Pathology and Pathogenesis of Chagas Heart Disease.


Journal

Annual review of pathology
ISSN: 1553-4014
Titre abrégé: Annu Rev Pathol
Pays: United States
ID NLM: 101275111

Informations de publication

Date de publication:
24 01 2019
Historique:
pubmed: 26 10 2018
medline: 21 4 2020
entrez: 26 10 2018
Statut: ppublish

Résumé

Chagas heart disease is an inflammatory cardiomyopathy that develops in approximately one-third of people infected with the protozoan parasite Trypanosoma cruzi. One way T. cruzi is transmitted to people is through contact with infected kissing bugs, which are found in much of the Western Hemisphere, including in vast areas of the United States. The epidemiology of T. cruzi and Chagas heart disease and the varied mechanisms leading to myocyte destruction, mononuclear cell infiltration, fibrosis, and edema in the heart have been extensively studied by hundreds of scientists for more than 100 years. Despite this wealth of knowledge, it is still impossible to predict what will happen in an individual infected with T. cruzi because of the tremendous variability in clonal parasite virulence and human susceptibility to infection and the lack of definitive molecular predictors of outcome from either side of the host-parasite equation. Further, while several distinct mechanisms of pathogenesis have been studied in isolation, it is certain that multiple coincident mechanisms combine to determine the ultimate outcome. For these reasons, Chagas disease is best considered a collection of related but distinct illnesses. This review highlights the pathology and pathogenesis of the most common adverse sequela of T. cruzi infection-Chagas heart disease-and concludes with a discussion of key unanswered questions and a view to the future.

Identifiants

pubmed: 30355152
doi: 10.1146/annurev-pathol-020117-043711
pmc: PMC7373119
mid: NIHMS1609251
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

421-447

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI054578
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI136031
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL075822
Pays : United States

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Auteurs

Kevin M Bonney (KM)

Liberal Studies, Faculty of Arts and Sciences, New York University, New York, NY 10003, USA; email: kevin.bonney@nyu.edu.

Daniel J Luthringer (DJ)

Department of Pathology and Laboratory Medicine and Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA; email: daniel.luthringer@cshs.org , stacey.kim3@cshs.org , david.engman@csmc.edu.

Stacey A Kim (SA)

Department of Pathology and Laboratory Medicine and Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA; email: daniel.luthringer@cshs.org , stacey.kim3@cshs.org , david.engman@csmc.edu.

Nisha J Garg (NJ)

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555-1070, USA; email: nigarg@utmb.edu.

David M Engman (DM)

Department of Pathology and Laboratory Medicine and Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA; email: daniel.luthringer@cshs.org , stacey.kim3@cshs.org , david.engman@csmc.edu.

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