Parasites and Heart Diseases Assignment
Parasites play a key role in causing heart diseases. The parasites such as the Toxoplasma gondii, Trypanosoma cruzi, and Trypanosomiasis brucei rhodesiense are some of the most prevalent ones that cause heart diseases. These parasites apply different mechanisms to cause infections in the heart. Some of them are spread by vectors while others find their entry into the body through different mechanisms. These parasites target the same organ. It is important to study their mechanisms of invasion and how they spread the infections to the heart. The paper explores whether the Toxoplasma gondii, Trypanosoma cruzi, and Trypanosomiasis brucei rhodesiense use the same mechanisms and vectors in their invasion. Therefore, it will help to form a better understanding of the mechanisms and the vectors involved in the process.Parasites and Heart Diseases Assignment
Introduction
Parasite infections are becoming rather prevalent in the world. It has been noted that even those parasitic infections that were associated with tropical conditions are now common worldwide. The new epidemiological trend could be associated with population migration and travelling.Parasites and Heart Diseases Assignment Human parasites are affecting a substantial number of people in the world. Whenever these parasites enter the human body, it leads to a series of clinical manifestations when they are migrating to the target organ. Some parasites are associated with a high prevalence of mortality and morbidity depending on the target organ. Unfortunately, the key organs such as the heart and lungs are the frequent targets of parasites. Toxoplasma gondii, Trypanosoma cruzi, and Trypanosomiasis brucei rhodesiense are some of the most prevalent parasites that cause heart diseases. Whenever thye affect the heart muscles, they may cause a generalized illness. However, in some cases, the parasites may have more serious consequences where they will affect the structures of the heart such as the myocardium leading to myocarditis and even cardiomyopathies. These parasites affect the pericardium; they may cause pericarditis and even cardiac tamponade. It is very evident that these parasites trigger a lot of heart infections. It is, therefore, important to have a deeper understanding of how they cause various infections. Their mode of action is also another area of interest that needs a deeper understanding.
Trypanosoma cruzi is a common zoonotic parasite that causes Chagas disease. There exist many members of the trypanosome, but it is only two subspecies that have the ability to cause the disease. Some people may not exhibit any clinical manifestations, but a significant proportion can develop a chronic Chagas heart disease. The symptoms may appear only after a long time. Most of the infections that are caused by the parasite are vector-borne, but they can also occur through organ transplantation and blood transfusion. It has been noted that some of the parasitic infections may reappear even after a organs transplantation. All the trypanosomes parasites that are associated with the various infections are transmitted by biting insects which are the carriers of the pathogens.
Other common trypanosomes such as Trypanosomiasis brucei rhodesiense are responsible for human African trypanosomiasis. The main vector is the tsetse fly which carries the trypanosomes. Whenever the trypanosomes are introduced to the body through a bite, they multiply rapidly, and they migrate to the various body organs. In most cases, the cardiac manifestations of the brucei are overshadowed by many neurological signs that are associated with the disease.
Toxoplasma gondii is another common parasitic organism that can infect most animals and birds. It is a single-celled parasite that infects the body and forms cysts that can affect the heart and even muscles. When these cysts rupture in the heart, they end up causing myocarditis.
From the above discussions, it is evident that the three parasites cause serious problems in the heart. However, it is important to form a deeper understanding of whether all these parasites use the same mechanism of developing the disease and whether they must be residing in the host for a disease to occur. The paper aims at forming a better understanding of the mechanisms and the vectors involved in the process.Parasites and Heart Diseases Assignment
The null hypothesis
Toxoplasma gondii, Trypanosome cruzi, and Trypanosomiasis brucei rhodesiense use similar mechanisms and vectors that lead to cardiac issues.
Alternative hypothesis
Toxoplasma gondii, Trypanosoma cruzi, and Trypanosomiasis brucei rhodesiense have different methods to cause cardiac abnormalities.
