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 found throughout Africa and South America, especially in Brazil, Venezuela, Surinam and Guyana. It also lives on several Caribbean islands such as Puerto Rico, St. Lucia, Martinique, and Guadeloupe. It is thought that the species may have been brought to the Western Hemisphere during the African slave trade when a number of susceptible snail hosts may have been introduced, possibly in the casks of drinking water that were brought with the slaves.
Biogeographic Regions: ethiopian (Native ); neotropical (Introduced )
- Bogitsh, B., C. Carter, T. Oeltmann. 2005. Human Parasitology. Burlington: Elsevier Academic Press.
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.
Schistosoma mansoni is a parasitic flatworm. An oral sucker surrounds the mouth of the adult, and a ventral sucker is immediately located posterior to the bifurcation of the gut. There is an esophagus with distinct esophageal glands, but no pharynx is present. Paired caeca come together posteriorly, forming a single caecum that extends the remaining length of the schistosome body. Schistosoma mansoni is dioecious and sexually dimorphic. The adult male (up to 10 mm in length) is more robust than the female and possesses a body groove called a gynaecophoral canal. The female, which is longer and more slender than the male (up to 10 to 14 mm in length), is held within the groove of the male. The tegument of males have tubercles on the dorsal surface, whereas the tegument of females is smooth. The male has 6 to 9 testes, and the male genital pore opens ventrally, immediately posterior to the ventral sucker. On the female, a single ovary is located in the anterior portion of the body. The uterus can be long or short, depending on the position of the ovary relative to the female genital pore.
Range length: 10 to 14 mm.
Sexual Dimorphism: male larger
Other Physical Features: ectothermic ; bilateral symmetry
Schistosoma mansoni adults are parasitic to humans and commonly reside in mesenteric venules and in the large intestine. During development, the miracidium larvae live in fresh water habitats in shallow coastal areas before infecting a snail intermediate host. The miracidium transforms into a sporocyst in the headfoot of the snail, and then moves to the digestive glands or gonads. Cercariae leave the sporocyst through a birth pore, pass through the tissues of the snail, then are released into fresh water before entering a human.
Habitat Regions: temperate ; tropical ; freshwater
Aquatic Biomes: lakes and ponds; rivers and streams
- Meyer, M., O. Olsen. 1971. Essentials of Parasitology. Dubuque, Iowa: Wm. C. Brown Company Publishers.
As a parasite, the dietary needs of Schistosoma mansoni are almost solely fulfilled by the host. The parasite mainly gains nourishment from the blood of the host, feeding on proteins and monosaccharides. Specifically, Schistosoma mansoni consumes a lot of glucose, which the parasite uses to generate energy that it requires for reproduction and other activities. If the host is malnourished, then there are negative effects on the development of the parasite. For example, males of Schistosoma mansoni have been known to have smaller testes when found in a malnourished host than when found in a well-nourished host. Similarly, the ovaries of females are smaller and less abundant when in a malnourished host.
Animal Foods: mammals; mollusks
Primary Diet: carnivore (Eats body fluids)
- Neves, R. 2001. Morphological aspects of Schistosoma mansoni adult worms isolated from nourished and undernourished mice: a comparative analysis by confocal laser scanning microscopy. Mem Inst Oswaldo Cruz, 96.7: 1013-1016.
Individuals of Schistosoma mansoni are found in freshwater environments. Location and distribution vary depending on region and time of year. They are predominantly found in bodies of fresh water with irrigation systems, because the environment remains generally stable. Because they are parasitic, they infect other species in the bodies of water in which they dwell. Most often, they initially infect snails in the family Planorbidae, particularly of the genus Biomphlaria. Other organisms such as monkeys, rats, and other rodents, can be infected themselves by ingesting infected snails. Humans tend to become infected through contact with contaminated water rather than by consumption of infected snails.
Ecosystem Impact: parasite
Species Used as Host:
- Snails, Biomphlaria
Predation on snails (genus Biomphlaria) that are infected with Schistosoma mansoni is not uncommon, but direct predation on the parasites themselves is not widely known. It has, however, been noted that free-living miracidia (prior to infecting a snail) are often preyed upon by certain annelids like those of the genus Chaetogaster.
