A<unk>  egg with the characteristic lateral spine Schistosome eggs, which may become lodged within the hosts tissues, are the major cause of pathology in schistosomiasis. Some of the deposited eggs reach the outside environment by passing through the wall of the intestine; the rest are swept into the circulation and are filtered out in the periportal tracts of the liver, resulting in periportal fibrosis. Onset of egg laying in humans is sometimes associated with an onset of fever (Katayama fever). This "acute schistosomiasis" is not, however, as important as the chronic forms of the disease. For<unk>  and S. japonicum, these are "intestinal" and "hepatic schistosomiasis", associated with formation of granulomas around trapped eggs lodged in the intestinal wall or in the liver, respectively. The hepatic form of the disease is the most important, granulomas here giving rise to fibrosis of the liver and hepatosplenomegaly in severe cases. Symptoms and signs depend on the number and location of eggs trapped in the tissues. Initially, the inflammatory reaction is readily reversible. In the latter stages of the disease, the pathology is associated with collagen deposition and fibrosis, resulting in organ damage that may be only partially reversible. Granuloma formation is initiated by antigens secreted by the miracidium through microscopic pores within the rigid egg shell, and the immune response to granuloma, rather than the direct action of egg antigens, causes the symptoms. The granulomas formed around the eggs impair blood flow in the liver and, as a consequence, induce portal hypertension. With time, collateral circulation is formed and the eggs disseminate into the lungs, where they cause more granulomas, pulmonary arteritis and, later, cor pulmonale. A contributory factor to portal hypertension is Symmers' fibrosis, which develops around branches of the portal veins. This fibrosis occurs only many years after the infection and is presumed to be caused in part by soluble egg antigens and various immune cells that react to them. Recent research has shown that granuloma size is consistent with levels of IL-13, which plays a prominent role in granuloma formation and granuloma size. IL-13 receptor α 2 (IL-13Rα2) binds IL-13 with high affinity and blocks the effects of IL-13. Thus, this receptor is essential in preventing the progression of schistosomiasis from the acute to the chronic (and deadly) stage of disease. Synthetic IL-13Rα2 given to mice has resulted in significant decreases in granuloma size, implicating IL-13Rα2 as an important target in schistosomiasis.<unk>  infection often occurs alongside those of viral hepatitis, either hepatitis B virus (HBV) or hepatitis C virus (HCV). This is due to high prevalence of schistosomiasis in areas where chronic viral hepatitis is prevalent. One important factor was the development of large reservoir of infection due to extensive schistosomiasis control programs that used intravenously administered tartar emetic since the 1960s. Co-infection is known to cause earlier liver deterioration and more severe illness. Evasion of host immunity Adult and larval worms migrate through the host's blood circulation avoiding the host's immune system. The worms have many tools that help in this evasion, including the tegument, antioxidant proteins, and defenses against host membrane attack complex (MAC). The tegument coats the worm and acts as a physical barrier to host antibodies and complement. Host immune defenses are capable of producing superoxide, but these are counterattacked by antioxidant proteins produced by the parasite. Schistosomes have four superoxide dismutases, and levels of these proteins increase as the schistosome grows. Antioxidant pathways were first recognised as a chokepoints for schistosomes, and later extended to other trematodes and cestodes. Targeting of this pathway with different inhibitors of the central antioxidant enzyme thioredoxin glutathione reductase (TGR) results in reduced viability of worms. Decay accelerating factor (DAF) protein is present on the parasite tegument and protects host cells by blocking formation of MAC. In addition, schistosomes have six homologues of human CD59 which are strong inhibitors of MAC. Diagnosis The presence of<unk>  is detected by microscopic examination of parasite eggs in stool. A staining method called Kato-Katz technique is used for stool examination. It involves methylene blue-stained cellophane soaked in glycerine or glass slides. A bit costlier technique called formalin-ether concentration technique (FECT) is often used in combination with the direct faecal<unk> ear for higher accuracy. Serological and immunological tests are also available. Antibodies and antigens can be detected in the blood using ELISA to identify infection. Adult worm antigens can be detected by indirect haemagglutination assays (IHAs). Polymerase chain reaction (PCR) is also used for detecting the parasite DNA. Circulating cathodic antigen (CCA) in urine can be tested with lateral flow immune-chromatographic reagent strip and point-of-care (POC) tests. Egg detection and immunologic tests are not that sensitive. Polymerase chain reaction (PCR) based testing is accurate and rapid. They, however, are not frequency used in countries were the disease is common due to the cost of the equipment and the technical experience required to run them. Using a microscope to detect eggs costs about US$0.40 per test well PCR is about $US7 per test as of 2019. Loop-mediated isothermal amplification (LAMP) are being studied as they are lower cost. LAMP testing is not commercially available as of 2019. Treatment The standard drug for<unk>  infection is praziquantel at a dose of 40 mg/kg. Oxamniquine is also used.
Schistosoma mansoni
Schistosoma japonicum
Taenia asiatica
Schistosoma haematobium
Taenia solium
Echinostoma cinetorchis
Taenia saginata
Trichuris trichiura