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... • Lower sperm concentration and motility [229] • Anti-sperm antibodies [230] Trichomonas vaginalis • Urethra [231] • Prostate [231][232][233] • Testis [234,235] • Epididymis [233,236] • Urethritis [231] • Prostatitis [231][232][233] • Orchitis [234] • Atrophic testes [234,235] • Epididymitis [233,236] • Low serum testosterone [234,235] • Hypogonadism and oligoasthenoteratozoospermia [234] • Azoospermia [235,236] • Decreased spermatozoa motility and morphological alterations [237] Trypanosoma brucei • No direct organ infection described • Atrophy of seminiferous tubules [238] • Reduction of testicular volume [239] • Testicular hypogonadism [240,241] • Lower testosterone plasma levels [240][241][242] • Impotency [239,[241][242][243] Trypanosoma cruzi • Testis [244][245][246] • Epididymo-orchitis [244] • Hypoplasia of germ cells [245,246] • Maturation arrest of germ cells [245,246] • Degeneration of Leydig cells [245,246] • Not directly reported however: ...
... • Lower sperm concentration and motility [229] • Anti-sperm antibodies [230] Trichomonas vaginalis • Urethra [231] • Prostate [231][232][233] • Testis [234,235] • Epididymis [233,236] • Urethritis [231] • Prostatitis [231][232][233] • Orchitis [234] • Atrophic testes [234,235] • Epididymitis [233,236] • Low serum testosterone [234,235] • Hypogonadism and oligoasthenoteratozoospermia [234] • Azoospermia [235,236] • Decreased spermatozoa motility and morphological alterations [237] Trypanosoma brucei • No direct organ infection described • Atrophy of seminiferous tubules [238] • Reduction of testicular volume [239] • Testicular hypogonadism [240,241] • Lower testosterone plasma levels [240][241][242] • Impotency [239,[241][242][243] Trypanosoma cruzi • Testis [244][245][246] • Epididymo-orchitis [244] • Hypoplasia of germ cells [245,246] • Maturation arrest of germ cells [245,246] • Degeneration of Leydig cells [245,246] • Not directly reported however: ...
... Chagas disease, caused by Trypanosoma cruzi, affects 6-7 million people who mainly live in Latin America [261]. Even if male infertility is not especially mentioned in the literature, Chagas, who gave his name to this American trypanosomiasis, identified parasites in the testicles of acutely or chronically infected men often in association with epididymo-orchitis [244]. In addition, hypoplasia or maturation arrest of testicular germ cells, as well as degeneration of Leydig cells, were described in chronic Chagas disease patients. ...
Background:
Infertility affects one couple out of six worldwide. Male infertilty can result from congenital or acquired factors, of which pathogens that reach the genital tract through sexual contact or blood dissemination. The impact of major viral, bacterial and parasitic infections on the male genital tract and fertility has been summarized.
Results and conclusions:
A systematic review of articles published in the Google Scholar and PubMed databases was conducted. It turns out that viruses, as well as bacteria and parasites are major inducers of male genital tract infections and ensuing infertility through damage to the organs and subsequent loss of function and/or through direct damage to the sperm cells. Moreover, not only male infertility results from such infections but these can also be transmitted to women and even to the offspring, thus highlighting the need to efficiently detect, treat and prevent them.
... Over a century ago the Brazilian physician Carlos Chagas described the American trypanosomiasis, named after him the "Chagas disease" [1]. Fritz Koberle, one of the very founders of our department, investigated for decades the Chagas disease hypothesizing the "neurogenic theory" [2]. ...
... While Chagas had previously observed that the brainstem undergo inflammatory degeneration due to the Trypanossoma cruzi (T. cruzi) infection [1], Koberle proposed the T. cruzi-related degeneration of the peripheral nervous system promote the "gross enlargement of the oesophagus, colon, and heart" [2]. A careful reading of the original Chagas' manuscript reveals he might catch a glimpse of the relationship between the trypanosomiasis-induced neuronal degeneration and Chagas heart disease, which, in fact, was proven by Koberle [1,2]. ...
... cruzi) infection [1], Koberle proposed the T. cruzi-related degeneration of the peripheral nervous system promote the "gross enlargement of the oesophagus, colon, and heart" [2]. A careful reading of the original Chagas' manuscript reveals he might catch a glimpse of the relationship between the trypanosomiasis-induced neuronal degeneration and Chagas heart disease, which, in fact, was proven by Koberle [1,2]. ...
Trypanosomiasis induces a remarkable myenteric neuronal degeneration leading to megacolon. Very little is known about the risk for colon cancer in chagasic megacolon patients. To clarify whether chagasic megacolon impacts on colon carcinogenesis, we investigated the risk for colon cancer in Trypanosoma cruzi (T. cruzi) infected patients and rats.
Colon samples from T. cruzi-infected and uninfected patients and rats were histopathologically investigated with colon cancer biomarkers. An experimental model for chemical myenteric denervation was also performed to verify the myenteric neuronal effects on colon carcinogenesis. All experiments complied the guidelines and approval of ethical institutional review boards.
No colon tumors were found in chagasic megacolon samples. A significant myenteric neuronal denervation was observed. Epithelial cell proliferation and hyperplasia were found increased in chagasic megacolon. Analyzing the argyrophilic nucleolar organiser regions within the cryptal bottom revealed reduced risk for colon cancer in Chagas' megacolon patients. T. cruzi-infected rats showed a significant myenteric neuronal denervation and decreased numbers of colon preneoplastic lesions. In chemical myenteric denervated rats preneoplastic lesions were reduced from the 2nd wk onward, which ensued having the colon myenteric denervation significantly induced.
Our data suggest that the trypanosomiasis-related myenteric neuronal degeneration protects the colon tissue from carcinogenic events. Current findings highlight potential mechanisms in tropical diseases and cancer research.
... Human trypanosomiasis is characterized by two clinically distinct stages. The acute phase has a short duration of approximately two months and can be asymptomatic or symptomatic [9]. After the acute phase, the patient progresses to the chronic phase, with different clinical manifestations, from the lack of symptoms to severe cardiac or gastrointestinal (GI) disorders. ...
... Approximately 70% of the infected individuals remain asymptomatic [10] in the indeterminate phase of the disease, which can last two or more decades [11]. The chronic digestive form, which is the focus of our study, can involve the presence of megaesophagus and megacolon in severe human cases [9,12,13]. These conditions are characterized by significant morphological changes, including dilatation and hypertrophy of the intestinal wall, and physiological disorders that affect predominantly the sigmoid region, with loss of the organ's motor coordination [14]. ...
