Epidemiology Of Chagas Disease

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.

Chagas disease is an illness caused by the parasite Trypanosoma cruzi. This parasite infects triatomine bugs, which are common in Mexico, Central America, and South America. These bugs spread the disease to humans through contact with their feces. This may be through bites from the bugs, or the parasite can enter the body through mucous membranes or small cuts in the skin.

Hello Nathan, I enjoyed your post. Chagas is a major disease and I must say it will be interesting to see how the house projects research goes. It is apparent that this aid the Latin America countries in need while including their socio-economical status. Use resources indigoes to the population of countries at hand. It is apparent that close living quarters within humans to humans such as over crowding, and close living of humans to animals aids not just Chagas disease but many. Chagas disease is a disease that can be stopped but is an extremely challenging challenge.

Mexico is one of the 21 Latin American countries where Chagas disease is found endemic and will be the purpose of this analysis. This country is ranked number three in terms of number of infected individuals with Chagas disease in the Western Hemisphere, where 99% of the cases are present (Bern 2011). Also, according to Carabarin-Lima (2013), 96% of the transmission of Chagas in Mexico is vector borne and the greatest percentage of the triatomine bugs is present in rural areas. According to Tonantzin (2013), it is estimated that one million people suffer from Chagas in Mexico, while the population at risk is 5.5 million people (Carabarin-Lima, 2013).

This document will discuss how demographics disease trends affect the delivery of health care. Starting with current age composition of the United States population and how future changes will occur in the next 10 to 20 years. Next will be identifiable factors that support environmental and changing demographic trends. Providing examples of relevant diseases and how the aging trend will increase or decrease health issues and how to reduce health complications because of age. The current rate of obesity will be discussed and how it will change in the next 10 to 20

Cells move from the blood into the intestines and produce inflammation which is a normal immune system response. The inflammation does not subside, leading to chronic inflammation, ulceration, thickening of the intestinal wall, and eventually causing patient symptoms.

Chorea-Acanthocytosis (ChAc) is a neurological disease that is extremely rare to come across, affecting only about 500-1000 people worldwide (GHR). ChAc is one of a handful of uncommon diseases named neuroacanthocytosis (GARD).

The Infectious Diseases Society of America (IDSA) has recently noted several model antibiotic-resistant bacteria strains with redesigned capabilities in pathogenesis, transmission and resistance. These several strains, Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species, have been given the acronym-based title of the ESKAPE Pathogens. These strains of bacteria compromise one of the biggest threats faced by physicians today not because of the infectious and devastating illnesses they lead to, but because of their ability to resist antibiotics in the healthcare setting. Failure for industries, academia and government to cooperate and develop research/development operations has left healthcare providers one-step behind in the fight against these new brands of infectious diseases. A lack of research/development operations has left the healthcare industry with antiquated antibiotics no longer capable of targeting and eradicating these microorganisms in human systems.

In 1854 cholera swiftly took over in just one street in London killing over 600 people in a little more than a week. Cholera first started in India and spread to England when the british arrived there. Now that you know this let’s find out what cholera even is first of all.

The enteric nervous system (ENS) is an essential, independent system of monitoring and control regulating nutrient absorption, secretion, motility, blood flow, and sensation in the gastrointestinal (GI) tract (reviewed by Beattie and Smith, 2008; Molderings, 2012). The ENS consists of more than 100 million neurons scattered throughout the gut in clusters called ganglia, which innervate adjacent tissues and organs, including the esophagus, stomach, intestines, pancreas, and gallbladder. At the molecular level, more than 30 transmitters and cotransmitters have been identified, including serotonin. As is the case with the central nervous system (CNS) (reviewed by Gillette, 2006), the main role that serotonin plays in the gut is neuromodulatory (reviewed by Molderings, 2012). In particular, the enteric serotonergic pathways are important for regulating smooth muscle tone, peristalsis, secretion, and sensation (reviewed by Beattie and Smith, 2008).

