Relevant bibliographies by topics / South American trypanosomiasis

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Academic literature on the topic 'South American trypanosomiasis'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "South American trypanosomiasis"

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Dias, João Carlos Pinto. "The Treatment of Chagas Disease (South American Trypanosomiasis)." Annals of Internal Medicine 144, no. 10 (May 16, 2006): 772. http://dx.doi.org/10.7326/0003-4819-144-10-200605160-00012.

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Jiménez-Coello, M., K. Y. Acosta-Viana, E. Guzman-Marin, and A. Ortega-Pacheco. "American Trypanosomiasis Infection in Fattening Pigs from the South-East of Mexico." Zoonoses and Public Health 59 (September 2012): 166–69. http://dx.doi.org/10.1111/zph.12016.

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Hudson, Leslie, and Veronica Britten. "IMMUNE RESPONSE TO SOUTH AMERICAN TRYPANOSOMIASIS AND ITS RELATIONSHIP TO CHAGAS' DISEASE." British Medical Bulletin 41, no. 2 (1985): 175–80. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072046.

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SÁNCHEZ, LAURA VIVIANA, and JUAN DAVID RAMÍREZ. "Congenital and oral transmission of American trypanosomiasis: an overview of physiopathogenic aspects." Parasitology 140, no. 2 (September 25, 2012): 147–59. http://dx.doi.org/10.1017/s0031182012001394.

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SUMMARYChagas disease or American trypanosomiasis is a pathology affecting about 8–11 million people in Mexico, Central America, and South America, more than 300 000 persons in the United States as well as an indeterminate number of people in other non-endemic countries such as USA, Spain, Canada and Switzerland. The aetiological agent isTrypanosoma cruzi, a protozoan transmitted by multiple routes; among them, congenital route emerges as one of the most important mechanisms of spreading Chagas disease worldwide even in non-endemic countries and the oral route as the responsible of multiple outbreaks of acute Chagas disease in regions where the vectorial route has been interrupted. The aim of this review is to illustrate the recent research and advances in host-pathogen interaction making a model of how the virulence factors of the parasite would interact with the physiology and immune system components of the placental barrier and gastrointestinal tract in order to establish a response againstT. cruziinfection. This review also presents the epidemiological, clinical and diagnostic features of congenital and oral Chagas disease in order to update the reader about the emerging scenarios of Chagas disease transmission.
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García. "A NEW PCR-RFLP FOR SPECIES-SPECIFIC DIAGNOSIS OF SOUTH AMERICAN ANIMAL TRYPANOSOMIASIS." American Journal of Animal and Veterinary Sciences 9, no. 2 (February 1, 2014): 128–36. http://dx.doi.org/10.3844/ajavsp.2014.128.136.

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Guhl, F. "Purified Trypanosoma cruzi specific glycoprotein for discriminative serological diagnosis of South American trypanosomiasis (Chagas' disease)." Memórias do Instituto Oswaldo Cruz 85, no. 4 (December 1990): 531–32. http://dx.doi.org/10.1590/s0074-02761990000400026.

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Siemens, Tobias August, Miguel Carlos Riella, Thyago Proença de Moraes, and Cristian Vidal Riella. "APOL1 risk variants and kidney disease: what we know so far." Brazilian Journal of Nephrology 40, no. 4 (December 2018): 388–402. http://dx.doi.org/10.1590/2175-8239-jbn-2017-0033.

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ABSTRACT There are striking differences in chronic kidney disease between Caucasians and African descendants. It was widely accepted that this occurred due to socioeconomic factors, but recent studies show that apolipoprotein L-1 (APOL1) gene variants are strongly associated with focal segmental glomerulosclerosis, HIV-associated nephropathy, hypertensive nephrosclerosis, and lupus nephritis in the African American population. These variants made their way to South America trough intercontinental slave traffic and conferred an evolutionary advantage to the carries by protecting against forms of trypanosomiasis, but at the expense of an increased risk of kidney disease. The effect of the variants does not seem to be related to their serum concentration, but rather to local action on the podocytes. Risk variants are also important in renal transplantation, since grafts from donors with risk variants present worse survival.
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Cox, F. E. G. "History of Human Parasitology." Clinical Microbiology Reviews 15, no. 4 (October 2002): 595–612. http://dx.doi.org/10.1128/cmr.15.4.595-612.2002.