We developed a novel murine model of long-term infection with Trypanosoma cruzi with the aim to elucidate the pathogenesis of megacolon and the associated adaptive and neuromuscular intestinal disorders. Our intent was to produce a chronic stage of the disease since the early treatment should avoid 100% mortality of untreated animals at acute phase. Treatment allowed animals to be kept infected and alive in order to develop the chronic phase of infection with low parasitism as in human disease. A group of Swiss mice was infected with the Y strain of T. cruzi. At the 11th day after infection, a sub-group was euthanized (acute-phase group) and another sub-group was treated with benznidazole and euthanized 15 months after infection (chronic-phase group). Whole colon samples were harvested and used for studying the histopathology of the intestinal smooth muscle and the plasticity of the enteric nerves. In the acute phase, all animals presented inflammatory lesions associated with intense and diffuse parasitism of the muscular and submucosa layers, which were enlarged when compared with the controls. The occurrence of intense degenerative inflammatory changes and increased reticular fibers suggests inflammatory-induced necrosis of muscle cells. In the chronic phase, parasitism was insignificant; however, the architecture of Aüerbach plexuses was focally affected in the inflamed areas, and a significant decrease in the number of neurons and in the density of intramuscular nerve bundles was detected. Other changes observed included increased thickness of the colon wall, diffuse muscle cell hypertrophy, and increased collagen deposition, indicating early fibrosis in the damaged areas. Mast cell count significantly increased in the muscular layers. We propose a model for studying the long-term (15 months) pathogenesis of Chagasic megacolon in mice that mimics the human disease, which persists for several years and has not been fully elucidated. We hypothesize that the long-term inflammatory process mediates neuronal damage and intramuscular and intramural denervation, leading to phenotypic changes in smooth muscle cells associated with fibrosis. These long-term structural changes may represent the basic mechanism for the formation of the Chagasic megacolon.
... Chagas disease (CD) was first described by the Brazilian scientist Carlos Chagas in 1909 1,2 . It remains a public health problem in Latin America 3 , with a potential expansion to non-endemic countries 4 . ...
Patients with Chagas disease have reduced health-related quality of life (HRQoL). Hence, we aimed to identify the factors that mostly affected their HRQoL. This was a systematic review of qualitative studies. The Latin American and Caribbean Health Sciences Literature, Medical Literature Analysis and Retrieval System Online, Excerpta Medica Database, Web of Science, and SciVerse Scopus databases were searched for relevant studies without language or date restrictions. The search and data analysis were performed by independent reviewers; all qualitative studies that reported the factors that had an impact on the HRQoL of patients with Chagas disease were included. The risk of bias was assessed using the Critical Appraisal Skills Program Qualitative Study Checklist; confidence in the evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation-Confidence in the Evidence from Reviews of Qualitative approach. Five studies were included in this review: four in Brazil and one in California, United States, with immigrants from Central and South America. The sample consisted of 207 patients with chronic Chagas disease. Stigma, physical limitations, work absenteeism, emotional or mental aspects, fear of treatment, and fear of the future had the strongest impact on the HRQoL. All items showed moderate confidence except for fear of treatment (low confidence). The physical, emotional, mental, and cultural aspects affected the HRQoL of patients with chronic Chagas disease. Identification of these factors is important in the development of strategies aimed at improving the HRQoL of this population.
Keywords:
Chagas disease; Quality of life; Qualitative research; Systematic review
... An acute, diffuse, and intense myocardiopathy with high levels of parasites is the basic anatomopathological substrate found in the acute form of chagasic heart disease. [6][7][8][9][10][11] The mortality of acute Chagas disease stems from the occurrence of acute heart disease associated or not with meningoencephalopathy due to Schizotrypanum infection. 12 According to Dias 3 in his anthological longitudinal study in Bambuí, more than 75% of the recorded deaths in the acute phase of the disease refer to children aged less than 3 years, with lethality varying between 1.3% and 45% of the published cases (3) . ...
... De acordo com Chagas (1916), os indivíduos que adquirem a Doença de Chagas (DC), na sua fase aguda, podem ser distinguidos em dois grandes grupos, cujo critério principal da distinção seria a expressão da sintomatologia e prognóstico. ...
O presente artigo tem por objetivo apresentar dados referentes a Região Norte (RN) do Brasil quanto ao número de casos novos de Doença de Chagas Aguda (DCA) entre 2010 a 2019, nos estados que constituintes (Acre, Amazonas, Amapá, Pará, Rondônia, Roraima e Tocantins), correlacionados com fatores sociais que atuam para a persistência da enfermidade em determinadas localidades. Trata-se de um estudo do tipo descritivo, qualitativo e quantitativo. Foram coletados, analisados e organizados dados referentes ao número de casos de DCA pelas cinco regiões do Brasil (Centro-oeste, Nordeste, Norte, Sudeste e Sul) no período de 2010 a 2019, com enfoque nos estados que compõe a RN, por meio do tabulador que opera na internet (TABNET) do Departamento de Informática do Sistema Único de Saúde (DATASUS). Os dados coletados de Doença de Chagas (DC) nas diferentes regiões brasileiras apontaram que o maior número de casos novos da DC no período de 2010 a 2019 concentravam-se na RN, com expressivo número dos incidentes localizados no estado do Pará. Entre os notificados 54,27% dos diagnosticados foram do sexo masculino, a escolaridade na maioria dos casos foi informada como ignorada (91,67%) e o modo de infecção mais provável foi a oral com 78,54%. Nesse sentido, A DC ainda ameaça basicamente as regiões mais vulneráveis da América Latina. Torna-se, portanto, de extrema importância a promoção de ações públicas que visem atenuar esse problema de saúde pública, tendo base a equidade e promoção de qualidade de vida para a população.
... The first case description of human trypanosomiasis by Carlos Chagas was Berenice's case, a two-year-old girl, who presented with fever of 39.4°C, palpebral edema, adenomegaly, hepatomegaly and presence of T. cruzi in peripheral blood, with subsequent remission of the signs and symptoms [68]. ...
This review is a perspective on the history of Chagas disease, and it adopts a novel approach from literary studies, historical documents and the science and epidemiology of the nature of the disease. From this analysis, comes the review's working definition of the Contact Zone (CZ): “the space in which geographically and historically separated people come into contact with each other and establish long-lasting relationships, which usually involve coercive conditions, radical inequality and intolerable conflict.”
In the Patient-Physician CZ, we verified the triple transition phenomena: the American trypanosomiasis shifted from a rural, acute, and vectorial transmitted disease to an urban, chronic and non-vectorial disease.
