Neglected tropical cardiomyopathies: I. Chagas disease

Sophie Yacoub; Ana Olga Mocumbi; Magdi H Yacoub

doi:10.1136/hrt.2007.132316

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Education in Heart

Myocardial disease

Neglected tropical cardiomyopathies: I. Chagas disease

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Chagas Disease: a neglected cardiomyopathy
Alfonso J. Rodriguez-Morales
Published on: 27 January 2008

Published on: 27 January 2008
Chagas Disease: a neglected cardiomyopathy
- Alfonso J. Rodriguez-Morales, Physician Researcher
- Other Contributors:
  Mayra A. Rivas, Cardiology Service, Childrens Hospital J.M. De Los Ríos, Caracas, Venezuela; Jesus A. Benitez, Chagas Disease Program, Ministry of Health, Maracay, Venezuela.
Dear Editor,
Recently, Yacoub et al,[1] reviewed for the section Education in Heart of the journal Heart, different clinical but also epidemiological, diagnostic, therapeutic and other aspects of Chagas disease, “a neglected tropical cardiomyopathy”. Although it should be acknowledge the importance of such reviews, particularly in a topic that has been neglected in many aspects, including research as well intern...
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Dear Editor,
Recently, Yacoub et al,[1] reviewed for the section Education in Heart of the journal Heart, different clinical but also epidemiological, diagnostic, therapeutic and other aspects of Chagas disease, “a neglected tropical cardiomyopathy”. Although it should be acknowledge the importance of such reviews, particularly in a topic that has been neglected in many aspects, including research as well international education, some aspects needs further comments and discussion.
As Yacoub et al stated Chagas disease is caused by the protozoan parasite Trypanosoma cruzi, its transmission (more than the spread) is due to different species of hematophagous reduviidae bugs, that include Triatoma infestans, but also Rhodnius prolixus, Triatoma dimidiata, and Panstrongylus megistus, among others.[2] About the geographical distribution is important to state that currently Chagas disease is endemic in Latin America, ranging from Argentina to Mexico, but in North America is present in also southern states of USA, including Texas,[3] Oklahoma,[4] Alabama,[5] and more recently in Louisiana due to Triatoma sanguisuga,[6] but also in western states such as Arizona,[7] New Mexico,[8] California.[9]
Secondly, although the latin American immigration of patients with Chagas disease to north America is one of the most important, recently this phenomena has been increasingly relevant in other countries in Europe, particularly to Spain,[10] but also France,[11] Germany,[12] Switzerland,[13] among others. Even in the United Kingdom a patient from this country returned from Argentina with Chagas disease.[14] In Australia, Chagas disease in immigrants has been also reported.[10] In the case of USA, although up to year 2000 just five cases were reported, the diagnose of these cases included PCR,[15] and in 2007, when the autochthonous transmission of T. cruzi occurred in Louisiana, the patient had positive test results from 2 serologic tests and hemoculture at the Centers for Disease Control, Atlanta, Georgia, and the Triatoma sanguisuga (18) collected were positive for T. cruzi by PCR in 56%.[6] Then, Chagas disease could be an emergent disease in the United States.
About the life cycle of the parasite, this involves many morphologically distinct stages – more than described for any other genus in the Family Trypanosomatidae. In the mammalian host, intracellularly multiplying amastigotes develop via epi- and promastigote intermediate stages to nonreplicative blood trypomastigotes. These trypomastigotes are ingested by the insect vectors and transform in the lumen of the digestive tract into dividing and nonreplicative amastigotes and spheromastigotes and dividing epimastigotes. Later, nonreplicative infective trypomastigotes develop. If the main intermediate stages are also considered, more than 18 different forms can be classified in the vector.[16]
Clinically, an area of inflammation at the site of inoculation, called chagoma, when involves conjunctival inoculation could lead to the triad of conjunctivitis, periorbital edema, and preauricular satellite lymphadenopathy; and this is what is known as the Romaña sign.[17]
Regard to the pathology we consider that those developments recently achieved in demonstrating that T. cruzi could be found in the myocardium during the chronic phase of Chagas disease, should be acknowledged citing some of them.[18, 19]
Finally, in the XXI century when HIV/AIDS pandemics is affecting the human being worldwide, the interaction between T. cruzi and this retrovirus, should be also considered, because produce a different clinical spectrum. Chagas disease has been well recognized as an opportunistic infection associated with AIDS.[20, 21] To date, the cases reported largely represent reactivation of chronic infection, which is expected because of the differing patterns of epidemiological risk for these infections; T. cruzi infection occurs primarily in rural regions, and HIV infection occurs primarily in urban regions, but this pattern is changing and less rural and more urban pattern is now observed in different countries allowing the geographical overlapping between both entities.[22, 23] Clinical reactivation generally occurs in persons with CD4+ T cell counts <200 cells/mm3 and most commonly involves the CNS. Lesions are often multiple, with preferential involvement of the white matter. Hemorrhagic foci can produce mass effects simulating brain tumors. Histologically, brain lesions exhibit necrosis, hemorrhage, and inflammatory infiltrates. Amastigote forms of the parasite are abundant in glial cells and macrophages. Myocarditis is a common autopsy finding in persons who have died of meningoencephalitis. Such myocarditis is often clinically silent. When present, clinical manifestations include arrhythmias and congestive heart failure.[20]
Cardiac manifestations previously seen only in resource-constrained countries, including certain parasitic infections such as Chagas disease, can be currently diagnosed anywhere in the globe. These epidemiologic transitions have been favored by multiple factors: growing travel and immigration, worldwide spread of HIV/AIDS epidemic, and growing number of organ transplantation, increased use of immunosuppressive agents, and blood transfusions.[23] Clinicians anywhere in the globe need to be aware of the potential cardiac manifestations of parasitic diseases, such as the American Trypanosomiasis, but also those related to other neglected diseases.
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Neglected tropical cardiomyopathies: I. Chagas disease: myocardial disease.
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Genetic variation, population structure, and phylogenetic relationships of Triatoma rubida and T. recurva (Hemiptera: Reduviidae: Triatominae) from the Sonoran Desert, insect vectors of the Chagas' disease parasite Trypanosoma cruzi.
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Chagas disease of the colon and rectum.
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17. Prata A.
Clinical and epidemiological aspects of Chagas disease.
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18. Anez N, Carrasco H, Parada H, et al.
Myocardial parasite persistence in chronic chagasic patients.
The American journal of tropical medicine and hygiene 1999;60:726-32.
19. Schijman AG, Vigliano CA, Viotti RJ, et al.
Trypanosoma cruzi DNA in cardiac lesions of Argentinean patients with end-stage chronic chagas heart disease.
The American journal of tropical medicine and hygiene 2004;70:210-20.
20. Karp CL, Auwaerter PG.
Coinfection with HIV and tropical infectious diseases. I. Protozoal pathogens.
Clin Infect Dis 2007;45:1208-13.
21. Vaidian AK, Weiss LM, Tanowitz HB.
Chagas' disease and AIDS.
Kinetoplastid Biol Dis 2004;3:2.
22. Guzman-Tapia Y, Ramirez-Sierra MJ, Dumonteil E.
Urban Infestation by Triatoma dimidiata in the City of Merida, Yucatan, Mexico.
Vector borne and zoonotic diseases (Larchmont, NY 2007;7:597-606.
23. Franco-Paredes C, Rouphael N, Mendez J, et al.
Cardiac manifestations of parasitic infections part 1: overview and immunopathogenesis.
Clinical cardiology 2007;30:195-9.
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