Schistosomiasis

Common symptoms of schistosomiasis are intestinal inflammation and cachexia.

 

IL-23 is partial responsible for both conditions, and suppression of IL-23 p40 in acute schistosomiasis neutralizes both the inflammation and cachexia.

Three species associated with human disease: S mansoni, S hematobium, and S japonicum.

Long-lived infection by multicellular intravascular parasites involving one of five trematode species: Shistosoma japonicum, S. mansoni, S. haemoatobium, S intercalatum or S. mekongi.

S. mansoni-intestinal schistosomiasis transmitted through feces.

S.haematobium-urogenital schistosomiasis transmitted through urine.

Schistosoma haematobium and S. mansoni have the highest prevalence and cause the greatest burden of disease.

Approximately 90% of cases occur in sub-Saharan Africa.

Second most common tropical disease behind malaria

More than 100 million people are infected with Schistosoma hematobium causing disease of the urinary tract and pelvic organs.

Continues to spread with increasing frequency.

Acquired through contact with freshwater contaminated with larval helminths, known as cercariae, which are produced by intermediate snail hosts of the parasite.

Often a prolonged illness which may be decades long and associated with chronic inflammation, with severe anemia, malnutrition and poor performance in school and work.

Symptoms include anemia, fever, genital lesions, irreversible organ damage and stunting.

Parasitic transmission linked to developmental stages that occur in fresh water and a period of growth in an intermediate host snail, such that there is significant geographic localization of the disease.

In patients with intestinal disease late complications lead to fibrosis and portal hypertension with a substantial risk of life-threatening esophageal variceal bleeding.

With urinary Schistosomiasis late complications include urinary tract obstruction with renal failure and inflammatory related bladder cancer.

S. Japonicum induces the highest risk of infection related inflammation and other complications of the disease.

Urinary tract disease is a specific trait of infection with Schistosoma hematobium, while GI and liver disease are usually associated with Schistosoma mansoni and so Schistosoma japonicum, respectively.

Parasitic infection caused by trematode flatworms in the venous system of the intestines and bladder.

S japonicum adult worms inhabit the mesenteric and portal veins.

Man is the principal host of S japonicum.

Female worms occupy a groove in the lateral edge of the male worm’s body.

Female worms produce approximately 3,000 eggs per day and production begins 4-6 weeks after infection and continues for the 3-5 year life of the worm.

Eggs excreted into the lumen of the bowel or bladder and excreted in the feces (S mansoni and S japonicum)or urine (S hematobium).

Eggs that hatch into fresh water and release motile ciliated miracidia which penetrate the body of a host snail and asexually multiply and emerge as motile cercaria.

Cercaria enter humans by penetrating the skin, lose therapy tails and change into schistosomula before migrating to the liver and lungs.

After six weeks the schistosomula mature into adult worms, mate and go to the venous system for habitation.

Hematuria and dysuria are common in both early and late stage disease.

Hematuria is the first sign of established disease appearing 10-12 weeks after infection.

Can cause serious urinary tract complications, including hydronephrosis, renal failure, and bladder cancer due to the presence of schistosome eggs in the bladder and a vigorous inflammatory response as a result.

Principal cause of rectal prolapse in certain geographical areas of the world secondary to dysentery and schistosomal polyps on rectal mucosa.

In Egypt disease occurs in rural areas, among young men exposed to Nile irrigation water infested with S mansoni.

Hematobium infection occurs in tropical Africa, parts of North Africa, Arabian peninsula, Middle East, Madagascar and islands of the Indian Ocean.

Schistosoma haematobium is associated with contaminated water and is often seen in travelers or persons from areas in which this organism is endemic, such as the Middle East.

Schistosoma haematobium patients usually present with hematuria and the diagnosis is made by observing the trematode eggs in the urine (Badmos KB et al).

Spread by direct contact with fresh water contaminated with the parasites released in a larval stage from infected freshwater snails.

Humans encounter the larvae when they enter contaminated water while bathing, playing, swimming, washing, fishing, or simply walking through the water.

Sub-Saharan Africa site of majority of urinary schistosomiasis, with highest prevalence in school aged children, adolescents and young adults.

In North America and Europe most cases of urinary schistosomiasis found in immigrant populations.

In terms of socioeconomic in public health impact this is second only to malaria among parasitic diseases.

Continued loss of mucous and blood in stool can lead to severe anemia and rectal prolapse.

Symptoms result from chronic immune granulomatous response to schistosome eggs.

Granulomatous disease develops in the intestine, genitourinary tract and liver, the sites of maximal egg accumulations.

Granulomatous changes include inflammation, hyperplastic changes, ulcerations and development of polyps, which can lead the rectal prolapse.

Hypersplenism secondary to chronic granulomatous disease in the liver may result.

Praziquantel is the drug of choice.

Praziquantel distributed to school age children 5-15 years of age who have the highest infection burden and who can be reached efficiently through schools.

It is a preventive chemotherapy based on the prevalence of the infection.

The preventive chemotherapy management is determined by the prevalence of the infection: below 10% entails the administration of the drug every three years; 10 to 49% treatment every two years; and 50% or greater, treatment annually.

Praziquantel mainstay of treatment and cures 60-90% of patients.

For patients not cured, Praziquantel, can decreases worm burden and egg production.

The emergence of resistance to Praziquantel may be occurring.