Schistosoma japonicum is one of the three main Schistosoma trematode flatworms that infect humans and cause schistosomiasis (=bilharziasis), the other two being S. haematobium and S. mansoni (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. japonicum 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.
Various animals--including dogs, cats, rodents, pigs, horses, and goats--serve as reservoirs for S. japonicum. Pathology of S. japonicum 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 japonicum occurs in the Far East.
Schistosoma japonicum is found in China, Taiwan, the Philipines and Southeast Asia. (Roberts and Janovy 2000, WHO 1996)
Biogeographic Regions: palearctic (Native ); oriental (Native )
These parasitic worms have a complex life cycle with many stages.
The first stage, the egg, is round or oval and very small (about 80 by 60 micrometers), with a very small spur on one end.
The first stage that hatches from the egg is called a miracidium, and is not much bigger then the egg. It is free-swimming,ovoid, covered with cilia, and could easily be mistaken for protozoan. It has a complex of glands at the front end that are used to penetrate the skin of a snail host.
Once inside a snail, the miracidium sheds its skin and cilia, and metamorphoses into a different shape called a sporocyst. This stage has no mouth or gut, it takes its food directly from the snail it lives in. Each sporocyst reproduces asexually -- creating daughter sporocysts. These live and grow inside the snail host, completing another round of asexual reproduction, but this time the offspring have a different structure, and are called cercaria.
S. japonicum cercaria look like tiny flatworms with fishtails. The body is about 200 by 70 micrometers, the long thin tail is another 220 micrometers long, and has two "flukes" called furci that are each about 80 micrometers long. The front end is equipped with an array of glands and other structures for entering a new host. This stage leaves the snail and enters a bird or mammal (including humans) host and then transforms again, shedding it's tail and moving through the bloodstream.
The worm finally matures inside the intestinal veins of a mammal. It grows to about 15 mm in length. Males are shorter and stouter than females, and have a long groove on their underside in which the female (should one arrive) attaches herself. Both sexes have a strong sucker around the mouth, and another called an acetabulum, a little ways further down on the ventral side. The skin of the worms is coated with tiny spines, ridges and sensory organs that are probably involved in helping resist and avoid the host immune system.
Other Physical Features: ectothermic ; bilateral symmetry
This species must have snail and vertebrate hosts to survive. The snails it uses live in warm freshwater streams, ponds, and ditches.
Terrestrial Biomes: forest ; rainforest ; scrub forest
Aquatic Biomes: benthic
The source of the worm's nutrition is the host. The sporocyst stage absorbs nutrition through its skin, taking it directly from the tissues of its snail host. Adult worms feed on blood in the intestinal veins where they live (Roberts and Janovy 2000)
Life History and Behavior
This species reproduces sexually: a male and female worm must mate in the veins of the host before the female can lay eggs (many other flatworms can produce eggs without mating first). Female worms produce enormous numbers of offspring: a single mated pair may release 3,000 eggs per day, and live for over 20 years. Through a complex process involving secretions from the egg and the hosts' immune system, the eggs are moved through the wall of the vein and into the gut or bladder, where they are excreted by the host. Once they are exposed to freshwater the eggs hatch, and the miracidium emerges. This stage lives for only a few hours, and must find a snail in the genus Oncomelania to tunnel into or it will die. Inside the snail it becomes a sporocyst (larva). While in the snail the sporocysts reproduce asexually and become daughter sporocysts. The daughter sporcysts then reproduce asexually again, this time producing cercaria. It is in this stage that they enter humans and other vertebrates. The cercaria emerge from their snail host and swim in the water. If they contact a host, they quickly stick to the skin and shed their tail. Then they secrete digestive compounds that allow them to penetrate the skin of the host and enter the hosts' circulatory system. They transform again, this time into adult worms that live in the veins of the small intestine (all sources)
Parental Investment: no parental involvement
Molecular Biology and Genetics
Barcode data: Schistosoma japonicum
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 japonicum
Public Records: 21
Specimens with Barcodes: 21
Species With Barcodes: 1
There are currently no conservation efforts for this animal. Because of its negative effects on humans most efforts are aimed at destruction and containment. The World Health Organization is working on "...controlling morbidity...health education and provision of safe water." (WHO pg 3) The climate in which the flatworm is found dictates the types of control that we are able to exert in an effort to contain and eradicate it.