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
Schistosoma mansoni communicates through chemical means. Individuals have several receptors, including several ligand-gated channels that respond to chemical changes in the internal environment of their host. Once inside of their host, intermediate or definitive, they are not known to make many changes to its chemistry, but they are thought to protect themselves from localized immune system signals and enzymatic activity by releasing their own signals that lessen or weaken the signals of the host. Individuals live independently in freshwater during the miracidium stage for a short time. Under this condition, the parasite is sensitive to temperature and pressure changes.
Communication Channels: chemical
Perception Channels: chemical
Adults of Schostosoma mansoni live in mesenteric veins which drain the intestine of the host. The female will generally move to smaller venules before depositing her eggs. The enclosed miracidium is under-developed at time of oviposition, but will be well-formed before reaching the lumen of an infected organ. The egg must penetrate and traverse multiple tissues and mucosal lining before entering the lumen of the gut or the bladder to escape to the environment. The passage of eggs from the blood stream to the lumen of the infected organ are induced by secretions that are part of the immune response of the host. Once the egg has reached the intestinal lumen, the egg can exit the host organism in either feces or urine.
Upon reaching fresh water, the miracidia are activated to hatch, because they are no longer under the inhibitory osmolarity of the host's body fluids. Hatching occurs by rupturing the eggshell along the suture line. Free-swimming miracidia must find a suitable intermediate snail host quickly after hatching, or they will die. After a snail is penetrated, transformation into a sporocyst occurs in the headfoot. Another generation of sporocysts is produced, and these sporocysts migrate into the digestive gland or gonads. Cercariae exit the sporocyst through a birth pore and can be passed to the exterior. This passage is facilitated by secretions coming from a pair of escape glands in the cercaria.
Actively swimming cercariae possess distinctive forked tails and move in a figure-eight pattern. Secretions from the mammalian skin stimulate the cercariae to attach and penetrate the definitive host. Cercariae have five pairs of unicellular glands. Two preacetabular glands are anterior to the ventral sucker, while three postacetabular glands lie behind the ventral sucker. Each gland has a duct that empties at the anterior region of the oral sucker. Cercariae adhere using both their muscular suckers and mucoid secretions to attach to the skin of a human host. Because secretions from the preacetabular glands are highly enzymatic, they facilitate lysis of the host skin for penetration. Within the skin, cercariae burrow into the peripheral capillary bed or enter the lymphatic system, where the worms can migrate to the heart and enter the lungs. Three significant morphological changes occur in cercariae during the penetration process: loss of the tail, loss of the surface coat, and emptying of the contents of the penetration glands. The cercaria is referred to as a schistomule following this transformation.
Schistomules reside within pulmonary capillaries by the third day after penetration. On day four, juveniles begin feeding on host blood cells, which triggers a period of rapid growth and development. After 7 to 10 days, schistomules migrate through the pulmonary vein into the heart, and then into the systemic circulation. About three weeks later, the worms reach the hepatic portal veins, where sexual maturity is reached, and mating is possible after 40 days. Males that contain females in their body grooves move to venules at the definitive sites.
Development - Life Cycle: metamorphosis
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.
Once a schistosome enters the snail intermediate host, development requires 3 to 4 weeks on average. In the human host, the organism will generally live another 7 to 8 weeks. On average, Scistosoma mansoni lives about 80 days.
Status: wild: 80 days.
Schistosoma mansoni is a dioecious species, with the male and female individuals being separate. Females spend much of their time wrapped inside the body groove of male worms, resulting in near constant mating.
Mating System: monogamous
Female worms deposit 190 to 300 eggs daily, each measuring 114 to 175 micrometers long by 45 to 68 micrometers wide and bearing a prominent, lateral spine. At the time of fertilization, the sex of worms is genetically determined.
Breeding interval: Schistosoma mansoni breeds daily.
Breeding season: Schistosoma mansoni breeds year round.
Range number of offspring: 190 to 300.
Average age at sexual or reproductive maturity (female or asexual): 21 days.
Average age at sexual or reproductive maturity (male): 21 days.
Key Reproductive Features: iteroparous ; year-round breeding ; gonochoric/gonochoristic/dioecious (sexes separate); sexual ; fertilization (Internal )
There is no parental investment after the eggs are released. Post-hatching, the free swimming miracidia are on their own to penetrate a suitable snail host within a few hours or they will die.
