**4. Pathophysiology**

The *T. cruzi* parasite is a heterogeneous species with a diverse phenotypic diversity, circulates between vectors and hosts, and is classified into discrete typing units a term used to describe sets of stocks that are genetically similar to each other and have "tags" a molecular marker to identify each other DTU (TcI-TcIVI and Tcbat) [9]. The life cycle consists of three different forms, metacyclic trypomastigotes, the infection form of *T. cruzi*, which consists of a fusiform shape and measures 10–20 m in length and 1.3 m in width. The transmitted by feces while triatomines feed on blood they defecate on the skin and *T. cruzi* introduces itself through the opening made by the bite and enter to the bloodstream or by rubbing on the mucosae (nasal or conjunctival). In the body, they are phagocytosed by macrophages, in the cytosol of subcutaneous cellular tissue they differentiate into amastigotes. The amastigotes measure 1.5–5 m in diameter with an ovoid shape, they replicate by binary fission and cause cell lysis to turn back to trypomastigotes to go into the blood and lymphatic circulation, they have tropism for myocardiocytes, rhabdomyocytes, and leiomyocytes. In this phase, a vector without infection can ingest it, within triatomines, trypomastigotes move to the medial segment of the gastrointestinal tract, once there they differentiate into epimastigotes, which replicate again through binary fission. Epimastigotes travel toward the distal segment of the gastrointestinal tract where they anchor themselves to colon epithelium through their flagella, they transform back to trypomastigotes to be excreted with feces during the next ingestion of blood and infect another human [8, 10]. In addition to vector transmission, *T. cruzi* can be transmitted by routes other than direct inoculation. These transmission routes play a greater role in non-endemic countries and a significant growth in endemic areas. It is estimated that vertical transmission reaches a frequency of 4.7% (range 3.9–5.6%) and that frequency may be higher in endemic countries than in non-endemic countries (5 vs. 2.7%). The biological determinant for congenital transmission is maternal parasitemia, which can be greater than 31% when *T. cruzi* is detected by PCR, likewise, transmission is also possible although it presents negative PCR [11]. The parasite can also be transmitted through blood and its products, the frequency of transmission per unit of infected blood is estimated to be 10–25%. In solid organ transplants from an infected donor, it appears to be lower for kidney recipients (0–19%) than for liver recipients (0–29%) and heart recipients (75–100%) [11].

The acute phase of Chagas disease is characterized by strong inhibition of the host's immune response triggered by virulence factors of *T. cruzi*, which are crucial to create a persistent infection and establish chronic disease involving, among other things, the induction of anergy and clonal deletion in T cell compartments, together with strong polyclonal stimulation of type B cells which restrict antigen-specific lymphocytes. Membrane glycoproteins of *T. cruzi* are essential to dampen the host's protective immunity. These membranes are covered by mucin-like molecules attached to their terminal galactosyl residues, sialic acid residues that are transferred from host glycoconjugates by parasite trans-sialidase. Mucin-like molecules of *T. cruzi* are key players in host–parasite interaction, including invasion of the host and subversion of its immune system. Its sialylated forms are capable of protecting the antigenic

*Digestive Disorders in Chagas Disease: Megaesophagus and Chagasic Megacolon DOI: http://dx.doi.org/10.5772/intechopen.102871*

determinants of the parasite from host attack mediated by antigalactosyl antibodies and complement factor B. Likewise, they incapacitate dendritic cell function demonstrated by the inhibition of IL-12 production. This inhibition can occur at the transcriptional level of the IL-2 gene in T cells, which also occurs when T cell proliferation and activation are blocked in response to mitogens and antigens. Sialoglycoproteins also inhibit early events in T cell activation, particularly tyrosine phosphorylation of the adapter protein SLP-76 and tyrosine kinase ZAP-70 [12].
