Length and caliber of the rectosigmoid colon among patients with Chagas disease and controls from areas at different altitudes

Lopes, Gesner Pereira; Ferreira-Silva, Márcia Maria; A, Ramos; Moraes‐Souza, Helio; Prata, Áluízio; Correia, Dalmo

doi:10.1590/0037-8682-0247-2013

Cited by 10 publications

(8 citation statements)

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“…Nowadays, little is known about the influence of temperature and altitude on the incidence of Chagas disease in our country. A previous study has reported that altitude could be an important factor in the development of the rectosigmoid length in Andean patients with Chagas disease [ 21 ], which suggests a direct relation between altitude and the virulence of the strain. Moreover, De Fuentes-Vicente et al .…”

Section: Discussionmentioning

confidence: 99%

Evolution of incidence and geographical distribution of Chagas disease in Mexico during a decade (2007–2016)

et al. 2018

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Chagas disease, whose aetiological agent is the protozoan Trypanosoma cruzi, mainly occurs in Latin America. In order to know the epidemiology and the geographical distribution of this disease in Mexico, the present work analyses the national surveillance data (10 years) for Chagas disease issued by the General Directorate of Epidemiology (GDE). An ecological analysis of Chagas disease (2007–2016) was performed in the annual reports issued by the GDE in Mexico. The cases and incidence were classified by year, state, age group, gender and seasons. A national distribution map showing Chagas disease incidence was generated. An increase of new cases was identified throughout the country (rates from 0.37 to 0.81 per 100 000 inhabitants). Of the total cases accumulated (7388), the major cases were attributed to the states of Veracruz, Chiapas, Quintana Roo, Oaxaca, Morelos and Yucatán. The analysis per age groups and gender revealed that, in most age groups, the incidence was higher in the male population. The most number of cases was identified in spring and summer; a direct relationship between the environmental temperature increase and the number of new cases was identified. The analysis showed that the rate of Chagas disease increased presumably due to state programmes; the search for new cases has expanded and we speculate that the disease is associated with occupational activities. These results summarise and recall how important it is to implement the monitoring of Chagas disease mainly in south states of the Mexican Republic in order to implement strategies to control this disease.

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Section: Discussionmentioning

confidence: 99%

Evolution of incidence and geographical distribution of Chagas disease in Mexico during a decade (2007–2016)

et al. 2018

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“…Empowering deleterious factors in the acute phase of the disease by increasing the number of parasites in the inoculum contributed significantly to reducing the thickness of the muscular layer, event observed when we compared the medium and high groups. Morphological changes in intestinal tissue associated with Chagas disease are already known and widely studied in the chronic phase of the disease [ 13 , 25 , 26 ]; since the morphometric changes are associated with denervation of the muscle layer, which facilitates the dilation of the tissue, thereby decreasing its thickness. Accordingly, we add new information to the literature since we have demonstrated that a reduction in thickness also happens in the acute phase due to an increase in the inoculum.…”

Section: Discussionmentioning

confidence: 99%

“…To give an example, intestinal myenteric denervation caused by interferon-dependent nitric oxide production during the acute disease phase has been shown to be critical for the development of the digestive form of the disease during the chronic phase [ 12 ]. Moreover, altitude, ethnicity, drug use, and diet have also been suggested to influence the size and length of the rectal and sigmoid colon segments of the patient’s intestine [ 13 ]. Experimental morphometric studies that evaluated the effects of 2 different parasite inocula in Swiss mice demonstrated that reductions in the numbers of myenteric nerves occurred mainly between 30 and 75 days of infection; this finding was linked to the parasite inoculum and infection duration [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load

Vazquez

Miguel

et al. 2015

Parasites Vectors

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BackgroundChagas disease is caused by the protozoan Trypanosoma cruzi and is characterized by cardiac, gastrointestinal, and nervous system disorders. Although much about the pathophysiological process of Chagas disease is already known, the influence of the parasite burden on the inflammatory process and disease progression remains uncertain.MethodsWe used an acute experimental disease model to evaluate the effect of T. cruzi on intestinal lesions and assessed correlations between parasite load and inflammation and intestinal injury at 7 and 14 days post-infection. Low (3 × 102), medium (3 × 103), and high (3 × 104) parasite loads were generated by infecting C57BL/6 mice with “Y”-strain trypomastigotes. Statistical analysis was performed using analysis of variance with Tukey’s multiple comparison post-test, Kruskal–Wallis test with Dunn’s multiple comparison, χ2 test and Spearman correlation.ResultsHigh parasite load-bearing mice more rapidly and strongly developed parasitemia. Increased colon width, inflammatory infiltration, myositis, periganglionitis, ganglionitis, pro-inflammatory cytokines (e.g., TNF-α, INF-γ, IL-2, IL-17, IL-6), and intestinal amastigote nests were more pronounced in high parasite load-bearing animals. These results were remarkable because a positive correlation was observed between parasite load, inflammatory infiltrate, amastigote nests, and investigated cytokines.ConclusionsThese experimental data support the idea that the parasite load considerably influences the T. cruzi-induced intestinal inflammatory response and contributes to the development of the digestive form of the disease.

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“…According to Lopes et al ( 2013 ), who examined the longest radiological series of chagasic patients from endemic areas in Brazil and the Andes, the megacolon mostly starts with the lengthening of the sigmoid associated with an increase in the colon's diameter, at advanced stages of the disease. As shown for the esophagus (de Oliveira et al, 1995 ), colonic motility may reflect functional abnormalities in a stage preceding colon dilation (Santos et al, 2000 ).…”

Section: Discussionmentioning

confidence: 99%

Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease

Ricci

Béla

Moraes

et al. 2020

Front. Cell. Infect. Microbiol.

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There is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite's DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.

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Length and caliber of the rectosigmoid colon among patients with Chagas disease and controls from areas at different altitudes

Cited by 10 publications

References 10 publications

Evolution of incidence and geographical distribution of Chagas disease in Mexico during a decade (2007–2016)

Evolution of incidence and geographical distribution of Chagas disease in Mexico during a decade (2007–2016)

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load

Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease

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