Reactivation of Chagas' disease in a human immunodeficiency virus-infected patient leading to severe heart disease with a late positive direct microscopic examination of the blood.

Sartori, Ana Marli Christovam; Lopes, Marta Heloísa; Benvenuti, Luiz Alberto; Caramelli, Bruno; Pietro, A O Di; Nunes, E. V.; Ramírez, Luis Pita; Shikanai-Yasuda, Maria Aparecida

doi:10.4269/ajtmh.1998.59.784

Cited by 65 publications

(58 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, in the researched literature the Chagas disease reactivation occurred in individuals with the CD4 T cells of up to 382 cells/mm 3,23 . Other similar reports with CD4 T cells above 200 cells/mm 3 and confirmed reactivation by high parasitemia with T. cruzi detected on peripheral blood, pericardial fluid, myocardial and quantitative xenodiagnosis have been described 34,42 . The opposite is also found, that is, CD4 T cells count bellow 200 cells/mm 3 without reactivation 35 .…”

Section: Casesmentioning

confidence: 88%

“…Therefore, the neurological condition draws more the attention 25,52,65,66,87 that in most of the times has toxoplasmosis as the main diagnosis in view to the frequency that this condition happens in HIV infected individuals 33,37,68 . In the heart, the symptomatology and the physical aspects overlap those seen on the natural evolution of the chronic chagasic cardiopathy, hindering the diagnosis 22,27,34,42,88 .…”

Section: Casesmentioning

confidence: 99%

“…In relation to the clinical focus of each organ affected, this was nonspecific, ranging to the central nervous system from headache, signs of intracranial hypertension, seizures, motor location and coma, generating diagnostic confusion, mainly with toxoplasmosis and tumors of the central nervous system 37,65,66,75,84 . For the heart, it consists of triggering or exacerbating congestive heart failure, arrhythmias, atrioventricular, heart and fascicular blocks 22,27,34,42 . The fact that the clinical picture presented in the reactivation in the heart, usually occurred in the natural evolution of the chronic chagasic cardiopathy 88,102 making the diagnosis difficult, unlike the central nervous system which does not present exuberant symptomatology in the chronic phase of the disease.…”

Section: Casesmentioning

confidence: 99%

See 2 more Smart Citations

Co-infection Trypanosoma cruzi/HIV: systematic review (1980 - 2010)

Almeida

Ramos

Correia

et al. 2011

Rev. Soc. Bras. Med. Trop.

114

View full text Add to dashboard Cite

Introduction:The co-infection Trypanosoma cruzi/HIV has been described as a clinical event of great relevance. The objective of this study was to describe clinical and epidemiological aspects published in literature. Methods: It is a systematic review of a descriptive nature from the databases Medline, Lilacs, SciELO, Scopus, from 1980 to 2010. Results: There were 83 articles (2.8 articles/year) with a total of 291 cases. The co-infection was described in 1980 and this situation has become the defining AIDS clinical event in Brazil. This is the country with the highest number of publication (51.8%) followed by Argentina (27.7%). The majority of cases are amongst adult men (65.3%) native or from endemic regions with serological diagnosis in the chronic stage (97.9%) and indeterminate form (50.8%). Both diseases follow the normal course, but in 41% the reactivation of the Chagas disease occurs. The most severe form is the meningoencephalitis, with 100% of mortality without specific and early treatment of the T. cruzi. The medication of choice was the benznidazole on doses and duration normally used for the acute phase. The high parasitemia detected by direct or indirect quantitative methods indicated reactivation and its elevation is the most important predictive factor. The lower survival rate was related to the reactivation of the Chagas disease and the natural complications of both diseases. The role of the antiretroviral treatment on the co-infection cannot yet be defined by the knowledge currently existent. Conclusions: Despite the relevance of this clinical event there are still gaps to be filled.

show abstract

Section: Casesmentioning

confidence: 88%

Section: Casesmentioning

confidence: 99%

Section: Casesmentioning

confidence: 99%

See 1 more Smart Citation

Co-infection Trypanosoma cruzi/HIV: systematic review (1980 - 2010)

Almeida

Ramos

Correia

et al. 2011

Rev. Soc. Bras. Med. Trop.

114

View full text Add to dashboard Cite

show abstract

“…Host and pathogen will then live in equilibrium, similar to other parasitic infections, such as leishmaniases and toxoplasmosis. This equilibrium may be broken, for instance, in a state of immunosuppression, when patent parasitism may reappear (Sartori et al 1998, Galhardo et al 1999. The evaluation of the factors responsible for the development or control of pathogenic responses has been hindered by the high variability of the parasite: different T. cruzi strains display distinct biological behaviors (Andrade and Magalhães 1996).…”

Section: T Cruzi Infection and The Murine Modelmentioning

confidence: 99%

The pathogenesis of Chagas' disease: when autoimmune and parasite-specific immune responses meet

Soares

Pontes-de-Carvalho

Ribeiro-dos-Santos

2001

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

Chagas' disease is a major health problem in Latin America, where it constitutes one of the leading causes of heart failure. About one fourth of Trypanosoma cruzi-infected individuals develop chronic chagasic cardiomyopathy (CChC), the most severe form of the disease. CChC is histologically characterized by the presence of multifocal inflammatory infiltrates in the heart, composed mainly by mononuclear cells, usually adhered to myocytes and leading to myocytolysis, and frequently by interstitial fibrosis. The pathogenesis of CChC is still unclear, despite intense investigations both in human beings and in animal models of the disease. Although tissue parasitism is rare in the chronic phase of infection, an immune response targeted to persistent parasites or parasite antigens is suggested, by some authors, as the pathogenic mechanism of CChC. Other researchers affirm that the lack of correlation between tissue parasitism and intensity of inflammation suggests, along with the presence of autoreactive immune responses, that CChC results from the action of an autoimmune response. Herein we review reports from the literature and our own data, which together indicate, on one hand, the participation of parasite-specific immune responses and, on the other hand, clearly demonstrate the participation of heart-specific immune responses in the pathogenesis of CChC. Moreover, multiple factors may determine whether an individual in the indeterminate form of the disease will develop CChC. The mechanisms by which T. cruzi breaks immunological tolerance to heart antigens are also discussed.

show abstract

“…Microscopically, fungal lesions have variable inflammatory infiltrates and necrosis and a specific diagnosis is made by iden tifying yeast forms or hyphae of specific organ isms, aided by standard histological stains such as Gomori methenamine silver or periodic acid Schiff [10][11][12] .The near absence of an inflam matory infiltrate accompanying fungal organisms is a manifestation of immune system failure with progression of AIDS to a late stage when oppor tunistic infections are more likely to be widely disseminated to organs such as the heart [10][11][12] . Patients living in endemic areas for Trypano soma cruzi may rarely develop a pronounced myocarditis 13,14 . Mycobacterium avium-complex infection can be widely disseminated and in volve the heart with microscopic lesions charac terized by clusters of large macrophages filled with numerous acid-fast rod-shaped organisms [10][11][12] .…”

Section: Nonviral Myocarditismentioning

confidence: 99%