Journal articles: '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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GarcÃa. "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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Hudson, L., F. Guhl, N. de Sanchez, D. Bridge, C. A. Jaramillo, and A. Young. "Longitudinal studies of the immune response of Colombian patients infected with Trypanosoma cruzi and T. rangeli." Parasitology 96, no. 3 (June 1988): 449–60. http://dx.doi.org/10.1017/s0031182000080094.

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SUMMARYTwo groups of patients were examined for anti-Trypanosoma cruzi antibodies by immunofluorescence and ELISA (i) inhabitants of the village and surrounding rural area of Tibu, Norte de Santander, Colombia (n = 327) and (ii) employees of the Empresa Colombiana de Petroleos (ECOPETROL, n = 849). The latter group had a lower rate of positive serology (12 as compared to 29%) but the distributions of antibody titres were very similar in the two groups. A total of 119 serum samples (37 village and 82 ECOPETROL, including 25 seronegative controls) were analysed for their ability to immunoprecipitate the 7 major polypeptides of T. cruzi trypomastigotes of Mr > 72 kDa. Although 10 sera from positive patients showed no immunoprecipitation, all of the remaining positive sera contained antibodies which reacted with the 150, 90 and 85 kDa polypeptides. When the T. cruzi immunofluorescence positive, immunoprecipitation negative sera were retested by ELISA using GP90, all were negative thus suggesting that the patients had had a misdiagnosed T. rangeli infection. The new diagnosis was confirmed by immunofluorescence and ELISA with T. rangeli epimastigotes. Longitudinal studies were carried out on 19 patients from the ECOPETROL group for up to 3–5 years. Five seropositive patients showed a change in their anti-trypomastigote immunoprecipitation profiles over this period; one by loss of a previously recognized high molecular weight band and four others by conversion from a negative to a positive immunoprecipitation profile. These latter patients presented initially with uncomplicated T. rangeli infection but then acquired a T. cruzi superinfection. These patients represent the nucleus of a group in which prospective studies will identify the effect of T. rangeli infection on the course of subsequent South American trypanosomiasis and Chagas' disease.

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Carrington, Mark. "Slippery customers: How African trypanosomes evade mammalian defences." Biochemist 31, no. 4 (August 1, 2009): 8–11. http://dx.doi.org/10.1042/bio03104008.

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African trypanosomes are excellent parasites and can maintain an infection of a large mammalian host for months or years. In endemic areas, Human African Trypanosomiasis, also called sleeping sickness, has been largely unaffected by the advent of modern medicine, and trypanosomiasis of domestic livestock is a major restraint on productivity in endemic areas and is arguably the major contributor to the institutionalized poverty in much of rural sub-Saharan Africa1,2. A simple way of visualizing the effect of the livestock disease is to compare maps showing the distribution of livestock (www.ilri.org/InfoServ/Webpub/Fulldocs/Mappoverty/index.htm) and tsetse flies, the insect vector (www.fao.org/ag/AGAinfo/programmes/en/paat/maps.html): the lack of overlap is remarkable. Tsetse flies are only present in sub-Saharan Africa, and this probably restricted the spread of African trypanosomiasis until historical times. Livestock infections are now present in much of South Asia and South America, a product of long distance trade and adaptation of the trypanosomes to mechanical transmission3. The majority of research is on Trypanosoma brucei as this includes the human infective subspecies. This article provides a description of progress in the understanding the molecular details of how the trypanosome interacts with the mammalian immune system and how these studies have extended beyond this to fundamental aspects of eukaryotic cell biology.

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Magez, Stefan, Joar Esteban Pinto Torres, Seoyeon Oh, and Magdalena Radwanska. "Salivarian Trypanosomes Have Adopted Intricate Host-Pathogen Interaction Mechanisms That Ensure Survival in Plain Sight of the Adaptive Immune System." Pathogens 10, no. 6 (May 31, 2021): 679. http://dx.doi.org/10.3390/pathogens10060679.

