placed in host plasma, sporocysts acquire plasma antigens, and within 3 h host plasma antigens are present on the surface at near steady state. Though a wide variety of peptides is acquired, there is selection. Furthermore, some differences occur in the peptides acquired from the plasma of susceptible and resistant strains of snail. Acquired antigens are rapidly processed, and are predominantly undetectable in tegumental extracts after a few hours. In contrast, rabbit antibody on sporocysts remains in situ for at least 48 h, so under some conditions there is stable expression of certain tegumental antigenic determinants.These data, obtained using antibodies to snail plasma antigens and to sporocyst tegumental antigens, are discussed in the light of current ideas on the cellular and molecular basis of susceptibility and resistance in this host#parasite system.

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Abou-El-Naga, Iman F. "Heat shock protein 70 (Hsp70) in Schistosoma mansoni and its role in decreased adult worm sensitivity to praziquantel." Parasitology 147, no. 6 (March 4, 2020): 634–42. http://dx.doi.org/10.1017/s0031182020000347.

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AbstractSchistosoma mansoni is the most common species causing schistosomiasis. It has a complex life cycle involving a vertebrate definitive host and a snail intermediate host of the genus Biomphalaria. Each stage encounters a plethora of environmental stresses specially heat stress. Another sort of stress arises from repeated exposure of the parasite to praziquantel (PZQ), the only drug used for treatment, which leads to the development of resistance in the fields and the labs. Heat shock protein 70 (Hsp70) is found in different developmental stages of S. mansoni. It is immunogenic and regulate cercarial invasion besides its chaperone function. In the Biomphalaria/S. mansoni interaction, epigenetic modulations of the Hsp70 gene underscore the susceptibility phenotype of the snail. Hsp70 is up-regulated in adult S. mansoni with decreased sensitivity to PZQ. This could be due to the induction of oxidative and endoplasmic reticulum stress, induction of apoptosis, exposure to the stressful drug pressure and increase influx of calcium ions. Up-regulation of Hsp70 might help the worm to survive the schistosomicidal effect of the drug mainly by dealing with misfolded proteins, inhibition of apoptosis, induction of autophagy, up-regulation of the P-glycoprotein transporter and attenuation of the signalling from G protein coupled receptors.

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De Jong-Brink, M., M. Elsaadany, and M. S. Soto. "The occurrence of schistosomin, an antagonist of female gonadotropic hormones, is a general phenomenon in haemolymph of schistosome-infected freshwater snails." Parasitology 103, no. 3 (December 1991): 371–78. http://dx.doi.org/10.1017/s0031182000059886.

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In haemolymph of Lymnaea stagnalis, parasitized with the digenetic trematode parasite Trichobilharzia ocellata, a neuropeptide (schistosomin) occurs which antagonizes female gonadotropic hormones, e.g. calfluxin (CaFl). By means of an ultracytochemical hormone-assay, the CaFl assay, it was demonstrated that the occurrence of schistosomin is a general phenomenon in schistosome-infected freshwater snails. Haemolymph of the schistosomiasis-transmitting snail species Biomphalaria glabrata and B. pfeifferi, parasitized with Schistosoma mansoni, also appeared to contain an antagonizing factor, i.e. schistosomin. In contrast, in haemolymph of L. stagnalis parasitized with Diplostomum spathaceum (Diplostomatidae) no schistosomin could be found. This suggests that schistosomin may only occur in snails infected with parasites belonging to the Schistosomatidae. The effect of schistosomin is rather specific. Haemolymph of B. glabrata parasitized with S. mansoni had not the capacity to inhibit the response to CaFl in the target organs for CaFl, the albumen glands of L. stagnalis and Bulinus truncatus. The same holds true for haemolymph of infected L. stagnalis: it did not inhibit the CaFl response in glands of B. glabrata and B. truncatus and even not in those of a related species (L. ovata). Schistosomins in haemolymph of infected B. glabrata and B. pfeifferi, on the other hand, seem more related. Both appeared to inhibit the hormone response in glands of the two Biomphalaria species studied. The results indicate that schistosomin in haemolymph of schistosome-infected pulmonate snails, although functionally related, may differ structurally.

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TCHUEM TCHUENTÉ, L. A., V. R. SOUTHGATE, A. THÉRON, J. JOURDANE, A. LY, and B. GRYSEELS. "Compatibility of Schistosoma mansoni and Biomphalaria pfeifferi in Northern Senegal." Parasitology 118, no. 6 (June 1999): 595–603. http://dx.doi.org/10.1017/s0031182099004345.

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The construction of the Diama dam on the Senegal River and the ensuing ecological changes have led to a massive outbreak of Schistosoma mansoni infection in Northern Senegal, associated with very high intensity of infections, due to extremely intense transmission. The vectorial capacity of Biomphalaria pfeifferi from Ndombo, near Richard-Toll was investigated in order to assess the role of the snail–parasite relationship in this particular epidemiological situation. The results revealed an unusually high compatibility between the Senegalese S. mansoni strain and its local snail intermediate host, B. pfeifferi. The snail infection rate after exposure to a single miracidium per snail was 87%. The cercarial production of infected snails was very high, with a mean total production of 50456 cercariae per snail. No significant difference was found in the total cercarial output between snails exposed to 1 miracidium and those exposed to 5 miracidia. The increase in the rate of cercarial output was significantly greater in snails exposed to 5 miracidia, but there was a higher mortality in this group. The chronobiological cercarial production pattern showed a peak around mid-day. The implications of these findings on the epidemiology of schistosomiasis in Northern Senegal are discussed.

