Schistosoma mansoni
Schistosoma mansoni | |
---|---|
Schistosomes copulating | |
Scientific classification | |
Domain: | Eukaryota |
Kingdom: | Animalia |
Phylum: | Platyhelminthes |
Class: | Trematoda |
Order: | Diplostomida |
Family: | Schistosomatidae |
Genus: | Schistosoma |
Species: | S. mansoni
|
Binomial name | |
Schistosoma mansoni Sambon, 1907
|
Schistosoma mansoni is a
Unlike other flukes (
The life cycle of schistosomes includes two hosts: humans as definitive hosts, where the parasite undergoes sexual reproduction, and snails as intermediate hosts, where a series of asexual reproduction takes place. S. mansoni is transmitted through water, where freshwater snails of the genus Biomphalaria act as intermediate hosts. The larvae are able to live in water and infect the hosts by directly penetrating the skin. Prevention of infection is done by improved sanitation and killing the snails. Infection is treated with praziquantel.
S. mansoni was first noted by Theodor Maximillian Bilharz in Egypt in 1851, while discovering S. haematobium. Sir Patrick Manson identified it as unique species in 1902. Louis Westenra Sambon gave the name Schistosomum mansoni in 1907 in honour of Manson.[2][3][4]
Structure
Adult
Schistosomes, unlike other trematodes, are long and cylindrical worms and are
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). It has the general appearance of a
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.
Sex
S. mansoni and other schistosomes are the only flukes or
Eggs
The eggs are oval-shaped, measuring 115–175 µm long and 45–47 µm wide, and ~150 µm diameter on average. They have pointed spines towards the broader base on one side, i.e. lateral spines. This is an important diagnostic tool because co-infection with S. haematobium (having a terminal-spined eggs) is common, and they are hard to distinguish.[21] When the eggs are released into the water, a lot of them are immature and unfertilised so that they do not hatch. When the eggs are larger than 160 µm in diameter, they also fail to hatch.[22][23]
Larva
The miracidium (from the Greek word μειράκιον, meirakion, meaning youth) is pear-shaped, and gradually elongates as it ages. It measures about 136 μm long and 55 μm wide. The body is covered by anucleate epidermal plates separated by epidermal ridges. The epidermal cells give off numerous hair-like cilia on the body surface. There are 17–22 epidermal cells. Epidermal plate is absent only at the extreme anterior called apical papilla, or terebratorium, which contains numerous sensory organelles.[24] Its internal body is almost fully filled with glycogen particles and vesicles.[25]
The cercaria has a characteristic bifurcated tail, classically called furcae (Latin for fork); hence, the name (derived from a Greek word κέρκος, kerkos, meaning tail). The tail is highly flexible and its beating propels the cercaria in water.[26] It is about 0.2 mm long and 47 μm wide, somewhat loosely attached to the main body. The body is pear-shaped and measures 0.24 mm in length and 0.1 mm in width.[27] Its tegument is fully covered with spine. A conspicuous oral sucker is at the apex. As a non-feeding larva, there are no elaborate digestive organs, only oesophagus is distinct. There are three pairs of mucin glands connected to laterally to the oral sucker at the region of the ventral sucker.[28][29]
Physiology
Feeding and nutrition
Developing Schistosoma mansoni worms that have infected their definitive hosts, prior to the sexual pairing of males and females, require a nutrient source in order to properly develop from cercariae to adults. The developing parasites lyse host red blood cells to gain access to nutrients and also makes its own fungi from its waste it is hard to detect; the hemoglobin and amino acids the blood cells contain can be used by the worm to form proteins.[30] While hemoglobin is digested intracellularly, initiated by salivary gland enzymes, iron waste products cannot be used by the worms, and are typically discarded via regurgitation.[31]
Kasschau et al. (1995) tested the effect of temperature and pH on the ability of developing S. mansoni to lyse red blood cells.[30] The researchers found that the parasites were best able to destroy red blood cells for their nutrients at a pH of 5.1 and a temperature of 37 °C.[30]
Locomotion
Schistosoma mansoni is locomotive in primarily two stages of its life cycle: as cercariae swimming freely through a body of freshwater to locate the epidermis of their human hosts, and as developing and fully-fledged adults, migrating throughout their primary host upon infection.[31] Cercariae are attracted to the presence of fatty acids on the skin of their definitive host, and the parasite responds to changes in light and temperature in their freshwater medium to navigate towards the skin.[32] Ressurreicao et al. (2015) tested the roles of various protein kinases in the ability of the parasite to navigate its medium and locate a penetrable host surface.[32] Extracellular signal-regulated kinase and protein kinase C both respond to changes in medium temperature and light levels, and the stimulation of p38 mitogen-activated protein kinase, associated with recognition of parasite host surface, results in a glandular secretion that deteriorates the host epidermis, and allows the parasite to burrow into its host.
