Schistosoma mansoni is one of the three main Schistosoma trematode flatworms that infect humans and cause schistosomiasis (=bilharziasis), the other two being S. haematobium and S. japonicum (in some regions, S. mekongi and S. intercalatum also infect humans and cause schistosomiasis). Other schistosome species, which parasitize birds and non-human mammals, can cause cercarial dermatitis in humans.
The life cycle of S. mansoni and related schistosomes is complex. Eggs are eliminated from a human host with feces or urine. Under optimal conditions, the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The life stages within the snail include two generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host, and shed their forked tail, becoming schistosomulae (human contact with water is thus necessary for infection by schistosomes). The schistosomulae migrate through several tissues and stages to their residence in the veins. Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species. For example, S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine and S. mansoni occurs more often in the superior mesenteric veins draining the large intestine. However, both species can occupy either location, and they are capable of moving between sites, so it cannot be stated unequivocally that either is found only in one location or another. Schistosoma haematobium most often occurs in the venous plexus of bladder, but can also be found in the rectal venules. The females (7 to 20 mm in length, slightly larger than males) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S. mansoni and S. japonicum) and of the bladder and ureters (S. haematobium), and are eliminated with feces or urine, respectively.
Pathology of S. mansoni schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas, Symmers' pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord.
Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East.
- Urinary schistosomiasis - parasites progressively damaging the bladder, ureters and kidneys.
- Intestinal schistosomiasis - parasites progressively enlarging the liver and spleen, damaging the intestine and causing hypertension of the abdominal blood vessels.
Schistosoma mansoni is a parasite that is found in Africa, Madagascar, parts of South America (such as Venezuela and Brazil), Puerto Rico and the West Indies.
Biogeographic Regions: ethiopian (Native ); neotropical (Native )
Distribution and ecology
Schistosoma mansoni is a parasitic organism. Different stages of the life cycle live in different hosts
- Adults live in human blood vessels
- Miracidium live for a short time in fresh water before infecting snails
- Cercariae develop in the snail and are released in to freshwater before infecting humans.
During its lifetime, this parasite lives in the bodies of two different hosts. The first, the intermediate host, is usually a freshwater snail from the family Planorbidae. The ciliated larvae mature into sporocysts in these snails, making the snail a producer of cercariae for the remainder of its life. Adults mature and reproduce in the mesenteric portal system of a wide variety of hosts such as man, mice and hamsters. They thrive in tropical and equatorial environments because there are more people and a wide range of molluscs to act as hosts, as well as many rivers to transfer and carry the miracidia and cercariae.
Aquatic Biomes: lakes and ponds; rivers and streams
Shistosomula (the tail-less larvae of the worm) mature and reproduce in the hepatic portal system of their definitive (final) host. The blood in this system is rich in soluble food materials such as amino acids and monosaccharides. The shistosome worms ingest blood from the hepatic and mesenteric veins. Females feed more actively than males because the nutritional requirements of egg production are much greater than the nutritional requirements needed for sperm production.
Diseases and Parasites
- Eggs that do not pass through the wall of the intestine are circulated in the blood. Initially the eggs may produce a fever (Katayama fever), but symptoms may be hard to recognise.
- Eggs trapped in the liver cause an immune response that damages the liver over time and cause further severe complications.
- Eggs lodged in the intestine wall can cause a reaction leading to intestine blockage and blood loss.
Life History and Behavior
Mature adult Schistosoma mansoni are about 1 cm long. The male and female form a reproductive pair, with the female held by the male within a groove. Females release eggs, into the blood vessels. A pair may live for years within the host, the female producing thousands of eggs during this time.
- passed out through the wall of the host's intestine.
- circulating in the blood cause much of the pathology associated with schistosomiasis, as they become trapped in the liver and other internal organs.
- swim about in the water, propelled by the many cilia that cover them.
