Parasites are organisms found in almost every niche and some species have evolved to the point of developing characteristics for intracellular survival, which is the case of the parasite Trypanosoma cruzi that causes Chagas disease. T. cruzi is transmitted to the vertebrate host through the feces of triatomine bugs in which the infective forms, metacyclic trypomastigotes, are inoculated after the insect bite. The establishment of T. cruzi infection depends on a number of factors that begins with the invasion of host cells, which mobilizes various effector mechanisms of the immune system, such as the activation of factors related to innate immunity and acquired immunity. This research paper aims to answer what are the types of immune response used by the infected host during the developmental stages of the parasite, as well as what are the possible evasion mechanisms used by the T. cruzi that allows its survival in a hostile environment created by the response of the host immune system.
American trypanosomiasis or Chagas disease was discovered by the Brazilian physician Carlos R. J. Chagas in 1909. Chagas disease is caused by the flagellated protozoan Trypanosoma cruzi, which is mostly transmitted during a meal blood of blood‑sucking triatomine insects (kissing bugs). Triatomine insects have wide variety of hosts such as skunks, dogs, cats, armadillos, goats, sheep, which serve as a reservoir of the disease (Nouvellet et al. 2013). Inside of the triatomine insects occurs the
Gut worms are a type of roundworm that infect cattle in their stomach by causing eggs to form in their feces. Also known as Parasitic Gastroenteritis (PGE), this disease causes the cattle industry to lose millions of dollars each year.
Fever, swelling around initial infection site, parasites in blood, sometimes asymptomatic, rarely debilitating or life threatening problems can occur.
Nature never ceases to amaze. Who would have thought that such a small and insignificant single celled organism can do so much? Who would have thought that this organism can affect our precious brains in a way that we can hardly detect? We previously thought that our brains cannot be controlled by anyone. T. Gondii took that assumption and blew it to pieces. T. Gondii is able to trick our bodies and our brains into doing what is best for it to survive. Toxoplasma Gondii is manipulating the behavior of people in Kuwait.
In the chronic phase, because of low and probably intermittent parasitemia, diagnosis relies on serologic detection of specific immunoglobulin G (IgG) antibodies that bind to T cruzi antigens (see Fig. 4A). Enzyme-linked immunosorbent assay, indirect immunofluorescence, and indirect hemagglutination are most common methods used. Two positive results from any of these 3 conventional techniques are recommended for a final diagnosis.
Chagas disease, also known as American Trypanosomiasis, is a tropical disease caused by the parasite Trypanosoma cruzi, transmitted to humans through contact with the feces of an infected triatomine bug. The triatomine bug known as the kissing bug is a subspecies of the Reduviidae family. The bug itself does not cause the disease. Through contact with the fecal matter from the kissing bug, which is excreted near the bite wound, the parasite enters the bloodstream and begins to develop and reproduce.
Our plan is to run blood tests on individuals who exhibit symptoms of FSGS to confirm if they express the APOL1 gene. The individuals whose blood we use, since we have to take both likelihood of affliction and ancestry into consideration, will be from people who are of West African descent. In order to confirm if the individual expresses the APOL1 gene, we will first take the individual’s blood sample, large enough to have a detectable amount of HDL cholesterol (potentially formed into an APOL1-HDL complex). We will then acquire a sample of the parasite. The parasite will be acquired by gathering the various species of Tsetse flies which serve as vectors for trypanosomes in West Africa. We can then cultivate a live axenic sample of
This bacterium has developed a unique way to evade the human immune system and starts evading right from moment the bite occurs. It has learned to survive in the human body and sometimes even heavy doses of medicines fail to generate results against the bacteria.