In the Academic CZ, we describe the original disagreements which denied the existence of the disease and the current controversies about pathogenic mechanisms and etiological treatment.
From the News from Latin America, and in the Original CZ, we will review the evolution of different forms of transmission.
As in any good story, research across broad disciplines is necessary to reveal historical perspectives, scientific approaches, and the epidemiology of the disease, which has a prequel of 9000 years and an open ending: thus, we explore across the Global CZ, with its multiple and unexpected actors.
... Although cardiac and gastrointestinal forms of CD are better known and studied, it has been evidenced that the disease, especially in its acute phase, affects Section Editor: Hiroshi Sato * Aline Silva Miranda mirandas.aline@gmail.com almost all organs, including the adrenal gland (Chagas 1916;Barbosa Jr. and Andrade 1984;Correa-de-Santana et al. 2006). Recently, our research group reported local changes in renin angiotensin system (RAS) components in heart and brain tissues of rats infected by T. cruzi (Miranda et al. 2019;Rachid et al. 2019). ...
Chagas disease (CD) is a tropical zoonosis caused by the protozoan Trypanosoma cruzi. Severe autonomic dysfunction like reduced cardiac catecholamine-containing or acetylcholinesterase-positive innervation have been reported in CD. Renin-angiotensin system (RAS) seems to participate in the regulation of adrenal catecholamine secretion by adrenal medullary chromaffin cells, which might be dependent of nitric oxide (NO) pathways. To investigate the levels of RAS components in the adrenal gland during the acute infection with Y strain T. cruzi and in response to acute administration of an inhibitor of the enzyme NO synthase, L-NAME. Male Holtzman rats were inoculated intraperitoneally with Y strain T. cruzi and received L-NAME or tap water from one day before the infection until 13 or 17 days post-inoculation (dpi). The concentration of RAS molecules in the adrenal tissue was evaluated by ELISA immunoassay. Angiotensin converting enzyme 1 (ACE1) levels were significantly lower at 17 dpi when compared to 13 dpi. No significant differences were found compared with baseline, and no changes were detected in adrenal tissue levels of angiotensin converting enzyme 2 (ACE2), angiotensin II, or angiotensin-(1-7). Moreover, the treatment with L-NAME did not influence the levels of RAS components in adrenal tissue during the course of T. cruzi infection. We provided the first evidence that levels of RAS molecules change in the adrenal gland during acute phase of T. cruzi infection. Future studies are necessary to fully address the role of NO in RAS-associated adrenal gland function in CD.
... Chagas disease (CD) is an anthropozoonosis caused by the protozoan Trypanosoma cruzi and is typically transmitted by triatomines, vectors of the Triatominae family (Hemiptera: Reduviidae), known as kissing bugs [1][2][3] . ...
Introduction:
Chagas disease is caused by the protozoa Trypanosoma cruzi. Its main reservoir is the domestic dog, especially in rural areas with favorable characteristics for vector establishment and proliferation. The aims of this study were to collect data, survey and map the fauna, and identify T. cruzi infection in triatomines, as well as to assess the presence of anti-T. cruzi antibodies in dogs in rural areas of the municipality of Mossoró, Brazil.
Methods:
An active entomologic research was conducted to identify adult specimens through an external morphology dichotomous key. The analysis of natural infection by T. cruzi in the insects was performed by isolation in culture and polymerase chain reaction. The antibody testing for T. cruzi in dogs was performed by enzyme-linked immunosorbent assay and indirect immunofluorescence assay.
Results:
A total of 68 triatomines were captured, predominantly the Triatoma brasiliensis brasiliensis (Neiva 1911) species. The vector mapping displayed areas with greater risk for parasite transmission. Of the examined triatomines (51 specimens), 41.2% (21/51) were positive on polymerase chain reaction, and all were negative on culture. In the serum testing, 11% (25/218) of dogs were seropositive, but no association was found between the serologic results and the presence and infection by T. cruzi in triatomines.
Conclusions:
This study demonstrated the movement of T. cruzi in the studied area, by the presence of vectors and naturally infected domestic reservoirs. The mapping of the studied rural area demonstrates the risk of disease transmission.
... Trypanosoma cruzi (T. cruzi) infection induces Chagas disease, a condition named after the Brazilian scientist Carlos Chagas [1]. Treatment for the 10 million people infected with T. cruzi currently costs about US$ 7.2 billion per year worldwide [2]. ...
Background:
Trypanosoma cruzi (T. cruzi) infects millions of Latin Americans each year and can induce chagasic megacolon. Little is known about how serotonin (5-HT) modulates this condition. Aim We investigated whether 5-HT synthesis alters T. cruzi infection in the colon.
Materials and methods:
Forty-eight paraffin-embedded samples from normal colon and chagasic megacolon were histopathologically analyzed (173/2009). Tryptophan hydroxylase 1 (Tph1) knockout (KO) mice and c-KitW-shmice underwent T. cruzi infection together with their wild-type counterparts. Also, mice underwent different drug treatments (16.1.1064.60.3).
Results:
In both humans and experimental mouse models, the serotonergic system was activated by T. cruzi infection (p < 0.05). While treating Tph1KO mice with 5-HT did not significantly increase parasitemia in the colon (p > 0.05), rescuing its synthesis promoted trypanosomiasis (p < 0.01). T. cruzi-related 5-HT release (p < 0.05) seemed not only to increase inflammatory signaling, but also to enlarge the pericryptal macrophage and mast cell populations (p < 0.01). Knocking out mast cells reduced trypanosomiasis (p < 0.01), although it did not further alter the neuroendocrine cell number and Tph1 expression (p > 0.05). Further experimentation revealed that pharmacologically inhibiting mast cell activity reduced colonic infection (p < 0.01). A similar finding was achieved when 5-HT synthesis was blocked in c-KitW-shmice (p > 0.05). However, inhibiting mast cell activity in Tph1KO mice increased colonic trypanosomiasis (p < 0.01).
Conclusion:
We show that mast cells may modulate the T. cruzi-related increase of 5-HT synthesis in the intestinal colon.
... Doença de Chagas Humana (DCH), também conhecida como tripanossomíase americana, é uma zoonose causada pelo protozoário Trypanosoma cruzi.1 Trata-se de uma patologia endêmica nas Américas Central e do Sul, onde se encontram aproximadamente 17 milhões das pessoas infectadas e outros 100 milhões de indivíduos com risco de infecção.2 ...