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SUMMARY Humans are hosts to nearly 300 species of parasitic worms and over 70 species of protozoa, some derived from our primate ancestors and some acquired from the animals we have domesticated or come in contact with during our relatively short history on Earth. Our knowledge of parasitic infections extends into antiquity, and descriptions of parasites and parasitic infections are found in the earliest writings and have been confirmed by the finding of parasites in archaeological material. The systematic study of parasites began with the rejection of the theory of spontaneous generation and the promulgation of the germ theory. Thereafter, the history of human parasitology proceeded along two lines, the discovery of a parasite and its subsequent association with disease and the recognition of a disease and the subsequent discovery that it was caused by a parasite. This review is concerned with the major helminth and protozoan infections of humans: ascariasis, trichinosis, strongyloidiasis, dracunculiasis, lymphatic filariasis, loasis, onchocerciasis, schistosomiasis, cestodiasis, paragonimiasis, clonorchiasis, opisthorchiasis, amoebiasis, giardiasis, African trypanosomiasis, South American trypanosomiasis, leishmaniasis, malaria, toxoplasmosis, cryptosporidiosis, cyclosporiasis, and microsporidiosis.
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Dias, João Carlos Pinto, Emmanuel Dias, and Genard Carneiro da Cunha Nóbrega. "Long-term follow-up of a patient since the acute phase of Chagas disease (South American trypanosomiasis): further treatment and cure of the infection." Revista da Sociedade Brasileira de Medicina Tropical 48, no. 5 (October 2015): 629–32. http://dx.doi.org/10.1590/0037-8682-0073-2015.

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Oliveira, Gerlandes Fernandes de, Mariane Albuquerque Lima Ribeiro, Gabriela Vieira de Souza Castro, André Luiz Rodrigues Menezes, Renato Abreu Lima, Romeu Paulo Martins Silva, and Dionatas Ulises De Oliveira Meneguetti. "Retrospective study of the epidemiological overview of the transmission of Chagas disease in the State of Acre, South-Western Amazonia, from 2009 to 2016." Journal of Human Growth and Development 28, no. 3 (November 28, 2018): 329–36. http://dx.doi.org/10.7322/jhgd.152187.

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Introduction: Chagas disease (CD), also known as American Trypanosomiasis, is an infectious parasitic disease caused by the etiologic agent Trypanosoma cruzi. It is considered endemic in the low-income population and is classified by the WHO as a neglected tropical disease. In the state of Acre, there is almost no scientific data regarding the epidemiology of CD, even though the first autochthonous case was registered in the 1980s. Objective: To analyze the epidemiological panorama of the transmission of Chagas disease in the State of Acre, Brazil, from 2009 to 2016. Methods: A survey of the occurrence of Chagas disease in the State of Acre was performed using public domain secondary data from the Brazil’s Notifiable Diseases Information System of SUS (publicly funded health care system), and from the SUS Database of the Health Surveillance Foundation of the State of Acre. Data were collected from the following variables: gender, age group, form of contagion, distribution by region and municipality, perimeter and seasonality. Result: Forty-two cases of CD were confirmed, with an increase of more than 300% from 2015 to 2016 and a frequency coefficient of 3.06 cases per 100,000 people, and in the Tarauacá/Envira region, the probability of a person contracting CD was 600% higher than the state mean. Conclusion: We found that in the state of Acre, in the period from 2009 to 2016, most cases of CD occurred in 2016, in the Tarauacá/Envira region, mainly in the municipality of Feijó, in the rural zone, from July to October, in the age group of 0 to 30 years, being the oral form the main route of transmission and presenting no statistical difference between men and women.
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Dissertations / Theses on the topic "South American trypanosomiasis"

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Silva, Laura Denise Mendes da. "Papel dos receptores TLR2 e TLR4 na produção de citocinas em pacientes chagásicos crônicos." Botucatu, 2016. http://hdl.handle.net/11449/136189.

