(schis•to•so•mi•a•sis) noun
(also known as bilharzia, bilharziosis or snail fever)
By Haitham Mekkawi M.D.
Etiology and Epidemiology
caused by several species of fluke (Trematods) of the genus Schistosoma.
It is most commonly found in Asia, Africa, and South America, especially in areas with water that is contaminated with freshwater snails, which may carry the parasite.
Schistosomiasis affects over 200 milion people in the tropics and subtropics, most of whom live in Sub-Saharan Aafrica, Chronic infection cause significant morbidity,
After Malaria it has the most socio-economic impact of any parasitic disease.
Schistosomiasis is usually disease of rural and poor areas but has also been associated with Development projects such as dams and irrigations schemes.
Parasitology and Pathogenesis
There are many species of Schistosoma that cause the disease, Schistosoma Mansoni, Schistosoma haematobium Schistosoma Japonicum Schistosoma Intercalatum and Schistosoma Mekongi.
The first three are the most common pathogen in man.
Note that. Schistosoma haematobium cause urinary schistosomiasis
Schistosoma mansoni and Schistosoma intercalatum cause intestinal schistosomiasis,
Schistosoma japonicum and Schistosoma mekongi cause Asian intestinal schistosomiasis
Life cycles
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1- In Fresh water parasite eggs are released into the environment from infected individuals, the hatch on contact with fresh water and release the free-swimming miracidium. 2- In Snails Miracidia infect fresh-water snails , After infecting the sniail, the miracidium transforms into a primar(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. |
Source CDC Click picture to Enlarge |
3- In Human body
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 faeces. 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.
Clinical Features
Cercarial penetration of the skin may cause local dermatitis (swimmer’s itch), After the the symptom free period likely 3 to 4 weeks , systemic allergic reaction may develop, Allergic symptoms may include fever, rash, mayalgia, and pneumonitis (Katayama fever), the allergic reactions is typical for visitors and people coming from abroad but in local population its not typical population who are exposed to earlier infection in their childhood.
S. haematobium infection (Bihjarzia)
The early symptom is usually painless terminal haematuria, as the inflammation progress there is increase if urination frequency and groin pain, obstruction uropathy may develop leading to hydronephrosis, renal failure, and recurrent Urinary tract infection, it has been found that urinary schistomiasis is directly linked with squamous cell carcinoma of the bladder, the genitalia may also be effected and ectopic eggs may cause pulmonary or neurological disease.
S. Mansoni
Usually effects the large intestine in the early stages there is superficial mucosal changes associated with blood stained diarrhea, with the progression of the disease the damges of the mucosal damage became more profound and polyps and fibrosis may be seen and finally fibrosis and stricture formation.
Ectopic eggs are carried to the liver where they can cause intense granulomatous response, hepatitis followed by progressive periportal fibrosis leading to portal hypertension, esophageal varices and splenomegaly, liver function usually but not always preserved.
S. Japanicum
Unlike other species it has tendancy to infect numerous mammals apart of man,
Its clinical findings are similer to those of S. Mansoni but it infect both small and large intestine it produce more amounts of eggs than S. Mansoni therefore the disease tend to be more severe and progress rapidly hepatic involvement is more common neurological involvement is observed in 5% of the patients.
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Diagnosis Allergic reaction with signs of penetration in expats is suggestive to Schistosomiasis can be after exposure to fresh water in endemic areas, note that esenophilia may be present but non-specific but its highley suggestive if other parasitic infection could be excluded. Ova or eggs can be found in terminal urine sample some time ova can be found in semen, 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. Photomicrography of bladder in S. hematobium infection, showing clusters of the parasite eggs with intense eosinophilia, Source: CDCTissue 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. |
the Ova of S. Mansoni (eggs)
The Ova of S.hematobium
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Treatment Praziquantel is the drug of choice the dose is 40mg/kg the dose can be divided into two doses given apart for S. Japanicom the dose is 60mg/kg given in three doses each dose 20mg/kg at 4 hours interval |
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Salam Alikum wa rahamato Allah..
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Osman
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