Chagas Disease (American Trypanosomiasis)
- Author: Louis V Kirchhoff, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD more...
Chagas disease, also known as American trypanosomiasis, is caused by infection with the protozoan parasite Trypanosoma cruzi. The organism T cruzi and infection in humans were first described in 1909 by the Brazilian physician Carlos R. J. Chagas. T cruzi is found mostly in blood-sucking triatomine insects (kissing bugs) and small mammals in a sylvatic cycle that is enzootic from the southern and southwestern United States to central Argentina and Chile. T cruzi infection in humans occurs in a spotty distribution throughout the range of the sylvatic cycle.
New cases of vector-borne T cruzi infection usually occur in persons who live in primitive houses in areas where the sylvatic cycle is active. The living quarters are invaded by infected triatomines, which become domiciliary. Infected insects take blood meals from humans and their domestic animals and deposit parasite-laden feces. The parasites are then transmitted via contact with breaks in the skin, mucosal surfaces, or the conjunctivas. Transmission can also occur congenitally, via blood transfusion and organ transplantation, and by ingestion of food and drink contaminated with feces from infected bugs.
T cruzi infection is life-long. A minority of persons with long-standing T cruzi infection develop the serious cardiac and gastrointestinal problems that characterize chronic symptomatic Chagas disease.
T cruzi is a member of the family Trypanosomatidae in the order Kinetoplastida and belongs to a special section called Stercoraria. The infective forms of T cruzi are contained in the feces of the insect vectors and gain entry into its mammalian hosts through contamination. This mechanism of transmission contrasts with that of the two subspecies of African trypanosomes that cause human disease, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, which are transmitted via the saliva of their vectors, and with the mechanism by which the nonpathogenic trypanosome found in the Americas, Trypanosoma rangeli, is transmitted to its mammalian hosts.
As with other parasites that infect both mammalian and insect hosts, the life cycle of T cruzi is complex (see image below).
The T cruzi life cycle consists of 3 main developmental forms. Epimastigotes are an extracellular and noninfective form of the parasite found in the midgut of insect vectors, where they multiply by binary fission. As epimastigotes (depicted in the first image below) move to the hindgut, they differentiate into metacyclic trypomastigotes (depicted in the second image below), which are nondividing forms resistant to mammalian complement that have the capacity to infect mammalian cells. They then enter local cells through breaks in the skin, mucous membranes, or the conjunctivas and transform into the third morphologic form, amastigotes. Amastigotes multiply intracellularly until the host cell is overwhelmed, at which point they transform into bloodstream trypomastigotes.
As the host cells rupture, the trypomastigotes are released into the lymphatics and bloodstream, through which they spread to distant sites and invade new host cells. See image below.
This process continues asynchronously for the life of the host. Small numbers of trypomastigotes may be ingested in blood meals taken by uninfected triatomines. The trypomastigotes transform into epimastigotes in the midgut of these insects, thus completing the cycle.
T cruzi can also be transmitted when mammalian hosts ingest infected insects, and this mechanism of transmission may play a major role in maintaining the sylvatic cycle.
Numerous biological, biochemical, and molecular studies have shown that the population of T cruzi is highly diverse.[2, 3, 4, 5] Although T cruzi is a diploid organism in which some genetic exchange may occur in insect vectors, its genetic and phenotypic diversity is thought to result from the clonal multiplication of the epimastigote and amastigote forms. The current consensus is that T cruzi can be divided into 6 discrete taxonomic units (DTUs; TcI through TcVI). The strains in each DTU show variability in geographic, epizootic, epidemiologic, and pathogenic characteristics.[7, 8]
Vectors of T cruzi
Triatomines, which transmit T cruzi, belong to the family Reduviidae in the order Hemiptera. Reduviidae has 22 subfamilies, including the Triatominae. Although the vectors of T cruzi are occasionally referred to as reduviids, this term is not appropriate since the vast majority of the species in the family Reduviidae are phytophagous or insectivorous and do not transmit the parasite.
All triatomine species are able to transmit T cruzi to humans, but only a handful become domiciliary to any great extent and are important as T cruzi vectors. Many more triatomine species are involved in the widespread sylvatic cycles. Triatomines have 5 nymphal stages (instars), all of which can harbor and transmit T cruzi.
The three vector species most important in the transmission of T cruzi to humans include Triatoma infestans, Rhodnius prolixus (see image below), and Triatoma dimidiata. Historically, T infestans has been by far the most important, as it has been the primary vector in the sub-Amazonian endemic regions. Since the early 1990s, under the aegis of the Southern Cone Initiative (SCI), which is supported by the World Health Organization (WHO) and the Pan American Health Organization (PAHO), Chagas disease control programs in Argentina, Bolivia, Brazil, Chile, Paraguay, and Uruguay have focused on eliminating domiciliary T infestans.
These efforts have been widely successful, so much so that Uruguay, Chile, and, most recently, Brazil have been declared transmission-free by the PAHO.
Major progress in vector control has also been achieved in Argentina, Paraguay, and Bolivia. Programs similar to the SCI have been implemented in the Andean nations and Central America, where R prolixus is typically found. The range of T dimidiata is similar but also extends far into Mexico. Other domiciliary species occupy more restricted areas and play less-important roles in the transmission of T cruzi to humans. The sylvatic species can also colonize human dwellings and thus present a potential risk for transmission.
Mammalian hosts of T cruzi
T cruzi infection has been found in more than 100 mammalian species throughout the range mentioned above, which includes the southern and southwestern United States. Mammals typically involved in sylvatic cycles of transmission include opossums, armadillos, raccoons, monkeys, wood rats, and coyotes, among many others.
Pets such as dogs and cats can become infected in enzootic regions, likely as they eat parasitemic prey or ingest infected insects.[12, 13, 14] It is of interest that Carlos Chagas observed T cruzi in the blood of wild marmosets and a domestic cat before he discovered the parasite in the blood of his first infected patient, Berenice. In some situations, dogs have been shown to be an important link in the maintenance of the domiciliary cycle and consequent transmission to humans.
Livestock have occasionally been found to be infected with T cruzi, but the parasite is not known to affect the health of livestock. Birds, amphibians, and reptiles are naturally resistant to T cruzi infection; however, in some situations, birds may be important sources of blood meals for triatomines.
The modes of transmission of T cruzi to humans
Historically, most transmissions of T cruzi to humans have resulted from the contamination of vulnerable surfaces (eg, breaks in the skin, mucosae, and the conjunctivas) with the feces of infected vectors. However, as noted, vector-borne transmission has been reduced markedly in many endemic countries. Transfusion transmission was a major public health problem in endemic countries for decades, but, as accurate serologic assays for T cruzi infection were developed and screening of blood donors became mandatory and were implemented throughout the endemic range, this problem has been all but eliminated.[16, 17]
Not surprisingly, T cruzi can also be transmitted via transplantation of organs obtained from persons with chronic infection, and occasional reports of this in Latin America[18, 19] and in the United States[20, 21] have appeared.