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Salivarian trypanosomes are extracellular parasites affecting humans, livestock and game animals. Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense are human infective sub-species of T. brucei causing human African trypanosomiasis (HAT—sleeping sickness). The related T. b. brucei parasite lacks the resistance to survive in human serum, and only inflicts animal infections. Animal trypanosomiasis (AT) is not restricted to Africa, but is present on all continents. T. congolense and T. vivax are the most widespread pathogenic trypanosomes in sub-Saharan Africa. Through mechanical transmission, T. vivax has also been introduced into South America. T. evansi is a unique animal trypanosome that is found in vast territories around the world and can cause atypical human trypanosomiasis (aHT). All salivarian trypanosomes are well adapted to survival inside the host’s immune system. This is not a hostile environment for these parasites, but the place where they thrive. Here we provide an overview of the latest insights into the host-parasite interaction and the unique survival strategies that allow trypanosomes to outsmart the immune system. In addition, we review new developments in treatment and diagnosis as well as the issues that have hampered the development of field-applicable anti-trypanosome vaccines for the implementation of sustainable disease control.

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GIORDANI, FEDERICA, LIAM J. MORRISON, TIM G. ROWAN, HARRY P. DE KONING, and MICHAEL P. BARRETT. "The animal trypanosomiases and their chemotherapy: a review." Parasitology 143, no. 14 (October 10, 2016): 1862–89. http://dx.doi.org/10.1017/s0031182016001268.

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SUMMARYPathogenic animal trypanosomes affecting livestock have represented a major constraint to agricultural development in Africa for centuries, and their negative economic impact is increasing in South America and Asia. Chemotherapy and chemoprophylaxis represent the main means of control. However, research into new trypanocides has remained inadequate for decades, leading to a situation where the few compounds available are losing efficacy due to the emergence of drug-resistant parasites. In this review, we provide a comprehensive overview of the current options available for the treatment and prophylaxis of the animal trypanosomiases, with a special focus on the problem of resistance. The key issues surrounding the main economically important animal trypanosome species and the diseases they cause are also presented. As new investment becomes available to develop improved tools to control the animal trypanosomiases, we stress that efforts should be directed towards a better understanding of the biology of the relevant parasite species and strains, to identify new drug targets and interrogate resistance mechanisms.

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Botoni, Fernando A., Antonio Luiz P. Ribeiro, Carolina Coimbra Marinho, Marcia Maria Oliveira Lima, Maria do Carmo Pereira Nunes, and Manoel Otávio C. Rocha. "Treatment of Chagas Cardiomyopathy." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/849504.

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Chagas' disease (ChD), caused by the protozoaTrypanosoma cruzi(T. cruzi), was discovered and described by the Brazilian physician Carlos Chagas in 1909. After a century of original description, trypanosomiasis still brings much misery to humanity and is classified as a neglected tropical disease prevalent in underdeveloped countries, particularly in South America. It is an increasing worldwide problem due to the number of cases in endemic areas and the migration of infected subjects to more developed regions, mainly North America and Europe. Despite its importance, chronic chagas cardiomyopathy (CCC) pathophysiology is yet poorly understood, and independently of its social, clinical, and epidemiological importance, the therapeutic approach of CCC is still transposed from the knowledge acquired from other cardiomyopathies. Therefore, the objective of this review is to describe the treatment of Chagas cardiomyopathy with emphasis on its peculiarities.

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Magri, Alice, Roberta Galuppi, and Marialetizia Fioravanti. "Autochthonous Trypanosoma spp. in European Mammals: A Brief Journey amongst the Neglected Trypanosomes." Pathogens 10, no. 3 (March 13, 2021): 334. http://dx.doi.org/10.3390/pathogens10030334.

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The genus Trypanosoma includes flagellated protozoa belonging to the family Trypanosomatidae (Euglenozoa, Kinetoplastida) that can infect humans and several animal species. The most studied species are those causing severe human pathology, such as Chagas disease in South and Central America, and the human African trypanosomiasis (HAT), or infections highly affecting animal health, such as nagana in Africa and surra with a wider geographical distribution. The presence of these Trypanosoma species in Europe has been thus far linked only to travel/immigration history of the human patients or introduction of infected animals. On the contrary, little is known about the epidemiological status of trypanosomes endemically infecting mammals in Europe, such as Trypanosomatheileri in ruminants and Trypanosomalewisi in rodents and other sporadically reported species. This brief review provides an updated collection of scientific data on the presence of autochthonous Trypanosoma spp. in mammals on the European territory, in order to support epidemiological and diagnostic studies on Trypanosomatid parasites.