- never feed
- live for about a day
The spororcyst produces cercariae through asexual reproduction, so that one miracidium can produce many thousands of genetically identical cercariae. Somewhere around 3-4 weeks after being infected, the snail begins to shed cercariae into the water. Like miracidia, cercariae
- do not feed
- live for about a day
- propel themselves with an actively
beating tail, swimming tail-first through the water.
Schistosoma mansoni are a unusual among flatworms because they are dioecious (separate sexes). The male is much larger and broader than the female and the female fits into a groove in his body. Copulation takes place in the veins of the liver and mesentery, and they copulate quite frequently. The female lays eggs in the small veins without leaving her mate. The eggs are unique and easily identifiable because of the singular spine that they possess on the lateral side of the egg. The female can lay about 300 eggs per day. There is also a sporocyst stage in the larval stage of the life cycle of S. mansoni, which allows it to produce a very large quantity of offspring from a single zygote.
Molecular Biology and Genetics
Barcode data: Schistosoma mansoni
There are 51 barcode sequences available from BOLD and GenBank. Below is a sequence of the barcode region Cytochrome oxidase subunit 1 (COI or COX1) from a member of the species. See the BOLD taxonomy browser for more complete information about this specimen and other sequences.
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Download FASTA File
Statistics of barcoding coverage: Schistosoma mansoni
Public Records: 21
Specimens with Barcodes: 34
Species With Barcodes: 1
The recovery of eggs from a 5,000 year old Egyptian mummy has shown that the disease, schistosomiasis, caused by this parasite has been present since prehistoric times. The recent report of newly discover strains illustrates the continuing versatality of these parasites.
Relevance to Humans and Ecosystems
Economic Importance for Humans: Negative
In countries affected by Schistosoma mansoni, such as Egypt, where the climate is very dry, agricultural development is hindered because they can not irrigate the land. The most detrimental effect of the parasite, however, is schistosomiasis. It occurs in many third world or underdeveloped countries, and it has a serious negative economic impact. The disease spreads rapidly people are ignorant of the danger of the parasite and the disease caused by it. The disease not only affects humans but animals and lifestock as well. Animals are needed for their meat as well as for manual labor for farmers. When the disease afflicts animals, human food sources are affected as well. Another negative effect of the parasite is that the government must put a substantial amount of funding into the purification of water. This can be a time consuming and expensive project if it is possible at all
Economic Importance for Humans: Positive
Research in the area of contolling this parasite is a major source of income. Many governmental research laboratories in the countries affected by this parasite, such as the National Research Center in Dokki, Egypt, focus on schistosomiasis. Because schistosomiasis is so easily spread through contact with contaminated water, the water in the countries affected by the disease is virtually unusable. This provides an industry centered around water purification andthe production of bottled, purified water.
Schistosoma mansoni is a significant parasite of humans, a trematode that is one of the major agents of the disease schistosomiasis. The schistosomiasis caused by Schistosoma mansoni is intestinal schistosomiasis.
Schistosomes are atypical trematodes in that the adult stages have two sexes (dioecious) and are located in blood vessels of the definitive host. Most other trematodes are hermaphroditic and are found in the intestinal tract or in organs, such as the liver. The lifecycle of schistosomes includes two hosts: a definitive host (i.e. human) where the parasite undergoes sexual reproduction, and a single intermediate snail host where there are a number of asexual reproductive stages. S. mansoni is named after Sir Patrick Manson, who first identified it in Formosa (Taiwan).
Morphology of adult schistosomes
Schistosomes, unlike other trematodes, are long and slim worms. The male S. mansoni is approximately 1 cm long (0.6–1.1 cm)  and is 0.1 cm wide. It is white, and it has a funnel-shaped oral sucker at its anterior end followed by a second pediculated sucker. The external part of the worm is composed of a double bilayer, which is continually renewed as the outer layer, known as the membranocalyx, is shed continuously. The tegument bears a large number of small tubercules. The suckers have small thorns in their inner part as well as in the buttons around them. The male genital apparatus is composed of 6 to 9 testicular masses, situated dorsally. There is one deferent canal beginning at each testicle which is connected to a single deferent that dilates into a reservatory, the seminal vesicle, located at the beginning of the gynacophoric canal. The copula happens through the coaptation of the male and female genital orifices.
