Parasites and Heart Diseases

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.


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. 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.

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.

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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).

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.

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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.

Trypanosomiasis Brucei

The trypanosomiasis brucei also uses the same mechanisms as T cruzi. The parasite must reside in the body of the host for some time. It must pass through a vector for it to undergo a cycle that will transform it into an active form. Without the vector, the parasite cannot find its way into the human body. However, there are differences in the mode of transmissions and the vectors. The tsetse flies are the major vectors of the parasite, and they are responsible for the getting of the disease into human beings (Hidron et al., 2010). Whenever a tsetse fly bites an animal that has been infected, it ingests the trypomastigotes which later multiply into metacyclic trypomastigotes. In case there is another tsetse fly bite, the trypomastigotes are introduced into the lymphatic system. A systematic infection occurs at the point of the bite (Hidron et al., 2010). Trypanosomiasis brucei rhodesiense is one of the main flagellate parasites that cause the human African trypanosomiasis. The disease results from tsetse fly bites (MacLean et al., 2010). After the bite, the tsetse flies spread the metacyclic trypanosomes that multiply very fast and then migrate to other parts of the body. The incubation period of the disease can vary but after the incubation, the common symptoms include arthralgia, lymphadenopathy as well as neurological symptoms. The symptoms continue to manifest until treatment is intiated (Hidron et al., 2010). The cardiac manifestations of the T.brucei are not very prominent. Although the cardiac manifestations have been ignored in many writings, it is an area that is worth studying and deserves a deeper analysis.

Pancarditis is an infection associated with T. Brucei. At the early stages, the cardiac layers are infiltrated by lymphocytes and plasma cells (MacLean et al., 2010). The macrophages and the polymorph nuclear are also infiltrated at the advanced stages. The infiltration is also associated with a high prevalence of trypanosomes in the interstitium (Hidron et al., 2010). At the advanced stages, the infiltrate and the parasites can also be observed in the heart valves and even the lymphatic drainage system of the heart. In the pericardium, there is the presence of bloody fluid that contains a high concentration of fibrin and trypanosomes (MacLean et al., 2010). At the advanced stages of the disease, macroscopically biventricular dilation as well as pericardial fat occur (Morrison, 2013).

In a post-mortem study of the human beings, there can be found a chronic pancarditis that is characterized by lymph homonuclear cell infiltration. Pancarditis can cause death because of its severability. Epicarditis and degenerative changes with cellular infiltration in the heart system have also been described. The patients who have died as a result of HAT were reported to have a normal heart but there is valvular fibrosis. There is an increased pericardial fluid and cardiomegaly in some cases.

At the early stages of HAT infection, Band T lymphocytes can easily respond to VSG molecules. This results in antibodies, and it becomes so easy to remove the various organisms from the blood system. The most important feature of the parasites is that they have a strong ability to escape the responses of the immune system (MacLean et al., 2010). The parasites can change their VSG molecules. By the time the body produces antibodies to fight the trypanosome, the trypanosome will present a new surface that is not antibody specific. The trypanosome achieves this through gene conversion and DNA rearrangement. The parasites are able to suppress the immune system by limiting specific antibodies. With this ability, they are capable of perpetuating infection. The parasite macrophages, in turn, can depress the T-cell proliferative responses to the VSG (MacLean et al., 2010).

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The parasite also generates the antigens, which makes it hard for the host to fight the parasite; thus, the chances of parasites’ survival increase (Elliott et al., 2013). Patients in the last stage of the infection tend to exhibit a lot of clinical manifestations. In human beings, signs of heart failure are so prevalent (MacLean et al., 2010). The histology has also evidenced myocardial involvement. Other major symptoms that have been observed are the enlargement of the cardiac, volume overload as well as peripheral edema. Other studies on heart failure among patients in the last stage of the T.b.rhodesiense HAT tend to exhibit symptoms such as a cough, heart murmurs, and even cardiac rhythms. Laboratory markers of heart failure such as NT-pro-BNP tend to be elevated among patients with HAT. Their electrocardiograms are abnormal.

Toxoplasma Gondii

Toxoplasma gondii is a common disease-causing agent that is affecting almost a third of the world population. Unlike the other two parasites discussed above, the Toxoplasma gondii is transmitted during the digestion of food and water that have been contaminated. After getting infected, the patients exhibit a less severe and asymptomatic condition or a systematic condition. Depending on the health condition of the hosts, the disease can manifest in various forms (Zhou et al., 2011). For example, people who have an immune deficiency can be seriously affected by the condition. In the US, the T.gondii is a parasite that resides in cat feces. Although the parasite exists in many warm-blooded animals, the cat serves as the key host (Alvarado-Esquivel, et al., 2016). However, cats will never show any signs of the disease. The parasite can enter the human body after one comes into contact with feces of an infected cat. The pregnant mothers are at a very high risk of spreading the disease to their unborn children.