US Federal List: no special status
CITES: no special status
Relevance to Humans and Ecosystems
S. japonicum is a parasite that uses humans as a primary host, and is a major cause of disease in the regions where it lives. Most of the harm it causes is due to the massive number eggs released. These trigger immune responses that in turn cause many health problems. As the eggs move through the host tissues, they cause fevers, weakness, liver and kidney damage, blood in the urine, and abdominal pain. In a few cases the eggs drift in the circulatory system and end up in other parts of the body, including the brain, causing even more severe damage. In places where this species occurs, many rural people are afflicted with this condition, called schistosomiasis (All Sources).
This animal does not benefit humans.
Schistosoma japonicum is an important parasite and one of the major infectious agents of schistosomiasis.This parasite has a very wide host range, infecting at least 31 species of wild mammals, including 9 carnivores, 16 rodents, one primate (Human), two insectivores and three artiodactyls and therefore it can be considered a true zoonosis.
Schistosoma japonicum is the only human blood fluke that occurs in China. It is the cause of schistosomiasis japonica, a disease that still remains a significant health problem especially in lake and marshland regions. Schistosomiasis is an infection caused mainly by three schistosome species; Schistosoma mansoni, Schistosoma japonicum and Schistosoma haematobium. S. japonicum being the most infectious of the three species. Infection by schistosomes is followed by an acute Katayama fever. Historical accounts of Katayama disease dates back to the discovery of S. Japonicum in Japan in 1904. The disease was named after an area it was endemic to, Katayama district, Hiroshima, Japan. If left untreated, it will develop into a chronic condition characterized by hepatosplenic disease and impaired physical and cognitive development. The severity of S. japonicum arises in 60% of all neurological diseases in schistosomes due to the migration of schistosome eggs to the brain.
The S. japonicum worms are yellow or yellow-brown. The males of this species are slightly larger than the other Schistosomes and they measure ~ 1.2 cm by 0.5 mm. The females measure 2 cm by 0.4 mm. The adult worms are longer and narrower than the related S. mansoni worms.
By electron microscopy there are no bosses or spines on the dorsal surface of the male, which is ridged and presents a spongy appearance. Many spines cover the inner surface of the oral sucker and extend to the pharyngeal opening. The oral sucker shows a rim with spines of variable size and sharpness inward and outward from the rim. The ventral sucker possesses many spines which are smaller than in the oral sucker. The lining of the gynecophoric canal is roughened by minute spines. The integument of the female is ridged and pitted and possesses fewer spines than in the oral sucker, the ventral sucker, and the gynecophoric canal of the male. Anterior to the acetabulum, the integumental surfaces are devoid of spines. However, in the other areas, spines are equally distributed except for the vicinity of the excretory pore.
The ova are about 55 - 85 μm by 40 - 60 μm, oval with a minute lateral spine or knob.
The life cycles of Schistosoma japonicum and Schistosoma mansoni are very similar. In brief, eggs of the parasite are released in the feces and if they come in contact with water they hatch into free-swimming larva, called miracidia. The larva then has to infect a snail of the genus Oncomelania such as species of Oncomelania hupensis within one or two days. Inside the snail, the larva undergo asexual reproduction through a series of stages called sporocysts. After the asexual reproduction stage cercaria (another free-swimming larva) are generated in large quantities, which then leave (shed into the environment) the snail and must infect a suitable vertebrate host. Once the cercaria penetrates the skin of the host it loses its tail and becomes a schistosomule. The worms then migrate through the circulation ending at the mesenteric veins where they mate and start laying eggs. Each pair deposits around 1500 – 3500 eggs per day in the vessels of the intestinal wall. The eggs infiltrate through the tissues and are passed in the feces.
Once the parasite has entered the body and begun to produce eggs, it uses the hosts' immune system (granulomas) for transportation of eggs into the gut. The eggs stimulate formation of granuloma around them. The granulomas, consisting of motile cells, carry the eggs to the intestinal lumen. When in the lumen, granuloma cells disperse leaving the eggs to be excreted within feces. Unfortunately, about two-thirds of eggs are not excreted, instead they build up in the gut. Chronic infection can lead to characteristic Symmer's fibrosis (also known as "clay pipe stem" fibroses, these occur due to intrahepatic portal vein calcification which assume the shape of a clay pipe in cross section). S. japonicum is the most pathogenic of the schistosoma species because it produces up to 3,000 eggs per day, ten times greater than that of S. mansoni..