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Théron, André, Hélène Moné, and Claudia Gérard. "Spatial and energy compromise between host and parasite: The Biomphalaria glabrata-Schistosoma mansoni system." International Journal for Parasitology 22, no. 1 (February 1992): 91–94. http://dx.doi.org/10.1016/0020-7519(92)90084-x.

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MARTINS-SOUZA, R. L., C. A. J. PEREIRA, P. M. Z. COELHO, O. A. MARTINS-FILHO, and D. NEGRÃO-CORRÊA. "Flow cytometry analysis of the circulating haemocytes from Biomphalaria glabrata and Biomphalaria tenagophila following Schistosoma mansoni infection." Parasitology 136, no. 1 (January 2009): 67–76. http://dx.doi.org/10.1017/s0031182008005155.

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SUMMARYAiming to further characterize the haemocyte subsets in Biomphalaria snails, we have performed a detailed flow cytometric analysis of whole haemolymph cellular components using a multiparametric dual colour labelling procedure. Ethidium bromide/acridine orange fluorescence features were used to first select viable haemocytes followed by flow cytometric morphometric analysis based on the laser scatter properties (forward scatter-FSC and side scatter-SSC). Our findings demonstrated that B. glabrata (BG-BH, highly susceptible to S. mansoni) and 2 strains of B. tenagophila (BT-CF, moderately susceptible and BT-Taim, resistant to S. mansoni) have 3 major circulating haemocyte subsets, referred to as small, medium and large haemocytes. The frequency of small haemocytes was higher in BG-BH, while medium haemocytes were the most abundant cell-type in both B. tenagophila strains. Schistosoma mansoni infection resulted in early reduction of large and medium circulating haemocytes followed by an increase of small haemocytes. Although parasite infection induced haemocyte alterations in all Biomphalaria strains, the response was particularly intense in BT-Taim, the parasite-resistant snail. Interestingly, the trematode infection induces changes in haemocytes with less granular rather than in those with more granular profile. The results indicated that, in B. tenagophila of Taim strain, circulating haemocytes, especially the medium and high subset with less granular profile, are very reactive cells upon S. mansoni infection, suggesting that this cell subset would participate in the early parasite destruction observed in this snail strain.

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Minchella, D. J., K. M. Sollenberger, and C. Pereira De Souza. "Distribution of schistosome genetic diversity within molluscan intermediate hosts." Parasitology 111, no. 2 (August 1995): 217–20. http://dx.doi.org/10.1017/s0031182000064970.

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SUMMARYNaturally infected Biomphalaria glabrata snails were collected at two sites near Belo Horizonte, Brazil, and Schistosoma mansoni cercariae isolated from single snails were used to infect individual mice. Genetic comparison of single worm DNA was accomplished by hybridization of Southern blots to a polymorphic repetitive DNA element. Genetic profiles of parasite individuals revealed a diverse array of parasite genotypes in naturally infected intermediate hosts. The observed distribution of schistosome genotypes among intermediate hosts indicates that over half of the infected snails harbour multiple miracidia. Snails were more likely to carry multiple infections than expected by chance. This degree of overdispersion combined with high levels of genetic variability facilitates multi-genotype transmission and helps maintain parasite genetic diversity.

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Jones, Isabel J., Susanne H. Sokolow, Andrew J. Chamberlin, Andrea J. Lund, Nicolas Jouanard, Lydie Bandagny, Raphaël Ndione, et al. "Schistosome infection in Senegal is associated with different spatial extents of risk and ecological drivers for Schistosoma haematobium and S. mansoni." PLOS Neglected Tropical Diseases 15, no. 9 (September 27, 2021): e0009712. http://dx.doi.org/10.1371/journal.pntd.0009712.

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Schistosome parasites infect more than 200 million people annually, mostly in sub-Saharan Africa, where people may be co-infected with more than one species of the parasite. Infection risk for any single species is determined, in part, by the distribution of its obligate intermediate host snail. As the World Health Organization reprioritizes snail control to reduce the global burden of schistosomiasis, there is renewed importance in knowing when and where to target those efforts, which could vary by schistosome species. This study estimates factors associated with schistosomiasis risk in 16 villages located in the Senegal River Basin, a region hyperendemic for Schistosoma haematobium and S. mansoni. We first analyzed the spatial distributions of the two schistosomes’ intermediate host snails (Bulinus spp. and Biomphalaria pfeifferi, respectively) at village water access sites. Then, we separately evaluated the relationships between human S. haematobium and S. mansoni infections and (i) the area of remotely-sensed snail habitat across spatial extents ranging from 1 to 120 m from shorelines, and (ii) water access site size and shape characteristics. We compared the influence of snail habitat across spatial extents because, while snail sampling is traditionally done near shorelines, we hypothesized that snails further from shore also contribute to infection risk. We found that, controlling for demographic variables, human risk for S. haematobium infection was positively correlated with snail habitat when snail habitat was measured over a much greater radius from shore (45 m to 120 m) than usual. S. haematobium risk was also associated with large, open water access sites. However, S. mansoni infection risk was associated with small, sheltered water access sites, and was not positively correlated with snail habitat at any spatial sampling radius. Our findings highlight the need to consider different ecological and environmental factors driving the transmission of each schistosome species in co-endemic landscapes.

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Johnson, Pieter T. J., Peder J. Lund, Richard B. Hartson, and Timothy P. Yoshino. "Community diversity reduces Schistosoma mansoni transmission, host pathology and human infection risk." Proceedings of the Royal Society B: Biological Sciences 276, no. 1662 (January 20, 2009): 1657–63. http://dx.doi.org/10.1098/rspb.2008.1718.