Various studies have revealed that there is a close relationship between coronary ischemia and other infectious agents. Atherosclerosis which is a chronic inflammatory disease plays a key role in initiating and even spreading of pathophysiology in atherosclerotic lesions. T.gondii infection in the acute phase causes the synthesis of the IL-I2 alongside other cytokines, which leads to the synthesis of IFN-y by the NK cells. The CD4+ and CD8+ are also formed. During the chronic phase, the levels of the proinflammatory cytokines go down (Zhou et al., 2011). The THl CD4+ T lymphocytes continue producing IFN-y which is a key component that is responsible for host infection. The growth of T gondii depends on the host cholesterol. The cholesterol of the host in the blood decreases; the plasma low-density lipoprotein also decreases, and this poses a significant risk for developing atherosclerosis. T.gondii infection results in THl systematic inflammatory response in the target organ (Alvarado-Esquivel et al., 2016). The same is a proinflammatory stimulus which could promote the pro-atherogenic environment.

Other studies on the relationship between the heart disease and the T.gondii have also revealed that patients with heart disease have had an exposure to T.gondii. However, such studies have concluded that a chronic infection of T.gondii could be associated with heart disease rather than an acute infection (Zhou et al., 2011). The same is a clear indication that T.gondii is a major causative factor of heart diseases.

In the case of T.brucei and T. Cruzi, it is notable that the disease becomes so severe among the immunodeficient individuals. It is a life-threatening infection that can easily lead to death. For example, babies can easily develop a serious infection because of their weak immune system. However, there are not so many reported cases of the infection since lot of people have a strong immune system that can help in forming a strong resistance to the parasite (Zhou et al., 2011).

Although the parasite has severe effects, the problem is that the disease is not widely reported even in developed countries because the infection causes no symptoms. Most people who are infected with the parasite are not even aware of it (Zhou et al., 2011). Those with a good immune system will not exhibit the symptoms again. Another notable characteristics of the parasite is that it cannot spread from one person to another. However, this can occur in case when there is a donation of an organ from an infected person or a maternal transfer from a mother to a child.

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Heart Diseases Caused by Parasites


There are some heart diseases that are caused by parasites. Toxoplasma gondii, Trypanosoma cruzi, and Trypanosomiasis brucei rhodesiense are some of the most common parasites that cause heart diseases. Unfortunately, these parasites have been ignored in literature and textbooks despite their harmful effects. They affect the different parts of the heart and tend to exhibit different mechanisms in their invasion. One of the most common similarities in the three parasites is that the parasite must reside in the body of the host. The Toxoplasma gondii, Trypanosoma cruzi, and Trypanosomiasis brucei rhodesiense can only have an impact on the person after they have been introduced in the body (Nagajyothi et al., 2014). Mostly, they exist in an inactive form outside the host, but they become active and cause severe damages after invasion. From the hypothesis, the main purpose was to determine whether Toxoplasma gondii, Trypanosoma cruzi and Trypanosomiasis brucei rhodesiense have the same mechanism and vectors. From the literature, it is evident that they do not rely on the same factor. In the case of T.brucei, the tsetse fly is the main vector (Nagajyothi et al., 2014). Whenever an infected person is bitten by a tsetse fly, it transmits the inactive form of the T.brucei which later develops to metacyclic trypomastigotes. The metacyclic trypomastigotes are then introduced into a healthy body through a bite. On the other hand, T cruzi is spread through the triatomine parasite. The vector that is responsible is the Triatomine bugs. The above finding helps in forming a good conclusion that the three parasites do not use the same vectors. The researcher rejects the null hypothesis as the three parasites use the same vectors in spreading the disease. The researcher accepts the alternative hypothesis since it is evident that the discussed parasites have different vectors and different mechanisms of causing infections (Nagajyothi et al., 2014).

Another common feature is that the parasites can be spread from one person to another through an organ transplant from an individual who is infected. On the other hand, it is notable that a strong immune system can play a role in preventing the adverse effects of the parasites in the body.

The chronic Chagas cardiomyopathy is one of the most common manifestations of the Chaga,s disease. The T.cruzi can cause irreversible changes to the heart muscles that leads to the thinning of the myocardium and hypertrophy. The T.cruzi is very resistant to the immune system being a very adaptive parasite. It changes its DNA so quickly such that even if the host’s immune system tries to fight it, it changes to a form that is not compatible with the antigens. The T.gondii does not have a vector. The parasite does not cause any infection when one has a strong immunity. The main controversy in the literature review is that the epidemiological impact of the T.gondii parasite has not been well elaborated and needs a deeper study. In the future studies, it is important to consider the risk factors associated with the parasite since they have not been covered in the literature. The main literature controversy surrounding the Chagas disease is that there has been a lot of focus on neurological impacts of the disease and less attention has been paid to the heart diseases. The literature review of Trypanosomiasis brucei rhodesiense also raises a controversy since there has been more focus on sleeping sickness, and the heart disease literature has been overlooked.

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In conclusion, the three parasites cause heart diseases by affecting the various parts of the heart. From the literature review, there is a need to carry out a detailed research so as to determine the epidemiological effect that results from the exposure to T.gondii. The research paper shows a need for further studies on the characteristics and impacts of T.gondii. In the case of the other two parasites, there is a need to carry out a deep study as a way of determining the risk factors associated with the disease and how they cause the various heart diseases. It is, therefore, important to focus on these diseases as a way of forming a deeper understanding of their mechanisms and processes involved. Their vectors are not the same, and they do not use same mechanisms.

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