The female has a cylindrical body, longer and thinner than the male (1.2 to 1.6 cm long by 0.016 cm wide). The female parasite is darker, and it looks gray. The darker color is due to the presence of a pigment (hemozoin) in its digestive tube. This pigment is derived from the digestion of blood. The ovary is elongated and slightly lobulated and is located on the anterior half of the body. A short oviduct conducts to the ootype which continues with the uterine tube. In this tube it is possible to find 1 to 2 eggs (rarely 3 to 4) but only 1 egg is observed in the ootype at any one time. The genital pore opens ventrally. The posterior two-thirds of the body contain the vittelogenic glands and their winding canal, which unites with the oviduct a little before it reaches the ootype.
The digestive tube begins at the anterior extremity of the worm, at the bottom of the oral sucker. The digestive tube is composed of an esophagus which divides in two branches (right and left) and that reunite in a single cecum. The intestines end blindly, meaning that there is no anus.
Schistosoma mansoni infects about 83.31 million people worldwide, causing the disease intestinal schistosomiasis (schistosomiasis caused by all the Schistosoma species infects over 200 million people.)
S. mansoni is the most widespread of the human-infecting schistosomes, and is present in 54 countries. These countries are predominantly in South America and the Caribbean, Africa including Madagascar, and the Middle East.
After the eggs of the human-dwelling parasite are emitted in the faeces and into the water, the ripe miracidium hatches out of the egg. The hatching happens in response to temperature, light and dilution of faeces with water. The miracidium searches for a suitable freshwater snail (Biomphalaria glabrata, Biomphalaria straminea, Biomphalaria tenagophila or Biomphalaria sudanica) to act as an intermediate host and penetrates it. Following this, the parasite develops via a so-called mother-sporocyst and daughter-sporocyst generation to the cercaria. The purpose of the growth in the snail is the numerical multiplication of the parasite. From a single miracidium result a few thousand cercaria, every one of which is capable of infecting man.
The cercaria emerge from the snail during daylight and they propel themselves in water with the aid of their bifurcated tail, actively seeking out their final host. When they recognise human skin, they penetrate it within a very short time. This occurs in three stages, an initial attachment to the skin, followed by the cercaria creeping over the skin searching for a suitable penetration site, often a hair follicle, and finally penetration of the skin into the epidermis using cytolytic secretions from the cercarial post-acetabular, then pre-acetabular glands. On penetration, the head of the cercaria transforms into an endoparasitic larva, the schistosomule. Each schistosomule spends a few days in the skin and then enters the circulation starting at the dermal lymphatics and venules. Here they feed on blood, regurgitating the haem as hemozoin. The schistosomule migrates to the lungs (5–7 days post-penetration) and then moves via circulation through the left side of the heart to the hepatoportal circulation (>15 days) where, if it meets a partner of the opposite sex, it develops into a sexually mature adult and the pair migrate to the mesenteric veins. Such pairings are monogamous.
Male schistosomes undergo normal maturation and morphological development in the presence or absence of a female, although behavioural, physiological and antigenic differences between males from single-sex, as opposed to bisex, infections have been reported. On the other hand, female schistosomes do not mature without a male. Female schistosomes from single-sex infections are underdeveloped and exhibit an immature reproductive system. Although the maturation of the female worm seems to be dependent on the presence of the mature male, the stimuli for female growth and for reproductive development seem to be independent from each other.
The adult female worm resides within the adult male worm's gynaecophoric canal, which is a modification of the ventral surface of the male forming a groove. The paired worms move against the flow of blood to their final niche in the mesenteric circulation where they begin egg production (>32 days). The S. mansoni parasites are found predominantly in the small inferior mesenteric blood vessels surrounding the large intestine and caecal region of the host. Each female lays approximately 300 eggs a day (one egg every 4.8 minutes), which are deposited on the endothelial lining of the venous capillary walls. Most of the body mass of female schistosomes is devoted to the reproductive system. The female converts the equivalent of almost her own body dry weight into eggs each day. The eggs move into the lumen of the host's intestines and are released into the environment with the faeces.
