or '''bilharzia''' is a
Disease affecting many people in
Developing Countries . It is also called '''snail fever''' but is not to be confused with
Swimmer's Itch . In certain African communities the process of overcoming Schistosomiasis is an important
Rite Of Passage . Although it has a low
Mortality Rate , schistosomiasis can be very debilitating. ('''Bilharzia''', or '''bilharziosis''', is a largely obsolete eponym, after
Theodor Bilharz , who first described the cause of urinary schistosomiasis in 1851.)
There are five
Species of
Flatworm s that cause schistosomiasis. Each causes a different clinical presentation of the
Disease . Schistosomiasis may 'metastasize' to different parts of the body, and this does not depend on its particular clinical profile.
The disease is found in
Tropic al countries in
Africa ,
Caribbean , eastern
South America , east
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 focally in
Southeast Asia and central
West Africa , respectively.
An estimated 200 million people have the disease, 120 million symptomatic. A few countries have eradicated the disease, and many more are working towards it. The
World Health Organization is working towards this goal. Controlled urbanization has reduced exposure sites, with a subsequent decrease in new infections. The most common way of getting schistosomiasis in developing countries is by swimming in lakes, ponds and other bodies of water which are infested with the
Snail s (usually of the ''
Biomphalaria '' or ''
Oncomelania '' genus) that are the
Natural Reservoir s of the ''Schistosoma'' pathogen.
Schistosomes have a typical . 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 motile, alternating between vigorous upward movement and sinking to maintain their position in the water. Cercarial activity is particularly stimulated by water turbulence, shadows and human skin chemicals. 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 1-2 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 6-8 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 male. She is wholly dependent upon the male for nutrition. Adult worms are about 10 mm long. Worm pairs relocate to the
Mesenteric or rectal veins. ''S. haematobium'' schistosomula ultimately migrate from the liver to the perivesical venous plexus through the hemorrhoidal plexus. Once they have fully matured, adult schistosomes are unable to undergo any further migration through the body.
Parasites reach maturity in 6-8 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 faeces. ''S. haematobium'' eggs pass through the bladder wall and into the urine. Only mature eggs are capable of crossing into the digestive tract, possibly through the release of
Proteolytic enzymes. Up to half the eggs released by the worm pairs become trapped in the mesenterice veins, or will be washed back into the liver, where they will become lodged. Worm pairs can live in the body for up to five 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.
Above all, schistosomiasis is a chronic disease. Pathology of ''S. mansoni'' and ''S. japonicum'' schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg ,
Scar ring,
Calcification ,
Squamous Cell Carcinoma , and occasional embolic egg granulomas in brain or spinal cord.
Bladder Cancer diagnosis and mortality are generally elevated in afflicted areas.
Many infections are
Asymptomatic . Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by ''S. mansoni'' and ''S. japonicum''. Manifestations include:
Occasionally 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:
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 (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. Investigation of ''S. japonicum'' should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection.
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.
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 (e.g., recent infections) and for
Epidemiologic surveys.
Schistosomiasis is readily treated using a single oral megadose of the drug
Praziquantel . While Praziquantel is safe and highly effective in curing an infected patient, it does not prevent re-infection by cercariae and is thus not an optimum treatment for people living in endemic areas. As with other major parasitic diseases, there is ongoing and extensive research into developing a vaccine that will prevent the parasite from completing its life cycle in humans.
Antimony has been used in the past to treat the disease. In low doses this
Toxic metalloid bonds to
Sulfur atoms in
Enzymes used by the bug and kills it without harming the host. This treatment is not referred to in present-day
Peer-review scholarship;
Praziquantel is universally used. Outside of the US, there is a second drug available for treating Schistosoma mansoni (exclusively) called
Oxamniquine .
The main focus of prevention is eliminating the water-borne snails which are
Natural Reservoir s for the disease. This is usually done by identifying bodies of water, such as lakes, ponds, etc., which are infested, forbidding or warning against swimming and adding
Acrolein ,
Copper Sulfate , etc., to the water in order to kill the snails.
In 1989,
Aklilu Lemma and
Legesse Wolde-Yohannes received the
Right Livelihood Award for their research on the
Sapindus -Plant (''Phytolacca dodecandra''), as a preventative measure for the disease.
Recent studies have indicated the possibility of biocontrol of the parasite. Introducing or adding to existing populations of crayfish in the ponds and rivers where the parasite is prevalent would keep host snail populations down, thus significantly reducing the parasite population.
