scholarly journals Unprecedented incidence of Trypanosoma cruzi infections in a cohort of dogs directly detected through longitudinal tracking at multi-dog kennels, Texas, USA

2021 ◽  
Author(s):  
Rachel E Busselman ◽  
Alyssa C Meyers ◽  
Italo B Zecca ◽  
Lisa D Auckland ◽  
Andres H Castro ◽  
...  

Canine Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is increasingly recognized as a health concern for dogs in the USA, and infected dogs may signal geographic regions of risk for human disease. Dogs living in multi-dog kennel environments where triatomine vectors are endemic may be at high risk for infection. We monitored a cohort of 64 T. cruzi -infected and uninfected dogs from across 10 kennels in Texas, USA, to characterize changes in infection status over time. We used robust diagnostic criteria in which reactivity on multiple independent platforms was required to be considered positive. Among the 30 dogs enrolled as serologically- and/or PCR-positive, all but one dog showed sustained positive T. cruzi diagnostic results over time. Among the 34 dogs enrolled as serologically- and PCR-negative, 10 new T. cruzi infections were recorded over a 12-month period. The resulting incidence rate was 30.7 T. cruzi infections per 100 dogs per year. This study highlights the risk of T . cruzi infection to dogs in kennel environments, despite multiple vector control methods employed by kennel owners. To protect both dog and human health, there is an urgent need to develop more integrated vector control methods as well as prophylactic and curative antiparasitic treatment options for T. cruzi infection in dogs.

2021 ◽  
Vol 15 (11) ◽  
pp. e0009935
Author(s):  
Rachel E. Busselman ◽  
Alyssa C. Meyers ◽  
Italo B. Zecca ◽  
Lisa D. Auckland ◽  
Andres H. Castro ◽  
...  

Canine Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is increasingly recognized as a health concern for dogs in the USA, and infected dogs may signal geographic regions of risk for human disease. Dogs living in multi-dog kennel environments (kennels with more than one dog) where triatomine vectors are endemic may be at high risk for infection. We monitored a cohort of 64 T. cruzi-infected and uninfected dogs across 10 kennels in Texas, USA, to characterize changes in infection status over one year. We used robust diagnostic criteria in which reactivity on multiple independent platforms was required to be considered positive. Among the 30 dogs enrolled as serologically- and/or PCR-positive, all but one dog showed sustained positive T. cruzi diagnostic results over time. Among the 34 dogs enrolled as serologically- and PCR-negative, 10 new T. cruzi infections were recorded over a 12-month period. The resulting incidence rate for dogs initially enrolled as T. cruzi-negative was 30.7 T. cruzi infections per 100 dogs per year. This study highlights the risk of T. cruzi infection to dogs in kennel environments. To protect both dog and human health, there is an urgent need to develop more integrated vector control methods as well as prophylactic and curative antiparasitic treatment options for T. cruzi infection in dogs.


2022 ◽  
Vol 12 ◽  
Author(s):  
Carolina V. Poncini ◽  
Alejandro F. Benatar ◽  
Karina A. Gomez ◽  
Gabriel A. Rabinovich

Trypanosoma cruzi, the protozoan parasite causative agent of Chagas disease, affects about seven million people worldwide, representing a major global public health concern with relevant socioeconomic consequences, particularly in developing countries. In this review, we discuss the multiple roles of galectins, a family of β-galactoside-binding proteins, in modulating both T. cruzi infection and immunoregulation. Specifically, we focus on galectin-driven circuits that link parasite invasion and inflammation and reprogram innate and adaptive immune responses. Understanding the dynamics of galectins and their β-galactoside-specific ligands during the pathogenesis of T. cruzi infection and elucidating their roles in immunoregulation, inflammation, and tissue damage offer new rational opportunities for treating this devastating neglected disease.


2020 ◽  
Vol 5 (2) ◽  
pp. 87
Author(s):  
Aaron W. Tustin ◽  
Ricardo Castillo-Neyra ◽  
Laura D. Tamayo ◽  
Renzo Salazar ◽  
Katty Borini-Mayorí ◽  
...  

Blood-sucking triatomine bugs transmit the protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease. We measured the prevalence of T. cruzi infection in 58,519 Triatoma infestans captured in residences in and near Arequipa, Peru. Among bugs from infected colonies, T. cruzi prevalence increased with stage from 12% in second instars to 36% in adults. Regression models demonstrated that the probability of parasite acquisition was roughly the same for each developmental stage. Prevalence increased by 5.9% with each additional stage. We postulate that the probability of acquiring the parasite may be related to the number of feeding events. Transmission of the parasite does not appear to be correlated with the amount of blood ingested during feeding. Similarly, other hypothesized transmission routes such as coprophagy fail to explain the observed pattern of prevalence. Our results could have implications for the feasibility of late-acting control strategies that preferentially kill older insects.