... T. cruzi has the ability to invade and replicate inside almost any type of nucleated mammalian cell in vitro. The broad range of infected organs was noted in the earliest autopsy studies of fatal acute T. cruzi infection [40]. Analyses of acutely infected mice have shown that diverse parasite strains indeed infect a huge array of cell types in virtually any tissue [16,[20][21][22]26,33,[41][42][43][44][45][46][47]. ...
In chronic Trypanosoma cruzi infections, parasite burden is controlled by effective, but nonsterilising immune responses. Infected cells are difficult to detect because they are scarce and focally distributed in multiple sites. However, advances in detection technologies have established a link between parasite persistence and the pathogenesis of Chagas heart disease. Long-term persistence likely involves episodic reinvasion as well as continuous infection, to an extent that varies between tissues. The primary reservoir sites in humans are not definitively known, but analysis of murine models has identified the gastrointestinal tract. Here, we highlight that quantitative, spatial, and temporal aspects of T. cruzi infection are central to a fuller understanding of the association between persistence, pathogenesis, and immunity, and for optimising treatment.
... As manifestações gerais são de febre, mal-estar, cefaléia, astenia, hiporexia, hipertrofia de linfonodos, hepatoesplenomegalia e com pouca frequência meningoencefalite. Os sinais mais característicos da fase aguda são: o Chagoma que é um inchaço na região da picada (Argolo et al., 2008) e o sinal de Romana que é um edema bipalpebral quando a transmissão ocorre pelo olho(Chagas, 1916), as duas aparecem de sete a dez dias após a infecção e permanecem por cerca de dois a quatro meses(Pereira et al.,1989;Mirtha et al., ...
Os triatomíneos são insetos largamente difundidos nas Américas, encontrados desde o sul dos Estados Unidos até o sul da Argentina. São de grande importância, pois podem transmitir a Tripanossomíase americana, também denominada doença de Chagas. O presente estudo objetivou avaliar o panorama da infecção de triatomíneos por tripanosomatídeos e sua presença em reservatórios diversos na região do município de Ouro Preto do Oeste, Rondônia, com o intuito de criar plataforma geradora de subsidio para atenção primaria à saúde, e desenvolver novas estratégias de educação popular para a profilaxia da doença de chagas na região. A pesquisa ocorreu em dois ambientes distintos, um de mata primária e outro de área de pastagem. Foram realizadas duas coletas mensais, uma em cada ambiente, no período de fevereiro de 2009 a janeiro de 2010, totalizando 24 coletas. Em cada coleta foi dissecada uma O. speciosa (babaçu) na busca de triatomíneos. Os triatomíneos coletados foram separados de acordo com seu estágio ninfal, sendo encaminhados em caixas térmicas, com temperatura ambiente para o laboratório de microscopia do Centro Universitário Luterano de Ji-paraná, onde foram preparados esfregaços em lâminas e lamínulas do conteúdo do tubo digestivo dos triatomínios, diluídos em soro fisiológico e examinados com ocular 16x e objetiva 40x. Os exames foram minuciosos, abrangendo toda a lamínula, sendo positivo quando se encontrou o parasito com sua forma alongada e flagelo móvel. Posteriormente os esfregaços foram fixados em metanol, corados com Giemsa e observados novamente em microscopia óptica, para confirmação de positividade quanto à presença dos tripanosomatídeos. A maior ocorrência de triatomíneos foi na área de pastagem, no período chuvoso e no estágio ninfa-3, com maior positividade em adulto com índice acima de 70% de contaminação para tripanosomatídeos. Constatou-se que o panorama da infecção de triatomíneos por tripanosomatídeos no município de Ouro Preto do Oeste – Rondônia é preocupante, devido a altos índices de contaminação dos mesmos, e a sua presença cada vez mais constante em residências. O estudo revelou que boa parte da população e das autoridades em saúde do estado desconhecia a existência dos triatomíneos. A pesquisa teve uma grande repercussão, sendo lançadas diversas notas em jornais de noticia e graças a essa divulgação, a Secretaria Estadual de Saúde, viabilizou a distribuição do guia de identificação de triatomíneos do estado de Rondônia, sendo criada a primeira estratégia de educação popular para a profilaxia da doença de Chagas na região.
... Several phenotypic and genetic studies on different species in different ecotopes have demonstrated variations among these species, regarding the sensilla of the insects' antenna, the size of the head and wings, genetic simplification in relation to wild, peridomestic and domestic habits and geographical distribution (Dujardin 1998, Catalá & Dujardin 2001, Cabajal de la Fuente & Catalá 2002, Hernández et al. 2008, 2013 (Chagas 1909); B, C: Trypanosoma cruzi (Chagas 1909); D: armadillo Dasypus novemcinctus (Chagas 1912); E: acute cases of Chagas disease (Chagas 1916). ...
Chagas disease is maintained in nature through the interchange of three cycles: the wild, peridomestic and domestic cycles. The wild cycle, which is enzootic, has existed for millions of years maintained between triatomines and wild mammals. Human infection was only detected in mummies from 4,000-9,000 years ago, before the discovery of the disease by Carlos Chagas in 1909. With the beginning of deforestation in the Americas, two-three centuries ago for the expansion of agriculture and livestock rearing, wild mammals, which had been the food source for triatomines, were removed and new food sources started to appear in peridomestic areas: chicken coops, corrals and pigsties. Some accidental human cases could also have occurred prior to the triatomines in peridomestic areas. Thus, triatomines progressively penetrated households and formed the domestic cycle of Chagas disease. A new epidemiological, economic and social problem has been created through the globalisation of Chagas disease, due to legal and illegal migration of individuals infected by Trypanosoma cruzi or presenting Chagas disease in its varied clinical forms, from endemic countries in Latin America to non-endemic countries in North America, Europe, Asia and Oceania, particularly to the United States of America and Spain. The main objective of the present paper was to present a general view of the interchanges between the wild, peridomestic and domestic cycles of the disease, the development of T. cruzi among triatomine, their domiciliation and control initiatives, the characteristics of the disease in countries in the Americas and the problem of migration to non-endemic countries.
... 0 REVISTA DE PATOLOGIA TROPICAL O relatório de 150 páginas foi publicado em 1916, no fascículo 3, do volume 8, das Memórias do Instituto Oswaldo Cruz. No número anterior, no fascículo 2 do mesmo volume, no artigo sobre "Tripanosomose Americana -Forma aguda da moléstia", Chagas faz a única referência ao mal de engasgo de toda sua obra, propondo sua possível causa, o Trypanosoma cruzi (19). ...
