Schistosomiasis (also known as bilharzia, bilharziosis or snail fever) is a parasitic disease caused by several species of fluke of the genus ''Schistosoma''.
Although it has a low mortality rate, schistosomiasis often is a chronic illness that can damage internal organs and, in children, impair growth and cognitive development.
Species of Schistosoma that can infect humans:
- ''Schistosoma mansoni'' (ICD-10 B65.1) and ''Schistosoma intercalatum'' (B65.8) cause intestinal schistosomiasis
- ''Schistosoma haematobium'' (B65.0) causes urinary schistosomiasis
- ''Schistosoma japonicum'' (B65.2) and ''Schistosoma mekongi'' (B65.8) cause Asian intestinal schistosomiasis
Species of Schistosoma that can infect other animals:
- S. bovis - (normally infecting cattle, sheep and goats in Africa, parts of Southern Europe and the Middle East)
- S. mattheei - (normally infecting cattle, sheep and goats in Central and Southern Africa)
- S. margrebowiei - (normally infecting antelope, buffalo and waterbuck in Southern and Central Africa)
- S. curassoni - (normally infecting domestic ruminants in West Africa) has been reported.
- S. rodhaini - (normally infecting rodents and carnivores in parts of Central Africa).
Above all, schistosomiasis is a chronic disease. Many infections are subclinically symptomatic, with mild anemia and malnutrition being common in endemic areas. Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by ''S. mansoni'' and ''S. japonicum''. Manifestations include:
- Abdominal pain
- Eosinophilia - extremely high eosinophil granulocyte (white blood cell) count.
- Hepatosplenomegaly - the enlargement of both the liver and the spleen.
- Genital sores - lesions that increase vulnerability to HIV infection. Lesions caused by Schistosomiasis may continue to be a problem after control of the Schistosomiasis infection itself. Early treatment, especially of children, which is relatively inexpensive, prevents formation of the sores.
- Skin symptoms: At the start of infection, mild itching and a papular dermatitis of the feet and other parts after swimming in polluted streams containing cercariae.
Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic ''S. japonicum'' eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from ''S. mansoni'' and ''S. haematobium'' infections may result in a transverse myelitis with flaccid paraplegia.
Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include:
- Colonic polyposis with bloody diarrhea (''Schistosoma mansoni'' mostly);
- Portal hypertension with hematemesis and splenomegaly (''S. mansoni'', ''S. japonicum'');
- Cystitis and ureteritis (''S. haematobium'') with hematuria, which can progress to bladder cancer;
- Pulmonary hypertension (''S. mansoni'', ''S. japonicum'', more rarely ''S. haematobium'');
- Glomerulonephritis; and central nervous system lesions.
Bladder Cancer diagnosis and mortality are generally elevated in affected areas.
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive host.
The life cycles of all five human schistosomes are broadly similar: parasite eggs are released into the environment from infected individuals, hatching on contact with fresh water to release the free-swimming miracidium. Miracidia infect fresh-water snails by penetrating the snail's foot. After infection, close to the site of penetration, the miracidium transforms into a primary (mother) sporocyst. Germ cells within the primary sporocyst will then begin dividing to produce secondary (daughter) sporocysts, which migrate to the snail's hepatopancreas. Once at the hepatopancreas, germ cells within the secondary sporocyst begin to divide again, this time producing thousands of new parasites, known as cercariae, which are the larvae capable of infecting mammals.
Cercariae emerge daily from the snail host in a circadian rhythm, dependent on ambient temperature and light. Young cercariae are highly mobile, alternating between vigorous upward movement and sinking to maintain their position in the water. Cercarial activity is particularly stimulated by water turbulence, by shadows and by chemicals found on human skin.
Penetration of the human skin occurs after the cercaria have attached to and explored the skin. The parasite secretes enzymes that break down the skin's protein to enable penetration of the cercarial head through the skin. As the cercaria penetrates the skin it transforms into a migrating schistosomulum stage.
The newly transformed schistosomulum may remain in the skin for 2 days before locating a post-capillary venule; from here the schistosomulum travels to the lungs where it undergoes further developmental changes necessary for subsequent migration to the liver. Eight to ten days after penetration of the skin, the parasite migrates to the liver sinusoids. ''S. japonicum'' migrates more quickly than ''S. mansoni'', and usually reaches the liver within 8 days of penetration. Juvenile ''S. mansoni'' and ''S. japonicum'' worms develop an oral sucker after arriving at the liver, and it is during this period that the parasite begins to feed on red blood cells. The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the shorter male. Adult worms are about 10 mm long. Worm pairs of ''S. mansoni'' and ''S. japonicum'' relocate to the mesenteric or rectal veins. ''S. haematobium'' schistosomula ultimately migrate from the liver to the perivesical venous plexus of the bladder, ureters, and kidneys through the hemorrhoidal plexus.