Parental Investment: no parental involvement
- Bogitsh, B., C. Carter, T. Oeltmann. 2005. Human Parasitology. Burlington: Elsevier Academic Press.
- Harrison, F., B. Bogitsh. 1991. Microscopic Anatomy of Invertebrates. New York: Wiley-Liss Inc..
Molecular Biology and Genetics
Barcode data: Schistosoma mansoni
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
Relevance to Humans and Ecosystems
Schistosoma mansoni is the parasite responsible for schistosomiasis, a disease that affects nearly 300,000,000 people. Early on, the disease causes rashes, fever, and muscle aches, while chronic infections can lead to bladder cancer, damaged organs, and in children it can cause developmental issues. In regions where rate of infection is high, over $3,000,000 in medical costs can be made annually to help those infected. Humans become infected through contact with contaminated water, and often in regions of high infection there is little knowledge and education of these parasites. Prevention is costly for those attempting to create cleaner freshwater environments. For many regions, freshwater irrigation systems are a way of sustaining life, and for most of these regions there is not much capital to spare. Cleaning and filtering irrigation systems is expensive and thus cannot happen in most areas.
Negative Impacts: injures humans (causes disease in humans )
- Center for Disease Control, 2012. "Parasites - Schistosomiasis" (On-line). Center for Disease Control. Accessed April 11, 2013 at http://www.cdc.gov/parasites/schistosomiasis/.
Schistosoma mansoni was one of the first flatworms to have a fully mapped genome, thus allowing much genetic research about the disease schistosomiasis and its prevention/cure. By creating so many research opportunities, Schistosoma mansoni has inadvertently stimulated the economy.
Positive Impacts: research and education
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 (now 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 continuously renewed as the outer layer, known as the membranocalyx, and 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's (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.
S. mansoni is commonly found in places with poor sanitation. Because of the parasite's fecal-oral transmission, bodies of water that contain human waste can be infectious. Water that contains large populations of the intermediate host snail species is more likely to cause infection. Young children living in these areas are at greatest risk because of their tendency to swim and bathe in cercaria-infected waters longer than adults . Any one travelling to the areas described above, and who is exposed to contaminated water, is at risk of schistosomiasis.
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 capable of infecting a human.
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 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 to 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 lifecycle 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, as a consequence, 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 occurs only many years after the infection and is presumed to be caused in part by soluble egg antigens and various immune cells that 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). In rare instances, 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 that 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, in general praziquantel is considered the first option for treatment. The recommended dose is: praziquantel, 1 to 5 600 mg tablets by height from ≥94 cm for children up to 15 years old, and 40 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 cases of suspected schistosomiasis should be treated regardless of presentation because the adult parasite can live in the host for years.
- Birch, CA (1974). "Schistosoma mansoni. Sir Patrick Manson, 1844-1922.". The Practitioner 213 (1277): 730–2. PMID 4156405.
- Swanner, Yann A. Meunier ; with contributions from Michael Hole, Takudzwa Shumba & B.J. (2014). Tropical Diseases : a Practical Guide for Medical Practitioners and Students. Oxford: Oxford University Press, USA. p. 40. ISBN 9780199997909.
- 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. doi:10.1590/s0036-46651995000500010. 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.
- "DPDx - Schistosomiasis risk and Epidemiology Factors". CDC. Retrieved 2013-11-05.
- 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.
- Danso-Appiah, A; Olliaro, PL; Donegan, S; Sinclair, D; Utzinger, J (Feb 28, 2013). "Drugs for treating Schistosoma mansoni infection". The Cochrane database of systematic reviews 2: CD000528. doi:10.1002/14651858.cd000528.pub2. PMID 23450530.
- WHO (2006). "Preventive Chemotherapy guidelines. Report of a WHO expert committee.". World Health Organization. Geneva, Switzerland.
- Brinkmann, UK; Werler, C; Traoré, M; Doumbia, S; Diarra, A (Jun 1988). "Experiences with mass chemotherapy in the control of schistosomiasis in Mali". Tropical medicine and parasitology: official organ of Deutsche Tropenmedizinische Gesellschaft and of Deutsche Gesellschaft fur Technische Zusammenarbeit (GTZ) 39 (2): 167–74. PMID 3140359.
- Abou-El-Naga IF (2013) Biomphalaria alexandrina in Egypt: Past, present and future. J Biosci 38(3):665-672
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