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Orientador: Sueli Aparecida Calvi
Resumo: A doença de Chagas (DC), causada pelo protozoário Trypanosoma cruzi (T. cruzi), é uma doença negligenciada e considerada um grave problema de saúde pública. A sua evolução no individuo infectado ocorre em duas fases distintas: a fase aguda que dura de 2 a 4 meses, caracterizada pela alta parasitemia, mas ausência de sinais e sintomas específicos, o que dificulta sua detecção, e a fase crônica na qual a maioria dos indivíduos é diagnosticada. Nessa fase, uma boa parte dos indivíduos apresenta a forma indeterminada ou assintomática da doença. No entanto, cerca de 30 a 40% dos indivíduos infectados desenvolvem a DC sintomática, que pode se apresentar na forma de doença cardíaca ou doença digestiva. Um dos desafios mais importantes no estudo da DC é a determinação dos mecanismos relacionados à resposta imune do hospedeiro que levam a essas diferentes apresentações clinicas. A resposta imune celular via liberação das citocinas pró-inflamatórias como IFN-y, TNF-α e IL-17 é considerada determinante na resistência do hospedeiro. No entanto, um fino controle da liberação dessas citocinas deve ocorrer para que a resposta não se intensifique ou não se perpetue e resulte em lesão tecidual, o que ocorre através da ativação de citocinas anti-inflamatórias como a IL-10 e o TGF-y. Esse controle de resposta seria responsável pelo não aparecimento de sintomas nos indivíduos com doença de Chagas assintomática. Os receptores de reconhecimento padrão (PRRs), particularmente os Toll-Like Receptors... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Chagas disease (CD), caused by the protozoan Trypanosoma cruzi (T. cruzi), is a neglected disease and considered a serious problem of public health. Its evolution in a infected host occurs in two distinct stages: the acute stage which lasts 2 to 4 months and is characterized by high parasitemia, but no detection of specific signs and symptoms, which difficult its detection, and the chronic stage in which most individuals are diagnosed. At this second stage, most individuals present the indeterminate or asymptomatic chronic disease. However, about 30 to 40% of them become symptomatic and present the cardiac or digestive disease. One of the most important challenges in the CD study is to determine the mechanisms related to the host immune response that lead to these different clinical manifestations. The cellular immune response characterized by the release of pró-inflammatory cytokines such as IFN-y, TNF-α and IL-17 is considered crucial in host resistance. However, it is suggested that a fine control of this response must occur in order to avoid a perpetuated inflammatory process which results in tissue injury. This control was found to be responsible by the absence of clinical symptoms in individuals with the indeterminate chronic form and depends on activation of anti-inflammatory cytokines such as IL-10 and TGF-β. The pattern recognition receptors (PRRs), particularly the Toll-Like Receptors (TLRs) are extremely important in defining the cytokine profile that will be relea... (Complete abstract click electronic access below)
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Lascano, Segundo Mauricio. "Molecular Epidemiology of Trypanosoma (Herpetosoma) rangeli (Kinetoplastida: Trypanosomatidae) in Ecuador, South America, and Study of the Parasite Cell Invasion Mechanism in vitro." Ohio : Ohio University, 2009. http://www.ohiolink.edu/etd/view.cgi?ohiou1258469326.

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Books on the topic "South American trypanosomiasis"

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Sakhuja, Vinay, and Harbir Singh Kohli. Leishmaniasis and trypanosomiasis. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0184_update_001.

