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1

Schistosomes: Development, reproduction, and host relations. New York: Oxford University Press, 1991.

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2

Walker, Tina Kay. Genetic variation in schistosomes. Uxbridge: Brunel University, 1987.

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3

Comité OMS d'experts sur la schistosomiase et les géohelminthiases : prévention et lutte. Schistosomiase et géohelminthiases: Prévention et lutte. Genève: Organisation mondiale de la santé, 2004.

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4

Agrawal, Prof Mahesh Chandra. Schistosomes and Schistosomiasis in South Asia. India: Springer India, 2012. http://dx.doi.org/10.1007/978-81-322-0539-5.

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5

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Schistosomes, liver flukes and helicobacter pylori. Lyon, France: IARC, 1994.

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6

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1994 Lyon, France). Schistosomes, liver flukes and Helicobacter pylori. Geneva: The Agency, 1994.

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7

Jean-Philippe, Chippaux, ed. La lutte contre les schistosomoses en Afrique de l'Ouest. Paris: Éditions IRD, 2000.

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8

D, Rollinson, and Simpson Andrew J. G, eds. The Biology of schistosomes: From genes to latrines. London: Academic Press, 1987.

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9

Ngueyap, Ferdinand. La schistosomiase urinaire au Cameroun: Pratiques contagieuses, morbidité et demande de soins. Yaoundé: l'Institut de formation et de recherche démographiques, 1998.

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10

Celia, Holland, ed. The impact of helminth infections on human nutrition: Schistosomes and soil-transmitted helminths. London: Taylor & Francis, 1987.

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11

ICGEB/TDR Symposium (1990 Shanghai, China). Immunodiagnostic approaches in schistosomiasis: Proceedings of ICGEB/TDR Symposium, Shanghai, 1990. Chichester [England]: Wiley, 1992.

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12

Carabin, Hélène, Maria V. Johansen, Jennifer F. Friedman, Stephen T. McGarvey, Henry Madsen, Zhou Xiao-Nong, and Steven Riley. Zoonotic schistosomosis (schistosomiasis). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0062.

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Asiatic schistosomiosis is a very old disease with Schistosoma japonicum eggs found in human remains > 2000 years old from Hunan and Hubei provinces in China (Mao and Shao 1982). The original description of Asiatic schistosomiosis was made by Fujii in 1847 (Sasa 1972). The life cycle was fi rst described by Kawanashi (1904) who noted trematode-like eggs in cat faeces. The same year, Katsurada recovered adult worms from a cat from Katayama, Japan (Okabe 1964). Fujinami and Nakamura (1909) first reported skin infection with S. japonicum cercariae of different mammals, and Miyairi and Suzuki (1914) discovered that Oncomelania hupensis served as intermediate host where miracidia developed into sporocysts and further into cercariae (Jordan 2000). The snail hosts of S. japonicum were discovered in China by Faust and Meleney (1923), The Philippines by Tubangui (1932) and in Indonesia by Carvey et al. (1973). In addition to the skin as the principal route of infection, Suda (1924) described oral infection and several authors described the intrauterine route of infection. (Okabe 1964; Sasa 1972).Following the understanding of the lifecyle, control measures including wearing closely woven clothing, composting of faeces with urine for at least 14 days, replacing cattle with horses, killing of rodents especially rats, killing of snails by lime, copper sulphate or salt water, were proven to have some efficacy. In Japan, an effective integrated control programme started after Second World War with the last human case being reported in 1978 (Jordan 2000 ). The National Schistosomiosis Control Programme in China started in 1955 and at that time more than 10 million people were infected with S. japonicum (Wu 2002). Emetine and antimony potassium tartrate were among the first drugs with proven efficacy against schistosomiosis in humans. Later antimony and finally praziquantel and artemether have been introduced as highly effective drugs with only minor adverse effects (Wu 2002).
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13

Schistosomes And Schistosomiasis In South Asia. Springer India, 2012.

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14

Agrawal, Prof Mahesh Chandra. Schistosomes and Schistosomiasis in South Asia. Springer London, Limited, 2012.

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15

Agrawal, Prof Mahesh Chandra. Schistosomes and Schistosomiasis in South Asia. Springer, 2014.

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16

Rollinson, David. The Biology of Schistosomes: From Genes to Latrines. Academic Press, 1988.

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17

Rollinson, David. The Biology of Schistosomes: From Genes to Latrines. Academic Press, 1988.

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18

Jurberg, Arnon Dias, and Paul J. Brindley, eds. Gene function in schistosomes: recent advances towards a cure. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-556-5.

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19

The Impact of Helminth Infections on Human Nutrition: Schistosomes and Soil Transmitted Helminths. Taylor & Francis, 1987.

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20

Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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Abstract:
AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.
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