Life cycle of Trypanosoma cruzi in invertebrate and vertebrate reservoirs
There are many species of protozoa in the genus Trypanosoma, but only Trypanosoma cruzi, Trypanosoma gambiencei and Trypanosoma rhodesiae cause disease in humans.
Trypanosoma cruzi, a protozoan parasite Hemoflagella vexaliensis, is the causative agent of Chagas disease, while Trypanosoma bresona gambia and Trypanosoma rhodes cause African trypanosomiasis.
Chagas disease, also known as Chagas disease, affects millions of people throughout the Americas. In 1909, Carlos Chagas first described the disease by discovering the parasite in the blood of a Brazilian child suffering from swollen lymph nodes, anemia and fever.
Trypanosoma cruzi is a member of the family Trypanosomatidae kinematics and belongs to a subspecies called feces. The development of fecal parasites occurs in the intestine of invertebrate carriers, and infection of vertebrates occurs through feces.
Trypanosoma cruzi is carried in the internal organs of Trypanosoma cruzi and spreads when infected feces contaminate the bite site or intact mucous membranes.
During feeding, infected triatomine insects absorb a large amount of blood in their digestive system, which forces the removal of large amounts of accumulated excrement that are usually deposited on the surface of the skin.
The released feces contain posterior circulation trypanomalums, which actively penetrate the skin through active movement and release of tissue-lytic enzymes. Other patterns of Trypanosoma cruzi transmission include organ transplantation, blood transfusion, and congenital transmission.
Mechanism of transmission Trypanosoma cruzi contrasts with three subspecies of African trypanosomiasis that cause human and animal African trypanosomiasis, Trypanosoma bredeii, Trypanosoma bredesii and Trypanosoma brucei, which are transmitted by the saliva of their vectors, and have the mechanism of transmission of Trypanosoma cruzi to its mammalian host, a non-pathogenic Trypanosoma found in the Americas.
In addition to colonizing in the stomach of its invertebrate carrier, the salivary parasite migrates to the salivary gland of the vector, where the vertebrate form of infection forms but never spreads to the intestine.
In the process of vehicle acquisition of blood meal, infection of vertebrates occurs through saliva. Like tsetse flies, trypanosoma vectors ingest circulating trypanoflagellates when they draw blood meal from infected mammalian hosts. Trypanosoma cruzi infects vertebrate and invertebrate hosts at specific stages of its life cycle.
The posterior ring parasite form expresses a group of surface glycoproteins that interact with mammalian cells. One of these glycoproteins, a post-cycle stage-specific 82-kDa glycoprotein, is involved in host cell invasion.
The gp82 glycoprotein is an adhesion molecule that binds to host cells in a receptor-mediated manner and triggers Ca2+ mobilization, which is essential for parasite infiltration.
Other glycoproteins expressed in and adhered to mammalian cells in bloodstream or tissue culture-derived pyramidal flagellates are gp83, gp85, and Tc-85. GP83 signals the entry of Trypanosoma upmodulatii into macrophages via the mitogen-activated protein kinase pathway. Surface glycosinositol phospholipids of parasites have been shown to be involved in the attachment process.
The description of the occurrence of metacycles can be divided into two parts, with the first part leading to the second part. Trypanosomas sense the loss of sugar in the environment and respond by lengthening their cell bodies and flagella and activating their mitochondria, which results in sterol-rich and more hydrophobic trypanosoma flagella lengthening.
The elongation of the flagella allows trypanosomes to adhere to hydrophobic surfaces, and it is this interaction that triggers metaphytes to occur. The trigger for this metacellgenesis is cyclic adenosine monophosphate-mediated.
Cyclic AMP plays an important role in controlling lower eukaryote differentiation. The relative amount of cyclic AMP can vary depending on the surrounding environment, allowing the organism to quickly adapt to new conditions.
The differential balance of cAMP may lead to activation of protein kinases, transcription of specific genes, and changes in the structure of the cytoskeleton, ultimately leading to changes in morphological cells.
The circulating AMP balance may change with environmental changes, leading to differential gene expression and morphological changes that allow the parasite to go through its life cycle.
The developmental stages of Trypanosoma cruzi alternate between infectious and non-infectious forms. Amastigote and epimastigote are non-infectious in the gut of mammalian hosts and insect vectors, respectively.
The flow-flow pyramidal flagellates found in vertebrate host blood and the posterior circulation pyramidal flagellates found in the rectum of insect invertebrate carriers are considered to be two distinct pyramidal flagellates that are infectious, but non-replicant, stages of development.
The insect sucks the blood of the vertebrate mammalian host infected with the bloodflow pyramidal flagellates and begins circulation, and inside the stomach of the insect, the ingested pyramidal flagellates are transformed into upper flagellates that replicate strongly in the midgut.
Epimastigotes are converted into metacyclictrypomastigotes in the hindgut of the insect host, and when the insect vector sucks up blood meal from an uninfected host, they are eliminated by feces.
Trypanoma flagella excreted from damaged skin caused by insect bites leads to Trypanosoma cruzi infection.
Once metacyclictrypomastigote enters the mammalian host, it invades host cells at the seeding site and transforms into a replicating amastigote form, which transforms back into the bloodstream trypomastigote form as intracellular amastigote after completing the replication cycle.
Trypanosoma cruzi is covered by a dense layer of mucin-type molecules, which are the main surface glycoproteins of Trypanosoma cruzi. These proteins are widely distributed in different developmental forms of cell bodies, flagella bags, and flagella, and play a key role in parasite protection and the regulation of infectious and host immune responses throughout the parasite's life cycle.
The mucin of Trypanosoma cruzi is divided into two gene families, TcMUC and TcSMUG, and these proteins are divided into several groups according to their central domain: TcMUC is divided into TcMUCI, TcMUCII, and TcMUCIII.
