LF Disease Pathogenesis Paper

While this infection does cause harm to the lymphatic system, it still affects the integumentary system (skin). The skin and lymphatic system go hand in hand when this infection is present in the individual. This is seen when the skin reacts to the decreased function of the lymphatic system due to the parasitic worm.

The Human Body is an oasis of life. Still, every waking moment of our lives, our bodies endure vicious attacks. Bacteria, viruses, fungi, microbes, toxins, and parasites - I like to think of them as invaders from the outside world. Each invader is equipped with its own specialized method of attack. On a microscopic level, our bodies fight a life-long war. As the battle rages, our immune system kicks in and protects us against the perils of illness. The immune system is not made up of one particular tissue or organ. Instead, an arsenal of defense cells; including lymphocytes, bone marrow, and leukocytes join forces to keep us healthy. Besides the occasional times we get caught in the crossfire with a common cold, a healthy immune system keeps

After the parasites enter your body, they can cause any number of symptoms. People have developed skin rashes, aches, fevers, chills, coughs, inflammation, scarring, anemia, malnutrition, and learning difficulties. They can also affect the lungs, bladder, liver, and intestines. Less often, the eggs can induce paralysis, seizures, or even spinal cord inflammation.

Much of our understanding of immune interactions with T. gondii is through studies on rodents, and the rodent immune system shows some specific adaptations in this area. Indeed, rodents express a set of toll-like-receptors (TLRs) to deal with recognizing protozoan parasites; studies have identified that the cell surface receptors TLR-2 and TLR-4 (which respond to glycosylphosphatidylinositols), and the endosomal receptors TLR-7, TLR-9, TLR-11 and TLR-12 are required 6, 17. The most compelling evidence suggests that the endosomal TLR-11 (possibly in conjunction with TLR-12) is part of a specific murine response that recognizes the protein profilin which is secreted from motile parasites 18-20. Evidence suggests that the innate immune response in mice

Parasites. They’re not the typical topic of table conversation, but they are still an important thing to research and be knowledgeable about. While there are many, many different kinds of parasites, in this paper we will be zooming in on and talking all about the internal parasite that is the tapeworm.

Hookworms; also describe as the intestinal parasites are a serious infection that affects both humans and animals. The hookworms are very small species that develop based on blood-feeding. Those harmful species not only hook to the intestinal’ mucosa and suck the whole-body nutrition but also they conceal some antigens that cause a hold off to the immune resistance and eliminate the hemoglobin. As a result, the body undergo a series of intestinal hemorrhaging stats with extreme decrease in healthy blood cells. In other, the patient

It is considered as a hypersensitivity reaction to the migrating larvae of stomach worms Habronema microstoma, H. muscae and Dreschia megastoma. Both the stable and house fly deposit their larvae on manure, which injest the stomach worm larvae and serves as intermediate host. The adult flies deposit stomach worm larvae wherever they feed like mucocutaneus junction, wounds and other moist regions of the animal’s body. The larvae deposited near mouth or lips complete their life cycle and become adult in the stomach. The larvae can penetrate wounds and moistened skin lesions and may reach to dermal and subcutaneous tissues and eventually die (Rebhun, 1996; Yarmut et al.,2008). The disease occurs more in the fly season with warm weather and regress during winters. Calcification and deposition of sulfur granules are the characterstic for stomach worm lesion (Pusturela et al.,2003). The larvae deposited on the mucous membranes or on injured tissue do not complete their life cycle and induce a local inflammatory reaction causing cutaneous (summer sores) or ophthalmic habronemiasis (Traversa et al.,

target larger parasites, typically worms (Graham, et al., 2005). Some of the first studies of Type 1 cytopathic immune responses were with Tumor Necrosis Factor (Tracey and Cerami, 1994). Tumor Necrosis Factor (TNF), a cytokine produced in response to invasion by a parasite, was found to cause tissue damage to the host during its response to a viral invasion, causing a reaction very similar to septic shock (Tracey and Cerami, 1994). For larger infections, Type 2 cytokines are the most common immune response (Graham et al., 2005). While attempting to repair tissue damage caused by worms, these cytokines can often overcorrect the problem, causing fibrosis (Graham et al., 2005).

TNFa is an endogenous pyrogen, thus is capable of inducing inflammation, fever, apoptotic cell death and, inhibition of tumorigenesis. (Kleef and Hager, 2000) One of the most potent stimuli for TNFa is a bacterial endotoxin (lipopolysaccharide) or (LPS) which is derived from the outer cell wall of gram-negative bacteria. (Verhoef et al., 1999) LPS is a major component of the outer membrane of gram-negative bacteria, and contributes greatly to the structural integrity of the bacteria. (Kaszowska, 2004) Large amounts of TNFa are released in

Researchers such as Ralston and colleagues supported the hypothesis that trogocytosis is a mechanism in which cells receive nutrition from other cells, however, in the transaction parasites and host cells, the parasites virulence is enhanced killing the host cells. In the processes of amoebiasis, ingested E. histolytica settles in the colon of the individual, releases its mucus and interacts with the exposed enterocyte cells lining in colon causing cell death by lysis. Other models suggested that parasite attached themselves to host cells in order to kill through unclear mechanism involving releasing substances into the cell membranes. Additionally there was also a model indicating that pathogens engulf and ingest dying enterocytes by phagocytosis. However, this latter model is not consistent with the finding that parasites nibble on host cells through consistent actions causing cell death, then moving on once death is

The organism T. brucei is responsible for the vector-borne disease known as Trypanomiasis also known as African sleeping sickness which affects millions of people in 36 sub-Saharan countries. Parasites enter the body through bites from the tsetse fly. Its life cycle starts, when an infected tsetse fly bites human skin. While it is feeding on blood, metacyclic trypomastigotes are transmitted to the skin from the salivary glands of the fly. The parasites get into the bloodstream by entering lymphatic or blood vessels. They travel in different body fluids (such as blood, lymphatic or spinal fluid), transform into bloodstream trypomastigotes and

Copeland et al. (1) evaluated inflammatory responses and compared the responses in both humans and mice. Specifically, the researchers examined the acute inflammatory response to endotoxin, which is a component of the cell wall in gram-negative bacteria (1). The mice and humans had similar responses for multiple variables, including levels of tumor necrosis factor (TNF), interleukin-6 (IL-6), and CXC chemokines (1). Chemokines are a type of signaling

For effective control and prevention strategy of malaria, there is a need to understand the pathogenesis of the parasite (mechanisms for parasite invasion and host defence). There are four human malaria parasites; Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, and Plasmodium ovale. However, the plasmodium falciparum is the most common across much of Sub-Saharan Africa. It accounts for all the malaria mortality in sub Saharan Africa and also over 90% of the global Plasmodium falciparum burden. (Joy et al. 2003).

Pro-inflammatory cytokines are those which – among several other negative consequences – promote inflammation and tissue destruction

Hookworms in humans is caused by a helminth infection caused by a nematode parasite Necator americanus and Ancylostoma duodenale. Humans are exposed to the infection when their skin comes in contact with larvae in the soil which was contaminated by human feces. The larvae penetrates the skin and enters the bloodstream, lungs and mouth. Once the larvae enters the mouth it is swallowed and ends up in the intestines. Once it reaches the intestines the larvae receives its nutrients from the host blood. Feeding on human blood supply, hookworms inevitably end up causing anemia in that individual. Other symptoms of the infection include a skin rash, weight loss, wheezing and cough, fever, stomach pain, diarrhea, heart failure or even death if the infection is left untreated.