A disfagia espasmódica é uma doença que foi revelada em 1740 por F. Hoffmann. Desde então apareceu em pontos imprevistos por todo o mundo e, consequentemente, o interesse em desvendá-la foi crescendo. Porém, tudo não passou de um conhecimento de sua patologia, sem maiores benefícios para os atingidos pela doença. No Brasil, um mal semelhante, embora mencionado anteriormente, teve sua primeira abordagem médica, em 1857, numa descrição no livro Brazil and brazilians, de dois missionários norte-americanos, Kidder e Fletcher(l), que reproduzem as observações de um Dr. ... (nome não revelado) que, em l" de julho de 1855, em seu consultório em Limeira, São Paulo, lhes dá notícia de uma nova doença e descreve detalhadamente os sintomas, a gravidade e sua marcha progressiva, terminando com a morte por pura fome, devido à impossibilidade da passagem dos alimentos para o estômago. Os autores presenciaram a consulta de dois casos atendidos e ficaram sabendo que a doença, além de grassar em Limeira, atacava numa ampla região do sertão. O Dr. ... conta que atendeu um paciente a 80 milhas de distância e, para sua surpresa, encontrou na mesma casa mais nove portadores dessa "nova" doença -o mal de engasgo -que, dizem, grassava pelo sertão adentro até em Goiás. Faculdade de Medicina de Ribeirão Preto, perto de Limeira. Numa sucessão de eventos detetivescos, com outros participantes, Meneghelli acabou conhecendo por acaso uma descendente direta do procurado médico e tudo se esclareceu (2). Tratava-se do médico norte-americano Dr. Joseph Cooper Reinhardt que, depois de perambular pela Ásia e pela Oceania, se fixara em Limeira e, por último, em Campinas, onde faleceu em 1873, aos 63 anos, deixando descendência. A segunda abordagem médica do agora conhecido mal de engasgo aparece na edição em português da Geographia Physica do Brasil Refundida de J. E. Wappoeus (Edição Condensada), publicada por J. Capistrano de Abreu e A. do Valle Cabral -Rio de Janeiro, 1884. Nesta edição adaptada à nossa patologia há uma nova e detalhada informação sobre o mal de engasgo, de autoria do Prof. Martins Costa que diz textualmente: Há também nessas regiões [o autor refcre-se a Curvelo, MG] uma moléstia endémica, a que seus habitantes chamam mal de engasgo e que consiste, diz o Dr. A. Idelfonso Gomes, em uma 'paralisia da faringe'; os que padecem esta moléstia não podem engolir alimento; cada bolo é empurrado por alguns goles de água.
Chagas disease, discovered over a century ago, continues to pose a global health challenge, affecting millions mainly in Latin America. This historical review with commentary outlines the disease's discovery, its evolution into a global concern due to migration, and highlights significant advances in diagnostics and treatment strategies. Despite these advancements, the paper discusses ongoing challenges in eradication, including vector control, congenital transmission, the disease's asymptomatic nature, and socioeconomic barriers to effective management. It calls for a multidisciplinary approach, enhanced diagnostics, improved treatment accessibility, and sustained vector control efforts. The review emphasizes the importance of global collaboration and increased funding to reduce Chagas disease's impact.
The discovery of Chagas disease is one of the most brilliant and significant in the
history of medicine, particularly, of the Brazilian medicine and science. Carlos Chagas is
exhibited in the literature as a great scientist who discovered a disease that silently
afflicted the backlands of Brazil. From that discovery, the "health look" turns to the most
vulnerable populations in the rural and less developed depths of the country. Little has
been written about the context that led to that breakthrough, and which conditions made
possible such event. Moreover, why that happened in that specific period.
At this end of curse paper, we aimed to know which aspects were paramount for
the discovery of Chagas disease. It is well understood, a priori, that political and economic issues in the First Republic created a favorable context for its discovery. However, which other elements preceded these questions? Among them, we can list the change in the paradigm of scientific thinking that led to the emergence of positivist philosophy, causing shifts in the direction of actions in the scientific field, unveiling a new coping model for situations in areas of education and health. Therefore, the present work tries to analyze a probable relationship between the discovery of Chagas disease and modern scientific thinking, which emerged in the 19th century, and the positivist ideal, established in Brazil from 1840 on. Likewise, this work aims to characterize the context of Carlos Chagas' education and professional career and what paths he took to qualify as the protagonist of this important outcome, namely, the discovery of an unprecedented disease relevant to the public health of the young Brazilian Republic. Consequently, we intended to elucidate two questions: Did the construction of a positivist ethos in the second half of the 19th-century favor the discovery of Chagas disease? Were Carlos Chagas' academic background and professional environment decisive for this discovery of Chagas' disease?
Chagas disease began millions of years ago as an enzootic disease of wild animals and started to be transmitted to man accidentally in the form of an anthropozoonosis when man invaded wild ecotopes. Endemic Chagas disease became established as a zoonosis over the last 200-300 years through forest clearance for agriculture and livestock rearing and adaptation of triatomines to domestic environments and to man and domestic animals as a food source. It is estimated that 15 to 16 million people are infected with Trypanosoma cruzi in Latin America and 75 to 90 million people are exposed to infection. When T. cruzi is transmitted to man through the feces of triatomines, at bite sites or in mucosa, through blood transfusion or orally through contaminated food, it invades the bloodstream and lymphatic system and becomes established in the muscle and cardiac tissue, the digestive system and phagocytic cells. This causes inflammatory lesions and immune responses, particularly mediated by CD4+, CD8+, interleukin-2 (IL) and IL-4, with cell and neuron destruction and fibrosis, and leads to blockage of the cardiac conduction system, arrhythmia, cardiac insufficiency, aperistalsis, and dilatation of hollow viscera, particularly the esophagus and colon. T. cruzi may also be transmitted from mother to child across the placenta and through the birth canal, thus causing abortion, prematurity, and organic lesions in the fetus. In immunosuppressed individuals, T. cruzi infection may become reactivated such that it spreads as a severe disease causing diffuse myocarditis and lesions of the central nervous system. Chagas disease is characterized by an acute phase with or without symptoms, and with entry point signs (inoculation chagoma or Romaña's sign), fever, adenomegaly, hepatosplenomegaly, and evident parasitemia, and an indeterminate chronic phase (asymptomatic, with normal results from electrocardiogram and x-ray of the heart, esophagus, and colon) or with a cardiac, digestive or cardiac-digestive form. There is great regional variation in the morbidity due to Chagas disease, and severe cardiac or digestive forms may occur in 10 to 50% of the cases, or the indeterminate form in the other asymptomatic cases, but with positive serology. Several acute cases have been reported from Amazon region most of them by T. cruzi I, Z3, and a hybrid ZI/Z3. We conclude this article presenting the ten top Chagas disease needs for the near future.