The rate of congenital (transplacental) transmission from mothers with chronic T cruzi infection to their newborns is 1%-15%.[22, 23] To date, no measures have been defined to reduce or eliminate this form of transmission.[24, 25, 26] As transmission by vectors and through transfusion of contaminated blood have been reduced, the proportion of new T cruzi infections that result from congenital transmission has increased. Nonetheless, the overall number of instances of congenital transmission certainly has decreased as seroprevalence rates have fallen.
In contrast to Toxoplasma gondii, vertical transmission of T cruzi is possible with successive pregnancies. Transmission of T cruzi via breast milk appears to be extremely rare. Several instances of transmission of T cruzi to groups of people via ingestion of food or drink presumably contaminated with the feces of infected vectors have been reported.[28, 29, 30, 31, 32, 33] Finally, the facility of producing infective forms of T cruzi in the laboratory has resulted in numerous accidental transmissions in this context.
An inflammatory lesion caused by T cruzi that may appear at the site of entry in patients with acute Chagas disease is called a chagoma. Histologic changes may include interstitial edema, lymphocytic infiltration, and reactive hyperplasia of adjacent lymph nodes due to intracellular parasitism of muscle and other subcutaneous tissues. When parasitized host cells rupture, trypomastigotes are released and can often be detected by microscopic examination of anticoagulated blood. As the infection spreads systemically, muscles, including the myocardium, and various other tissues become parasitized.
Acute myocarditis, consisting of patchy areas of necrosis and infected cells, may develop (see image below).[37, 38] The pseudocysts occasionally seen in sections of infected tissues are intracellular aggregates of amastigotes. The patent parasitemias of the acute illness may be accompanied by lymphocytosis, and transaminase levels may be elevated. The cerebrospinal fluid may contain parasites.
The heart is the most commonly affected organ in persons with chronic Chagas disease. Autopsy may reveal marked bilateral ventricular enlargement, often involving the right side more than the left, in the heart of patients who die of chagasic heart failure (see image below). The ventricular walls are often thin, and mural thrombi and apical aneurysms may be present. In addition, diffuse interstitial fibrosis, widespread lymphocytic infiltration, and atrophy of myocardial cells may all be present.
T cruzi parasites are rarely found during microscopic examination of stained sections of myocardial tissue; however, in numerous studies, T cruzi ‑specific polymerase chain reaction (PCR) assays have demonstrated parasites in areas of focal inflammation.[41, 42, 43, 44] Pathologic changes in the conduction systems of chronic chagasic hearts are also common and often correlate with dysrhythmias. Chronic inflammatory lesions and dense fibrosis frequently involve the right branch and the left anterior branch of the bundle of His, but lesions may also be found in other segments of the conduction system.
Salient features on gross examination of the colon or esophagus in patients with chronic chagasic gastrointestinal disease (megadisease) include dilatation and muscular hypertrophy of the affected organs (see images below).[46, 47] Focal inflammatory lesions with lymphocytic infiltration are visible on microscopy. The number of neurons in the myenteric plexus is often markedly reduced, and periganglion and intraganglion fibrosis with accompanying Schwann cell proliferation, along with lymphocytosis, are present. In most patients with megadisease, the functional effects of this parasympathetic denervation are limited to the esophagus or colon, but clinically manifest dysfunction of the ureters, biliary tree, and other hollow viscera has been reported.
The pathogenesis of cardiac and gastrointestinal lesions of chronic Chagas disease has been a focus of debate for decades.[48, 49, 50] During the last 20 years, however, convincing evidence has shown that low levels of parasites in chronically affected tissue, detectable with molecular methods, provokes a chronic inflammatory response that eventually leads to the pathologic changes observed microscopically and organ dysfunction.[43, 51]
Despite the presence of the sylvatic cycle of T cruzi transmission in the southern and southwestern United States, only 23 cases of autochthonous transmission of the parasite have been reported.[37, 52, 53] Although some cases of T cruzi infection probably go unnoticed or unreported, autochthonous acute Chagas disease is rare in the United States. This concept is supported by the extreme rarity of T cruzi infection among US blood donors who were not born in or who have not traveled extensively in endemic countries. The rarity of vector‑borne transmission of T cruzi to humans in the United States is likely due to the overall sparsity of vectors and the generally higher housing standards, which help prevent the vectors from becoming domiciliary.
In contrast, the epidemiology of chronic T cruzi infection in the United States has changed markedly in the last few decades owing to the large number of people from endemic countries who have moved to the United States. According to one recent estimate, 23 million persons from endemic countries now live in the United States, 300,000 of whom have chronic T cruzi infection.[54, 55] Approximately two thirds of these immigrants from endemic countries are from Mexico, where the overall prevalence of T cruzi infection is 0.5%-1%.
Five cases of transfusion-associated transmission of T cruzi were reported in the United States prior to the implementation of donor screening in 2007,[57, 58] all of which occurred in immunocompromised patients. Two additional such cases were found through trace-back studies after screening started.
Two tests are currently being used to screen US blood donors for Chagas disease: the Ortho T cruzi ELISA Test System (Ortho Clinical Diagnostics, Rochester, NY)[61, 62] and the Abbott Prism Chagas assay (Abbott Laboratories, Abbott Park, IL). Donor samples positive in either of the two screening assays generally undergo confirmatory testing in the Chagas RIPA (performed by Quest Diagnostics, Inc., Chantilly, VA) or the Abbott Enzyme Strip Assay (ESA) Chagas.[65, 66]
The data accumulated to date indicate that about 1 in every 13,000 US blood donors is infected with T cruzi (ie, repeat reactive in the Ortho or Abbott screening assays and positive in the Chagas RIPA or the Abbott ESA), which is consistent with estimates by groups familiar with the epidemiology of T cruzi in the United States prior to the initiation of screening. No instances of transfusion transmission of T cruzi in the United States are known to have occurred since donor screening was implemented.
Five recipients of organ transplants from 3 donors with T cruzi infection developed acute Chagas disease in the United States, one of whom died of the illness.[20, 21]
T cruzi is found only in the Americas, except in isolated cases in which infected persons have carried the parasites to other regions (eg, the Far East, Australia, Europe).[67, 68, 69, 70, 71] The PAHO estimates that, in 2006, 7.7 million persons had T cruzi infection in the 21 endemic countries, which had a total population of 532 million. The PAHO also estimated that there were approximately 41,200 new vector‑borne cases of T cruzi infection per year and that 14,400 infants were born with congenital Chagas disease annually.
