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| classis = [[Trematoda]]
| classis = [[Trematoda]]
| ordo = [[Strigeidida]]
| ordo = [[Strigeidida]]
| familia = [[Schistosomatidae]]
| family = [[Schistosomatidae]]
| genus = ''[[Schistosoma]]''
| genus = ''[[Schistosoma]]''
| species = '''''S. mansoni'''''
| species = '''''S. mansoni'''''

Revision as of 09:46, 25 August 2015

This article is about the organism. For the infection, see Schistosomiasis.

Schistosoma mansoni
Schistosomes copulating
Scientific classification
Kingdom:
Animalia
Phylum:
Platyhelminthes
Class:
Trematoda
Order:
Strigeidida
Genus:
Schistosoma
Species:
S. mansoni
Binomial name
Schistosoma mansoni
Sambon, 1907

Schistosoma mansoni is a significant parasite of humans, a trematode that is one of the major agents of the disease schistosomiasis which is one type of helminthiasis, a neglected tropical disease. 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).[1][2]

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) [3] 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.[4] 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.[5]

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.

Epidemiology

Schistosoma mansoni infects about 83.31 million people worldwide,[6] causing the disease intestinal schistosomiasis (schistosomiasis caused by all the Schistosoma species infects over 200 million people.)[7][8]

S. mansoni is the most widespread of the human-infecting schistosomes, and is present in 54 countries.[citation needed] 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 .[9] Any one travelling to the areas described above, and who is exposed to contaminated water, is at risk of schistosomiasis.

Life cycle

Schistosoma mansoni life cycle

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[10]) 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.

Libora et al. (2010)[11] have detected in Venezuela, that a land snail Achatina fulica can also serve as a host of Schistosoma mansoni.[11]

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.[12] 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.[13] Such pairings are monogamous.[14]

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.[15] 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.

Genome

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.[16]

In 2000, the first BAC library of Schistosome was constructed.[17] 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.[18] 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.[19]

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.[20][21]

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.[22]

Pathology

A Schistosoma mansoni egg with the characteristic lateral spine

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.[23] 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.[24]

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).[25]

Tegument

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 [26] 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 [27]

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.

Symptoms

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.

Katayama fever

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.

Intestinal schistosomiasis

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).[28]

Currently there are two drugs available, praziquantel and oxamniquine, for the treatment of schistosomiasis.[29] They are considered equivalent in relation to efficacy and safety.[30] 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;[31] 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.[32]

Notes

Schistosoma mansoni reached Egypt via infected slaves and baboons from the Land of Punt through migrations that occurred possibly as early as the Vth Dynasty.[33]

References

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  24. ^ 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. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  25. ^ 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.
  26. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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  30. ^ Danso-Appiah, A; Olliaro, PL; Donegan, S; Sinclair, D; Utzinger, J (September 21, 2013). "Drugs for treating Schistosoma mansoni infection". The Cochrane database of systematic reviews. 2: CD000528. doi:10.1002/14651858.cd000528.pub2. PMID 23450530.
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  32. ^ 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.
  33. ^ Abou-El-Naga IF (2013) Biomphalaria alexandrina in Egypt: Past, present and future. J Biosci 38(3):665-672
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