Chagas disease remains an endemic disease especially in South and Central American countries. Approximately 40% of infected patients will ultimately develop clinical symptoms. Chagasic colopathy is presented in 70% of symptomatic patients, more commonly associated with Chagasic megaesophagus. Clinical history includes chronic constipation which progressively becomes worsen. It may be diagnosed with or without megacolon, mainly depending on the stage of the disease (Chagasic colopathy presents initially as an elongated followed by a dilated sigmoid colon). The mechanism for developing chronic constipation are: internal anal sphincter achalasia and the loss of synchronic bowel contraction. The diagnosis of Chagasic colopathy is difficult when a radiological megacolon is not presented. Anal manometry plays an important role as it may determine whether the rectoanal inhibitory reflex is absent.
The digestive form of Chagas is characterized by alterations in motor, secretory, and absorptive functions of the gastrointestinal tract seen in chronic phase of the disease. It is related to denervation of the enteric nervous system that may occur along the entire digestive tract. As a result of this denervation, digestive motility disturbances occur, leading to loss of coordination of peristalsis and relaxation of the sphincters, resulting in progressive dilation—megaformations, notably in the esophagus and colon, known as chagasic megaesophagus and megacolon. The main esophageal symptom is slowly progressive dysphagia, even for years. In chagasic colopathy, the main symptom is constipation. The most common method used to evaluate chagasic esophagopathy and colopathy has been radiological examination. Esophageal manometry has been widely performed in evaluating chagasic esophagopathy and less in colopathy. More recently, high-resolution manometry has been applied in the assessment of esophageal involvement in Chagas disease.
Chagas disease, formerly confined to the Latin-American sub-continent, is now diagnosed in vast numbers of T. cruzi chronically infected individuals living in the United States, Canada, virtually all European countries, Asia, and Oceania, because of recent population migratory and globalization patterns.
Unicellular eukaryotes of the Trypanosomatidae family include human and animal pathogens that belong to the Trypanosoma and Leishmania genera. Diagnosis of the diseases they cause requires the sampling of body fluids (e.g., blood, lymph, peritoneal fluid, cerebrospinal fluid) or organ biopsies (e.g., bone marrow, spleen), which are mostly obtained through invasive methods. Body fluids or appendages can be alternatives to these invasive biopsies but appropriateness remains poorly studied. To further address this question, we perform a systematic review on clues evidencing the presence of parasites, genetic material, antibodies, and antigens in body secretions, appendages, or the organs or proximal tissues that produce these materials. Paper selection was based on searches in PubMed, Web of Science, WorldWideScience, SciELO, Embase, and Google. The information of each selected article (n = 333) was classified into different sections and data were extracted from 77 papers. The presence of Trypanosomatidae parasites has been tracked in most of organs or proximal tissues that produce body secretions or appendages, in naturally or experimentally infected hosts. The meta-analysis highlights the paucity of studies on human African trypanosomiasis and an absence on animal trypanosomiasis. Among the collected data high heterogeneity in terms of the I 2 statistic (100%) is recorded. A high positivity is recorded for antibody and genetic material detection in urine of patients and dogs suffering leishmaniasis, and of antigens for leishmaniasis and Chagas disease. Data on conjunctival swabs can be analyzed with molecular methods solely for dogs suffering canine visceral leishmaniasis. Saliva and hair/bristles showed a pretty good positivity that support their potential to be used for leishmaniasis diagnosis. In conclusion, our study pinpoints significant gaps that need to be filled in order to properly address the interest of body secretion and hair or bristles for the diagnosis of infections caused by Leishmania and by other Trypanosomatidae parasites.
https://www.jstor.org/stable/10.7476/9788526815018
It has been estimated that there are between six and seven million people in the world infected with Trypanosoma cruzi, the parasite that causes Chagas disease, most of them in Latin America. The vector-borne transmission is produced through insects of the subfamily Triatominae carrying the parasite. The most important species in the Southern Cone of the Americas is Triatoma infestans. Currently, this route of infection is observed in the Americas.
We present the first documented case of Trypanosoma cruzi‐induced orchitis in a rhesus macaque. Additionally, we describe an in situ hybridization–based assay to confirm T. cruzi infection in formalin‐fixed tissues.
Resumo Harold Howard Shearme Wolferstan Thomas foi um pesquisador da Escola de Medicina Tropical de Liverpool que teve fugaz destaque na medicina britânica na época em que foi deslocado para a Amazônia (1905). Cinco anos antes, uma expedição da mesma Escola estivera na região para investigar a febre amarela. Thomas e Anton Breinl viajaram para Manaus ainda com o objetivo de estuda essa doença. Naquele intervalo, transcorreram processos muitos dinâmicos na medicina tropical, em particular no tocante às tripanossomíases. Thomas ganhou projeção ao demonstrar que o atoxyl era eficaz no tratamento de animais e humanos infectados por tripanossomos. No presente artigo, Thomas é o fio que conduz a uma trama formada por diferentes atores e doenças na América, Europa e África, cujas sinergias revelam contornos da medicina tropical e o lugar nela ocupado pela região amazônica no começo do século XX. Enfatizaremos especialmente as tripanossomíases. Até sua morte em Manaus, em 1931, Thomas envolveu-se com outros problemas de saúde locais e com médicos que lideravam a saúde pública e a medicina experimental no Amazonas - curso discrepante daquele tomado pela maioria dos médicos europeus que participaram de missões em colônias e áreas de influência das metrópoles imperiais. Nos anos 1950, Thomas foi ‘redescoberto’, ao receber (postumamente) parte de um prêmio conferido aos descobridores da cura da doença do sono. Sua memória teve outros revivals em ambientes acadêmicos.
RESUMO Órgão oficial da Associação Médica de Goiás, a Revista Goiana de Medicina ultrapassou suas fronteiras originais e tornou-se veículo de divulgação das pesquisas dos médicos do Brasil Central, dando-lhes muita visibilidade. O destaque conferido em sua linha editorial à doença de Chagas, grave endemia rural que ameaçava o interior do país em meados do século XX, é fator determinante da proeminência por eles alcançada. Com base na análise de artigos e correspondência institucional, e tomando o periódico em questão como fonte e objeto de pesquisa, busca-se refletir simultaneamente sobre a importância da revista goiana para a institucionalização da medicina local e sua relevância entre os estudiosos da tripanossomíase.