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Global biodiversity loss and disease emergence are two of the most challenging issues confronting science and society. Recently, observed linkages between species-loss and vector-borne infections suggest that biodiversity may help reduce pathogenic infections in humans and wildlife, but the mechanisms underlying this relationship and its applicability to a broader range of pathogens have remained speculative. Here, we experimentally evaluated the effects of host community structure on transmission of the human pathogen, Schistosoma mansoni , which alternates between snail intermediate hosts and vertebrate definitive hosts. By manipulating parasite exposure and community diversity, we show that heterospecific communities cause a 25–50 per cent reduction in infection among snail hosts ( Biomphalaria glabrata ). Infected snails raised alongside non-host snails ( Lymnaea or Helisoma sp.) also produced 60–80 per cent fewer cercariae, suggesting that diverse communities could reduce human infection risk. Because focal host density was held constant during experiments, decreases in transmission resulted entirely from diversity-mediated pathways. Finally, the decrease in infection in mixed-species communities led to an increase in reproductive output by hosts, representing a novel example of parasite-mediated facilitation. Our results underscore the significance of community structure on transmission of complex life-cycle pathogens, and we emphasize enhanced integration between ecological and parasitological research on the diversity–disease relationship.

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JANNOTTI-PASSOS, Liana Konovaloff, and Cecilia Pereira de SOUZA. "Susceptibility of Biomphalaria tenagophila and Biomphalaria straminea to Schistosoma mansoni infection detected by low stringency polymerase chain reaction." Revista do Instituto de Medicina Tropical de São Paulo 42, no. 5 (October 2000): 291–94. http://dx.doi.org/10.1590/s0036-46652000000500010.

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In order to determine Schistosoma mansoni infection rates in Biomphalaria tenagophila and B. straminea, low stringency polymerase chain reaction (LS-PCR) technique was used as a complementary method to light exposure technique. LS-PCR has already been standardized in our laboratory to detect the trematode DNA in B. glabrata. Higher S. mansoni infection rates were detected using conventional method and LS-PCR. The parasite DNA profile was detected in both species after 7-day exposure to miracidia, using LS-PCR. This technique enables early detection of schistosomiasis transmission focuses, in endemic areas, before the beginning of cercariae shedding.

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Theron, A., A. Rognon, B. Gourbal, and G. Mitta. "Multi-parasite host susceptibility and multi-host parasite infectivity: A new approach of the Biomphalaria glabrata/Schistosoma mansoni compatibility polymorphism." Infection, Genetics and Evolution 26 (August 2014): 80–88. http://dx.doi.org/10.1016/j.meegid.2014.04.025.

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Paraense, W. Lobato, and Lygia R. Corrêa. "A potential vector of Schistosoma mansoni in Uruguay." Memórias do Instituto Oswaldo Cruz 84, no. 3 (September 1989): 281–88. http://dx.doi.org/10.1590/s0074-02761989000300001.

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Susceptibily experiments were carried out with a Biomphalaria straminea-like planorbid snail (Biomphalaria aff. straminea, species inquirenda) from Espinillar, near Salto (Uruguay), in the area of the Salto Grande reservoir, exposed individually to 5 miracidia of Schistosoma mansoni (SJ2 and BH2 strains). Of 130 snails exposed to the SJ2 strain, originally infective to Biomphalaria tenagophila, 30 became infected (23%). The prepatent (precercaria) period ranged from 35 to 65 days. The cercarial output was irregular, following no definite pattern, varying from 138 to 76,075 per snail (daily average 4.3 to 447.5 and ending up with death. Three specimens that died, without having shed cercarie, on days 69 (2) and 80 after exposure to miracidia, had developing secondary sporocysts in their tissues, justifying the prospect of a longer precercarial period in these cases. In a control group of 120 B. teangophila, exposed to the SJ2 strain, 40 became infected, showing an infection rate (33.3%) not significantly different from that of the Espinillar snail (X [raised to the power of] 2 = 3.26). No cercarie were produced by any of the Espinilar snails exposed to miracidia of the BH2 strain, originally infective to Biomphalaria glabrata. Four specimens showed each a primary sporocyst in one tentacle, which disappeared between 15 and 25 days post-exposure, and two others died with immature, very slender sporocysts in their tissues on days 36 and 54. In a control group of 100 B. glabrata exposed to BH2 miracidia, 94 shed cercariae (94%) and 6 remained negative. Calculation of Frandsen's (1979a, b) TCP/100 index shows that "Espinillar Biomphalaria-SJ2 S. mansoni" is a vector-parasite "compatible" combination. Seeing that tenagophila-borne schistosomiasis is prevalent in Rio de Janeiro and São Paulo states and has recently spread sothwards to Santa Catarina state, and the range of B. tenagophila overlaps taht of the Espinillar Biomphalaria, the possibility of schistosomiais establishing itself in Uruguay, although not imminent, is not to be disregarded.

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Gérard, Claudia. "Energy constraint exerted by the parasite Schistosoma mansoni on the locomotion of its snail host, Biomphalaria glabrata." Canadian Journal of Zoology 74, no. 4 (April 1, 1996): 594–98. http://dx.doi.org/10.1139/z96-068.

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The consequences of the constraint caused by the parasite Schistosoma mansoni on the locomotory activity of its snail host, Biomphalaria glabrata, were studied during the patent period. Rates of locomotion were determined 6 times per 24-h period for juvenile and adult snails with single-miracidium infections, then compared with those of healthy snails of the same age. The locomotory activity of infected snails was the same during the day and at night, whereas control snails moved less at night than during the day. The locomotion of snails infected when immature was similar to that of the controls during the day and superior at night. The locomotion of snails infected when mature decreased regularly during patency and clearly decreased in comparison with that of healthy snails. The results are interpreted in terms of energy constraint on the mode of resource allocation of the host due to the parasite.

