Biological Sciences
Chagas Disease
Chagas disease is a tropical parasitic infection caused by the Trypanosoma cruzi parasite. It is primarily transmitted to humans through the bite of infected triatomine bugs, but can also be spread through blood transfusions, organ transplantation, and from mother to baby during pregnancy. The disease can cause serious cardiac and gastrointestinal complications if left untreated.
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11 Key excerpts on "Chagas Disease"
- Richard L. Guerrant, David H. Walker, Peter F. Weller(Authors)
- 2011(Publication Date)
- Saunders(Publisher)
CHAPTER 99 American Trypanosomiasis (Chagas Disease)*Louis V. KirchhoffIntroduction
Access the complete reference list online at http://www.expertconsult.comAmerican trypanosomiasis (Chagas Disease) is a zoonosis caused by Trypanosoma cruzi , a protozoan parasite found only in the Americas. The geographic range of T. cruzi infection in humans and other mammalian hosts is primarily determined by the distribution of the various species of blood-sucking triatomine insects that act as its vectors. This range extends from the southern United States to Central Argentina (Fig. 99.1 ).Figure 99.1 Geographic distribution of human infection with Trypanosoma cruzi (Chagas Disease). Endemic countries in which the overall prevalence rate is ≥1% are shown in pink and those in which the prevalence rate is less than 1% are shown in yellow.The Agent
The genus Trypanosoma contains several dozen species, but only T. cruzi and the two African trypanosome subspecies (see Chapter 98 ), Trypanosoma brucei gambiense and T. b. rhodesiense , cause disease in humans.1 T. rangeli , found only in the Americas, can be transmitted to humans, but does not cause a persistent infection and is not pathogenic.2 T. cruzi was first described in 1909 by the Brazilian physician Carlos Chagas, who saw the motile parasites while doing microscopic examinations of dissected intestines of triatomine insects.3 The complex life cycle of T. cruzi involves insect vectors as well as mammalian hosts (Figs 99.2 and 99.3). Vectors become infected when they ingest blood from mammals that have circulating trypomastigotes, which are nondividing but infective forms of the parasite (Fig. 99.4 ). Once inside the midgut of an insect host, the parasites undergo transformation to epimastigotes, which are flagellates having a distinct morphology, and these organisms then multiply extracellularly. After migration to the hindgut, epimastigotes transform into nondividing metacyclic trypomastigotes, which are then discharged with the feces around the time of a subsequent blood meal. Transmission to a second mammalian host occurs when breaks in the skin, mucous membranes, or conjunctivae are contaminated with insect feces containing the infective metacyclic forms. Inside the new host, these parasites enter a variety of host cell types and, after transformation into amastigotes, multiply intracellularly. When proliferating amastigotes fill the host cell, they differentiate into trypomastigotes and the cell ruptures. The parasites released invade adjacent tissues and spread hematogenously to distant sites where they initiate further asynchronous cycles of intracellular multiplication, thus maintaining a parasitemia infective for vectors. T. cruzi can also be transmitted by transfusion of blood donated by infected persons,4 - 6 from mother to fetus,7 - 10 and in laboratory accidents.11, 12
- (Author)
- 2006(Publication Date)
- Elsevier Science(Publisher)
More than any other parasitic disease, Chagas Disease is closely linked to social and economic under-development: poor living conditions, limited access to health care and poor housing of rural endemic areas or on the outskirts of urban centres. A determining factor is the abundance of domestic animals, livestock enclosures, clay-walled vegetable plots, chicken runs and wood-burning stoves. However, the epide-miological picture of Chagas Disease has changed over the last decades; it is no longer restricted to rural areas of endemicity, as migration to urban centres has opened up new modes of transmission, mainly via blood transfusion and congenitally. Trypanosoma cruzi Taxonomy, developmental stages and life cycle T. cruzi belongs to the Kinetoplastida order and the Trypanosomatidae family. It is classified into a special section, designated Stercoraria, because it is the only human trypanosome to be transmitted by the faeces of its invertebrate vector. This pro-tozoan is widespread in the Americas, from the Great Lakes of the United States of America to the southern Patagonia of Argentina (approximately 42 1 N–46 1 S). Four main evolutive forms can be identified during the parasite life cycle: (1) The trypomastigote is the infective flagellate form of the parasite, which is found in (a) the bloodstream of the mammalian host, known as blood trypomastigote and (b) in the terminal portion of the digestive and urinary tracts of the vectors, named as metacyclic trypomastigote; (2) The epimastigote is the replicative form of the parasite in the reduviid bug as well as in the acellular culture medium; (3) The amastigote is the intracellular replicative form of the parasite in the vertebrate host; (4) The spheromastigote is the non-replicative form found in the stomach of the vector.