According to PAHO estimates at that time, the following are the countries most affected by Chagas disease: Bolivia (6.8% prevalence); Argentina (4.1%); El Salvador (3.4%); Honduras (3.1%); Paraguay (2.5%); Guatemala (2%); Ecuador (1.7%); French Guyana, Guyana, and Surinam (1.2%); Venezuela (1.2%); Nicaragua (1.1%); Brazil (1%); and Mexico (1%).
As noted above, in recent years, the epidemiology of T cruzi infection has improved markedly in many endemic countries, as blood bank and vector-control programs have been implemented. Because of the success of programs directed at domiciliary vector programs, prevalence rates in younger age groups have been decreasing in many areas.[73, 74, 75, 76] All endemic countries have statutory or regulatory mandates for screening donated blood for T cruzi, and, with a few notable exceptions, particularly Mexico,[54, 77, 78, 79] effective universal screening has been implemented.
In the author’s view, the enormous progress made in controlling Chagas disease in recent decades clearly indicates that the obstacles hindering the complete elimination of T cruzi transmission to humans are primarily economic and political. In this context, no additional major advances, such as a more detailed understanding of the pathogenesis of Chagas disease,[80, 81] further genetic analyses,[4, 82] novel diagnostic approaches, or breakthroughs in vaccine development, are necessary for its completion. Other investigators take an opposing view regarding the application of high-technology approaches to the problem of Chagas disease.
Approximately 12,000 deaths attributable to Chagas disease occur annually, typically due to heart disease[85, 86, 87, 88] or, much less frequently, megadisease or meningoencephalitis. In persons with chronic T cruzi infection, mortality is primarily due to the rhythm disturbances and congestive heart failure that result from the chronic inflammatory cardiomyopathy due to the persistence presence of parasites in the heart tissue. Embolization of intraventricular clots to the cerebrum and lungs can also contribute to mortality.
Individuals with severe megaesophagus who do not receive medical attention can die of malnutrition and/or chronic aspiration pneumonitis. Megacolon (depicted in the image below) can also result in death, usually when volvulus develops and is not resolved surgically.
T cruzi infection does not have a racial predilection.
T cruzi infection does not have a sexual predilection.
Morbidity during the acute phase of Chagas disease is more pronounced in children than in adults. The gastrointestinal and cardiac manifestations of chronic T cruzi infection become apparent many years or even decades after initial infection and thus occur almost exclusively in adults.
Chagas C. Nova tripanozomiase humana. Estudos sobre a morfologia e o ciclo evolutivo do Schizotrypanum cruzi n. gen., n. sp., agente etiológico de nova entidade mórbida do homem. Mem Inst Oswaldo Cruz. 1909. 1:159-218.
Llewellyn MS, Rivett-Carnac JB, Fitzpatrick S, Lewis MD, Yeo M, Gaunt MW, et al. Extraordinary Trypanosoma cruzi diversity within single mammalian reservoir hosts implies a mechanism of diversifying selection. Int J Parasitol. 2011 May. 41(6):609-14. [Medline]. [Full Text].
Yeo M, Mauricio IL, Messenger LA, Lewis MD, Llewellyn MS, Acosta N, et al. Multilocus sequence typing (MLST) for lineage assignment and high resolution diversity studies in Trypanosoma cruzi. PLoS Negl Trop Dis. 2011 Jun. 5(6):e1049. [Medline]. [Full Text].
Diosque P, Tomasini N, Lauthier JJ, Messenger LA, Monje Rumi MM, Ragone PG, et al. Optimized multilocus sequence typing (MLST) scheme for Trypanosoma cruzi. PLoS Negl Trop Dis. 2014 Aug. 8(8):e3117. [Medline]. [Full Text].
Fernández MD, Cecere MC, Lanati LA, Lauricella MA, Schijman AG, Gürtler RE, et al. Geographic variation of Trypanosoma cruzi discrete typing units from Triatoma infestans at different spatial scales. Acta Trop. 2014 Aug 1. 140C:10-18. [Medline].
Gibson W, Stevens J. Genetic exchange in the trypanosomatidae. Adv Parasitol. 1999. 43:1-46. [Medline].
Miles MA, Llewellyn MS, Lewis MD, Yeo M, Baleela R, Fitzpatrick S, et al. The molecular epidemiology and phylogeography of Trypanosoma cruzi and parallel research on Leishmania: looking back and to the future. Parasitology. 2009 Oct. 136(12):1509-28. [Medline].
Ramírez JD, Guhl F, Rendón LM, Rosas F, Marin-Neto JA, Morillo CA. Chagas cardiomyopathy manifestations and Trypanosoma cruzi genotypes circulating in chronic Chagasic patients. PLoS Negl Trop Dis. 2010 Nov 30. 4(11):e899. [Medline]. [Full Text].
Lent H, Wygodzinsky P. Revision of the Triatominae (Hemiptera, Reduviidae), and their significance as vectors of Chagas' disease. Bull Am Museum Natural History. 1979. 163:123-520.
Carbajal-de-la-Fuente AL, Yadón ZE. A scientometric evaluation of the Chagas disease implementation research programme of the PAHO and TDR. PLoS Negl Trop Dis. 2013 Nov. 7(11):e2445. [Medline]. [Full Text].
Bradley KK, Bergman DK, Woods JP, et al. Prevalence of American trypanosomiasis (Chagas disease) among dogs in Oklahoma. J Am Vet Med Assoc. 2000 Dec 15. 217(12):1853-7. [Medline].
Lizundia R, Picado A, Cordero M, Calderón A, Deborggraeve S, Montenegro VM, et al. Molecular and serological rapid tests as markers of Trypanosoma cruzi infection in dogs in Costa Rica. Trop Parasitol. 2014 Jul. 4(2):111-4. [Medline]. [Full Text].
Cohen JE, Gürtler RE. Modeling household transmission of American trypanosomiasis. Science. 2001 Jul 27. 293(5530):694-8. [Medline].
Schmunis GA, Cruz JR. Safety of the blood supply in Latin America. Clin Microbiol Rev. 2005 Jan. 18(1):12-29. [Medline].
Moncayo A, Silveira AC. Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy. Mem Inst Oswaldo Cruz. 2009 Jul. 104 Suppl 1:17-30. [Medline].
Barcan L, Luna C, Lunao C, et al. Transmission of T. cruzi infection via liver transplantation to a nonreactive recipient for Chagas' disease. Liver Transpl. 2005 Sep. 11(9):1112-6. [Medline].
