User:Checkoutchek/Schistosomiasis

Pathogenesis
The infectious stage starts when the free-swimming larval form of the schistosome, cercariae, penetrates the human skin using their suckers, proteolytic enzymes, and tail movements; the cercariae transformed into schistosomulae by losing its tail and subsequently travels to the heart and lungs through venous system until it eventually reach the liver where it will mature into the adult form. The diseases caused by the schistomes are characterized into acute schistosomiasis and chronic schistosomiasis, and they can vary dependent on the species of schistosome.

Acute Infection


 * Minutes to days after initial infection:
 * Cercerial dermatitis (Swimmer's itch) - swimmer's itch is caused by a localized allergic reaction at the sites of skin penetration by the cercariae causing an inflammatory reaction that is characterized by itchy red pimples and blisters.


 * Few weeks to months after initial infection:
 * Acute Schistosomiasis (Katayama's Fever) - the exact pathophysiology of this disease remains unknown. It has been hypothesized to be caused by a systemic immune response due to immune complex formation (Type III hypersensivity) with the foreign antigens on the migratory schistosomula and the eggs, and the subsequent deposition of these complexes on various tissues leading to activation of an autoimmune response. Acute schistosomiasis caused by S. mansoni and S. haematobium generally affect people who have been infected for the first time such as tourists visiting endemic regions. In contrast, cases of acute schistosomiasis caused by S. japonicum can occur in reinfection to population who reside in endemic regions, and they occur in higher incidences and can have worse prognosis. It was proposed that the large amount of egg antigens released by S. japonicum interact with antibodies leading to the formation of high volume of immune complexes, which cause enlargement of the lymph tissues. This sequence of events can lead to clinical manifestation of fever, enlargement of spleen and liver due to fibrosis, portal hypertension, and death.

Chronic Infection


 * The clinical manifestations of chronic infection is mainly caused by immune reaction to the eggs entrapment within tissues resulting in granuloma formation and chronic inflammation. Adult worms live together in pairs (one male and female), sexually reproduce, and lay eggs in the veins around the intestines and bladder depending on the species, and these eggs can rupture the wall of the veins to escape to the surrounding tissues. The eggs make their way through the tissues to the intestinal or bladder lumen with help of proteolytic enzymes, however, a large amount of eggs are unable to finish their journey and remained stuck within the tissues where they can elicit an immune response. The miracidia in these eggs can then release antigens that stimulate an inflammatory immune response. The miracidia within the eggs live for around 6-8 weeks before they die and stop releasing the antigens. The granulomatous response is a Type IV hypersensitivity reaction mediated by CD4+ T cells, macrophages, and monocytes, and this chronic inflammatory response elicited by the eggs can cause fibrosis, tissue destruction, and granuloma nodules that disrupt the functions of the organs involved. The specific clinical symptoms and severity of the disease this causes depends on the type of schistosome infection, duration of infection, number of eggs, the organ at which the eggs are deposited. The amount of eggs entrapped in the tissues will continue to increase if the schistosoma are not eliminated.