eBook - ePubRising Contagious Diseases
Basics, Management, and Treatments
- Seth Kwabena Amponsah, Ranjita Shegokar, Yashwant V. Pathak(Authors)
- 2023(Publication Date)
- Wiley(Publisher)
17 Chagas Disease: Historical and Current Trends Vivek Patel1 , Dhara Patel2 , Grishma Patel2 , and Jayvadan K. Patel3 1 Sun Pharmaceutical Industries Ltd., Vadodara, Gujarat, India 2 Pioneer Pharmacy College, Vadodara, Gujarat, India 3 Aavis Pharmaceuticals, Hoschton, GA, United States17.1 Introduction
Chagas Disease, also known as American trypanosomiasis caused by the protozoan flagellate Trypanosoma cruzi (T. cruzi), is an endemic illness that can be fatal and initially was identified in 1909 by Brazilian physician Carlos Ribeiro Justiniano Chagas (1879–1934) [1] . T. cruzi is a parasite that affects an estimated 6–7 million individuals globally and is responsible for about 10,000 disease‐related fatalities, 30,000–40,000 new cases each year, and 8600 newborns become infected during pregnancies. Around 75 million additional people worldwide reside in places where they are susceptible to infection [2] . According to WHO, it was one among the world's top 13 most neglected tropical diseases (NTDs) in 2005 [3] . Despite being identified more than 110 years ago, Chagas Disease is still one of the public health concerns for 21 countries in continental Latin America [4] . Due to population movement, urbanization, and emigration, the epidemiological spectrum of the disease has shifted in the previous 10 years from a rural to an urban illness. Due to the ongoing migration of individuals from endemic locations, Chagas Disease has become an alarm for non‐endemic areas such as Japan, Canada, Europe, the United States, and Australia [5] . It is usually referred to as a “silent and silenced disease” because the majority of persons who are affected show no symptoms or just very minor signs [6] . Despite advancements, there are still a number of issues with dealing with this illness: in addition to the absence of a vaccine, it is thought that less than 10% of those affected by Chagas Disease worldwide receive a diagnosis, and only about 1% have access to specialized care [7] . The currently available treatments, Benznidazole and Nifurtimox (the latter being used on a smaller scale), have questionable efficacy and demand constant observation. Furthermore, the need for long‐term administration of these compounds results in a number of side effects that may necessitate early treatment discontinuation. These compounds also have significant manufacturing costs and are exceedingly hazardous [8 , 9 ]. When medical attention is given right away after an infection, the disease can be cured. Chagas Disease, which has a propensity for digestive clinical symptoms, thrombotic vascular accidents, and neurological sequelae, can cause arrhythmias and dilated cardiomyopathy, which can result in sudden death or heart failure if undetected and untreated in its chronic phase. The most significant mortality and morbidity among parasite infections, chronic Chagas Disease, is a disabling disorder that costs USD $627.5 million in medical expenses worldwide each year [8] . The cost per patient is estimated to be $200 in the early stages of the infection, but it may rise to $400–$6000 throughout the chronic symptomatic phase [10] . Taking into account the fact that Chagas Disease is now impacting non‐endemic nations as well, in order to increase public awareness of the disease, the seventy‐second World Health Assembly decided in May 2019 to establish World Chagas Disease Day, which will be observed on 14 April (the day in 1909 when Carlos Chagas diagnosed the first human case of the illness, a two‐year‐old girl named Berenice). In order to meet the targets for eliminating Chagas Disease by 2030, the road map for neglected tropical diseases 2021–2030 lists primary goals; such as confirming the cessation of vectorial domestic transmission; interruption of blood transfusions transmission and organ transplants; eradicating the disease congenital form; and ensuring that 75% of the eligible population receives antiparasitic treatment [11]