Riarte A, Luna C, Sabatiello R, et al. Chagas' disease in patients with kidney transplants: 7 years of experience 1989-1996. Clin Infect Dis. 1999 Sep. 29(3):561-7. [Medline].
Centers for Disease Control and Prevention. Chagas disease after organ transplantation--United States, 2001. MMWR Morb Mortal Wkly Rep. 2002 Mar 15. 51(10):210-2. [Medline].
Centers for Disease Control and Prevention. Chagas disease after organ transplantation--Los Angeles, California, 2006. MMWR Morb Mortal Wkly Rep. 2006 Jul 28. 55(29):798-800. [Medline].
Congenital transmission of Chagas disease - Virginia, 2010. MMWR Morb Mortal Wkly Rep. 2012 Jul 6. 61(26):477-9. [Medline].
Burgos JM, Altcheh J, Petrucelli N, Bisio M, Levin MJ, Freilij H, et al. Molecular diagnosis and treatment monitoring of congenital transmission of Trypanosoma cruzi to twins of a triplet delivery. Diagn Microbiol Infect Dis. 2009 Sep. 65(1):58-61. [Medline].
Gürtler RE, Segura EL, Cohen JE. Congenital transmission of Trypanosoma cruzi infection in Argentina. Emerg Infect Dis. 2003 Jan. 9(1):29-32. [Medline].
Schijman AG, Altcheh J, Burgos JM, et al. Aetiological treatment of congenital Chagas' disease diagnosed and monitored by the polymerase chain reaction. J Antimicrob Chemother. 2003 Sep. 52(3):441-9. [Medline].
Bern C, Verastegui M, Gilman RH, Lafuente C, Galdos-Cardenas G, Calderon M, et al. Congenital Trypanosoma cruzi transmission in Santa Cruz, Bolivia. Clin Infect Dis. 2009 Dec 1. 49(11):1667-74. [Medline].
Santos FC, Amato N, V, Gakiya E, et al. Microwave treatment of human milk to prevent transmission of Chagas disease. Rev Inst Med Trop Sao Paulo. 2003. 45:41-42.
Di Primio, R. An outbreak of illness in Teutonia. Trop.Dis.Bull. Ref Type: Abstract. 1968. 65(4):400-401.
Shikanai-Yasuda MA, Marcondes CB, Guedes LA, et al. Possible oral transmission of acute Chagas' disease in Brazil. Rev Inst Med Trop Sao Paulo. 1991 Sep-Oct. 33(5):351-7. [Medline].
Steindel M, Kramer Pacheco L, Scholl D, et al. Characterization of Trypanosoma cruzi isolated from humans, vectors, and animal reservoirs following an outbreak of acute human Chagas disease in Santa Catarina State, Brazil. Diagn Microbiol Infect Dis. 2008 Jan. 60(1):25-32. [Medline].
Alarcón de Noya B, Díaz-Bello Z, Colmenares C, Ruiz-Guevara R, Mauriello L, Zavala-Jaspe R, et al. Large urban outbreak of orally acquired acute Chagas disease at a school in Caracas, Venezuela. J Infect Dis. 2010 May 1. 201(9):1308-15. [Medline].
Díaz-Bello Z, Thomas MC, López MC, Zavala-Jaspe R, Noya O, DE Noya BA, et al. Trypanosoma cruzi genotyping supports a common source of infection in a school-related oral outbreak of acute Chagas disease in Venezuela. Epidemiol Infect. 2014 Jan. 142(1):156-62. [Medline].
Xavier SC, Roque AL, Bilac D, de Araújo VA, Neto SF, Lorosa ES, et al. Distantiae transmission of Trypanosoma cruzi: a new epidemiological feature of acute Chagas disease in Brazil. PLoS Negl Trop Dis. 2014 May. 8(5):e2878. [Medline]. [Full Text].
Herwaldt BL. Protozoa and helminths. Fleming DO, Hunt DL, eds. Biological Safety: Principles and Practice. 4 ed. Washington, DC: American Society for Microbiology; 2006. 115-61.
Andrade ZA. Patologia da doença de Chagas [Portuguese]. Brener Z, Andrade ZA, Barral-Netto M, eds. Trypanosoma cruzi e Doença de Chagas. 2 ed. Rio de Janeiro: Guanabara Koogan; 2000. 201-30.
Bern C, Martin DL, Gilman RH. Acute and congenital Chagas disease. Adv Parasitol. 2011. 75:19-47. [Medline].
Ochs DE, Hnilica VS, Moser DR, et al. Postmortem diagnosis of autochthonous acute chagasic myocarditis by polymerase chain reaction amplification of a species-specific DNA sequence of Trypanosoma cruzi. Am J Trop Med Hyg. 1996 May. 54(5):526-9. [Medline].
Parada H, Carrasco HA, Anez N, et al. Cardiac involvement is a constant finding in acute Chagas' disease: a clinical, parasitological and histopathological study. Int J Cardiol. 1997 Jun 27. 60(1):49-54. [Medline].
Hoff R, Teixeira RS, Carvalho JS, et al. Trypanosoma cruzi in the cerebrospinal fluid during the acute stage of Chagas' disease. N Engl J Med. 1978 Mar 16. 298(11):604-6. [Medline].
Marin-Neto JA, Cunha-Neto E, Maciel BC, Simões MV. Pathogenesis of chronic Chagas heart disease. Circulation. 2007 Mar 6. 115(9):1109-23. [Medline].
Jones EM, Colley DG, Tostes S, et al. Amplification of a Trypanosoma cruzi DNA sequence from inflammatory lesions in human chagasic cardiomyopathy. Am J Trop Med Hyg. 1993 Mar. 48(3):348-57. [Medline].
Bellotti G, Bocchi EA, de Moraes AV, et al. In vivo detection of Trypanosoma cruzi antigens in hearts of patients with chronic Chagas' heart disease. Am Heart J. 1996 Feb. 131(2):301-7. [Medline].
Zhang L, Tarleton RL. Parasite persistence correlates with disease severity and localization in chronic Chagas' disease. J Infect Dis. 1999 Aug. 180(2):480-6. [Medline].
Basquiera AL, Sembaj A, Aguerri AM, et al. Risk progression to chronic Chagas cardiomyopathy: influence of male sex and of parasitaemia detected by polymerase chain reaction. Heart. 2003 Oct. 89(10):1186-90. [Medline].
Andrade ZA, Andrade SG, Oliveira GB, et al. Histopathology of the conducting tissue of the heart in Chagas' myocarditis. Am Heart J. 1978 Mar. 95(3):316-24. [Medline].
Kirchhoff LV. American trypanosomiasis (Chagas' disease). Gastroenterol Clin North Am. 1996 Sep. 25(3):517-33. [Medline].
