Trypanosoma_Cruzi_Paper

Trypanosoma cruzi Paper For a single-celled organism, Trypanosoma cruzi has caused an incredible amount of damage and death throughout Latin America and now even some parts of the United States. Its vector is referred to as the “assassin bug” because of its lethal and very surreptitious methods of infection and diffusion into the human body. The most common result of infection from this parasite is Chagas Disease, which can have serious implications for the heart and gastrointestinal system. The cure for this parasite has eluded scientists and experts for years because of T. Cruzi’s very clever life cycle. It has the ability to transform between three different forms, which makes it very difficult to cure. The parasite thrives best in substandard living conditions. The anatomy and physiology of T. Cruzi is very unique and complex, especially for a single-celled organism. It is heterotrophic and able to reproduce asexually, which becomes a critical factor in its dispersion into the bloodstream of humans. The parasite transforms back and forth from three different forms. Each serves its own purpose and can reappear when needed. The first form, called trypomastigote, doesn’t actually infect any tissue. It has a long body with centralized nucleus and an undulating membrane that runs along the exterior of the parasite. The next form is called epimastigote and while it is smaller than the trypomastigote, it is certainly just as powerful. Its main function is to survive when the parasite travels through the vector’s harsh intestines. The final form is referred to as amastigote. This is the smallest form, but the most harmful because they infect smooth muscle tissue, especially cardiac cells, and they multiply while being released into the bloodstream. T. Cruzi receives its energy from unlikely sources, which is another component to its makeup that intrigues and confuses scientists. It receives many nutrients from acid calcisomes and reservosomes, which is very rare for a trypanosoma parasite. The T. Cruzi life cycle is both very fascinating and brilliant. It can enter the host with little difficulty in their trypomastigote form and multiply in its amastigote form through the process of binary fission. When it enters, it does so by creating or finding a bug bite or exposed piece of skin and defecating on it. The expected reaction from the human is to itch the bite, which then allows the feces to enter the bloodstream. The parasite, which is currently in its amastigote form, multiplies and the original cell dies. The multiplied cells then transform into trypomastigote form once again. Once they enter the vector’s midgut, they change to their epimastigote form. They then differentiate into infective metacyclic trypomastigotes. The parasites intermediate and terminal hosts are limited. It mostly begins with the reduviid bug and directly infects the human. There have been cases of dogs or transfusions infecting a person, but the majority of cases have been from direct contact between the bug and the human. The primary and most prevalent vectors of the Trypanosoma Cruzi parasite are triatomine bugs. The most common is called the “kissing bug” or “assassin bug” and other reduviid bugs. Trypanosoma Cruzi and the assassin bug is found indigenously only in Latin America. These countries include: Mexico, Argentina, Belize, Bolivia, Brazil, Chile, Colombia, Costa Rica, El Salvador, Ecuador, French Guinea, Guatemala, Guyana, Honduras, Nicaragua, Panama, Paraguay, Peru, Suriname, Uruguay, and Venezuela. They were once thought to inhabit only Brazil, but the parasite soon spread quickly to many other countries in that area. It lives primarily in poor living conditions, particularly thatched roofs and mud walls. While the parasite is rare in the United States, but there have been several cases so far, but T.Cruzi isn’t believed to be indigenous to America. The majority of cases here belong to immigrants from Latin American countries who had already contracted the parasite. The effect of the parasite on the host can be minor and include flu-like symptoms, or can be chronic and lethal. The most common effect is called Chagas Disease. Unfortunately, many cases are asymptomatic following a period of flu like symptoms, which means they go undetected. This period can last anywhere from 10 years to 40 years. In the majority of chronic patients, their life expectancy was decreased by 9 years because of the parasite. Some of the most deadly effects of the parasite are its implications for the patient’s heart and 25-30% of chronic patients experience cardiomyothapy. The parasite is extremely adaptable and is able to resist damage even in inflamed cardiac tissue. The treatment and control of the disease is surprisingly limited and not extraordinarily effective. The CDC estimated that 18 to 20 million people are infected throughout the world and that about 300,000 people in the United States are infected as well. When detected early, a cure is sometimes effective, but the symptoms are so subtle and unnoticeable that cures are almost never provided early enough. When caught, there are some drugs such as nifurtimox and benznidazole that can help or even cure the disease, but scientists have found that the parasites have recently been able to resist these drugs. The tests done to check for the parasite also provide many false negatives. The chronic version of the parasite is the most lethal and also the subtlest. Right now, there are only ways to cope with the pain and heart problems the chronic version provides, but no cure or even preventative measures have been approved. Trypanosoma Cruzi has not received nearly as much attention as it should be garnering due to its large presence in many Latin American countries and its severe symptoms and negative effects on those infected. Though it is single-celled, this parasite is extremely complex and can transform effortlessly from one protective form to another, which allows it to thrive and avoid any possible conflicts from the human’s body and any drugs that are being used to combat its dispersion.