Glycosylation Patterns in Gut: Implications for the Development of Vector Control Strategies.

The primary mode of transmission for Chagas disease is vector-borne transmission, spread by hematophagous insects of the subfamily. In Mexico, the triatomine is particularly significant in the transmission of . This study focused on analyzing protein expression and modifications by glycosylation in different regions of the digestive tract of fifth-instar nymphs of .

Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection with .

L-arginine metabolism through arginases and inducible nitric oxide synthase (NOS2) constitutes a fundamental axis for the resolution or progression of Chagas disease. Infection with can cause a wide spectrum of disease, ranging from acute forms contained by the host immune response to chronic ones, such as the chronic chagasic cardiomyopathy. Here, we analyzed, in an in vitro model, the ability of two isolates, with different degrees of virulence, to regulate the metabolism of L-arginine through arginase 1 (Arg-1) and NOS2 in macrophages and through arginase 2 (Arg-2) and NOS2 in cardiomyocytes.

Expression of Proteins, Glycoproteins, and Transcripts in the Guts of Fasting, Fed, and -Infected Triatomines: A Systematic Review.

Chagas disease is caused by the hemoflagellate protozoan The main transmission mechanism for the parasite in endemic areas is contact with the feces of an infected triatomine bug. Part of the life cycle of occurs in the digestive tract of triatomines, where vector and parasite engage in a close interaction at a proteomic-molecular level. This interaction triggers replication and differentiation processes in the parasite that can affect its infectivity for the vertebrate host.

Main Cardiac Histopathologic Alterations in the Acute Phase of Infection in a Murine Model.

Symptoms in the acute phase of Chagas disease are usually mild and nonspecific. However, after several years, severe complications like dilated heart failure and even death may arise in the chronic phase. Due to the lack of specific symptoms in the acute phase, the aim of this work was to describe and analyze the cardiac histopathology during this phase in a CD1 mouse model by assessing parasitism, fibrotic damage, and the presence and composition of a cellular infiltrate, to determine its involvement in the pathogenesis of lesions in the cardiac tissue.

Immunopathological Mechanisms Underlying Cardiac Damage in Chagas Disease.

In Chagas disease, the mechanisms involved in cardiac damage are an active field of study. The factors underlying the evolution of lesions following infection by and, in some cases, the persistence of its antigens and the host response, with the ensuing development of clinically observable cardiac damage, are analyzed in this review.

Parasitemia and Differential Tissue Tropism in Mice Infected with Isolates Obtained from in the State of Oaxaca, Mexico.

is a parasite transmitted by the feces of triatomines. Many triatomine species are found in Mexico, and various variants have been isolated from these species, each showing very different virulence and cell tropism. The isolates were obtained from specimens in three localities in the state of Oaxaca, Mexico: Tehuantitla, Vixhana, and Guichivere.

Higher temperatures reduce the number of Trypanosoma cruzi parasites in the vector Triatoma pallidipennis.

Background: Relatively little is known about how pathogens transmitted by vector insects are affected by changing temperatures analogous to those occurring in the present global warming scenario. One expectation is that, like their ectothermic vectors, an increase in temperature could reduce their fitness. Here, we have investigated the effect of high temperatures on the abundance of Trypanosoma cruzi parasites during infection in the vector Triatoma pallidipennis.

Bacteria cultured from the gut of Meccus pallidipennis (Hemiptera: Reduviidae), a triatomine species endemic to Mexico.

The study of intestinal microbiota in vector insects like triatomines is paramount in parasitology because many parasitic species inhabit the vector's gut. Although knowledge on the gut microbiota in various vectors of the parasitic flagellate Trypanosoma cruzi has grown, research efforts have focused on South American triatomines. This study reports the isolation of bacterial microbiota in the anterior and posterior gut of Meccus pallidipennis (a triatomine species endemic to Mexico) by culture, as well as its identification by phenotypic and biochemical tests and its quantification by counting colony-forming units.

Response to Infection by in a Murine Model.

Cardiopathy is a common, irreversible manifestation of the chronic phase of Chagas disease; however, there is controversy as to how the causes for progression from the acute to the chronic phase are defined. In this work, the presence of the parasite is correlated with the occurrence of cell infiltration and fibrosis in cardiac tissues, as well as IgG detection and disease progression in a murine model. Fifty CD1 mice were infected intraperitoneally with , while 30 control were administered with saline solution.

Coinfection by and a fungal pathogen increases survival of Chagasic bugs: advice against a fungal control strategy.

Triatomine bugs carry the parasitic protozoa Trypanosoma cruzi, the causal agent of Chagas disease. It is known that both the parasite and entomopathogenic fungi can decrease bug survival, but the combined effect of both pathogens is not known, which is relevant for biological control purposes. Herein, the survival of the triatomine Meccus pallidipennis (Stal, 1872) was compared when it was coinfected with the fungus Metarhizium anisopliae (Metschnikoff) and T.

Zombie bugs? Manipulation of kissing bug behavior by the parasite Trypanosoma cruzi.

The parasite manipulation hypothesis states that the parasite modifies host's behavior thereby increasing the probability that the parasite will pass from an intermediate host to its final host. We used the kissing bugs Triatoma pallidipennis and T. longipennis and two isolates of the Trypanosoma cruzi parasite (Chilpancingo and Morelos) to test these ideas.