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Sandland, Gregory J., Alice V. Foster, Monika Zavodna, and Dennis J. Minchella. "Interplay between host genetic variation and parasite transmission in the Biomphalaria glabrata–Schistosoma mansoni system." Parasitology Research 101, no. 4 (June 13, 2007): 1083–89. http://dx.doi.org/10.1007/s00436-007-0593-9.

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Ibikounlé, M., G. Mouahid, R. Mintsa Nguéma, N. G. Sakiti, D. Kindé-Gasard, A. Massougbodji, and H. Moné. "Life-history traits indicate local adaptation of the schistosome parasite, Schistosoma mansoni, to its snail host, Biomphalaria pfeifferi." Experimental Parasitology 132, no. 4 (December 2012): 501–7. http://dx.doi.org/10.1016/j.exppara.2012.09.020.

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WEBSTER, J. P. "Compatibility and sex in a snail–schistosome system." Parasitology 122, no. 4 (April 2001): 423–32. http://dx.doi.org/10.1017/s0031182001007442.

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Knowledge of the genetics underlying resistance to parasitic infection has important repercussions for our understanding of infection dynamics and the mechanisms of host–parasite co-evolution. The aim here was to determine for a Biomphalaria glabrata–Schistosoma mansoni system whether (1) resistance is dominant over susceptibility, (2) it is possible to crossbreed snails to be simultaneously resistant and/or susceptible to more than one parasite strain and (3) compatibility genotype affects reproductive strategy. Using replicate snail strains artificially selected for either resistance or susceptibility to single replicate parasite strains, individual snails from each line were paired with a selected partner of matched or non-matched compatibility status and cross-breeding was identified by RAPD–PCR. The resulting compatibility phenotype of all offspring was determined. Support for all 3 hypotheses were obtained. The results are discussed in terms of their applied and theoretical implications.

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Camargo, E. A. F., J. T. F. Camargo, M. F. Neves, L. F. Simões, L. A. D. Bastos, L. A. Magalhães, and E. M. Zanotti-Magalhães. "Assessment of the impact of changes in temperature in Biomphalaria glabrata (Say, 1818) melanic and albino variants infected with Schistosoma mansoni (Sambon, 1907)." Brazilian Journal of Biology 77, no. 3 (September 26, 2016): 490–94. http://dx.doi.org/10.1590/1519-6984.16715.

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Abstract Fluctuations in population density of planorbid hosts of S. mansoni are influenced by climatic factors. The knowledge about interference from changes in water temperature in these populations is an important aspect of the epidemiology of schistosomiasis. In this experiment, it is explored the influence of different temperatures on the development of Schistosoma mansoni in Biomphalaria glabrata melanic and albino variants. The results indicated an intrinsic relationship between temperature and development of the parasite in the intramollusc phase, independent of the pigmentation of the mantle of the molluscs. The higher the temperature, the shorter the period necessary for the development of the parasite was while the higher the mortality of infected mollusks. It is concluded that, in the presence of climate change, the increasement of temperature in cold and flooded regions may encourage the establishment of new foci of transmission of schistosomiasis by changing the geographic extent and extending the epidemiological transmission potential. In warm climates, higher temperatures, however, could compromise the transmission of the disease because of biological stress suffered by parasite and host. Under these conditions, it can result in the death of the parasite or a change in their ability to infect new host species of molluscs in new areas. Mantle pigmentation patterns in molluscs have not shown significant interference in the development of the parasite.

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THERON, A., C. SIRE, A. ROGNON, F. PRUGNOLLE, and P. DURAND. "Molecular ecology of Schistosoma mansoni transmission inferred from the genetic composition of larval and adult infrapopulations within intermediate and definitive hosts." Parasitology 129, no. 5 (October 5, 2004): 571–85. http://dx.doi.org/10.1017/s0031182004005943.

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We investigated the genotypic composition of the digenetic parasite Schistosoma mansoni for its adult stages within the definitive host (the wild rat, Rattus rattus) and for the larval stages within the intermediate host (the snail, Biomphalaria glabrata) both collected at the same transmission site. Our analyses are based upon the recognition and distribution of 200 different multilocus genotypes generated by RAPD markers. While intramolluscan larval infrapopulations are characterized by a low infection rate (0·6% on average) and low intra-host genetic diversity (1·1 genotype on average per infected snail), adult infrapopulations within rats showed a high infection rate (94%) and a substantial intra-host genetic diversity (34 genotypes on average) linked to high intensities (160 worms per host on average). A single definitive host bearing 105 different genotypes harboured 52% of the total genetic diversity detected within the whole parasite population. Analysis of the genetic data allowed the identification of various ecological, behavioural and immunological factors which are likely to enhance transmission of multiple parasite genotypes towards the vertebrate hosts. From the distribution of repeated identical multilocus genotypes within the parasite population and among the hosts, we have inferred different parameters of the cercarial transmission efficiency as well as patterns and processes by which vertebrate hosts acquire infection in the field.

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Malishev, Matthew, and David J. Civitello. "Linking Bioenergetics and Parasite Transmission Models Suggests Mismatch Between Snail Host Density and Production of Human Schistosomes." Integrative and Comparative Biology 59, no. 5 (May 23, 2019): 1243–52. http://dx.doi.org/10.1093/icb/icz058.