The hindgut is not only a fermentation vat, but it also stimulates immune responses, protects against pathogens, production and neutralization of toxins, and gene expression in host epithelial tissues (Milinovich et al., 2010). The cecal microbiome is extremely sensitive and can be affected by factors like gastrointestinal disease and dietary changes, which can lead to systemic consequences and even death (Costa et al., 2012). Therefore, healthy and balanced microbiota is vital for the overall wellbeing of the animal. By understanding external factors and how they affect the gut microbiota, this could help in diagnosing medical conditions and provide better treatment and prognosis of gastrointestinal diseases resulting in

Within the tubular gastrointestinal tract, the ENS is formed by various interconnected networks, called plexuses, of enteric neurons, glial cells, and axons (Widmaier et al. 2014). The majority of these nerve cells are found within two different arrangements of ganglia (Fig. 1): the myenteric (Auerbach’s) plexus and the submucosal (Meissner’s) plexus (Furness 2006; Guyton and Hall 2006). The nerve cells’ axons either synapse with additional neurons in the plexus or innervate the smooth muscle of digestive organs (Furness 2006). Neural activity in one plexus can affect activity in the other since some axons in one plexus synapse with neurons in the other (Fig. 1) (Widmaier et al. 2014). Extrinsic nerve fibers from the parasympathetic and sympathetic systems can also synapse with neurons in each of the two plexuses (Fig. 1) (Guyton and Hall 2006). Though the ENS can function without these nerve pathways, the subsystems of the ANS can influence gastrointestinal activity (Guyton and Hall 2006; Widmaier et al. 2014). An example would include either inhibiting or enhancing the GI tract’s motility and secretory activity through the sympathetic and parasympathetic fibers (Widmaier et al. 2014).

This journal article was over how our bodies protect us from the internal and external environments. The host has three main “fences” that help with that protection, the skin, the gastrointestinal tract, and the respiratory tract. We are really interesting subjects, the internal and external surfaces of our bodies are constantly being introduced to new bacteria, microbes, and pathogens and yet we do not get sick. The barriers or fences protect us and are crucial for our immune response. There is still much not understood about the immune system but we do know with certainty that when a child is born he or she acquires around two thousand different species of bacteria that really help to get the child immune system started and running. The researchers also know that there is four dominate groups of bacteria phyla’s in the “intestinal niche”, Firmicutes, bacteroidetes, Actinobacteria, and proteobacteria. We are able to have our normal bacteria’s in and on us because our immune system has learned to co-exist with its symbiotic species. As one may wonder or even certainly expect, competition does occur between the host symbiotic organisms and potentially harmful bacterial cells. They compete mainly for nutrients but also for space, some microbes even engage in “chemical warfare” and possibly even killing its rivalry. Inflammatory disorders can possibly arise from the internal and superficial wars going on, that is why the immune system is constantly being monitored for comprises

In this experiment, the scientists compared the amount of autoantibodies present in the digestive system of BN rats and BNm rats. An extraction of sera from BNm rats revealed the presence of autoantibodies that recognize and attacked wall components of arterioles and venules, as well as muscular layers of the intestine (Chabod et al. 2012). Furthermore, the intestinal tracts of BNm rats were noticeably marked with macroscopic lesions, multifocal infiltration, and granulomas (Chabod et al. 2012). In comparison, BN rats lacked the same autoantibodies found the mutated rats and tended to have less intestinal abrasions and abnormalities (Chabod et al. 2012). To determine whether CD4 T cells contributed to the development of IBD, the researchers experiments with wild type BN rats that were thymectomized and given anti-CD4 treatment (Chabod et al. 2012). The experimented rats showed no signs of IBD, indicating that mutation in the Themis gene is required for the development of IBD seen in BNm rats (Chabod et al. 2012). This further supports the researchers’ notion that a mutated Themis gene, along with subsequent reduction of viable CD4 T cells, is closely related to the occurrence of

When there is a problem in the colon, and these cells are inflamed and infected, they