As a chronic disease, S. japonicum can lead to Katayama fever, liver fibrosis, liver cirrhosis, liver portal hypertension, splenomegaly, and ascites. Some eggs may pass the liver and enter lungs, nervous system and other organs where they can adversely affect the health infected individual.
Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected.
Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Since eggs may be passed intermittently or in small amounts, their detection will be enhanced by repeated examinations and/or concentration procedures (such as the formalin - ethyl acetate technique). In addition, for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique.
Eggs can be found in the urine in infections with S. haematobium (recommended time for collection: between noon and 3 PM) and with S. japonicum. Detection will be enhanced by centrifugation and examination of the sediment. Quantification is possible by using filtration through a Nucleopore membrane of a standard volume of urine followed by egg counts on the membrane. Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium) may demonstrate eggs when stool or urine examinations are negative.
Since the eggs of S. japonicum are small, concentration techniques may be required. Biopsies are mostly performed to test for chronic schistomiasis with no eggs. An ELISA test can be performed to test for antibodies specific to schistosomes. A positive result indicates a present or recent infection (within the past two years). Ultrasonographic examination can be performed to assess the extent of hepatic and spleen-related morbidity. The problems with immunodiagnostic methods are that 1) It is only positive a certain time after infection 2) They can cross interact with other helminthes infections.
The chemotherapy of choice is praziquantel, a quinolone derivative. Praziquantel is generally administered in an oral form in one or two doses from 40–60 mg/kg body weight.
Combination treatment may prevent morbidity due to schistosomiasis. Praziquantel is most active against adult worms. However, it has been found that artemether prevents the development of adult worms, thus decreasing egg production in the host. If both praziquantel and artemether can be used together, the entire lifespan of S. japonicum would be covered in the vertebrate host.
Human waste should be hygienically disposed of. Human waste in water with the Oncomelania snail intermediate host is a major cause to the perpetuation of schistosomiasis. To prevent this from occurring, human waste should never be used for nightsoiling (fertilization of crops with human waste) and unsanitary conditions should be improved. To avoid infection, individuals should avoid contact with water that is contaminated by human or animal waste, especially water sources that are endemic to Oncomelania snails.
If necessary to enter potentially infected water, cercarial repellants and cercaricidal ointments can be applied to the skin before entering the water. Barrier cream with a dimethicone base offered high levels of protection for at least 48 hours.
The search for a practical vaccine continues and could greatly benefit affected areas.
Control against infection of S. japonicum requires multiple efforts consisting of education, eliminating the disease from infected individuals, controlling the vector, and providing a protective vaccine.
Education can be highly effective, but difficult with lack of resources. Also, asking people to change customs, traditions and behaviors can prove a difficult task.
Controlling S. japonicum with molluscicide has proved ineffective because Oncomelania snails are amphibious and only frequent water to lay their eggs.
Individuals at risk to infection from S. japonicum are farmers who often wade in their irrigation water, fisherman that wade in streams and lakes, children that play in water, and people who wash clothes in streams.
Ablution is a religious requirement in some Moslem countries to achieve cleanliness by washing of the anal or urethral orifices after urination or defecation. However, this act leads to the transmission of schistosomiasis. The water source typically used for ablution is a contaminated river or canal from previously deposited human waste, thus furthering the contamination in the population.
Important factors to influence transmission are age, sex of an individual, as well as the economic and educational level of a population. Males show the highest rates of infection, as well as the most intense infections. This may be due to occupational risk. As was the case of Suriname, the highest prevalence occurs in both sexes where both male and females work in fields.
Climate change may have potential impact on the transmission of schistosomiasis in China. The development of S. japonicum in the intermediate host Oncomelania hupensis occurred at the threshold of 15.4°C. Previously, O. hupensis has been restricted to areas where the mean January temperature has been over 0°C. With rising climate change, it is predicted that by 2050, O. hupensis will be able to cover 8.1% of the surface area of China, thus leading to greater concern to new populations being at risk to schistosomiasis.
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