The cost of being a killer's accomplice: Trypanosoma cruzi impairs the fitness of kissing bugs.

Relatively little is known about the fitness effects and life history trade-offs in medically important parasites and their insect vectors. One such case is the triatomine bugs and the parasite Trypanosoma cruzi, the key actors in Chagas disease. Previous studies have revealed some costs but have not simultaneously examined traits related to development, reproduction, and survival or their possible trade-offs.

Activity of the prophenoloxidase system and survival of triatomines infected with different Trypanosoma cruzi strains under different temperatures: understanding Chagas disease in the face of climate change.

Background: Little is known about how human disease vectors will modify their life history patterns and survival capacity as a result of climate change. One case is that of Chagas disease, which has triatomine bugs and Trypanosoma cruzi as vectors and parasite, respectively. This work aimed to determine: (i) the activity of the prophenoloxidase system (prophenoloxidase and phenoloxidase activity, two indicators of immune ability) in three intestine regions (anterior midgut, posterior midgutand rectum) of the triatomine bug Meccus pallidipennis under three temperature conditions (20 °C, 30 °C and 34 °C) against two T.

Trypanosoma cruzi: A review of biological and methodological factors in Mexican strains.

Trypanosoma cruzi, responsible for Chagas disease, is a serious public health problem in Latin America with eight million people infected in the world. Clinical manifestations observed in humans due to T. cruzi infection are largely associated with the wide biological and genetic heterogeneity of the parasite.

Identification of -Glcnacylated Proteins in .

Originally an anthropozoonosis in the Americas, Chagas disease has spread from its previous borders through migration. It is caused by the protozoan . Differences in disease severity have been attributed to a natural pleomorphism in .

In vitro activity of steroidal dendrimers on Trypanosoma cruzi epimastigote form with PAMAM dendrons modified by "click" chemistry.

The increasing use of dendrimers shows promise for the treatment of inflammatory diseases, Chagas disease and other conditions such as cancer. In this study, the activity of 1st and 2nd generation dendrimers over T. cruzi in the epimastigote stage was tested.

[Enfermedad de Chagas en México].

Chagas disease, which is caused by Trypanosoma cruzi, is considered to be the most serious parasitic disease in America. It is transmitted mainly by triatominae ("kissing bugs"). Mazzoti reported the first two human cases in Mexico.

Effects on Meccus pallidipennis (Hemiptera: Reduviidae) Eggs Exposed to Entomopathogenic Fungi: Exploring Alternatives to Control Chagas Disease.

Meccus pallidipennis Stål is a vector for Chagas disease. The extensive use of pyrethroid insecticides to control triatomines in Mexico has resulted in the development of resistant populations. As an alternative control approach, the effects on M.

Effects of Trypanosoma cruzi on the phenoloxidase and prophenoloxidase activity in the vector Meccus pallidipennis (Hemiptera: Reduviidae).

Background: Triatomine insects are vectors of Trypanosoma cruzi, the causal agent of Chagas disease. The insect-parasite interaction has been studied in relation to the transmission and prevalence of this disease. For most triatomines, however, several crucial aspects of the insect immune response are still unknown.

Bacterial symbionts in human blood-feeding arthropods: Patterns, general mechanisms and effects of global ecological changes.

Due to their high impact on public health, human blood-feeding arthropods are one of the most relevant animal groups. Bacterial symbionts have been long known to play a role in the metabolism, and reproduction of these arthropod vectors. Nowadays, we have a more complete picture of their functions, acknowledging the wide influence of bacterial symbionts on processes ranging from the immune response of the arthropod host to the possible establishment of pathogens and parasites.

What makes an effective Chagas disease vector? Factors underlying Trypanosoma cruzi-triatomine interactions.

The Chagas disease is caused by the parasite Trypanosoma cruzi, which infect blood-feeding triatomine bugs to finally reach mammal hosts. Chagas disease is endemic in Latin America, and is ranked among the 13 neglected tropical diseases worldwide. Currently, an estimate of 7 million people is infected by T.

Th-17 cytokines are associated with severity of Trypanosoma cruzi chronic infection in pediatric patients from endemic areas of Mexico.

In Chagas disease the clinical, acute and chronic manifestations are the result of the interaction between the parasite and the host factors. The balance between inflammatory and anti-inflammatory immune responses is essential for the increase or resolution of the manifestations in individuals infected with T. cruzi.

Chagas Disease in Mexico: Report of 14 Cases of Chagasic Cardiomyopathy in Children.

Chagas disease is a parasitic infection mainly found in Latin America; it is transmitted by a triatomine, also known as assassin bug or kissing bug. In humans, the parasite causes mostly cardiac disorders. Two-thirds of the Mexican territory are regarded as risk areas for vector transmission of Trypanosoma cruzi, the causal agent.

Relationships between altitude, triatomine (Triatoma dimidiata) immune response and virulence of Trypanosoma cruzi, the causal agent of Chagas' disease.

Little is known about how the virulence of a human pathogen varies in the environment it shares with its vector. This study focused on whether the virulence of Trypanosoma cruzi (Trypanosomatida: Trypanosomatidae), the causal agent of Chagas' disease, is related to altitude. Accordingly, Triatoma dimidiata (Hemiptera: Reduviidae) specimens were collected at three different altitudes (300, 700 and 1400 m a.