eBook - PDF- Wanderley De Souza(Author)
- 2019(Publication Date)
- IntechOpen(Publisher)
1 Section 1 Basic Biology 3 Chapter 1 Introductory Chapter: Biology of Trypanosoma cruzi Wanderley de Souza 1. Introduction Trypanosoma cruzi , an important zoonotic protozoan that causes Chagas Disease, is the focus of this book. There are two major reasons for the significant interest in the study of this protozoan and the disease it causes. First, Chagas Disease is an important life-long infection in humans that can be divided into distinct clinical stages: the acute phase, where patient symptoms can vary from asymptomatic to severe; the indeterminate form, which is usually asymptomatic; and the chronic phase, where cardiomyopathy and/or digestive mega syndromes appear. In Latin America, at least 8 million people are infected with T. cruzi and 13,000 die each year. In addition, migration patterns are driving the globalization of the disease and there are around 300,000 and 120,000 people infected in the USA and Europe, respectively. Second, T. cruzi is an interesting biological model for studying processes such as: (a) cell differentiation, where a non-infective stage transforms into an infective one; (b) cell invasion, where the infective stages are able to penetrate into a mammalian host cell, where they multiply several times and thus amplify the infection; and (c) evasion from the immune system, using several mechanisms. To better understand the information presented in various chapters of this book, let us review some basic information about T. cruzi infection [1]. Figure 1 shows a general view of the life cycle of T. cruzi in both vertebrate and invertebrate hosts [2]. The three basic developmental stages (trypomastigote, amastigote, and epimas-tigote) are schematically shown in Figure 2a – c , based on images obtained using transmission electron microscopy [2]. The various structures and organelles found in the protozoan are indicated. Figure 3 shows a scheme, where the various phases of the interaction of the trypomastigote form of T.
eBook - PDF- Mark F Wiser(Author)
- 2010(Publication Date)
- Garland Science(Publisher)
Trypanosoma cruzi infects a wide range of vertebrates. It is transmitted by blood-sucking triatomine bugs and causes a human disease commonly referred to as Chagas’ disease . Carlos Chagas first discovered the trypano-some while studying the vectors and named it after his mentor Oswaldo Cruz. Chagas determined the life cycle and found that the parasite could infect a wide range of mammals, including humans, and subsequently described the salient features of the disease. Chagas’ disease exhibits a patchy distribution throughout the Americas ranging from southern United States to southern Argentina. It is predominantly found in poor rural areas of Central and South America and is the leading cause of heart disease in Latin America. Life Cycle T. cruzi is transmitted to humans via hematophagous (i.e., blood feeding) insects called triatomine bugs (Figure 9.1). Numerous species of triatomines are capable of transmitting T. cruzi . However, the most important vectors for human transmission are Triatoma infestans and Rhodnius prolixus . Some common names of triatomine bugs include assassin bugs, kissing bugs (in reference for its tendency to bite around the face), and conenose bugs (in reference to their pointed heads). In addition, they are called reduviid bugs in reference to being in the family Reduviidae or triatomine bugs in refer-ence to the subfamily Triatominae. The life cycle consists of five nymphal Disease(s) Chagas’ disease, American trypanosomiasis Etiological agent(s) Trypanosoma cruz i Major organ(s) affected Blood, heart, esophagus, colon Transmission mode or vector Triatomine bugs Geographical distribution Foci throughout South and Central America Morbidity and mortality A generally asymptomatic acute stage is followed by decades of latency before chronic symptoms involving the heart or gastrointestinal system emerge.