A decrepit, fungus infested, skeleton-man who’s both tormented and controlled by the reproductive organs of a parasitic fungal infection growing on his face. He hides in dark damp places, usually behind his victim’s toilets, muttering gibberish to himself and occasionally wailing out in bursts of intense pain. His victims mainly include children, who’s blood he ingests, then regurgitates back into the bloodstream imbued with infectious fungal spores. Shortly following infection, the victim may begin to display early flu-like symptoms. After about 4 days, several brown to black pigmented regions begin to appear in large patches on the skin and the flu-like symptoms intensify. At 5-6 days, foxfire may begin to emanate from the patches, along
How the disease was transmitted was further looked on by Nelson (1995). According to the said author, the disease was transmitted primarily by fleas and rats. The stomachs of the fleas were infected with bacteria known Y. Pestis. Nelson held that “the bacteria would block the "throat" of infected fleas so that no blood could reach their stomachs, and they grew ravenous since they were starving to death” (1995, par. 14). The bacteria would then attempt to suck up blood from their victims, only to disgorge it back into their preys' bloodstreams (Nelson, 1995). Now, however, the victims' blood was mixed with Y. Pestis. Fleas infected rats in this fashion, and the rats spread the disease to other rats and fleas before dying (Nelson, 1995). Without rodent hosts, the fleas then migrated to the bodies of humans and infected them in the same fashion as they had the rats .
The plasmodium parasite would be most susceptible to human antibodies between the moment of initial infection and the arrival of the larvae in the liver, as it travels through the bloodstream in the form of sporozytes. Here the parasite is fully exposed, not ensconced in liver cells or red blood cells as during later phases of its development. Though the lower numbers of parasites at this stage would trigger less of an antibody response, this lower plasmodium population would also be more effectively countered by the human body's natural defenses.
Biological transmission occurs when the pathogen reproduces within a biological vector that transmits the pathogen from one host to another . Arthropods are the main vectors responsible for biological transmission. For example, hemipterans (called “kissing bugs” or “assassin bugs”) transmit Chagas disease to humans by defecating when they bite, after which the hu-man scratches or rubs the infected feces into a mucous membrane or break in the
One of the main reasons, Adrian was infected with the Chagas disease was that he lived in an area where the disease vector was present. A description of Adrian’s house on the banana plantation “small wooden houses set on low stilts now lined cleared strips of land between the bananas and the forest edge. Cracks between the slats of the wooden walls and floor allowed dirt and insects to enter the house.”(Santanello and Rehg) The triatomine insects (carrying parasites) live in the cracks of defectively constructed houses in areas near the forest similar to Adrian’s residence. The bugs usually more active during the night and feed on humans around the eyes or mouth because the skin is thinner in those areas. The next section of this case will discuss the treatment of the Chagas disease.
Chagas disease is an endemic infection in Latin America caused by the parasite Trypanosoma cruzi. Nowadays, it affects millions of people worldwide including thousands in Europe and Oceania. Megacolon, that represents the most frequent complication of the digestive chronic form, happens due to lesions of the enteric nervous system, followed by motility disorders. The neuronal lesions seems to initiate right in the acute phase and persist for a long period during the chronic phase, being that the mechanisms involved on such process are still debated. Among the cells of the immune system possibly involved in this pathological process, we emphasize the mast cell (MC), due to its well known role in the bidirectional communication between the immune
If a pathogen breaches barriers: innate immune response result into an immediate effect of non- specific response. All Innate immune systems derived from plants and animals, when a pathogen evades the innate response, a third layer of protection is possessed by vertebrates in which activation of adaptive immune system takes place. The immune system response adopts itself within an infection and pathogen recognition is improved. As a result of the improved response, its then retains itself when the pathogen is eliminated in form of an immunological memory and allows the adaptive immune system to mount faster and stronger when pathogen is encountered each time.
Since Darwin’s “dangerous” idea in the nineteenth century, the causes and significances of evolution have been investigated unceasingly. One evident example of evolution is between parasite and host relationships, in which host and parasite partners maximize their own fitness, by evolving to reduce the fitness of the other. Parasites are hypothesized to evolve and cause hosts to evolve, as well as promoting sexual recombination. There are two major hypotheses of evolution pertaining to host-parasite relationships: the Red Queen hypothesis and the Red King model. The Red Queen hypothesis claims that there is a