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ADAMS, E. R., P. B. HAMILTON, A. C. RODRIGUES, I. I. MALELE, V. DELESPAUX, M. M. G. TEIXEIRA, and W. GIBSON. "NewTrypanosoma (Duttonella) vivaxgenotypes from tsetse flies in East Africa." Parasitology 137, no. 4 (December 7, 2009): 641–50. http://dx.doi.org/10.1017/s0031182009991508.

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SUMMARYSalivarian trypanosomes pose a substantial threat to livestock, but their full diversity is not known. To survey trypanosomes carried by tsetse in Tanzania, DNA samples from infected proboscides ofGlossina pallidipesandG. swynnertoniwere identified using fluorescent fragment length barcoding (FFLB), which discriminates species by size polymorphisms in multiple regions of the ribosomal RNA locus. FFLB identified the trypanosomes in 65 of 105 (61·9%) infected proboscides, revealing 9 mixed infections. Of 7 different FFLB profiles, 2 were similar but not identical to reference West AfricanTrypanosoma vivax; 5 other profiles belonged to known species also identified in fly midguts. Phylogenetic analysis of the glycosomal glyceraldehyde phosphate dehydrogenase gene revealed that the TanzanianT. vivaxsamples fell into 2 distinct groups, both outside the main clade of African and South AmericanT. vivax. These newT. vivaxgenotypes were common and widespread in tsetse in Tanzania. TheT. brucei-like trypanosome previously described from tsetse midguts was also found in 2 proboscides, demonstrating a salivarian transmission route. Investigation of mammalian host range and pathogenicity will reveal the importance of these new trypanosomes for the epidemiology and control of animal trypanosomiasis in East Africa.

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Kamidi, Christine M., Joanna Auma, Paul O. Mireji, Kariuki Ndungu, Rosemary Bateta, Richard Kurgat, Collins Ouma, Serap Aksoy, and Grace Murilla. "Differential virulence of camel Trypanosoma evansi isolates in mice." Parasitology 145, no. 9 (January 24, 2018): 1235–42. http://dx.doi.org/10.1017/s0031182017002359.

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AbstractThis study assessed the virulence of Trypanosoma evansi, the causative agent of camel trypanosomiasis (surra), affecting mainly camels among other hosts in Africa, Asia and South America, with high mortality and morbidity. Using Swiss white mice, we assessed virulence of 17 T. evansi isolates collected from surra endemic countries. We determined parasitaemia, live body weight, packed cell volume (PCV) and survivorship in mice, for a period of 60 days’ post infection. Based on survivorship, the 17 isolates were classified into three virulence categories; low (31–60 days), moderate (11–30 days) and high (0–10 days). Differences in survivorship, PCV and bodyweights between categories were significant and correlated (P < 0.05). Of the 10 Kenyan isolates, four were of low, five moderate and one (Type B) of high virulence. These findings suggest differential virulence between T. evansi isolates. In conclusion, these results show that the virulence of T. evansi may be region specific, the phenotype of the circulating parasite should be considered in the management of surra. There is also need to collect more isolates from other surra endemic regions to confirm this observation.

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Moraes, Carolina B., Gesa Witt, Maria Kuzikov, Bernhard Ellinger, Theodora Calogeropoulou, Kyriakos C. Prousis, Stefano Mangani, et al. "Accelerating Drug Discovery Efforts for Trypanosomatidic Infections Using an Integrated Transnational Academic Drug Discovery Platform." SLAS DISCOVERY: Advancing the Science of Drug Discovery 24, no. 3 (February 20, 2019): 346–61. http://dx.doi.org/10.1177/2472555218823171.