eBook - PDF- Lihua Xiao, Una Ryan, Yaoyu Feng, Lihua Xiao, Una Ryan, Yaoyu Feng(Authors)
- 2015(Publication Date)
- CRC Press(Publisher)
223 13 Trypanosoma cruzi Karen Signori Pereira, Flávio Luís Schmidt, Rodrigo Labello Barbosa, and Luiz Augusto Corrêa Passos 13.1 Introduction American trypanosomiasis (Chagas Disease) was discovered in 1909 by Brazilian researcher Carlos Ribeiro Justiniano das Chagas (1878–1934) in a municipality of the state of Minas Gerais called Lassance. On April 14, 1909, while examining a feverish 2-year-old child named Berenice, Carlos Chagas dis-covered in her blood the same protozoon found in “barbers” (hematophagous hemipteran insects) and several species of animals. Berenice is considered the first described clinical case of Chagas Disease in humans. 1,2 The disease involves a complex biological cycle (protozoan life cycle relies on two types of hosts) and transmission of Trypanosoma cruzi . The protozoan genus name is derived from the Greek trypano (= drill, auger) and soma (= body) because of their corkscrew-like motion. The specific epithet was an honor to Oswaldo Cruz, a renowned microbiologist and Carlos Chagas’ mentor. 3 Chagas Disease is among the most important parasitic diseases. The World Health Organization (WHO) estimates that about seven to eight million people worldwide are infected with T. cruzi , mostly in Latin America. 4,5 In South America, especially Brazil, Ecuador, Chile, Paraguay, Uruguay, Bolivia, Argentina, and Venezuela, Chagas Disease is a severe and alarming public health problem. Since it affects mainly people in developing countries, it is a neglected disease, receiving little funding for diag-nosis, treatment, and prevention. However, in the past decades, it has been increasingly detected in the United States, Canada, and many European and some Western Pacific countries. 5 More than a century after the disease was discovered and described, a cure is still unavailable, and many aspects of the pathogen and disease still need elucidation.
eBook - ePubAmerican Trypanosomiasis Chagas Disease
One Hundred Years of Research
- Jenny Telleria, Michel Tibayrenc(Authors)
- 2017(Publication Date)
- Academic Press(Publisher)
1 History of the discovery of the American Trypanosomiasis (Chagas Disease) T. Araujo-Jorge 1, J. Telleria 2, 3 and J.R. Dalenz 4, 1 Fundação Oswaldo Cruz, Rio de Janeiro, Brazil, 2 Institute for Research for Development (IRD), Montpellier, France, 3 Pontifical Catholic University of Ecuador, Quito, Ecuador, 4 Universidad Mayor de San Andrés, La Paz, Bolivia Abstract American Trypanosomiasis was named Chagas Disease in honor of its discoverer, Carlos Chagas (1878–1934). In 1909 he produced a unique and exceptional work in the history of medicine. He discovered a new species of flagellated protozoa (1) in the intestines of hematophageous insects, (2) in the blood of various domestic animals, and (3) in the blood of a little girl. This new species was called “Trypanosoma cruzi” in honor of Professor Oswaldo Cruz. His discovery gradually spread among different Latin America countries. Salvador Mazza (Argentina) profoundly marked this history. Cecilio Romanha discovered the early pathognomonic sign of Chagas Disease (the Romanha sign) and Rafael Torrico is considered to be the father of Chagas Disease in Bolivia
eBook - PDF- Zlatan Delic(Author)
- 2012(Publication Date)
- IntechOpen(Publisher)
8 Globalization and Chagas Disease João Carlos Pinto Dias 1 and José Rodrigues Coura 2 1 Minas Gerais Academy of Medicine, Belo Horizonte 2 National Academy of Medicine, Rio de Janeiro 1,2 Oswaldo Cruz Foundation, Brasil 1. Introduction Globalization and Chagas Disease reflect several historic and social situations in Latin America (LA), with important influences and repercussions in the general society and between themselves. Originally, the disease was restricted to LA, with a socio-political context strongly marked by poverty, migration and the progressive enfeeblement of the State. (CNBB 2003, Macedo 1997, Schmunis 1997, Schmunis & Dias, 2000). In general, Chagas Disease emerges from a bio ecological context, deeply engaged with the people way of living and with the natural history of its etiological agent, the protozoan Trypanosoma (Schizotrypanum) cruzi ( T.cruzi ), circulating among several mammalian reservoirs and intermediate vectors, occurring in different sylvan sceneries of the Continent. Later on, this trypanosomiasis began to affect the human being in the so called domestic cycle, involving man invasion of natural environment, people migration, very poor dwellings and multiple situations of anthropic character (Dias & Coura, 1997, WHO, 2002).