Schistosoma mansoni has 8 pairs of chromosomes (2n = 16)—7 autosomal pairs and 1 sex pair. The female schistosome is heterogametic, or ZW, and the male is homogametic, or ZZ. Sex is determined in the zygote by a chromossomal mechanism. The Schistosoma genome is approximately 270 MB with a GC content of 34%, 4–8% highly repetitive sequence, 32–36% middle repetitive sequence and 60% single copy sequence. Numerous highly or moderately repetitive elements have been identified, and their frequency in genomic sequence data also suggests at least 30% repetitive DNA. Chromosomes range in size from 18 to 73 MB and can be distinguished by size, shape and C banding. There are estimated to be 15–20 thousand expressed genes. 
In 2000, the first BAC library of Schistosome was constructed. In June 2003, a ~5x whole genome shotgun sequencing project was initiated at the Sanger Institute. Together with the shotgun data being generated by TIGR, an ~8x coverage of the genome will be obtained, assembled and annotated.  Also in 2003, 163,000 ESTs (expressed sequence tags) were generated (by a consortium headed by the University of São Paulo) from six selected developmental stages of this parasite, resulting in 31,000 assembled sequences and an estimated 92% of the 14,000-gene complement. 
In 2009 the genomes of both S. mansoni and S. japonicum were published, with each describing 11,809 and 13,469 genes respectively. Analysis of the S. mansoni genome highlighted expansions in protease families and deficiencies in lipid anabolism; both observations can be directly related S. mansoni's parasitic lifestyle. The former included the invadolysin (host penetration) and cathepsin (blood feeding) gene families, while the latter encompassed several enzymes required for the de novo synthesis of fatty acids and sterols (so the worm must rely on its host for these products). The results open the way for research on new targeted treatments.
In 2012 an improved version of the S. mansoni genome was published, with only 885 scaffolds and more than 81% of the bases organised into chromosomes. In the same study the authors have also used transcriptome sequencing (RNA-seq) from four time points in the parasite’s life cycle to refine 45% gene predictions and profile their expression levels. 
Schistosome eggs, which may become lodged within the hosts tissues, are the major cause of pathology in schistosomiasis. Some of the deposited eggs reach the outside environment by passing through the wall of the intestine; the rest are swept into the circulation and are filtered out in the periportal tracts of the liver resulting in periportal fibrosis. Onset of egg laying in humans is sometimes associated with an onset of fever (Katayama fever). This "acute schistosomiasis" is not, however, as important as the chronic forms of the disease. For S. mansoni and S. japonicum these are "intestinal" and "hepatic schistosomiasis", associated with formation of granulomas around trapped eggs lodged in the intestinal wall or in the liver, respectively. The hepatic form of the disease is the most important, granulomas here giving rise to fibrosis of the liver and hepatosplenomegaly in severe cases. Symptoms and signs depend on the number and location of eggs trapped in the tissues. Initially, the inflammatory reaction is readily reversible. In the latter stages of the disease, the pathology is associated with collagen deposition and fibrosis resulting in organ damage that may be only partially reversible.
Granuloma formation is initiated by antigens secreted by the miracidium through microscopic pores within the rigid egg shell, and there is strong evidence that the vigorous granulomatous response, rather than the direct action of parasite egg antigens, is responsible for the pathologic tissue manifestations in schistosomiasis. The granulomas formed around the eggs impair blood flow in the liver and consequently induce portal hypertension. With time, collateral circulation is formed and the eggs disseminate into the lungs, where they cause more granulomas, pulmonary arteritis and, later, cor pulmonale. A contributory factor to portal hypertension is Symmers' fibrosis, which develops around branches of the portal veins. This fibrosis occur only many years after the infection and apparently is caused in part by soluble egg antigens and various immune cells which react to them.