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Visceral leishmaniasis, also known as kala-azar, has an insidious onset with constitutional features. Subsequently the intense parasitism of the reticuloendothelial system causes hepatosplenomegaly, anaemia, leucopenia, and thrombocytopaenia as well as hypergammaglobulinaemia. Kidney involvement manifests with proteinuria up to 1 g/24 hours, micro/macrohaematuria, and leucocyturia. Kidney involvement is generally mild and reversible with the treatment of infection. Biopsy appearances of diffuse proliferative glomerulonephritis, mesangial proliferation, and occasionally focal necrotizing glomerulonephritis with crescents have been described. Defects of urinary concentration and acidification have also been observed. Acute kidney injury (AKI) may be seen in one-third of patients and is associated with increased mortality.Trypanosomiasis has two forms. It causes sleeping sickness in Africa (T. brucei, transmitted by tsetse flies) or Chagas disease in South America (T. cruzei, transmitted by reduvid bugs). There is no direct association of these conditions with nephropathy, although there is in experimental models. AKI may occur, typically as a manifestation of multi-organ failure in African trypanosomiasis. APOL1 genotypes that confer susceptibility to FSGS are protective against T. brucei infection.
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Book chapters on the topic "South American trypanosomiasis"

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Domachowske, Joseph, and Manika Suryadevara. "Chagas Disease: South American Trypanosomiasis." In Clinical Infectious Diseases Study Guide, 301–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50873-9_49.

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Toth, Joseph F., and Joseph Domachowske. "Chagas Disease: South American Trypanosomiasis." In Introduction to Clinical Infectious Diseases, 385–91. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-91080-2_36.

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"South American trypanosomiasis." In Dermatology Therapy, 535. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_2521.

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Beinart, William, and Lotte Hughes. "Tsetse and Trypanosomiasis in East and Central Africa." In Environment and Empire. Oxford University Press, 2007. http://dx.doi.org/10.1093/oso/9780199260317.003.0016.

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Disease, we have argued, influenced patterns of colonization, especially in West Africa, the Americas, and Australia (Chapter 2). In turn, imperial transport routes facilitated the spread of certain diseases, such as bubonic plague. This chapter expands our discussion of environmentally related diseases by focusing on trypanosomiasis, carried by tsetse fly, in East and Central Africa. Unlike plague, this disease of humans and livestock was endemic and restricted to particular ecological zones in Africa. But as in the case of plague, the changing incidence of trypanosomiasis was at least in part related to imperialism and colonial intrusion in Africa. Coastal East Africa presented some of the same barriers to colonization as West Africa. Portugal maintained a foothold in South-East Africa for centuries, and its agents expanded briefly onto the Zimbabwean plateau in the seventeenth century, but could not command the interior. Had these early incursions been more successful, southern Africa may have been colonized from the north, rather than by the Dutch and British from the south. Parts of East Africa were a source of slaves and ivory in the eighteenth and early nineteenth centuries. The trading routes, commanded by Arab and Swahili African networks, as well as Afro-Portuguese further south, were linked with the Middle East and the Indian Ocean. In the early decades of the nineteenth century, slave-holding expanded within enclaves of East Africa, such as the clove plantations of Zanzibar. When Britain attempted to abolish the slave trade in the early nineteenth century, and policed the West African coast, East and Central African sources briefly became more important for the Atlantic slave trade. African slaves from these areas were taken to Latin America and the Spanish Caribbean. Britain did not have the same intensity of contact with East Africa as with West and southern Africa until the late nineteenth century. There was no major natural resource that commanded a market in Europe and British traders had limited involvement in these slave markets. But between the 1880s and 1910s, most of East and Central Africa was taken under colonial rule, sometimes initially as protectorates: by Britain in Kenya and Uganda; Germany in Tanzania; Rhodes’s British South Africa Company in Zimbabwe, Zambia, and Malawi; and by King Leopold of Belgium in the Congo.
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