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Abstract The consequences of parasite infection for individual hosts depend on key features of host–parasite ecology underpinning parasite growth and immune defense, such as age, sex, resource supply, and environmental stressors. Scaling these features and their underlying mechanisms from the individual host is challenging but necessary, as they shape parasite transmission at the population level. Translating individual-level mechanisms across scales could inherently improve the way we think about feedbacks among parasitism, the mechanisms driving transmission, and the consequences of human impact and disease control efforts. Here, we use individual-based models (IBMs) based on general metabolic theory, Dynamic Energy Budget (DEB) theory, to scale explicit life-history features of individual hosts, such as growth, reproduction, parasite production, and death, to parasite transmission at the population level over a range of resource supplies focusing on the major human parasite, Schistosoma mansoni, and its intermediate host snail, Biomphalaria glabrata. At the individual level, infected hosts produce fewer parasites at lower resources as competition increases. At the population level, our DEB–IBM predicts brief, but intense parasite peaks early during the host growth season when resources are abundant and infected hosts are few. The timing of these peaks challenges the status quo that high densities of infected hosts produce the highest parasite densities. As expected, high resource supply boosts parasite output, but parasite output also peaks at modest to high host background mortality rates, which parallels overcompensation in stage-structured models. Our combined results reveal the crucial role of individual-level physiology in identifying how environmental conditions, time of the year, and key feedbacks within host–parasite ecology interact to define periods of elevated risk. The testable forecasts from this physiologically-explicit epidemiological model can inform disease management to reduce human risk of schistosome infection.

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Allan, Euan R. O., Stephanie Bollmann, Ekaterina Peremyslova, and Michael Blouin. "Neither heat pulse, nor multigenerational exposure to a modest increase in water temperature, alters the susceptibility of Guadeloupean Biomphalaria glabrata to Schistosoma mansoni infection." PeerJ 8 (April 23, 2020): e9059. http://dx.doi.org/10.7717/peerj.9059.

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There are increasing concerns regarding the role global climate change will have on many vector-borne diseases. Both mathematical models and laboratory experiments suggest that schistosomiasis risk may change as a result of the effects of increasing temperatures on the planorbid snails that host schistosomes. Heat pulse/heat shock of the BS90 strain of Biomphalaria glabrata was shown to increase the rate of infection by Schistosoma mansoni, but the result was not replicable in a follow up experiment by a different lab. We characterised the susceptibility and cercarial shedding of Guadeloupean B. glabrata after infection with S. mansoni under two temperature regimes: multigenerational exposure to small increases in temperature, and extreme heat pulse events. Neither long-term, multigenerational rearing at elevated temperatures, nor transient heat pulse modified the susceptibility of Guadeloupean B. glabrata to infection (prevalence) or shedding of schistosome cercaria (intensity of infection). These findings suggest that heat pulse-induced susceptibility in snail hosts may be dependent on the strain of the snail and/or schistosome, or on some as-yet unidentified environmental co-factor.

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Elias, Marian, Rasha S. Hanafi, Samia El-Bardicy, Ebtisam A. Hafez, and Rashika El Ridi. "Resistance of Biomphalaria alexandrina to Schistosoma mansoni and Bulinus truncatus to Schistosoma haematobium Correlates with Unsaturated Fatty Acid Levels in the Snail Soft Tissue." Journal of Parasitology Research 2020 (November 1, 2020): 1–14. http://dx.doi.org/10.1155/2020/8852243.

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Only a fraction of the Biomphalaria and Bulinus snail community shows patent infection with schistosomes despite continuous exposure to the parasite, indicating that a substantial proportion of snails may resist infection. Accordingly, exterminating the schistosome intermediate snail hosts in transmission foci in habitats that may extend to kilometres is cost-prohibitive and damaging to the ecological equilibrium and quality of water and may be superfluous. It may be more cost effective with risk less ecological damage to focus on discovering the parameters governing snail susceptibility and resistance to schistosome infection. Therefore, laboratory bred Biomphalaria alexandrina and Bulinus truncatus snails were exposed to miracidia of laboratory-maintained Schistosoma mansoni and S. haematobium, respectively. Snails were examined for presence or lack of infection association with soft tissue and hemolymph content of proteins, cholesterol, and triglycerides, evaluated using standard biochemical techniques and palmitic, oleic, linoleic, and arachidonic acid, assayed by ultraperformance liquid chromatography-tandem mass spectrometry. Successful schistosome infection of B. alexandrina and B. truncatus consistently and reproducibly correlated with snails showing highly significant (up to P < 0.0001 ) decrease in soft tissue and hemolymph content of the monounsaturated fatty acid, oleic acid, and the polyunsaturated fatty acids, linoleic, and arachidonic acids as compared to naïve snails. Snails that resisted twice infection had soft tissue content of oleic, linoleic, and arachidonic acid similar to naïve counterparts. High levels of soft tissue and hemolymph oleic, linoleic, and arachidonic acid content appear to interfere with schistosome development in snails. Diet manipulation directed to eliciting excessive increase of polyunsaturated fatty acids in snails may protect them from infection and interrupt disease transmission in a simple and effective manner.

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SIRE, C., A. ROGNON, and A. THERON. "Failure of Schistosoma mansoni to reinfect Biomphalariaglabrata snails: acquired humoral resistance or intra-specific larval antagonism?" Parasitology 117, no. 2 (August 1998): 117–22. http://dx.doi.org/10.1017/s0031182098002923.