Rezende JM, Moreira H. Forma digestiva da doença de Chagas [Portuguese]. Brener Z, Andrade ZA, Barral-Netto M, eds. Trypanosoma cruzi e Doença de Chagas. 2 ed. Rio de Janeiro: Guanabara Koogan; 2000:. 297-343.
Tarleton RL. Chagas disease: a role for autoimmunity?. Trends Parasitol. 2003 Oct. 19(10):447-51. [Medline].
Tarleton RL, Zhang L, Downs MO. "Autoimmune rejection" of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue. Proc Natl Acad Sci U S A. 1997 Apr 15. 94(8):3932-7. [Medline].
Hyland KV, Engman DM. Further thoughts on where we stand on the autoimmunity hypothesis of Chagas disease. Trends Parasitol. 2006 Mar. 22(3):101-2; author reply 103. [Medline].
Añez N, Carrasco H, Parada H, et al. Myocardial parasite persistence in chronic chagasic patients. Am J Trop Med Hyg. 1999 May. 60(5):726-32. [Medline].
Cantey PT, Stramer SL, Townsend RL, Kamel H, Ofafa K, Todd CW, et al. The United States Trypanosoma cruzi Infection Study: evidence for vector-borne transmission of the parasite that causes Chagas disease among United States blood donors. Transfusion. 2012 Sep. 52(9):1922-30. [Medline].
Kirchhoff LV, Paredes P, Lomelí-Guerrero A, et al. Transfusion-associated Chagas disease (American trypanosomiasis) in Mexico: implications for transfusion medicine in the United States. Transfusion. 2006 Feb. 46(2):298-304. [Medline].
Carabarin-Lima A, González-Vázquez MC, Rodríguez-Morales O, Baylón-Pacheco L, Rosales-Encina JL, Reyes-López PA, et al. Chagas disease (American trypanosomiasis) in Mexico: an update. Acta Trop. 2013 Aug. 127(2):126-35. [Medline].
Centers for Disease Control and Prevention. Blood donor screening for chagas disease--United States, 2006-2007. MMWR Morb Mortal Wkly Rep. 2007 Feb 23. 56(7):141-3. [Medline].
Bern C, Montgomery SP, Katz L, Caglioti S, Stramer SL. Chagas disease and the US blood supply. Curr Opin Infect Dis. 2008 Oct. 21(5):476-82. [Medline].
Young C, Losikoff P, Chawla A, et al. Transfusion-acquired Trypanosoma cruzi infection. Transfusion. 2007 Mar. 47(3):540-4. [Medline].
Kessler DA, Shi PA, Avecilla ST, Shaz BH. Results of lookback for Chagas disease since the inception of donor screening at New York Blood Center. Transfusion. 2013 May. 53(5):1083-7. [Medline].
Trypanosoma cruzi (T. cruzi), Whole Cell Lysate Antigen, ORTHO® T. cruzi ELISA Test System (Package insert). Ortho-Clinical Diagnostics, Inc. 2006.
Tobler LH, Contestable P, Pitina L, et al. Evaluation of a new enzyme-linked immunosorbent assay for detection of Chagas antibody in US blood donors. Transfusion. 2007 Jan. 47(1):90-6. [Medline].
Chang CD, Cheng KY, Jiang LX, Salbilla VA, Haller AS, Yem AW, et al. Evaluation of a prototype Trypanosoma cruzi antibody assay with recombinant antigens on a fully automated chemiluminescence analyzer for blood donor screening. Transfusion. 2006 Oct. 46(10):1737-44. [Medline].
Kirchhoff LV, Gam AA, Gusmao RA, et al. Increased specificity of serodiagnosis of Chagas' disease by detection of antibody to the 72- and 90-kilodalton glycoproteins of Trypanosoma cruzi. J Infect Dis. 1987 Mar. 155(3):561-4. [Medline].
Cheng KY, Chang CD, Salbilla VA, Kirchhoff LV, Leiby DA, Schochetman G, et al. Immunoblot assay using recombinant antigens as a supplemental test to confirm the presence of antibodies to Trypanosoma cruzi. Clin Vaccine Immunol. 2007 Apr. 14(4):355-61. [Medline]. [Full Text].
Shah DO, Chang CD, Cheng KY, Salbilla VA, Adya N, Marchlewicz BA, et al. Comparison of the analytic sensitivities of a recombinant immunoblot assay and the radioimmune precipitation assay for the detection of antibodies to Trypanosoma cruzi in patients with Chagas disease. Diagn Microbiol Infect Dis. 2010 Aug. 67(4):402-5. [Medline].
Frank M, Hegenscheid B, Janitschke K, et al. Prevalence and epidemiological significance of Trypanosoma cruzi infection among Latin American immigrants in Berlin, Germany. Infection. 1997 Nov-Dec. 25(6):355-8. [Medline].
Nishimura A, Ueno Y, Fujiwara S, et al. [An autopsy case of sudden death due to Chagas' disease]. Nihon Hoigaku Zasshi. 1997 Feb. 51(1):39-43. [Medline].
Piron M, Verges M, Munoz J, et al. Seroprevalence of Trypanosoma cruzi infection in at-risk blood donors in Catalonia (Spain). Transfusion. 2008 Sep. 48(9):1862-8. [Medline].
Schmunis GA. Epidemiology of Chagas disease in non-endemic countries: the role of international migration. Mem Inst Oswaldo Cruz. 2007 Oct 30. 102 Suppl 1:75-85. [Medline].
Lescure FX, Canestri A, Melliez H, et al. Chagas disease, France. Emerg Infect Dis. 2008 Apr. 14(4):644-6. [Medline].
Estimación cuantitativa de la enfermedad de Chagas en las Américas. Geneva, Organización Panamericana de Salud. Ref Type: Pamphlet. Department of Control of Neglected Tropical Diseases (NTD). 2006.
Schofield CJ, Jannin J, Salvatella R. The future of Chagas disease control. Trends Parasitol. 2006 Dec. 22(12):583-8. [Medline].
Sabino EC, Goncalez TT, Salles NA, et al. Trends in the prevalence of Chagas' disease among first-time blood donors in São Paulo, Brazil. Transfusion. 2003 Jul. 43(7):853-6. [Medline].
Segura EL, Cura EN, Estani SA, et al. Long-term effects of a nationwide control program on the seropositivity for Trypanosoma cruzi infection in young men from Argentina. Am J Trop Med Hyg. 2000 Mar. 62(3):353-62. [Medline].
Dias JC. Elimination of Chagas disease transmission: perspectives. Mem Inst Oswaldo Cruz. 2009 Jul. 104 Suppl 1:41-5. [Medline].
