Schistosomiasis
A tropical helminth infection spread by contaminated freshwater snails.
Schistosomiasis, also known as snail fever, bilharzia, and Katayama fever, is a tropical helminth infection caused by parasitic flatworms of the genus Schistosoma. It affects the urinary tract or intestines and is spread through contact with fresh water contaminated by parasites released from infected freshwater snails. The disease is classified as a neglected tropical disease and is second only to malaria in economic significance among parasitic diseases in tropical regions.
Quick Facts
- Field
- Infectious disease
- Symptoms
- Abdominal pain
- diarrhea
- bloody stool
- blood in the urine
- Causes
- Schistosomes from freshwater snails
- Diagnosis
- Finding eggs of the parasite in urine or stool, antibodies in blood
- Prevention
- Access to clean water
- Medication
- Praziquantel
- Frequency
- 252 million (2015)
- Deaths
- 4,400–200,000
Facts from the source article.
Did You Know?
- A case in Germany was reported where a man contracted schistosomiasis from an infected snail in his aquarium.
- The drug praziquantel eliminates adult schistosomes but does not kill eggs or immature worms; live eggs can be excreted for weeks after treatment.
Signs and symptoms
Many people with schistosomiasis show no signs at all. When symptoms do appear, they usually start four to six weeks after infection, often with a vague sense of being unwell. Within the first half-day, a person may develop swimmer's itch, a rash at the spot where the parasite entered the skin. This rash can look like scabies and, in someone who has never been infected before, is usually mild and prickly, fading on its own. In those previously infected, the rash can turn into raised red bumps or fluid-filled blisters up to three centimeters wide. A more serious reaction, Katayama fever, can arise two to eight weeks later, bringing fever, muscle aches, cough, bloody diarrhea, chills, swollen lymph nodes, and sometimes trouble breathing. If parasite eggs reach the brain or spinal cord, seizures, paralysis, or inflammation may follow. Long-term infection can harm the liver, kidneys, and bladder, or cause infertility. In children, it can stunt growth and cause learning problems.
Transmission and life cycle
Infected individuals release Schistosoma eggs into water through feces or urine. After hatching, free-swimming larvae called miracidia infect specific freshwater snails: Bulinus for S. haematobium and S. intercalatum, Biomphalaria for S. mansoni, and Oncomelania for S. japonicum. Inside the snail, the larvae undergo two generations of sporocysts, then develop into fork-tailed cercariae that leave the snail and enter the water. Cercariae can survive in water for only 48 hours without a mammalian host. Humans become infected when cercariae penetrate the skin during activities such as bathing, swimming, washing, fishing, or walking through contaminated water. Once inside, cercariae lose their tails, become schistosomulae, and travel through venous circulation to the lungs and heart, eventually reaching the liver to mature into adult worms. After mating, adult worms produce eggs that enter the bladder or intestine and are excreted in urine or feces, continuing the cycle. Eggs that are not excreted can become embedded in body tissues, causing immune reactions and organ damage.
Pathogenesis
Infection begins when cercariae penetrate human skin using suckers, proteolytic enzymes, and tail movements, then transform into schistosomulae by losing their tail. The schistosomulae travel through the venous system to the heart and lungs, eventually reaching the liver to mature into adult worms. The disease is categorized as acute or chronic schistosomiasis, with manifestations varying by species. Minutes to days after infection, cercarial dermatitis (swimmer's itch) occurs as a localized allergic reaction at penetration sites, producing itchy red pimples and blisters. Weeks to months later, acute schistosomiasis (Katayama fever) may develop, thought to result from a systemic immune response involving immune complex formation (Type III hypersensitivity) against migratory schistosomula and eggs, leading to tissue deposition and autoimmune activation. Acute schistosomiasis from S. mansoni and S. haematobium typically affects first-time infected individuals such as tourists, while S. japonicum can cause acute disease in reinfected residents of endemic areas, with higher incidence and worse prognosis due to abundant egg antigens forming large immune complexes that enlarge lymph tissues, potentially causing fever, splenomegaly, hepatomegaly, portal hypertension, and death.
Diagnosis
Diagnosis is confirmed by identifying Schistosoma eggs in stool or urine. For S. mansoni or S. japonicum, stool examination is performed; for S. haematobium, urine examination is used, with collection recommended between noon and 3 PM. Eggs may be present in stool for all species. Detection is enhanced by repeated examinations or concentration procedures. The Kato-Katz technique, a semiquantitative stool examination using 20–50 mg of fecal material, is commonly used for field surveys and quantification. Other diagnostic methods include enzyme-linked immunosorbent assay, circumoval precipitation test, and alkaline phosphatase immunoassay. Tissue biopsy (rectal biopsy for all species, bladder biopsy for S. haematobium) may reveal eggs when stool or urine tests are negative. Urine reagent strips to confirm microhematuria are more accurate than circulating antigen tests for identifying active schistosomiasis in endemic areas. Antibody detection can be useful for travelers to endemic regions when eggs are not found in stool or urine, though test sensitivity and specificity vary widely depending on antigen preparations and test procedures.
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