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Failure of snail reinfection by Schistosoma mansoni has been demonstrated in susceptible Biomphalaria glabrata infected with 1 miracidium and subsequently re-exposed to 1 or 5 homologous parasite larvae. The acquisition of ‘resistance’ to secondary parasite infection was time dependent since complete inhibition was observed at 2 weeks and longer following monomiracidial exposure. This phenomenon was still observed in snails challenged 8 weeks after primary infection. Histological observations revealed that sporocysts from the challenge infection were free of encapsulation, their development was stopped and they degenerated slowly in the absence of haemocytic reaction of the host. Under the hypothesis of an acquired homologous resistance mechanism, this strongly suggests that 1 or several unidentified humoral factors are responsible for the non-development of the sporocysts from the challenge infection. However, considering the time-dependent nature of the phenomenon, an intraspecific larval antagonism process between sporocysts resulting from the primary infection and those from the challenge infection may be involved.

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PAN, S. Chia-Tung. "Review: SCHISTOSOMA MANSONI: THE ULTRASTRUCTURE OF LARVAL MORPHOGENESIS IN BIOMPHALARIA GLABRATA AND OF ASSOCIATED HOST-PARASITE INTERACTIONS." Japanese Journal of Medical Science and Biology 49, no. 4 (1996): 129–49. http://dx.doi.org/10.7883/yoken1952.49.129.

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VERMEIRE, J. J., and T. P. YOSHINO. "Antioxidant gene expression and function in in vitro-developing Schistosoma mansoni mother sporocysts: possible role in self-protection." Parasitology 134, no. 10 (April 20, 2007): 1369–78. http://dx.doi.org/10.1017/s0031182007002697.

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SUMMARYThe ability of the larval forms of Schistosoma mansoni to invade and parasitize their molluscan host, Biomphalaria glabrata, is determined by a multitude of factors. In this study we sought to elucidate the possible mechanisms by which the invading larvae are able to counteract the potentially harmful oxidative environment presented by the host upon initial miracidial infection. This was attempted by examining the gene expression profile of parasite antioxidant enzymes of the linked glutathione-(GSH) thioredoxin (Trx) redox pathway during early intramolluscan larval development. Three such enzymes, the peroxiredoxins (Prx1, Prx2 and Prx3) were examined as to their activity and sites of expression within S. mansoni miracidia and in vitro-cultured mother sporocysts. Results of these studies demonstrated that the H2O2-reducing enzymes Prx1 and 2 are upregulated during early mother sporocyst development compared to miracidia. Immunolocalization studies further indicated that Prx1 and Prx2 proteins are expressed within the apical papillae of miracidia and tegumental syncytium of sporocysts, and are released with parasite excretory-secretory proteins (ESP) during in vitro larval transformation. Removal of Prx1 and Prx2 from larval ESP by immunoabsorption significantly reduced the ability of ESP to breakdown exogenous H2O2, thereby directly linking ESP Prx proteins with H2O2-scavenging activity. Moreover, exposure of live sporocysts to exogenous H2O2 stimulated an upregulation of Prx1 and 2 gene expression suggesting the involvement of H2O2–responsive elements in regulating larval Prx gene expression. These data provide evidence that Prx1 and Prx2 may function in the protection of S. mansoni sporocysts during the early stages of infection.

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Gregory, T. Ryan. "Genome size estimates for two important freshwater molluscs, the zebra mussel (Dreissena polymorpha) and the schistosomiasis vector snail (Biomphalaria glabrata)." Genome 46, no. 5 (October 1, 2003): 841–44. http://dx.doi.org/10.1139/g03-069.

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The haploid genome sizes of two important molluscs were assessed by Feulgen image analysis densitometry. The genome size of the zebra mussel (Dreissena polymorpha), a prolific invader of North American lakes, was estimated to be 1C = 1.70 ± 0.03 pg, and that of the freshwater snail Biomphalaria glabrata, the predominant intermediate vector of the human parasite Schistosoma mansoni, was estimated at 0.95 ± 0.01 pg. These estimates will be important in future efforts in molluscan genomics, which at present lags far behind work being carried out with vertebrate and arthropod models. B. glabrata in particular, which has one of the smallest known gastropod genomes, is recommended as a highly suitable target for future genome sequencing.Key words: densitometry, DNA content, DNA sequencing, Feulgen, image analysis, Great Lakes, invading species, molluscs, Schistosoma mansoni.

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Rapado, Ludmila Nakamura, Priscila Orechio de Moraes Lopes, Lydia Fumiko Yamaguchi, and Eliana Nakano. "OVICIDAL EFFECT OF PIPERACEAE SPECIES ON Biomphalaria glabrata, Schistosoma mansoni HOST." Revista do Instituto de Medicina Tropical de São Paulo 55, no. 6 (December 2013): 421–24. http://dx.doi.org/10.1590/s0036-46652013000600009.

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SUMMARY Schistosomiasis is a neglected disease with public health importance in tropical and subtropical regions. An alternative to the disease control is the use of molluscicides to eliminate or reduce the intermediate host snail population causing a reduction of transmission in endemic regions. In this study nine extracts from eight Piperaceae species were evaluated against Biomphalaria glabrata embryos at blastula stage. The extracts were evaluated in concentrations ranging from 100 to 10 mg/L. Piper crassinervium and Piper tuberculatum extracts were the most active (100% of mortality at 20 mg/L and 30 mg/L respectively).

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Knight, Matty, Eba Ongele, and Fred A. Lewis. "Molecular studies of Biomphalaria glabrata, an intermediate host of Schistosoma mansoni." International Journal for Parasitology 30, no. 4 (April 2000): 535–41. http://dx.doi.org/10.1016/s0020-7519(99)00182-4.

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IBRAHIM, AMINA, OLFAT HAMMAM, and SHADIA EL-DAFRAWY. "INFECTED FRESHWATER SNAILS, BIOMPHALARIA ALEXANDRINA, THE INTERMEDIATE HOST OF SCHISTOSOMA MANSONI." Journal of the Egyptian Society of Parasitology 48, no. 3 (December 1, 2018): 503–7. http://dx.doi.org/10.21608/jesp.2018.76544.