eBook - PDFChagas Disease
Basic Investigations and Challenges
- Veeranoot Nissapatorn, Helieh S. Oz, Veeranoot Nissapatorn, Helieh S. Oz(Authors)
- 2018(Publication Date)
- IntechOpen(Publisher)
Modelling congenital transmission of Chagas, dis -ease. Bio Systems. 2010; 99 :215-222 [91] Massad E. The elimination of Chagas Disease from Brazil. Epidemiology and Infection. 2008; 136 :1153-1164 [92] Cordovéz JM, Rendon LM, Gonzalez C, Guhl F. Using the basic reproduction num -ber to assess the effects of climate change in the risk of Chagas Disease transmission in Colombia. Acta Tropica. 2014; 129 :74-82 [93] Ayala S. Distribución especial del riesgo de transmisión vectorial de la enfermedad de Chagas basada en la estimación del número reproductivo básico (R0). Tesis Magister en Salud Pública. Facultad de Medicina, Universidad de Chile: 2017; 73 pp Chagas Disease - Basic Investigations and Challenges 94 Chapter 7 Chagas Cardiomyopathy: Role of Sustained Host-Parasite Interaction in Systemic Inflammatory Burden Rodolfo A Kölliker-Frers, Matilde Otero-Losada, Gabriela Razzitte, Mariela Calvo, Justo Carbajales and Francisco Capani Additional information is available at the end of the chapter http://dx.doi.org/10.5772/intechopen.77980 Abstract The economic and social burden associated with Chagas Disease morbidity and mortality is regrettably large in Latin America causing more deaths than does any other parasitic disease. Inflammatory dilated cardiomyopathy is, by far, the most important clinical consequence of Trypanosoma cruzi infection. The insidious persistence of this parasite determines chronic myocarditis progression. The clinical outcome is multifactorial and depends on the particular parasite strain and virulence factors, the infective load and route of infection, the parasite ability to by-pass the protective immune response, the intensity and type of immune response during the acute infective phase, and the host genetic background. From the immunological viewpoint, host control of T. cruzi has been shown to depend on both humoral and cell-mediated adaptive responses and from the innate immune system.
- Alfonso J. Rodriguez-Morales(Author)
- 2018(Publication Date)
- IntechOpen(Publisher)
Infectious Diseases. 2nd ed. Philadelphia: Lippincott, Williams & Wilkins; 2004. pp. 2327-2334 [8] Teixeira ARL, Nascimento R, Sturm NR. Evolution and pathology in Chagas Disease— A review. Memórias do Instituto Oswaldo Cruz. 2006; 101 :463-491. DOI: 10.1590/ S0074-02762006000500001 [9] Costa RS, Monteiro RC, Lehuen A, Joskowicz M, Noël LH, Droz D. Immune complex-mediated glomerulopathy in experimental Chagas' disease. Clinical Immunology and Immunopathology. 1991; 58 :102-114. DOI: 10.1016/0090-1229(91)90152-Z [10] Oliveira GM, Masuda MO, Rocha NN, Schor N, Hooper CS, Araújo-Jorge TC, Henriques-Pons A. Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection. Memórias do Instituto Oswaldo Cruz. 2009; 104 :1063-1071. DOI: 10.1590/S0074-02762009000 800002 [11] Cumbinho LC, Pizzini CC, Oliveira FS, Batista W, Oliveira GM. Cardiorenal interaction during the acute phase of experimental Trypanosoma cruzi infection: The influence of aldosteron and the AT1 receptor on mortality. Journal of Experimental and Integrative Medicine. 2012; 2 :199-206. DOI: 10.5455/jeim.070512.or.029 [12] Lemos JRD, Rodrigues WF, Miguel CB, Parreira RC, Miguel RB, Rogerio AP, et al. Influence of parasite load on renal function in mice acutely infected with Trypanosoma cruzi . PLoS One. 2013; 8 :e71772 [13] Oliveira GM, da Silva TM, Batista WS, Franco M, Schor N. Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice. Parasitology Research. 2009; 106 :111-120. DOI: 10.1371/journal.pone.0071772 [14] Bruijn JA, Oemar BS, Ehrich JH, Oemar BS, Ehrich JM. Anti-basement membrane glomer -ulopathy in experimental trypanosomiasis. Journal of Immunology. 1987; 139 :2482-2488 [15] Van Velthuysen MLF, Bruijn JA, Van Leer EHG, Fleuren GJ. Pathogenesis of trypano -somiasis-induced glomerulonephritis in mice. Nephrology, Dialysis, Transplantation. 1992; 7 :507-515 [16] Rickman WJ, Cox HW.