Trypanosome Cruzi
Trypanosoma cruzi is associated with the Chagas disease. The triatomine parasite transmits most of the infections that are caused it. However, the parasite can also enter the body through organ transplant and blood transfusion. Mother-to-infant infection can also occur and in rare cases; the parasite can be transmitted through food or accidents among laboratory workers. In the case of vector-borne transmission, the parasite is spread through the metacyclic trypomastigotes which are active forms of the parasite (Bonney &Engman, 2008). The parasites enter into the body through mucous membranes and the broken tissues. When the trypomastigotes get into the host cells, they form there amastigotes and later multiply within the cells. The amastigotes form trypomastigotes through growing flagella (Deborggraeve, et al., 2009). The trypomastigotes invade the adjacent tissues where they spread through blood and lymphatic to other sites. The whole cycle is completed when the reduviid bug is ingested through the host blood. When patients are infected with the parasite, they start developing symptoms within 4-8 weeks. 30-40 percent of the patients who harbor the parasite are at a high risk of developing cardiac and even chronic Chagas disease (Deborggraeve, et al., 2009).
The parasites increase in number during the acute phase. At this stage, there is a massive tissue damage, and myocarditis is observed. Myocytolysis also occurs due to the parasites-related immune damage. There is hyaline degeneration of the muscles fibers due to the heavy infestations of the amastigotes (Bonney & Engman, 2008). The chronic Chagas cardiomyopathy is the most severe manifestation of this condition. There is a transition from the indeterminate form of the parasite. The parasite later causes serious damages to heart tissues. The pathology and pathogenesis of the T. cruzi infection are mainly derived in the cell culture experiments and animal models. The outcome of a T.cruzi infection is mainly dependent on the host and the parasite (Gutierrez et al., 2009). Whenever there is an acute infection of the parasite, it leads to an inflammatory reaction that includes the leukocyte which has eosinophils and macrophages (Bonney &Engman, 2008). Whenever there is an infection, the cardiovascular system experiences an elevated level of cytokines, chemokines endothelin, and even nitric oxide (Deborggraeve, et al., 2009).Parasites and Heart Diseases Assignment
CD4+ and the CD8+ are very common in the inflammatory infiltrate. In chronic Chagasic cardiomyopathy, the CD8+ T cells are the most prevalent. The blood from trypomastigotes accesses the cardiac myocytes due to the invasion of the endothelial cells, the interstitial areas and the myocardium (Junqueira et al., 2010). The cardiac myocytes are destroyed as a result of the invasion. The trypomastigote passes through the basal laminae areas and the extracellular areas. The expression and the activity of the metalloproteinases associated with myocardial zinc are up-regulated whenever an infection occurs (Rassi & Marin, 2009). The inhibition of the enzymes can significantly reduce the myocardium inflammation (Lewis et al., 2014). Inside the heart, the cardiac myocytes exist in three layers which meet at the apex. With the inflammation, the extracellular muscles start degrading. As a result, there is a slippage of the ventricular layers. This causes apical aneurysm formation and mural thinning. These are the most common features that are associated with the Chagas disease (Marin-Neto et al., 2009). The cardiac myocytes are replaced by the bands of fibrous tissue. The collagen tissues are the most common manifestations of the chagasic heart disease. The changes that are caused by the parasites are not reversible, and they lead to serious alterations of the heart functions (Deborggraeve, et al., 2009). As a result of the pathological changes, there is the thinning of the myocardium and hypertrophy (Bern et al., 2011).
Some of the key proteins that are involved are the endothelins. It is a 21 amino acid peptide secreted by endothelial cells. There is an increase in the active ET-1. Although ET-1 is found in many cells, the increased production could cause various types of hypertension. Eicosanoids are some of the important lipid mediators that play a role in vascular tone, developing ischemia and even inflamtaion. T.cruzi have the ability to synthesize the TXA2. This is an indication that TXA2 forms an important pathogenesis of T.cruzi.Parasites and Heart Diseases Assignment
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The spread of the T .cruzi mainly occurs through vector transmission. The parasite must be residing in the host for some time. The former indicates that if the parasite does not get access to the host, it cannot cause the disease. The triatomine bugs are the ones who are responsible for the spread of the disease. They ingest blood and pass the trypomastigotes which are left in the bitten area (Hidron et al., 2010). The bugs are found in tropical areas and areas with dense vegetation. In the transmission process, the vector injects the body of a human being with the parasite where it goes through the lifecycle to be an active form.Parasites and Heart Diseases Assignment