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OHLWEILER, Fernanda Pires, and Toshie KAWANO. "Biomphalaria tenagophila (Orbigny, 1835) (Mollusca): adaptation to desiccation and susceptibility to infection with Schistosoma mansoni Sambon, 1907." Revista do Instituto de Medicina Tropical de São Paulo 44, no. 4 (July 2002): 191–201. http://dx.doi.org/10.1590/s0036-46652002000400003.

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Experiments were carried out to test the susceptibility of Biomphalaria tenagophila to the infection with strain SJ of Schistosoma mansoni in the F1, F2 and non-selected parental generation. The potential adaptation of B. tenagophila to desiccation, in healthy mollusks and those exposed to the larvae of S. mansoni of the F1, F2 and non-selected parental generations was also studied. The presence of mucus and soil, at the shell opening, protected the snails against desiccation, favoring survival. The healthy mollusks performed more attempts against desiccation than those exposed to the larvae of the parasite. The mortality rate, during desiccation, was higher among mollusks that remained buried and with the shell opening unobstructed. During the desiccation period the stage of development of the parasite was influenced by the weight loss and the survival of the snails. The longer the period of desiccation, the greater was the weight loss observed, abbreviating survival. The non-selected parental generation was more sensitive to desiccation than the F1 and F2 generations, both in healthy mollusks and in those exposed to S. mansoni larvae. Healthy mollusks were more resistant to desiccation than those exposed to the larvae of the S. mansoni. Desiccation did not interrupt the development of S. mansoni larvae in mollusks, causing a delay in the cercariae elimination. The susceptibility of B. tenagophila to the SJ strain of S. mansoni, in mollusks maintained in water during the larvae incubation period, was similar in all three generations.

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Nguyen, Karena H., Philipp H. Boersch-Supan, Rachel B. Hartman, Sandra Y. Mendiola, Valerie J. Harwood, David J. Civitello, and Jason R. Rohr. "Interventions can shift the thermal optimum for parasitic disease transmission." Proceedings of the National Academy of Sciences 118, no. 11 (March 8, 2021): e2017537118. http://dx.doi.org/10.1073/pnas.2017537118.

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Temperature constrains the transmission of many pathogens. Interventions that target temperature-sensitive life stages, such as vector control measures that kill intermediate hosts, could shift the thermal optimum of transmission, thereby altering seasonal disease dynamics and rendering interventions less effective at certain times of the year and with global climate change. To test these hypotheses, we integrated an epidemiological model of schistosomiasis with empirically determined temperature-dependent traits of the human parasite Schistosoma mansoni and its intermediate snail host (Biomphalaria spp.). We show that transmission risk peaks at 21.7 °C (Topt), and simulated interventions targeting snails and free-living parasite larvae increased Topt by up to 1.3 °C because intervention-related mortality overrode thermal constraints on transmission. This Topt shift suggests that snail control is more effective at lower temperatures, and global climate change will increase schistosomiasis risk in regions that move closer to Topt. Considering regional transmission phenologies and timing of interventions when local conditions approach Topt will maximize human health outcomes.

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PEREIRA, Adriany Duarte, Pedro Luiz Silva PINTO, Juliana de Souza Almeida Aranha CAMARGO, Juliana Bianca Rocha de SOUZA, Carlos Antônio AMANTE, Viviane Krominski Graça de SOUZA, Luiz Ricardo Lopes de SIMONE, and Luís Marcelo Aranha CAMARGO. "Potential for shistosomiasis in a municipality of Rondônia, Brazilian Amazon." Acta Amazonica 46, no. 4 (December 2016): 377–82. http://dx.doi.org/10.1590/1809-4392201600483.

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ABSTRACT Schistossomiasis is a parasitic disease, caused by helminths of the genus Schistosoma and transmitted in Brazil by snails of the genus Biomphalaria. The municipality of Ouro Preto do Oeste, Rondônia, in the Brazilian Amazon Region, has unusually registered more than 900 cases of schistosomiasis in the last 10 years. The aim of this study was to investigate de potential of transmission of schsitosomiasis in Ouro Preto do Oeste. A total of 1,196 people in a risk area for the disease transmission were requested to answer a clinical-epidemiological survey and to collect feces samples for examination. All the samples that underwent examination resulted negative for S. mansoni. Two hundred and sixty-eight snails were collected in the locality of Ouro Preto do Oeste in 32 different locations. Among these, 44% were classified as belonging to the genus Biomphalaria. Another sample of snails (146 specimens), collected at the same sites, were submitted to an in vitro challenge with Schistosoma mansoni, and none of them were able to transmit the parasite. Finally, we discuss the epidemiological importance of these findings and the lack of attention to a patient with the disease in a non-endemic area. We failed to detected any association between shistossomiasis and the snails from the genus Biomphalaria, that exists in the local, as the planorbids were unable to transmit Shistosoma mansoni. Perhaps the small sample and/or the stool examination technique can have contributed to the results. Further studies, in other localities of Rondônia and with a greater sample could put some light in this question.

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Roger, Emmanuel, Christoph Grunau, Raymond J. Pierce, Hirohisa Hirai, Benjamin Gourbal, Richard Galinier, Rémi Emans, Italo M. Cesari, Céline Cosseau, and Guillaume Mitta. "Controlled Chaos of Polymorphic Mucins in a Metazoan Parasite (Schistosoma mansoni) Interacting with Its Invertebrate Host (Biomphalaria glabrata)." PLoS Neglected Tropical Diseases 2, no. 11 (November 11, 2008): e330. http://dx.doi.org/10.1371/journal.pntd.0000330.

