Introduction to Schistosomiasis:
- Schistosomiasis was once known as Bilharzia because it was discovered by Theodor Bilharz.
- Schistosoma belongs to class Trematoda of phylum Platyhelminthes. They are commonly called Blood flukes.
- The initial species discovered was S. haematobium.
- Evidence for human infection with these parasites can be found in mummified remains from ancient Egypt and China.
Etiology and Transmission:
Schistosomiasis manifests in both acute and chronic forms, with transmission occurring through contact with contaminated water during everyday tasks like farming, household chores, work, or leisure activities. Children, in particular, face heightened risk due to poor sanitation practices and frequent exposure to water bodies while swimming or fishing. The intestinal form of the disease is primarily triggered by Schistosoma mansoni, S. japonicum, S. mekongi, and S. intercalatum. The parasitic worm that causes urinary schistosomiasis is called Schistosoma haematobium.
Pathogenesis of Schistosomiasis:
All the stages of the parasite are pathogenic for humans, egg being the major pathogenic form.
Schistosomiasis is an immune disease.
Acute stage
Cercarial dermatitis
Cercarial dermatitis manifests as hypersensitivity reactions and maculopapular pruritic rashes because of innate immune responses. A Type I and IV allergic reactions called “Swimmer’s itch” occurs for a short period after cercaria penetration. This stage occurs in individuals exposed to human Schistosoma spp. infection for the first time. Swimmer’s itch is a type of cercarial dermatitis caused by cercariae stage of Schistosoma.
Following the successful maturity of the schistosomula and penetration of cercaria, the acute stage of symptoms starts. Acute symptomatic schistosomiasis, also known as Katayama syndrome or Katayama fever, typically emerges in individuals who have been recently infected, appearing anywhere from two weeks to three months post-exposure. The symptoms stem from an exaggerated immune response and the formation of antigen-antibody complexes, triggered by the movement of schistosomula through the body or the onset of egg-laying. Common signs include fever, muscle and joint aches, abdominal discomfort, diarrhea, and enlargement of the liver and spleen.
Established active infection
Acute schistosomiasis symptoms are rarely seen in most cases, particularly in endemic areas, and the disease progresses to an active infection stage with full adult worms and established egg production. Live eggs are expelled during this phase as feces or urine. Usually, the live adult worms that live in the blood vessels don’t directly create any symptoms or irritate the area. Antigenic glycoproteins, which are actively secreted by schistosome eggs, have the ability to trigger an inflammatory response that facilitates the eggs’ transit from the blood artery to the intestinal or bladder lumen. But these soluble egg antigens also cause granulomas to develop around eggs.
Late chronic infection
Worm burdens eventually decrease in the majority of individuals who are consistently exposed to infection in regions where schistosomiasis is endemic. Less fresh eggs are expelled or deposited in the tissue as a result of the decrease in worms. Immunological downregulation causes new granulomas to be smaller and less inflammatory, while the destruction of the eggs inside the old granulomas causes them to eventually disappear. Fibrous tissue subsequently replaces these granulomas, which lessens the intensity of the symptoms.
Diagnosis of Schistosomiasis:
A high threshold of suspicion is necessary to clinically diagnose infection because the majority of schistosomiasis patients are asymptomatic, particularly in regions where infection is rare.
Since most people infected with schistosomiasis are asymptomatic, a high index of suspicion is required to clinically identify infection, especially in geographic areas where infection is uncommon.
Examination of stool and urine
Stool samples are used to diagnose S. mansoni, S. japonicum, S. intercalatum, and S. mekongi. A variety of concentration techniques can be applied, such as the Kato method with glycolmalachite green, the merthiolate–iodine–formol method, and the formol–ether method. The most used approach for finding eggs in stool is the Kato–Katz thick smear method. The idea behind the Kato–Kato thick smear preparation is to use glycerol to make the feces sample clearer.
The eggs of S. mekongi and S. japonicum are spherical. The eggs of S. mansoni, and S. intercalatum are oval in shape. S. intercalatum eggs are expelled in urine and stool. The eggs of S. japonicum and S. mansoni have lateral spines.
The diurnal periodicity of S. haematobium egg urine output peaks between mid-morning and mid-afternoon. In order to concentrate the parasite eggs, urine collected during this time can either be passed through a cellulose filter or simply sedimented. The latter makes it possible to measure infection. Simple sedimentation or centrifugation methods are being replaced by filtration procedures that provide a quantitative evaluation of egg excretion. Eggs of S. haematobium are oval and have an apical spine.
Fig: Egg of S. mansoni in an unstained wet mount
Fig: Egg of S. haematobium in a wet mount of urine concentrates
Fig: Egg of S. japonicum in an unstained wet mount
Fig: Egg of S. intercalatum in a wet mount
Fig: Egg of S. mekongi
Antigen and Antibody Detection Methods
It includes detection of worm antigens, worm DNA and antischistosome-specific antibodies. Waste materials are regurgitated into the bloodstream by schistosomes when they feed on red blood cells. These products are called circulating anodic antigens (CAAs) and circulating cathodic antigens (CCAs) and they can be detected in serum and urine by enzyme-linked immunosorbent assay (ELISA) or monoclonal-antibody-based lateral flow assays. The detection of circulating anodic antigens (CAAs) or circulating cathodic antigens (CCAs) signals an ongoing schistosome infection, indicating the presence of living worms. Notably, these antigens can be found in the bloodstream even before the parasites begin laying eggs. In contrast, serological tests that identify antibodies specific to schistosome antigens are especially valuable for diagnosing infections in travelers who may have symptoms but shed few or no eggs. The immune system typically starts producing antibodies against adult worm proteins about 4 to 7 weeks post-exposure, with most individuals undergoing seroconversion within three months. However, in individuals residing in schistosomiasis-endemic regions, these antibodies can persist for years after treatment, making it difficult for serological tests to differentiate between active infection and past exposure.
References:
- Centers for Disease Control and Prevention. (2023, November 20). Schistosomiasis. U.S. Department of Health & Human Services. https://www.cdc.gov/dpdx/schistosomiasis/index.html
- Shaker, Y., Samy, N., & Ashour, E. (2014). Hepatobiliary Schistosomiasis. Journal of clinical and translational hepatology, 2(3), 212–216. https://doi.org/10.14218/JCTH.2014.00018
- McManus, DP., Dunne, DW & Sacko, M. Schistosomiasis (2018). Nat Rev Dis Primers, 4(13) https://doi.org/10.1038/s41572-018-0013-8
McManus, D. P., Bergquist, R., Cai, P., Ranasinghe, S., Tebeje, B. M., & You, H. (2020). Schistosomiasis-from immunopathology to vaccines. Seminars in immunopathology, 42(3), 355–371. https://doi.org/10.1007/s00281-020-00789-x