Parasites reach maturity in six to eight weeks, at which time they begin to produce eggs. Adult ''S. mansoni'' pairs residing in the mesenteric vessels may produce up to 300 eggs per day during their reproductive lives. ''S. japonicum'' may produce up to 3000 eggs per day. Many of the eggs pass through the walls of the blood vessels, and through the intestinal wall, to be passed out of the body in feces. ''S. haematobium'' eggs pass through the ureteral or bladder wall and into the urine. Only mature eggs are capable of crossing into the digestive tract, possibly through the release of proteolytic enzymes, but also as a function of host immune response, which fosters local tissue ulceration. Up to half the eggs released by the worm pairs become trapped in the mesenteric veins, or will be washed back into the liver, where they will become lodged. Worm pairs can live in the body for an average of four and a half years, but may persist up to 20 years.
Trapped eggs mature normally, secreting antigens that elicit a vigorous immune response. The eggs themselves do not damage the body. Rather it is the cellular infiltration resultant from the immune response that causes the pathology classically associated with schistosomiasis.
Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. The stool exam is the more common of the two. For the measurement of eggs in the feces of presenting patients the scientific unit used is epg or eggs per gram. 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. japonicum'' and with ''S. intercalatum'' (recommended time for collection: between noon and 3 PM). 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. Investigation of ''S. haematobium'' should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection.
Recently a field evaluation of a novel handheld microscope was undertaken in Uganda for the diagnosis of intestinal schistosomiasis by a team led by Dr. Russell Stothard who heads the Schistosomiasis Control Initiative at the Natural History Museum, London. His report abstract may be found here: biopsy (rectal biopsy for all species and biopsy of the bladder for ''S. haematobium'') may demonstrate eggs when stool or urine examinations are negative.
The eggs of ''S. haematobium'' are ellipsoidal with a terminal spine, ''S. mansoni'' eggs are also ellipsoidal but with a lateral spine, ''S. japonicum'' eggs are spheroidal with a small knob.
Antibody detection can be useful in both clinical management and for epidemiologic surveys.
Prevention is best accomplished by eliminating the water-dwelling snails that are the natural reservoir of the disease. Acrolein, copper sulfate, and niclosamide can be used for this purpose. Recent studies have suggested that snail populations can be controlled by the introduction of, or augmentation of existing, crayfish populations; as with all ecological interventions, however, this technique must be approached with caution.
In 1989, Aklilu Lemma and Legesse Wolde-Yohannes received the Right Livelihood Award for their research on the Sarcoca plant, as a preventative measure for the disease by controlling the snail. Concurrently, Dr Chidzere of Zimbabwe researched the similar Gopo Berry during the 1980s and found that it could be used in the control of infected freshwater snails. In 1989 he drew attention to his concerns that big chemical companies denigrated the Gopo Berry alternative for snail control. Reputedly Gopo Berries from hotter Ethiopia climates yield the best results. Later studies were conducted between 1993 and 1995 by the Danish Research Network for international health.
For many years from the 1950s onwards, civil engineers built vast dam and irrigation schemes, oblivious to the fact that they would cause a massive rise in water-borne infections from schistosomiasis. The detailed specifications laid out in various UN documents since the 1950s could have minimised this problem. Irrigation schemes can be designed to make it hard for the snails to colonize the water, and to reduce the contact with the local population.
This has been cited as a classic case of the Relevance paradox because guidelines on how to design these schemes to minimise the spread of the disease had been published years before, but the designers were blissfully unaware of them.
Schistosomiasis is readily treated using a single oral dose of the drug praziquantel annually. As with other major parasitic diseases, there is ongoing and extensive research into developing a schistosomiasis vaccine that will prevent the parasite from completing its life cycle in humans.
The World Health Organization has developed guidelines for community treatment of schistosomiasis based on the impact the disease has on children in endemic villages:
Experiments have shown medicinal castor oil as an oral anti-penetration agent to prevent schistosomiasis and that Praziquantel's effectiveness depended upon the vehicle used to administer the drug (e.g., Cremophor / Castor oil).
The disease is found in tropical countries in Africa, the Caribbean, eastern South America, southeast Asia and in the Middle East. ''Schistosoma mansoni'' is found in parts of South America and the Caribbean, Africa, and the Middle East; ''S. haematobium'' in Africa and the Middle East; and ''S. japonicum'' in the Far East. ''S. mekongi'' and ''S. intercalatum'' are found locally in Southeast Asia and central West Africa, respectively.
The disease is endemic to 74 countries, affecting an estimated 200 million people, half of whom live in Africa.
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