eBook - PDFTrypanosomiasis and Leishmaniasis
With Special Reference to Chagas' Disease
- Katherine Elliott, Maeve O'Connor, G. E. W. Wolstenholme, Katherine Elliott, Maeve O'Connor, G. E. W. Wolstenholme(Authors)
- 2009(Publication Date)
- Wiley(Publisher)
C. R. Seances SOC. Biol. Fil. 84,773-775 NATTAN-LARRIER, L. (1928) L‘hCredite de la maladie de Chagas. Bull. Acad. Mid. (Paris) NECHME, A. & SCHENONE, H. (1960) Resumen de veinte aiios de investigacion sobre la NEGHME, A., SCHENONE, H., REYES, H., CARRASCO, J. & ALFARO, E. (1960) Hallazgo de NEIVA, A. (1910) InformacKs sBbre a biolojia do Conorhinus megistus Burrn. Mem. Inst. NEIVA, A. (1913) Transmissiio do Trypanosoma cruzi pelo Rhipicephulus sanguineus (Latr.). 273-288 99, 98-99 enferrnedad de Chagas en Chile. Rev. Med. Chile 88,82-93 Triatoma infestans en vagones de ferrocarril. Bol. Chil. Parasitol. 15, 86-87 Oswaldo Cruz Rio de J. 2, 206-212 Bras.-Med. 21, 498 EPIDEMIOLOGY OF CHAGAS’ DISEASE 75 NEVES, D. P. (1971) Influencia da temperatura na evoluGiio do Trypanosoma cruzi em triato- mineos. Rev. Insr. Med. Trop. SGo Paul0 13, 155-161 NUSSENZWEIG, v., AMATO NETO, v., FREITAS, J. L. P. DE, SONNTAG, R. & BIANCALANA, A. (1955) Molestia de Chagas em bancos de sangue. Rev. Hosp. Clin. Fac. Med. Univ. ,960 Paul0 10,265-283 OLSEN, P. F., SHOEMAKER, J. P., TURNER, H. F. & HAYS, K. L. (1964) Incidence of Trypano- soma cruzi (Chagas) in wild vectors and reservoirs in East-Central Alabama. J. Parasitol. PELLEGRINO, J. (1949) Transmiss50 da doenp de Chagas pela transfusiio de sangue. Primeiras comprovacdes sorologicas em doadores e em candidatos a doadores de sangue. Rev. Bras. Med. 6, 297-301 PE~ALVER, L. M., RODR~CUEZ, M. I., BLOCH, M. & SANCHO, G. (1965) Tripanosomiasis en El Salvador. Arch. Col. Med. El Salv. 18, 97-134 PERLOWAGORA-SZUMLEWICZ, A. (1953) Ciclo evolutivo do Triatoma infestans em condiGdes de laboratorio. Rev. Bras. Malariol. Doencas Trop. 5, 35-47 PESS~A, S. B. (1958) Parasirologia Medica, 5th edn, Livraria Ed. Guanabara, Rio de Janeiro PESS~A, S. B. (1962) DomiciliaGiio dos triatomineos e epidemiologia da doenca de Chagas. Arq. Hig. Salide Publica (Srio Paulo) 27, 161-171 PHILLIPS, N.
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