Recent research has shown that granuloma size is consistent with levels of IL-13, which plays a prominent role in granuloma formation and granuloma size. IL-13 receptor α 2 (IL-13Rα2) binds IL-13 with high affinity and blocks the effects of IL-13. Thus, this receptor is essential in preventing the progression of schistosomiasis from the acute to the chronic (and deadly) stage of disease. Synthetic IL-13Rα2 given to mice has resulted in significant decreases in granuloma size, implicating IL-13Rα2 as an important target in schistosomiasis.
Evasion of host immunity
Adult and larval worms migrate through the host's blood circulation avoiding the host's immune system. The worms have many tools that help in this evasion, including the tegument, antioxidant proteins, and defenses against host membrane attack complex (MAC).
The tegument coats the worm and acts as a physical barrier to host antibodies and complement.
- Antioxidant proteins
Host immune defenses are capable of producing superoxide, which has a tremendous detrimental effect on the worm. However, they are able to produce a number of antioxidant proteins that block the effect of superoxide. Schistosomes have four superoxide dismutases, and levels of these proteins increase as the schistosome develops and matures.
Antioxidant pathways were first recognised as a chokepoints for Schistosomes  and later extended to other trematodes and cestodes. Targeting of this pathway with different inhibitors of the central antioxidant enzyme Thioredoxin Glutathione Reductase (TGR) results in reduced viability of worms 
- Defense against host MAC
Schistosomes have evolved ways to block host complement proteins. Immunocytochemistry techniques have found decay accelerating factor (DAF) protein on the tegument. DAF is found on host cells and protects host cells by blocking formation of MAC. It has also been found that the schistosome genome consists of human CD59 homologs. CD59 inhibits MAC.
Many individuals do not experience symptoms. If symptoms do appear, it usually takes four to six weeks from the time of infection. The first symptom of the disease may be a general ill feeling. Within twelve hours of infection, an individual may complain of a tingling sensation or light rash, commonly referred to as "swimmer's itch", due to irritation at the point of entrance. The rash that may develop can mimic scabies and other types of rashes. Other symptoms can occur two to ten weeks later and can include fever, aching, cough, diarrhea, or gland enlargement. These symptoms can also be related to avian schistosomiasis which does not cause any further symptoms in humans.
Another primary condition, called Katayama fever, may also develop from infection with these worms, and it can be very difficult to recognize. Symptoms include fever, lethargy, the eruption of pale temporary bumps associated with severe itching (urticarial) rash, liver and spleen enlargement, and bronchospasm.
In intestinal schistosomiasis, eggs become lodged in the intestinal wall and cause an immune system reaction called a granulomatous reaction. This immune response can lead to obstruction of the colon and blood loss. The infected individual may have what appears to be a potbelly. Eggs can also become lodged in the liver, leading to high blood pressure through the liver, enlarged spleen, the buildup of fluid in the abdomen, and potentially life-threatening dilations or swollen areas in the esophagus or gastrointestinal tract that can tear and bleed profusely (esophageal varices). Rarely, the central nervous system is affected. Individuals with chronic active schistosomiasis may not complain of typical symptoms.
Diagnosis and treatment
Diagnosis of infection is confirmed by the identification of eggs in stools. Eggs of S. mansoni are approximately 140 by 60 µm in size, and have a lateral spine. The diagnosis is improved by the use of the Kato-Katz technique (a semi-quantitative stool examination technique). Other methods which can be used are enzyme linked immunosorbent assay (ELISA), circumoval precipitation test (COPT) and alkaline phosphatase immunoassay (APIA).
Currently there are two drugs available, praziquantel and oxamniquine, for the treatment of  schistosomiasis. They are considered equivalent in relation to efficacy and safety. Due to its lower cost per treatment, praziquantel is generally considered the first option for treatment. The recommended dose is: praziquantel, 60 mg/kg of body weight for children up to 15 years old, and 50 mg/kg of body weight for adults; oxamniquine, 15 mg/kg for adults, and 20 mg/kg for children up to 15 years old. The treatment objective is to cure the disease and to prevent the evolution of the acute to the chronic form of the disease. All confirmed cases should be treated.