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According to the World Health Organization, more than 1 billion people are at risk of or are affected by neglected tropical diseases. Examples of such diseases include trypanosomiasis, which causes sleeping sickness; leishmaniasis; and Chagas disease, all of which are prevalent in Africa, South America, and India. Our aim within the New Medicines for Trypanosomatidic Infections project was to use (1) synthetic and natural product libraries, (2) screening, and (3) a preclinical absorption, distribution, metabolism, and excretion–toxicity (ADME-Tox) profiling platform to identify compounds that can enter the trypanosomatidic drug discovery value chain. The synthetic compound libraries originated from multiple scaffolds with known antiparasitic activity and natural products from the Hypha Discovery MycoDiverse natural products library. Our focus was first to employ target-based screening to identify inhibitors of the protozoan Trypanosoma brucei pteridine reductase 1 ( TbPTR1) and second to use a Trypanosoma brucei phenotypic assay that made use of the T. brucei brucei parasite to identify compounds that inhibited cell growth and caused death. Some of the compounds underwent structure-activity relationship expansion and, when appropriate, were evaluated in a preclinical ADME-Tox assay panel. This preclinical platform has led to the identification of lead-like compounds as well as validated hits in the trypanosomatidic drug discovery value chain.

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Tasdemir, Deniz, Marcel Kaiser, Reto Brun, Vanessa Yardley, Thomas J. Schmidt, Fatma Tosun, and Peter Rüedi. "Antitrypanosomal and Antileishmanial Activities of Flavonoids and Their Analogues: In Vitro, In Vivo, Structure-Activity Relationship, and Quantitative Structure-Activity Relationship Studies." Antimicrobial Agents and Chemotherapy 50, no. 4 (April 2006): 1352–64. http://dx.doi.org/10.1128/aac.50.4.1352-1364.2006.

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ABSTRACT Trypanosomiasis and leishmaniasis are important parasitic diseases affecting millions of people in Africa, Asia, and South America. In a previous study, we identified several flavonoid glycosides as antiprotozoal principles from a Turkish plant. Here we surveyed a large set of flavonoid aglycones and glycosides, as well as a panel of other related compounds of phenolic and phenylpropanoid nature, for their in vitro activities against Trypanosoma brucei rhodesiense, Trypanosoma cruzi, and Leishmania donovani. The cytotoxicities of more than 100 compounds for mammalian L6 cells were also assessed and compared to their antiparasitic activities. Several compounds were investigated in vivo for their antileishmanial and antitrypanosomal efficacies in mouse models. Overall, the best in vitro trypanocidal activity for T. brucei rhodesiense was exerted by 7,8-dihydroxyflavone (50% inhibitory concentration [IC50], 68 ng/ml), followed by 3-hydroxyflavone, rhamnetin, and 7,8,3′,4′-tetrahydroxyflavone (IC50s, 0.5 μg/ml) and catechol (IC50, 0.8 μg/ml). The activity against T. cruzi was moderate, and only chrysin dimethylether and 3-hydroxydaidzein had IC50s less than 5.0 μg/ml. The majority of the metabolites tested possessed remarkable leishmanicidal potential. Fisetin, 3-hydroxyflavone, luteolin, and quercetin were the most potent, giving IC50s of 0.6, 0.7, 0.8, and 1.0 μg/ml, respectively. 7,8-Dihydroxyflavone and quercetin appeared to ameliorate parasitic infections in mouse models. Generally, the test compounds lacked cytotoxicity in vitro and in vivo. By screening a large number of flavonoids and analogues, we were able to establish some general trends with respect to the structure-activity relationship, but it was not possible to draw clear and detailed quantitative structure-activity relationships for any of the bioactivities by two different approaches. However, our results can help in directing the rational design of 7,8-dihydroxyflavone and quercetin derivatives as potent and effective antiprotozoal agents.

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Capinera, John L. "Eastern Bloodsucking Conenose, Triatoma sanguisuga (LeConte) (Hemiptera: Reduviidae: Triatominae)." EDIS 2013, no. 10 (November 30, 2013). http://dx.doi.org/10.32473/edis-in1018-2013.

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The eastern bloodsucking conenose belongs to the subfamily Triatominae, known as the kissing bugs. Despite their affectionate vernacular name, they are particularly threatening “assassin bugs” who require blood meals to survive and reproduce. They are a known vector of American trypanosomiasis (or Chagas Disease) in South America, a debilitating illness caused by the parasite Trypanosoma cruzi. This disease is a problem in South and Central America and has been detected in the United States, but has not been found in Florida. This 4-page fact sheet was written by John L. Capinera, and published by the UF Department of Entomology and Nematology, November 2013. http://edis.ifas.ufl.edu/in1018

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Journal articles on the topic 'South American trypanosomiasis'

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