We have uncovered 80 medical files corresponding to original cases of Chagas' disease used for the classical description of the acute and cardiac forms of the disease. Sixty of them were diagnosed cardiac forms of the disease. The detailed clinical description of these 60 files is in excellent agreement with the nosography of progressive heart disease given by Chagas in his original 1922 paper. The reports we had access to, characterize a novel form of cardiac disease, dominated by progressive AV block, enlargement and displacement of the heart and sudden death, in relatively young adults including juveniles. In contrast to that remarkable clinical description, the assertion made by Chagas that this set of clinical signs was the consequence of an earlier infection by Trypanosoma cruzi rests on weak evidence, due to the difficulty to identify the parasite in most patients. Moreover, the association of thyroid dysfunction with cardiac disease emphasized by Chagas cannot be deduced from the files we have examined. Finally, the main reason why the disease had not been recognized for long as a defined clinical entity, is likely the absence of markedly distinctive clinical signs compared to most other parasitic diseases, poor sanitary conditions and the probable lack of clinical skills of the rare doctors working in the area where the disease was described.
A number of conditions lead to severe constipation. Christensen (1971)1 suggested that motility disorders of the gastrointestinal tract were due to one of three causes: either a defect in smooth muscle of the bowel, a defect in the intrinsic or extrinsic nerve supply or an abnormality of gastrointestinal hormones. The last of these is still ill-understood but hormones secreted by the intestinal neuroendocrine cells affect gastrointestinal motility and the subject is reviewed by Lluis and Thompson (1988)2. Lack of other hormones such as in myxoedema is well recognised to be associated with constipation (Abbasi et al., 1975)3. It seems appropriate to discuss in some detail diseases caused by apparent or presumed neurological or smooth muscle disorders.
Presently, the treatment of the infection by Trypanosoma cruzi has been considered unsatisfactory. The eradication of the infection and the interruption of the chronic disease evolution have not been reached by treatment in several clinic and experimental trials. To be unanimous, the indication of determined treatment it should be deposed of undesirable side effects and, even if it did not produce the cure (elimination) of the infection, it should at least stop its evolution. However, the treatment with anti-trypanosome nitro derivatives did not show a clear advantage, when cost and effectiveness were analyzed. Although millions of people with the acute T. cruzi infection do not present a clinic disease, the treatment is clearly indicated in several situations in which the patient's life is in danger. The controversy on the efficacy of the treatment of T. cruzi infection with the available drugs shows that this is one of the aspects of the investigation on Chagas disease that deserve research incentives. The suggestion that the pathogenesis of the disease is associated to the introduction of kDNA mutations from the parasite's genome to the host's defines the need of one or more drugs that are truly effective against the infection. The persistence of the infection, throughout the life of the patient may represent a source of kDNA which introduces cumulative mutations. The effect of these mutations on the evolution of the disease could be avoided with the infection elimination. Maybe, this is an aspect of scientific research with possibilities of generating real benefits to the 18 million people infected by T. cruzi, reminding that one third of them will present clinic manifestations of Chagas disease.
A century after the discovery of Chagas' disease, it can be said that the knowledge of several aspects of the immunopathology of this infection has advanced enormously. However, new aspects have begun to emerge, such as the immunoendocrine regulation of the illness. Hormones could influence immune response and may decisively affect the evolution of Chagas' disease. This article discusses findings on the role of the most important male hormone, testosterone, on different aspects of this infection.
Since more than 30 years, the hypothesis of autoimmunity is considered for chronic Chagas disease, especially for the most severe manifestation: the chronic Chagas heart disease. Actually, many studies were performed to sustain this hypothesis and successful outcomes reached to demonstrate molecular mimicry and presence of autoreactive T and B cells with potential pathological impact. The most severe pathology induced by Trypanosoma cruzi concerns the heart disease that affects 20–30% of the infected patients and leads to sudden death. Only 5–10% suffer from megaesophagus, megacolon, or peripheral neuropathies. The pathophysiology of Chagas heart disease is still not totally understood and two main mechanisms have been proposed; one is parasite-dependent myocardial damage and the other is impaired immunological responses associated to molecular mimicry. If the clinical features were well known since the beginning of the twentieth century, it remains to explore the mechanisms underlying the development of this chronic disease. Moreover, the recent researches have mostly focused on mechanisms of protection mediated by CD8+ T cells and definition of candidates for vaccination. Due to the restrictive rules of ethical approaches in humans, this chapter discusses the validity of the mouse model to learn about the pathological consequences of host-immune response to T. cruzi.
Die amerikanische Trypanosomose, verursacht durch das Trypanosoma cruzi (Chagas, 1909), war ursprünglich eine auf Wirbellose (Triatominae) beschränkte Parasitose, die sich nach Einbeziehung von Vertebraten in den parasitären Entwicklungscyclus auf zahlreiche Wirbeltierarten ausdehnte. Nachdem sich einige Überträger an die menschlichen Behausungen angepaßt hatten und dadurch auch der Mensch in den Entwicklungskreislauf des Trypanosoms eingeschlossen worden war, nahm sie schließlich den Charakter einer typischen Zoonose an (Chagas, 1912).
The term Molecular mimicry describes the sequence similarity between foreign (microorganism's peptides) and self peptides (the host's antigen). This phenomenon has been recently discovered as a one of the major mechanism in which there is a break-down of self-tolerance of the immune system following autoimmunity. After a short preface, the chapter contains examples of common infectious agents and their role in autoimmune diseases. Later on, it describes the autoimmune diseases in which there was found a relation to infectious agents via molecular mimicry mechanism. The data is summarized in two tables.
INTRODUÇÃO: No Estado do Maranhão, a doença de Chagas não apresenta o padrão clássico de transmissão endêmica. No entanto, inquérito entomológico prévio constata altos índices de infecção natural dos vetores e casos agudos têm sido registrados nas últimas décadas, o que motivou o presente estudo que tem por objetivo avaliar as condições sociodemográficas e ambientais envolvidas na transmissão. MÉTODOS: Foram estudados os casos agudos de doença de Chagas de 1994 a 2008. Os dados relacionados aos pacientes foram obtidos do banco de dados do Sistema de Informação de Agravos de Notificação, dos livros de registros de endemias da Fundação Nacional de Saúde e de prontuários médicos. Investigação entomológica foi realizada a partir de 2002. RESULTADOS: Foram identificados 32 casos, procedentes de 17 municípios, sendo 84,4%, da zona rural. O sexo masculino foi acometido em 67% dos casos. A ocupação mais frequente foi a de estudante (38,9%), seguida pela de lavrador e de caçador (27,8%). CONCLUSÕES: Os dados analisados sugerem que a transmissão foi, predominantemente, vetorial nos ambientes silvestre e peridomiciliar.