- Matthews, B. An Introduction to Parasitology. (Cambridge University Press.: 1998). ISBN 0-521-57691-1
- Machado-Silva JR, Galvao C, Oliveira RMF, Presgrave AF, Gomes DC (1995). "Schistosoma mansoni sambon, 1907: Comparative morphological studies of some Brazilian Strains". Rev. Inst. Med. Trop. Sao Paulo 37 (5): 441–447. PMID 8729755.
- Braschi S, Borges WC, Wilson RA (September 2006). "Proteomic analysis of the schistosome tegument and its surface membranes". Memórias Do Instituto Oswaldo Cruz 101 (Suppl 1): 205–12. doi:10.1590/S0074-02762006000900032. PMID 17308771.
- Rey, Luíz (1991). Parasitologia. Rio de Janeiro, RJ: Editora Guanabara Koogan S.A. pp. 351–62. ISBN 85-277-0189-8.
- Crompton DW (June 1999). "How much human helminthiasis is there in the world?". The Journal of Parasitology (The Journal of Parasitology, Vol. 85, No. 3) 85 (3): 397–403. doi:10.2307/3285768. JSTOR 3285768. PMID 10386428.
- Oliveira, G.; Rodrigues, N. B.; Romanha, A. J.; Bahia, D. (February 2004). "Genome and genomics of schistosomes". Canadian Journal of Zoology 82 (2): 375–390. doi:10.1139/z03-220.
- Jamison et al., ed. (2006). Disease Control Priorities in Developing Countries (2nd ed.). ISBN 0-8213-6179-1.
- Gatlin MR, Black CL, Mwinzi PN, Secor WE, Karanja DM, Colley DG (2009). "Association of the Gene Polymorphisms IFN-γ +874, IL-13 −1055 and IL-4 −590 with Patterns of Reinfection with Schistosoma mansoni". In King, Charles H. PLoS Neglected Tropical Diseases 3 (2): e375. doi:10.1371/journal.pntd.0000375. PMC 2631135. PMID 19190772.
- (Spanish) Libora M., Morales G., Carmen S., Isbelia S. & Luz A. P. (2010). "Primer hallazgo en Venezuela de huevos de Schistosoma mansoni y de otros helmintos de interés en salud pública, presentes en heces y secreción mucosa del molusco terrestre Achatina fulica (Bowdich, 1822). [First finding in Venezuela of Schistosoma mansoni eggs and other helminths of interest in public health found in faeces and mucous secretion of the mollusc Achatina fulica (Bowdich, 1822)]. Zootecnia Tropical 28: 383-394. PDF.
- Oliveira MF, d'Avila JC, Torres CR et al. (November 2000). "Haemozoin in Schistosoma mansoni". Molecular and Biochemical Parasitology 111 (1): 217–21. doi:10.1016/S0166-6851(00)00299-1. PMID 11087932.
- "DPDx - Schistosomiasis". CDC. Retrieved 2007-06-14.
- Beltran S, Boissier J (September 2008). "Schistosome monogamy: who, how, and why?". Trends in Parasitology 24 (9): 386–91. doi:10.1016/j.pt.2008.05.009. PMID 18674968.
- Loverde PT, Chen L (November 1991). "Schistosome female reproductive development". Parasitology Today 7 (11): 303–8. doi:10.1016/0169-4758(91)90263-N. PMID 15463396.
- "Schistosoma mansoni Genome Project". Sanger Institute. Retrieved 2007-06-14.
- Le Paslier MC, Pierce RJ, Merlin F et al. (April 2000). "Construction and characterization of a Schistosoma mansoni bacterial artificial chromosome library". Genomics 65 (2): 87–94. doi:10.1006/geno.2000.6147. PMID 10783255.