Becerril-Flores MA, Rangel-Flores E, Imbert-Palafox JL, et al. Human infection and risk of transmission of Chagas disease in Hidalgo State, Mexico. Am J Trop Med Hyg. 2007 Feb. 76(2):318-23. [Medline].
Gamboa-León R, Ramirez-Gonzalez C, Pacheco-Tucuch FS, O'Shea M, Rosecrans K, Pippitt J, et al. Seroprevalence of Trypanosoma cruzi among mothers and children in rural Mayan communities and associated reproductive outcomes. Am J Trop Med Hyg. 2014 Aug. 91(2):348-53. [Medline]. [Full Text].
Martínez-Tovar JG, Rebollar-Téllez EA, Fernández Salas I. Seroprevalence of T. cruzi infection in blood donors and Chagas cardiomyopathy in patients from the coal mining region of Coahuila, Mexico. Rev Inst Med Trop Sao Paulo. 2014 Mar-Apr. 56(2):169-74. [Medline]. [Full Text].
Nogueira LG, Santos RH, Fiorelli AI, Mairena EC, Benvenuti LA, Bocchi EA, et al. Myocardial gene expression of T-bet, GATA-3, Ror-?t, FoxP3, and hallmark cytokines in chronic Chagas disease cardiomyopathy: an essentially unopposed TH1-type response. Mediators Inflamm. 2014. 2014:914326. [Medline]. [Full Text].
Tomasini N, Lauthier JJ, Llewellyn MS, Diosque P. MLSTest: novel software for multi-locus sequence data analysis in eukaryotic organisms. Infect Genet Evol. 2013 Dec. 20:188-96. [Medline].
Farrow AL, Rachakonda G, Gu L, Krendelchtchikova V, Nde PN, Pratap S, et al. Immunization with Hexon modified adenoviral vectors integrated with gp83 epitope provides protection against Trypanosoma cruzi infection. PLoS Negl Trop Dis. 2014 Aug. 8(8):e3089. [Medline]. [Full Text].
Stuart K, Brun R, Croft S, et al. Kinetoplastids: related protozoan pathogens, different diseases. J Clin Invest. 2008 Apr. 118(4):1301-10. [Medline].
Maguire JH. Chagas' disease--can we stop the deaths?. N Engl J Med. 2006 Aug 24. 355(8):760-1. [Medline].
Rassi A Jr, Rassi A, Little WC, Xavier SS, Rassi SG, Rassi AG, et al. Development and validation of a risk score for predicting death in Chagas' heart disease. N Engl J Med. 2006 Aug 24. 355(8):799-808. [Medline].
Rassi A Jr, Rassi A, Marin-Neto JA. Chagas disease. Lancet. 2010 Apr 17. 375(9723):1388-402. [Medline].
Kirchhoff LV. Trypanosomiasis of the central nervous system. Scheld WM, Marra CM, Whitely RJ, eds. Infections of the Central Nervous System. 3 ed. 2004. 777-89.
Kirchhoff LV, Weiss LM, Wittner M, et al. Parasitic diseases of the heart. Front Biosci. 2004 Jan 1. 9:706-23. [Medline].
Mott KE, França JT, Barrett TV, Hoff R, de Oliveira TS, Sherlock IA. Cutaneous allergic reactions to Triatoma infestans after xenodiagnosis. Mem Inst Oswaldo Cruz. 1980 Jul-Dec. 75(3-4):3-10. [Medline].
Klotz JH, Dorn PL, Logan JL, Stevens L, Pinnas JL, Schmidt JO, et al. "Kissing bugs": potential disease vectors and cause of anaphylaxis. Clin Infect Dis. 2010 Jun 15. 50(12):1629-34. [Medline].
Dias E, Laranja FS, Miranda A, et al. Chagas' disease; a clinical, epidemiologic, and pathologic study. Circulation. 1956 Dec. 14(6):1035-60. [Medline].
Jorg ME, Freire RS, Orlando AS, et al. Disfunción cerebral mínima como secuela de meningoencefalitis aguda por Trypanosoma cruzi. Prensa Med Argentina. 1972. 59:1658-69.
Sartori AM, Ibrahim KY, Nunes Westphalen EV, et al. Manifestations of Chagas disease (American trypanosomiasis) in patients with HIV/AIDS. Ann Trop Med Parasitol. 2007 Jan. 101(1):31-50. [Medline].
Cordova E, Boschi A, Ambrosioni J, Cudos C, Corti M. Reactivation of Chagas disease with central nervous system involvement in HIV-infected patients in Argentina, 1992-2007. Int J Infect Dis. 2008 Nov. 12(6):587-92. [Medline].
Bern C. Chagas disease in the immunosuppressed host. Curr Opin Infect Dis. 2012 Aug. 25(4):450-7. [Medline].
Guiang KM, Cantey P, Montgomery SP, Ailawadhi S, Qvarnstrom Y, Price T, et al. Reactivation of Chagas disease in a bone marrow transplant patient: case report and review of screening and management. Transpl Infect Dis. 2013 Dec. 15(6):E264-7. [Medline].
Pinazo MJ, Espinosa G, Cortes-Lletget C, Posada Ede J, Aldasoro E, Oliveira I, et al. Immunosuppression and Chagas disease: a management challenge. PLoS Negl Trop Dis. 2013. 7(1):e1965. [Medline]. [Full Text].
Kirchhoff LV, Votava JR, Ochs DE, et al. Comparison of PCR and microscopic methods for detecting Trypanosoma cruzi. J Clin Microbiol. 1996 May. 34(5):1171-5. [Medline].
Freilij H, Altcheh J. Congenital Chagas' disease: diagnostic and clinical aspects. Clin Infect Dis. 1995 Sep. 21(3):551-5. [Medline].
Otani MM, Vinelli E, Kirchhoff LV, del Pozo A, Sands A, Vercauteren G, et al. WHO comparative evaluation of serologic assays for Chagas disease. Transfusion. 2009 Jun. 49(6):1076-82. [Medline].
Virreira M, Torrico F, Truyens C, et al. Comparison of polymerase chain reaction methods for reliable and easy detection of congenital Trypanosoma cruzi infection. Am J Trop Med Hyg. 2003 May. 68(5):574-82. [Medline].
Sabino EC, Lee TH, Montalvo L, Nguyen ML, Leiby DA, Carrick DM, et al. Antibody levels correlate with detection of Trypanosoma cruzi DNA by sensitive polymerase chain reaction assays in seropositive blood donors and possible resolution of infection over time. Transfusion. 2013 Jun. 53(6):1257-65. [Medline]. [Full Text].