1995 ◽  
Vol 52 (2) ◽  
pp. 183-187 ◽  
Author(s):  
Ana Lucia S. Sgambatti De Andrade ◽  
Jose Maria P. Souza ◽  
Celina Maria T. Martelli ◽  
Fabio Zicker ◽  
Ionizete G. Silva

2019 ◽  
Author(s):  
Ana G. Madrigal ◽  
Rachel Marcus ◽  
Robert Gilman ◽  
Alan L. Scott ◽  
Clive Shiff

AbstractChagas disease, caused by the protozoan parasite Trypanosoma cruzi, is a potentially life-threatening infection endemic to Latin America that has emerged as a global public health issue due to globalization and emigration patterns. Diagnosis of T. cruzi infection is complex, especially for the chronic phase of the disease that is characterized by a low to moderate burden of the difficult to detect, tissue-dwelling, intracellular form of the parasite. Diagnosis relies on a multistep indirect serological detection approach that requires positive results in at least two independent anti-T. cruzi antibody tests. With no gold standard diagnostic method for chronic T. cruzi, new approaches are needed that can more directly test for the presence of the parasite. Here, we report on of the potential utility of a noninvasive diagnostic approach that specifically detects T. cruzi-derived cell-free repeat DNA in the urine of patients who are both serologically positive and negative.


Acta Tropica ◽  
2010 ◽  
Vol 113 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Mariana Laura Moreno ◽  
Edgardo Moretti ◽  
Beatriz Basso ◽  
Maria Frias Céspedes ◽  
Silvia S. Catalá ◽  
...  

2004 ◽  
Vol 72 (12) ◽  
pp. 6817-6825 ◽  
Author(s):  
Thorsten Lieke ◽  
Sebastian E. B. Graefe ◽  
Ulricke Klauenberg ◽  
Bernhard Fleischer ◽  
Thomas Jacobs

ABSTRACT The protozoan parasite Trypanosoma cruzi circulates in the blood as trypomastigotes and invades a variety of cells to multiply intracellularly as amastigotes. The acute phase leads to an immune response that restricts the proliferation of the parasite. However, parasites are able to persist in different tissues, which causes the pathology of Chagas' disease. Natural killer (NK) cells play an important role in innate resistance to a variety of pathogens. In the present study we analyzed whether NK cells participated in the control of experimental T. cruzi infection. NK cells were depleted from C57BL/6 mice by antiasialo antibodies. This treatment caused an increased parasitemia during the acute phase, but tissue parasite burdens were not significantly altered according to quantitative real-time PCR. Our results demonstrated that NK cells were activated during the initial phase of a T. cruzi infection and exhibited a contact-dependent antiparasitic activity against extracellular parasites that was independent from perforin. Thus, NK cells limit the propagation of the parasite by acting on circulating T. cruzi trypomastigotes.


Author(s):  
Valeria Colombo ◽  
Andrea Giacomelli ◽  
Giovanni Casazza ◽  
Laura Galimberti ◽  
Cecilia Bonazzetti ◽  
...  

Abstract Background Chagas disease, as a consequence of globalization and immigration, is no more restricted to Central and Latin America. Therefore, congenital transmission represents a growing public health concern in non-endemic countries. Methods The aim of this study was to assess the prevalence of Trypanosoma cruzi infection in pregnant Latin American (LA) women living outside endemic countries and the rate of congenital transmission. Data were extracted from studies indexed in PubMed, Scopus, Embase, Lilacs and SciELO databases without language restriction. Two investigators independently collected data on study characteristics, diagnosis, prevalence of infection in pregnant women and congenital infection rate. The data were pooled using a random effects model. Results The search identified 1078 articles of which 29 were eligible regarding prevalence of T. cruzi infection among pregnant women and 1795 articles of which 32 were eligible regarding the congenital transmission rate. The estimated pooled prevalence of T. cruzi infection in LA pregnant women was 4.2% [95% confidence interval (CI): 3.0–5.5]. The prevalence of T. cruzi infection in pregnant women from Bolivia was 15.5% (95% CI: 11.7–19.7) and 0.5% (95% CI: 0.2–0.89) for those coming from all other LA countries. The estimated global rate of congenital transmission was 3.5% (95% CI: 2.5–4.5); excluding poor-quality studies, the rate of congenital transmission was 3.8% (95% CI: 2.4–5.1). Conclusions Prevalence of Chagas disease among LA pregnant women living outside endemic countries is high, particularly in Bolivian women. The rate of vertical transmission of T. cruzi infection is similar to the rate reported in South and Central American countries.


2007 ◽  
Vol 204 (4) ◽  
pp. 929-940 ◽  
Author(s):  
Anthony W. Ashton ◽  
Shankar Mukherjee ◽  
FNU Nagajyothi ◽  
Huan Huang ◽  
Vicki L. Braunstein ◽  
...  

Chagas' disease is caused by infection with the parasite Trypanosoma cruzi. We report that infected, but not uninfected, human endothelial cells (ECs) released thromboxane A2 (TXA2). Physical chromatography and liquid chromatography-tandem mass spectrometry revealed that TXA2 is the predominant eicosanoid present in all life stages of T. cruzi. Parasite-derived TXA2 accounts for up to 90% of the circulating levels of TXA2 in infected wild-type mice, and perturbs host physiology. Mice in which the gene for the TXA2 receptor (TP) has been deleted, exhibited higher mortality and more severe cardiac pathology and parasitism (fourfold) than WT mice after infection. Conversely, deletion of the TXA2 synthase gene had no effect on survival or disease severity. TP expression on somatic cells, but not cells involved in either acquired or innate immunity, was the primary determinant of disease progression. The higher intracellular parasitism observed in TP-null ECs was ablated upon restoration of TP expression. We conclude that the host response to parasite-derived TXA2 in T. cruzi infection is possibly an important determinant of mortality and parasitism. A deeper understanding of the role of TXA2 may result in novel therapeutic targets for a disease with limited treatment options.


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