- "Schistosoma mansoni Genome Project". The Institute for Genomic Research. Retrieved 2007-06-14.
- "Schistosoma mansoni EST Genome Project". University of São Paulo. Retrieved 2007-06-14.
- Berriman M, Haas BJ, LoVerde PT, Wilson RA, Dillon GP, Cerqueira GC, Mashiyama ST, Al-Lazikani B, Andrade LF, Ashton PD, Aslett MA, Bartholomeu DC, Blandin G, Caffrey CR, Coghlan A, Coulson R, Day TA, Delcher A, DeMarco R, Djikeng A, Eyre T, Gamble JA, Ghedin E, Gu Y, Hertz-Fowler C, Hirai H, Hirai Y, Houston R, Ivens A, Johnston DA, Lacerda D, Macedo CD, McVeigh P, Ning Z, Oliveira G, Overington JP, Parkhill J, Pertea M, Pierce RJ, Protasio AV, Quail MA, Rajandream MA, Rogers J, Sajid M, Salzberg SL, Stanke M, Tivey AR, White O, Williams DL, Wortman J, Wu W, Zamanian M, Zerlotini A, Fraser-Liggett CM, Barrell BG, El-Sayed NM. (July 2009). "The genome of the blood fluke Schistosoma mansoni". Nature 460 (7253): 352–8. doi:10.1038/nature08160. PMC 2756445. PMID 19606141.
- "Killer parasites' genes decoded". BBC News. July 16, 2009. Retrieved 2009-07-16.
- Anna V. Protasio, Isheng J. Tsai, Anne Babbage, Sarah Nichol, Martin Hunt, Nishadi De Silva, Tim J.C. Anderson, Richard C. Clark, Claire Davidson, Gary P. Dillon, Nancy E. Holroyd, Philip T. LoVerde, Christine Lloyd, Jacquelline McQuillan, Guilherme Oliveira,Thomas D. Otto, Sophia J. Parker-Manuel, Michael A. Quail, R. Alan Wilson, Adhemar Zerlotini, David W. Dunne, Matthew Berriman. (Jan 2012). "A systematically improved high quality genome and transcriptome of the human blood fluke Schistosoma mansoni.". PLoS Neglected Tropical Diseases 6 (1): 1455. doi:10.1371/journal.pntd.0001455. PMC 3254664. PMID 22253936.
- Boros DL (July 1989). "Immunopathology of Schistosoma mansoni infection". Clinical Microbiology Reviews 2 (3): 250–69. PMC 358119. PMID 2504481.
- Mentink-Kane MM, Cheever AW, Thompson RW et al. (January 2004). "IL-13 receptor α 2 down-modulates granulomatous inflammation and prolongs host survival in schistosomiasis". Proceedings of the National Academy of Sciences of the United States of America 101 (2): 586–90. doi:10.1073/pnas.0305064101. PMC 327191. PMID 14699044.
- Wilson RA, Coulson PS (September 2009). "Immune effector mechanisms against schistosomiasis: looking for a chink in the parasite's armour". Trends in Parasitology 25 (9): 423–31. doi:10.1016/j.pt.2009.05.011. PMID 19717340.
- Sayed AA, Simeonov A, Thomas CJ, Inglese J, Austin CP, Williams DL (April 2008). "Identification of oxadiazoles as new drug leads for the control of schistosomiasis". Nat. Med. 14 (4): 407–12. doi:10.1038/nm1737. PMC 2700043. PMID 18345010.
- Ross F, Hernández P, Porcal W, et al. (2012). "Identification of thioredoxin glutathione reductase inhibitors that kill cestode and trematode parasites". PLoS ONE 7 (4): e35033. doi:10.1371/journal.pone.0035033. PMC 3335049. PMID 22536349.
- "Clinical Aspects". University of Tsukuba School of Medicine. Retrieved 2007-06-14.
- "eMedicine - Schistosomiasis". eMedicine. Retrieved 2007-06-14.
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