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Gérard, Claudia, Hélène Moné, and André Théron. "Schistosoma mansoni – Biomphalaria glabrata: dynamics of the sporocyst population in relation to the miracidial dose and the host size." Canadian Journal of Zoology 71, no. 9 (September 1, 1993): 1880–85. http://dx.doi.org/10.1139/z93-268.

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The rate of invasion of snails and percentage of the digestive gland occupied by daughter sporocysts decrease when the snails are larger and the miracidial dose is smaller. Growth of the sporocyst population is influenced not only by the miracidial dose, but also by the changes in the growth rate of the host. The larger the host and (or) the smaller the miracidial dose, the more significant is the volume occupied by the sporocyst population. Biomass- and (or) density-dependent regulatory mechanisms of different patterns intervene to limit the volume of parasites. Rapid colonisation and intensive exploitation of the host correspond to an immature plurimiracidial system, whereas progressive colonisation and less exploitation correspond to a mature monomiracidial system. The results are discussed in terms of possible demographic strategies that can be used to optimize parasite fitness in various environments.

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Mone, Helene, Andre Theron, and Claude Combes. "Interaction between the Biomphalaria glabrata-Schistosoma mansoni Host-Parasite System and the Non-Target Molluscs: Influence on Cercarial Production." Journal of Parasitology 72, no. 3 (June 1986): 410. http://dx.doi.org/10.2307/3281681.

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Galinier, Richard, Guillaume Tetreau, Anaïs Portet, Silvain Pinaud, David Duval, and Benjamin Gourbal. "First characterization of viruses from freshwater snails of the genus Biomphalaria , the intermediate host of the parasite Schistosoma mansoni." Acta Tropica 167 (March 2017): 196–203. http://dx.doi.org/10.1016/j.actatropica.2016.12.021.

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Thornhill, Joyce A., Janet T. Jones, and J. R. Kusel. "Increased oviposition and growth in immature Biomphalaria glabrata after exposure to Schistosoma mansoni." Parasitology 93, no. 3 (December 1986): 443–50. http://dx.doi.org/10.1017/s0031182000081166.

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Abstract:

SUMMARYBiomphalaria glabrata snails are known to be castrated by infection with the trematode parasite Schistosoma mansoni 4–6 weeks post-infection. The pattern of oviposition in the first 35 days post-exposure (p.e.) was investigated, in snails aged 14 weeks and measuring 7–10 mm diameter which had not commenced egg-laying, by counting the numbers of eggs laid in 7-day intervals. A group of exposed snails was compared with a control non-exposed group. The exposed group included both parasitized and non-parasitized snails, and showed a significant increase in the median number of eggs laid during the periods 14–21 and 22–28 days p.e. Throughout the entire 35-day period exposed non-parasitized snails laid significantly more eggs than control snails, while parasitized snails laid significantly more eggs than controls during days 22–28 p.e. and significantly fewer during days 29–35 p.e. Parasitized snails also laid significantly more eggs/egg mass in the period 16–28 days p.e. than did control snails. Growth of the snails was measured. By day 28 p.e. the mean diameter of the exposed group was significantly greater than that of the control group. The increase in oviposition by snails soon after exposure is discussed in terms of a compensatory response for expected future suppression of egg-laying. The fact that parasitized and non-parasitized snails both show increased oviposition indicates that normal development of the parasite is not necessary to trigger the response.

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50

CARVALHO, O. S., R. L. CALDEIRA, A. J. G. SIMPSON, and T. H. D. A. VIDIGAL. "Genetic variability and molecular identification of Brazilian Biomphalaria species (Mollusca: Planorbidae)." Parasitology 123, no. 7 (November 2001): 197–209. http://dx.doi.org/10.1017/s0031182001008058.

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Abstract:

Freshwater snails belonging to the genus Biomphalaria are intermediate hosts of the trematode Schistosoma mansoni in the Neotropical region and Africa. In Brazil, one subspecies and ten species of Biomphalaria have been identified: B. glabrata, B. tenagophila, B. straminea, B. occidentalis, B. peregrina, B. kuhniana, B. schrammi, B. amazonica, B. oligoza, B. intermedia and B.t. guaibensis. However, only the first three species are found naturally infected with S. mansoni. The classical identification of these planorbids is based on comparison of morphological characteristics of the shell and male and female reproductive organs, which is greatly complicated by the extensive intra-specific variation. Several molecular techniques have been used in studies on the identification, genetic structure as well as phylogenetic relationships between these groups of organisms. Using the randomly amplified polymorphic DNAs (RAPD) analysis we demonstrated that B. glabrata exhibits a remarkable degree of intra-specific polymorphism. Thus, the genetics of the snail host may be more important to the epidemiology of schistosomiasis than those of the parasite itself. Using the simple sequence repeat anchored polymerase chain reaction (SSR-PCR) in intra-populational and intra-specific studies we have demonstrated that snails belonging to the B. straminea complex (B. straminea, B. kuhniana and B. intermedia) clearly presented higher heterogeneity. Using the low stringency polymerase chain reaction (LS-PCR) technique we were able to separate B. glabrata from B. tenagophila and B. tenagophila from B. occidentalis. To separate all Brazilian Biomphalaria species we used the restriction fragment length polymorphism (PCR-RFLP) of the internal transcribed spacer region (ITS) of the DNA gene. The method also proved to be efficient for the specific identification of DNA extracted from snail eggs. Recently we have sequenced the ITS2 region for phylogenetic studies of all Biomphalaria snails from Brazil.

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Journal articles on the topic 'Biomphalaria; Schistosoma mansoni; Host-parasite'

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