Moser DR, Kirchhoff LV, Donelson JE. Detection of Trypanosoma cruzi by DNA amplification using the polymerase chain reaction. J Clin Microbiol. 1989 Jul. 27(7):1477-82. [Medline].
Sturm NR, Degrave W, Morel C, et al. Sensitive detection and schizodeme classification of Trypanosoma cruzi cells by amplification of kinetoplast minicircle DNA sequences: use in diagnosis of Chagas' disease. Mol Biochem Parasitol. 1989 Mar 15. 33(3):205-14. [Medline].
Schijman AG, Bisio M, Orellana L, Sued M, Duffy T, Mejia Jaramillo AM, et al. International study to evaluate PCR methods for detection of Trypanosoma cruzi DNA in blood samples from Chagas disease patients. PLoS Negl Trop Dis. 2011 Jan 11. 5(1):e931. [Medline]. [Full Text].
Shikanai-Yasuda MA, Ochs DE, Tolezano JE, et al. Use of the polymerase chain reaction for detecting Trypanosoma cruzi in triatomine vectors. Trans R Soc Trop Med Hyg. 1996 Nov-Dec. 90(6):649-51. [Medline].
Mora MC, Sanchez Negrette O, Marco D, et al. Early diagnosis of congenital Trypanosoma cruzi infection using PCR, hemoculture, and capillary concentration, as compared with delayed serology. J Parasitol. 2005 Dec. 91(6):1468-73. [Medline].
Diez CN, Manattini S, Zanuttini JC, et al. The value of molecular studies for the diagnosis of congenital Chagas disease in northeastern Argentina. Am J Trop Med Hyg. 2008 Apr. 78(4):624-7. [Medline].
Russomando G, de Tomassone MM, de Guillen I, Acosta N, Vera N, Almiron M, et al. Treatment of congenital Chagas' disease diagnosed and followed up by the polymerase chain reaction. Am J Trop Med Hyg. 1998 Sep. 59(3):487-91. [Medline].
Pinto AY, Valente Vda C, Coura JR, Valente SA, Junqueira AC, Santos LC, et al. Clinical follow-up of responses to treatment with benznidazol in Amazon: a cohort study of acute chagas disease. PLoS One. 2013. 8(5):e64450. [Medline]. [Full Text].
Machado-de-Assis GF, Silva AR, Do Bem VA, Bahia MT, Martins-Filho OA, Dias JC, et al. Posttherapeutic cure criteria in Chagas' disease: conventional serology followed by supplementary serological, parasitological, and molecular tests. Clin Vaccine Immunol. 2012 Aug. 19(8):1283-91. [Medline]. [Full Text].
Lana Md, Lopes LA, Martins HR, Bahia MT, Machado-de-Assis GF, Wendling AP, et al. Clinical and laboratory status of patients with chronic Chagas disease living in a vector-controlled area in Minas Gerais, Brazil, before and nine years after aetiological treatment. Mem Inst Oswaldo Cruz. 2009 Dec. 104(8):1139-47. [Medline].
Bern C, Montgomery SP, Herwaldt BL, et al. Evaluation and treatment of chagas disease in the United States: a systematic review. JAMA. 2007 Nov 14. 298(18):2171-81. [Medline].
Altcheh J, Biancardi M, Lapena A, et al. [Congenital Chagas disease: experience in the Hospital de Niños, Ricardo Gutiérrez, Buenos Aires, Argentina]. Rev Soc Bras Med Trop. 2005. 38 Suppl 2:41-5. [Medline].
Sosa-Estani S, Segura EL. Etiological treatment in patients infected by Trypanosoma cruzi: experiences in Argentina. Curr Opin Infect Dis. 2006 Dec. 19(6):583-7. [Medline].
Braga MS, Lauria-Pires L, Arganaraz ER, et al. Persistent infections in chronic Chagas' disease patients treated with anti-Trypanosoma cruzi nitroderivatives. Rev Inst Med Trop Sao Paulo. 2000 May-Jun. 42(3):157-61. [Medline].
Lauria-Pires L, Braga MS, Vexenat AC, et al. Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives. Am J Trop Med Hyg. 2000 Sep-Oct. 63(3-4):111-8. [Medline].
Lauria-Pires L, Nitz N, Vexenat AC, et al. The treatment of Chagas disease patients with nitroderivative is unsatisfactory. Rev Inst Med Trop Sao Paulo. 2001. 43:175-81.
Sosa-Estani S, Cura E, Velazquez E, Yampotis C, Segura EL. Etiological treatment of young women infected with Trypanosoma cruzi, and prevention of congenital transmission. Rev Soc Bras Med Trop. 2009 Sep-Oct. 42(5):484-7. [Medline].
Cardinalli-Neto A, Bestetti RB, Cordeiro JA, Rodrigues VC. Predictors of all-cause mortality for patients with chronic Chagas' heart disease receiving implantable cardioverter defibrillator therapy. J Cardiovasc Electrophysiol. 2007 Dec. 18(12):1236-40. [Medline].
Barbosa MP, da Costa Rocha MO, de Oliveira AB, Lombardi F, Ribeiro AL. Efficacy and safety of implantable cardioverter-defibrillators in patients with Chagas disease. Europace. 2013 Jul. 15(7):957-62. [Medline].
Rassi A Jr, Rassi A. Another disappointing result with implantable cardioverter-defibrillator therapy in patients with Chagas disease. Europace. 2013 Sep. 15(9):1383. [Medline].
Gali WL, Sarabanda AV, Baggio JM, Ferreira LG, Gomes GG, Marin-Neto JA, et al. Implantable cardioverter-defibrillators for treatment of sustained ventricular arrhythmias in patients with Chagas' heart disease: comparison with a control group treated with amiodarone alone. Europace. 2014 May. 16(5):674-80. [Medline].
Fiorelli AI, Stolf NA, Honorato R, et al. Later evolution after cardiac transplantation in Chagas' disease. Transplant Proc. 2005 Jul-Aug. 37(6):2793-8. [Medline].
Fiorelli AI, Santos RH, Oliveira JL Jr, Lourenço-Filho DD, Dias RR, Oliveira AS, et al. Heart transplantation in 107 cases of Chagas' disease. Transplant Proc. 2011 Jan-Feb. 43(1):220-4. [Medline].
Bocchi EA, Bellotti G, Mocelin AO, et al. Heart transplantation for chronic Chagas' heart disease. Ann Thorac Surg. 1996 Jun. 61(6):1727-33. [Medline].
Campos SV, Strabelli TM, Amato Neto V, et al. Risk factors for Chagas' disease reactivation after heart transplantation. J Heart Lung Transplant. 2008 Jun. 27(6):597-602. [Medline].