The parasite's nervous system contains bilobed ganglia and several nerve cords which splay out to every surface of the body; serotonin is a transmitter distributed widely throughout the nervous system and plays an important role in nervous reception, and stimulating mobility.[33]
Life cycle
Intermediate host
After the eggs of the human-dwelling parasite are emitted in the faeces and into the water, the ripe
Miracidia directly penetrate the soft tissue of snail. Inside the snail, they lose their cilia and develop into mother sporocysts. The sporocysts rapidly multiply by asexual reproduction, each forming numerous daughter sporocysts. The daughter sporocysts move to the liver and gonads of the snail, where they undergo further growth.[38] Within 2–4 weeks, they undergo metamorphosis and give rise to fork-tailed cercariae. Stimulated by light, hundreds of cercariae penetrate out of the snail into water.[39]
Definitive host
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. In water, they can live for up to 12 hours, and their maximum infectivity is between 1 and 9 hours after emergence.
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
Genome
Schistosoma mansoni has 8 pairs of
In 2000, the first BAC library of Schistosome was constructed.
In 2009 the genomes of both S. mansoni and S. japonicum were published, with each describing 11,809 and 13,469 genes, respectively. S. mansoni genome has increased protease families and deficiencies in lipid anabolism; which are attributed to its parasitic adaptation. Proteases included the invadolysin (host penetration) and cathepsin (blood-feeding) gene families.[49][50]
In 2012, an improved version of the S. mansoni genome was published, which consisted of only 885 scaffolds and more than 81% of the bases organised into chromosomes.[51]
In 2019, Ittiprasert, Brindley and colleagues employed programmed CRISPR/Cas9 knockout of the gene encoding the T2 ribonuclease of the egg of Schistosoma mansoni, advancing functional genomics and reverse genetics in the study of schistosomes, and platyhelminths generally <https://doi.org/10.7554/eLife.41337>.
Pathology
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
Granuloma formation is initiated by antigens secreted by the miracidium through microscopic pores within the rigid egg shell, and the immune response to granuloma, rather than the direct action of egg antigens, causes the symptoms.
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.[55]
S. mansoni infection often occurs alongside those of viral hepatitis, either
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
Diagnosis
The presence of S. mansoni is detected by
Egg detection and immunologic tests are not that sensitive.[63] Polymerase chain reaction (PCR) based testing is accurate and rapid.[63] They, however, are not frequency used in countries were the disease is common due to the cost of the equipment and the technical experience required to run them.[63] Using a microscope to detect eggs costs about US$0.40 per test well PCR is about $US7 per test as of 2019.[64] Loop-mediated isothermal amplification (LAMP) are being studied as they are lower cost.[63] LAMP testing is not commercially available as of 2019.[64]
Treatment
The standard drug for S. mansoni infection is praziquantel at a dose of 40 mg/kg. Oxamniquine is also used.[65]
Epidemiology
As of 2021, 251.4 million people worldwide are having schistosomiasis due to different species of Schistosoma.[1] More than 75 million people were given medical treatment.[1] S. mansoni is the major species causing an annual death of about 130,000.[66] It is endemic in 55 countries and most prevalent in Africa, the Middle East, the Caribbean, Brazil, Venezuela and Suriname.[67] About 80-85% of schistosomiasis is found in sub-Saharan Africa, where S. haematobium, S. intercalatum and S. mansoni are endemic. Approximately 393 million Africans are at risk of infection from S. mansoni, of which about 55 million are infected at any moment. Annual death due to S. mansoni is about 130,000.[68] The prevalence rate in different countries of Africa are: 73.9% in northern Ethiopia, 37.9% in western Ethiopia, 56% in Nigeria, 60.5% in Kenya, 64.3% in Tanzania, 19.8% in Ghana, and 53.8% in Côte d'Ivoire.[69] In Egypt, 60% of the population in the Northern and Eastern parts of the Nile Delta and only 6% in the Southern part are infected.[70]
S. mansoni is commonly found in places with poor
History
The intermediate hosts Biomphalaria snails are estimated to originate in South America 95–110 million years ago. But the parasites Schistosoma originated in Asia. In Africa, the progenitor species evolved into modern S. mansoni and S. haematobium around 2–5 million years ago.[72][73]
A German physician Theodor Maximillian Bilharz was the first to discover the parasite in 1851, while working at Kasr el-Aini Hospital, a medical school in Cairo. Bilharz recovered them from autopsies of dead soldiers, and noticed two distinct parasites.[74] He described one of them as Distomum haematobium (now S. haematobium) in 1852,[75] but failed to identify the other. In one of his letters to his mentor Karl Theordor von Siebold, he mentioned some of the eggs were different in having terminal spines while some had lateral spines.[76] Terminal-spined eggs are unique to S. haematobium, while lateral spines are found only in S. mansoni. Bilharz also noted that the adult flukes were different in anatomy and number eggs they produced.[77] He introduced the terms bilharzia and bilharziasis for the name of the infection in 1856. A German zoologist David Friedrich Weinland corrected the genus name to Schistosoma in 1858; and introduced the disease name as schistosomiasis.[78]
The species distinction was first recognised by
References
- ^ a b c d "Schistosomiasis". www.who.int. World Health Organization. 1 February 2023. Archived from the original on 27 November 2023. Retrieved 27 November 2023.