Leishmaniasis and Chagas disease, caused by the kinetoplastid parasites Leishmania spp and Trypanosoma cruzi, respectively, are among the most important parasitic diseases, affecting millions of people and considered to be within the most relevant group of neglected tropical diseases. Chemotherapy is the main alternative to control such parasites, nevertheless, current treatments are far from satisfactory. This review outlines the current understanding on different drugs against leishmaniasis and Chagas disease and their mechanism of action. Recent approaches in the area of anti-leishmanial and trypanocidal therapies are also enumerated, as well as the search for new drugs.
This article analyzes the importance of ideas mobilized by medical doctors active in Brazilian public health to interpret society and in discussions of the national question over the first half of the 20th century. Texts from three different moments are assessed: in the context of the movement for rural sanitation in the 1910s; those composing the fieldwork promoted by the Yellow Fever Service of the Rockefeller Foundation in the 1930s; and those from one of the most persistent debates among social scientists during the 1940s and 1950s revolving around the question of development, cultural resistance to change, and the “folk culture of the Brazilian backlander.” The article argues that, in the Brazilian case, the authors who constructed the domain of public health fulfilled, among other roles, that of social interpreters, influencing the process of the development of sociological thought in the country.
Objctivando acrescentar algumas informacoes cientificas sobre o estabelecimento da etiologia chagasica do megaesofago. especialmeni0 nas duas decadas que precederam os trabalhos de Koberle. sao revistos alguns trabalhos feitos em Minas Gerais e Sao Paulo que foram pouco divulgados. Nota-se que havia preocupacao com o tema entre alguns grupos de pesquisa, a cpoca. inclusive com mencoes esparsas sobre o megacolon. Em geral, esses trabalhos pioneiros nao foram aprofundados ou continuados por causa de varias circunstâncias metodologicas e historico-inslitucionais. Vale notar que os dados sao bem trabalhados e coerentes com os conhecimentos atuais sobre a doenca e sua cpidemiologia, o que valori/a os estudos aqui apresentados.
Chagas disease cycle was fully elucidated by Carlos Chagas in 1909, when he reported his discovery to the scientific community in two seminal papers. Today remains innumerous factors that limit its therapeutic treatment. One of them is the lack of new drugs in the market since is well known that the existing drugs are poorly active with low efficacy and considerable side effects. Nowadays, many efforts have been done in combinatorial chemistry and synthesis of new compounds searching for new lead compounds. The present review intends to show that a wide variety of synthetic strategies are being used for the preparation of pharmaceutically active compounds against several strains of T. cruzi with a range of potential clinical applications.
Chagas disease is maintained in nature through the interchange of three cycles: the wild, peridomestic and domestic cycles. The wild cycle, which is enzootic, has existed for millions of years maintained between triatomines and wild mammals. Human infection was only detected in mummies from 4,000-9,000 years ago, before the discovery of the disease by Carlos Chagas in 1909. With the beginning of deforestation in the Americas, two-three centuries ago for the expansion of agriculture and livestock rearing, wild mammals, which had been the food source for triatomines, were removed and new food sources started to appear in peridomestic areas: chicken coops, corrals and pigsties. Some accidental human cases could also have occurred prior to the triatomines in peridomestic areas. Thus, triatomines progressively penetrated households and formed the domestic cycle of Chagas disease. A new epidemiological, economic and social problem has been created through the globalisation of Chagas disease, due to legal and illegal migration of individuals infected by Trypanosoma cruzi or presenting Chagas disease in its varied clinical forms, from endemic countries in Latin America to non-endemic countries in North America, Europe, Asia and Oceania, particularly to the United States of America and Spain. The main objective of the present paper was to present a general view of the interchanges between the wild, peridomestic and domestic cycles of the disease, the development of T. cruzi among triatomine, their domiciliation and control initiatives, the characteristics of the disease in countries in the Americas and the problem of migration to non-endemic countries.
RESUMO Objctivando acrescentar algumas informações científicas sobre o estabelecimento da etiologia chagásica do megaesôfago. especialmeni0 nas duas décadas que precederam os trabalhos de Koberle. são revistos alguns trabalhos feitos em Minas Gerais e São Paulo que foram pouco divulgados. Nota-se que havia preocupação com o tema entre alguns grupos de pesquisa, à cpoca. inclusive com menções esparsas sobre o megacólon. Em geral, esses trabalhos pioneiros não foram aprofundados ou continuados por causa de várias circunstâncias metodológicas e hístórico-inslitucionais. Vale notar que os dados são bem trabalhados e coerentes com os conhecimentos atuais sobre a doença e sua cpidemiologia, o que valori/a os estudos aqui apresentados. UNITERMOS: Doença de Chagas. Megaesôfago. Etiologia. Aspectos históricos. Esta pequena revisão pretende simplesmente aportar algumas informações adicionais às excelentes revisões históricas sobre o assunto, recentemente publicadas por Etzel (l I) e Rezende (24). Descoberta a doença em Minas Gerais, em 1909, coube ao próprio Carlos Chagas, em 1916, mencionar pela primeira vez que os muitos casos de "mal de engasgo" detectáveis na região do médio São Francisco poderiam ter etiologia esquisotripanósica (3). Chagas foi certamente alertado pelo relato minucioso da afeção que acometia "centenas de casos observados", feito por Neíva e Penna durante famosa expedição naquela área. No documento, esses autores estudam a nosologia, a fauna (com importantes informações sobre triatomíneos), a flora e os costumes regionais sem terem, entretanto, estabelecido ou mesmo sugerido uma relação entre o "mal de engasgo" e a l Pesquisador Titular do Ceniro de Pesquisas René Rachou. Fiocruz.
Foi verificada a transmissão sucessiva do T. cruzi em três gerações da cobaia Cavia porcellus sem a participação de triatomíneos. Embora não fosse determinado qual das vias, se placentária, leite, excreções ou contágio direto pelo qual o protozoário foi transmitido para os descendentes, chama-se atenção para a importância da manutenção de reservatórios da Doença de Chagas, mesmo na ausência de vetores invertebrados.The sucessive transmission of Trypanosoma cruzi among three generations of the guinea pig Cavia porcellus without the participation of triatomine bugs is verified. Although the mode of transmission, such as congenital, infected milk or other excretion or direct contagion was not defined, this maybe of importance in natural maintenance of reservoirs of T. cruzi without the invertebrate vectors.
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