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Schistosomiasis

From Academic Kids

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Skin vesicles created by the penetration of Schistosoma. Source: CDC

Schistosomiasis or bilharzia is a disease affecting many people in developing countries. It is also called snail fever or 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.

There are 5 species of flatworms that cause schistosomiasis. Each causes a different clinical presentation of the disease. It should be noted that schistosomiasis may 'metastize' to different parts of the body irrespective of its particular clinical profile.

  • Schistosoma mansoni and S. intercalatum cause intestinal schistosomiasis
  • Schistosoma haematobium causes urinary schistosomiasis
  • Schistosoma japonicum and S. mekongi cause Asian intestinal schistosomiasis
Contents

Geographical distribution and epidemiology

The disease is found in tropical 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 snails (usually of the Biomphalaria genus) that are the natural reservoirs of the Schistosoma pathogen.

Life cycle

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Schistosomiasis life cycle. Source: CDC

Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with man being the definitive host. The life cycles of all three human schistosomes are broadly similar: parasite eggs are released into the environment from infected individuals, rupturing on contact with fresh water to release the free-swimming miracidium. Miracidia infect fresh-water snails by penetrating the snail's foot. After infection, the miracidium divides into thousands of new parasites, known as cercariae, which are the infective larvae.

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 reamin 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 through the blood system to various sites around the body. Parasites either traverse capillary beds and re-enter the circulation, or become, particularly if crossing the hepatic portal vein, become lodged in a post-capillary venule. 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 depedent upon the male for nutrition. Adult worms are about 10 mm long. Worm pairs relocate to site is the mesenteric or rectal veins. S. haematobium schistosomula typically migrate from the site of penetration though the lungs to the vesical plexes of the bladder wall. 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 throught the intestingal 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 though the release of proteolytic enzymes. Up to half the eggs released by the worm pairs become trapped iun 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.

Pathology

Above all, schistosomiasis is a chronic disease. Pathology of S. mansoni and 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. Pathology of S. haematobium schistosomiasis includes: hematuria, scarring, 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.

Clinical features

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Photomicrography of bladder in S. hematobium infection, showing clusters of the parasite eggs with intense eosinophilia, Source: CDC

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 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:

Laboratory diagnosis

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. 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.

Antibody detection can be useful in both in clinical management (e.g., recent infections) and for epidemiologic surveys.

Treatment

Schistosomiasis is readily treated using a single oral megadose of the drug Praziquantel. Whilst Praziquantal 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 metal 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.

Prevention and hygiene

The main focus of prevention is eliminating the water-borne snails which are natural reservoirs for the disease. This is usually done by indentifying 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.

References

External links

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