- ^ a b Sambon, L.W. (1907). "Remarks on Schistosomum mansoni". Journal of Tropical Medicine and Hygiene. 10: 303–304.
- PMID 4156405.
- ISBN 9780199997909.)
{{cite book}}
: CS1 maint: multiple names: authors list (link - PMID 8729755.
- PMID 17308771.
- ISBN 978-85-277-0189-1.
- PMID 11087932.
- S2CID 20589225.
- PMID 15504538.
- PMID 31552097.
- PMID 19298820.
- PMID 3298599.
- PMID 17007463.
- doi:10.1139/z03-217.
- PMID 6502090.
- S2CID 23886925.
- ^ S2CID 20299817.
- S2CID 9587355.
- ^ PMID 23652002.
- PMID 19969774.
- PMID 2723933.
- PMID 2105231.
- S2CID 8968526.
- ^ Cort, W.W. (1919). "Notes on the eggs and miracidia of the human schistosomes". Univiversity of California Publications in Zoology. 18 (18): 509–519.
- .
- JSTOR 3271082.
- JSTOR 3270844.
- .
- ^ PMID 7722474.
- ^ ISBN 9781405107242.
- ^ PMID 26401028.
- PMID 24453972.
- PMID 1343914.
- ^ (in 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[dead link].
- ISBN 978-0-7020-5101-2.
- S2CID 16670424.
- PMID 25400499.
- PMID 22632645.
- S2CID 28975630.
- PMID 11087932.
- S2CID 36830557.
- PMID 18674968.
- PMID 15463396.
- Sanger Institute. Retrieved 2007-06-14.
- PMID 10783255.
- ^ "Schistosoma mansoni Genome Project". The Institute for Genomic Research. Retrieved 2007-06-14.
- S2CID 11387995.
- PMID 19606141.
- ^ "Killer parasites' genes decoded". BBC News. July 16, 2009. Retrieved 2009-07-16.
- PMID 22253936.
- ^ PMID 25685451.
- PMID 2504481.
- PMID 31040989.
- PMID 14699044.
- PMID 25889398.
- PMID 19717340.
- PMID 18345010.
- PMID 22536349.
- PMID 19717340.
- PMID 21586478.
- PMID 25843503.
- ^ PMID 25843503.
- ^ .
- PMID 23450530.
- ^ "Schistosomiasis: Epidemiology". WHO. Archived from the original on October 20, 2014. Retrieved 2021-06-05.
- PMID 10996119.
- PMID 12745133.
- PMID 25636189.
- PMID 25685449.
- CDC. Retrieved 2013-11-05.
- S2CID 23030603.
- S2CID 16670424.
- PMID 9566238.
- ISBN 9780521530606.
- ^ Lofty, W.M. (2009). "Human schistosomiasis in Egypt: Historical review, assessment of the current picture and prediction of the future trends". Journal of the Medical Research Institute. 30 (1): 1–7.
- ISBN 978-1-84826-733-6.
- PMID 17342284.
- ^ PMID 12364371.
- PMID 13821378.
- PMID 18597732.
- ^ Silva, Pirajá da (1917). Schistosomes in Bahia. Bahia, Brazil: Imprensa Official do Estado. p. 32.
- ISBN 978-94-010-5358-7.
External links
- Media related to Schistosoma mansoni at Wikimedia Commons