Bacal F, Silva CP, Pires PV, Mangini S, Fiorelli AI, Stolf NG, et al. Transplantation for Chagas' disease: an overview of immunosuppression and reactivation in the last two decades. Clin Transplant. 2010 Mar-Apr. 24(2):E29-34. [Medline].
Di Martino C, Nesi G, Tonelli F. Surgical treatment of chagasic megacolon with Duhamel-Habr-Gama technique modulated by frozen-section examination. Surg Infect (Larchmt). 2014 Aug. 15(4):454-7. [Medline].
Teixeira AR, Silva R, Cunha Neto E, et al. Malignant, non-Hodgkin's lymphomas in Trypanosoma cruzi-infected rabbits treated with nitroarenes. J Comp Pathol. 1990 Jul. 103(1):37-48. [Medline].
Teixeira AR, Cordoba JC, Souto Maior I, et al. Chagas' disease: lymphoma growth in rabbits treated with Benznidazole. Am J Trop Med Hyg. 1990 Aug. 43(2):146-58. [Medline].
Bocchi EA, Higuchi ML, Vieira ML, et al. Higher incidence of malignant neoplasms after heart transplantation for treatment of chronic Chagas' heart disease. J Heart Lung Transplant. 1998 Apr. 17(4):399-405. [Medline].
Centers for Disease Control and Prevention. The Global Surveillance Network of the ISTM and CDC. The GeoSentinel Newsletter: Information for Action. Infrequent Diagnoses & Their Geographic Exposures. 2008.
Virreira M, Truyens C, Alonso-Vega C, Brutus L, Jijena J, Torrico F, et al. Comparison of Trypanosoma cruzi lineages and levels of parasitic DNA in infected mothers and their newborns. Am J Trop Med Hyg. 2007 Jul. 77(1):102-6. [Medline].
Avila H, Goncalves AM, Nehme NS, et al. Schizodeme analysis of Trypanosoma cruzi stocks from South and Central America by analysis of PCR-amplified minicircle variable region sequences. Mol Biochem Parasitol. 1990 Sep-Oct. 42(2):175-87. [Medline].
Carlier Y. [Congenital Chagas disease: from the laboratory to public health]. Bull Mem Acad R Med Belg. 2007. 162(7-9):409-16; discussion 416-7. [Medline].
Dias JC, Silveira AC, Schofield CJ. The impact of Chagas disease control in Latin America: a review. Mem Inst Oswaldo Cruz. 2002 Jul. 97(5):603-12. [Medline].
El-Sayed NM, Myler PJ, Bartholomeu DC, et al. The genome sequence of Trypanosoma cruzi, etiologic agent of Chagas disease. Science. 2005 Jul 15. 309(5733):409-15. [Medline].
Engel JC, Dvorak JA, Segura EL, et al. Trypanosoma cruzi: biological characterization of 19 clones derived from two chronic chagasic patients. I. Growth kinetics in liquid medium. J Protozool. 1982 Nov. 29(4):555-60. [Medline].
Fabbro D, Velazquez E, Bizai ML, Denner S, Olivera V, Arias E, et al. Evaluation of the ELISA-F29 test as an early marker of therapeutic efficacy in adults with chronic Chagas disease. Rev Inst Med Trop Sao Paulo. 2013. 55(3):[Medline].
Fontanella GH, De Vusser K, Laroy W, et al. Immunization with an engineered mutant trans-sialidase highly protects mice from experimental Trypanosoma cruzi infection: a vaccine candidate. Vaccine. 2008 May 2. 26(19):2322-34. [Medline].
Gorlin J, Rossmann S, Robertson G, et al. Evaluation of a new Trypanosoma cruzi antibody assay for blood donor screening. Transfusion. 2008 Mar. 48(3):531-40. [Medline].
Haddad J, Raia A, Netto AC. [Colonic retro-rectal depression by perineal colostomy in the treatment of acquired megacolon. Modified Duhamel's operation]. Rev Assoc Med Bras. 1965 Mar. 11(3):83-8. [Medline].
Jackson Y, Myers C, Diana A, Marti HP, Wolff H, Chappuis F, et al. Congenital transmission of Chagas disease in Latin American immigrants in Switzerland. Emerg Infect Dis. 2009 Apr. 15(4):601-3. [Medline]. [Full Text].
Marin-Neto JA, Rassi A Jr, Morillo CA, Avezum A, Connolly SJ, Sosa-Estani S, et al. Rationale and design of a randomized placebo-controlled trial assessing the effects of etiologic treatment in Chagas' cardiomyopathy: the BENznidazole Evaluation For Interrupting Trypanosomiasis (BENEFIT). Am Heart J. 2008 Jul. 156(1):37-43. [Medline].
Mukherjee S, Nagajyothi F, Mukhopadhyay A, et al. Alterations in myocardial gene expression associated with experimental Trypanosoma cruzi infection. Genomics. 2008 May. 91(5):423-32. [Medline].
Pereira Nunes MC, Donnes W, Morillo C, Encina JJ, Ribeiro AL. Chagas Disease: an Overview of Clinical and Epidemiological Aspects. J Am Coll Cardiol. 2013 Jun 12. [Medline].
Schofield CJ, Dias JC. The Southern Cone Initiative against Chagas disease. Adv Parasitol. 1999. 42:1-27. [Medline].
Schofield CJ, Dujardin JP. Chagas disease vector control in Central America. Parasitol Today. 1997 Apr. 13(4):141-4. [Medline].
Siriano Lda R, Luquetti AO, Avelar JB, Marra NL, de Castro AM. Chagas disease: increased parasitemia during pregnancy detected by hemoculture. Am J Trop Med Hyg. 2011 Apr. 84(4):569-74. [Medline]. [Full Text].
Tanowitz HB, Machado FS, Jelicks LA, Shirani J, de Carvalho AC, Spray DC, et al. Perspectives on Trypanosoma cruzi-induced heart disease (Chagas disease). Prog Cardiovasc Dis. 2009 May-Jun. 51(6):524-39. [Medline]. [Full Text].
Tibayrenc M, Ayala FJ. [High correlation between isoenzyme classification and kinetoplast DNA variability in Trypanosoma cruzi]. C R Acad Sci III. 1987. 304(4):89-92. [Medline].
Yacoub S, Mocumbi AO, Yacoub MH. Neglected tropical cardiomyopathies: I. Chagas disease: myocardial disease. Heart. 2008 Feb. 94(2):244-8. [Medline].
Zafra G, Mantilla JC, Valadares HM, et al. Evidence of Trypanosoma cruzi II infection in Colombian chagasic patients. Parasitol Res. 2008 Jun 4. [Medline].