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of Amebiasis disease

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The nucleus has a “ring and dot appearance” which is composed of a peripheral chromatin and central eukaryote. IV. Life Cycle The ameba’s (trapezoids) normally live in the lumen of the large intestine, especially the transverse and descending colon, where they ingest bacteria and food particles and reproduce by simple asexual division. The lesions start as small ulcerations of the intestinal epithelium. Ameba’s within the lesions spread laterally as they encounter the deeper layers of the colon, sometimes producing flask-shaped ulcers that undermine the mucosa epithelium.

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As the call material passes down the intestine, the trapezoids eject any undigested food particles, and each individual rounds up and secretes a protective cyst-wall around itself. Cysts passed in the feces are about mum in diameter and can resist adverse environmental conditions for two or three weeks or for up to four weeks in water. Organisms may also spread through the portal circulation to produce abscesses in the liver and less commonly in the lung, brain, or other organs.

Despite their pathogenic potential, organisms in the intestinal tract often cause few or no symptoms. In addition, many humans carry non-pathogenic mambas that are morphologically indistinguishable from E. historical. V. Virulence Notable historical virulence is related to a number of amoebic components (elections, cytosine propitiates, and Ambrose) and host factors, such as intestinal bacterial flora. Trapezoids are selective in their interactions with bacteria, and the parasite recognition of coelenterates plays an important role in amoebic virulence. The virulence of E. Statistical has been proposed to be related to a number of amoebic components: (I) a family of calaboose (Gal)/N-acetic-d- agglomerations (Galena)-specific elections, which mediate the initial attachment f the parasite to the mucosa cells and enable resistance to Allis by serum complement; (ii) small amphibians proteins known as embargoes (App-a – Ambrose gene), which form pores in membranes of target cells as well as in the cell walls of ingested bacteria; and (iii) a family of six potent cytosine propitiates (CUPS) which have considerable sequence homology.

Although the specific role of each of these cytosine propitiates has not yet been established, their inhibition by antigens RNA has been shown to affect amoebic virulence. In addition to the amoebic components, there are various host factors which nutrient to and determine the virulence of E. historical trapezoids in the human host. One factor which has been suggested to play an important role in amoebic virulence is the bacterial flora of the intestine. E. Statistical trapezoids attach and ingest bacteria either by using their membrane- associated election specific for Gal and Galena or by having their manses containing cell surface components serve as receptors for the manses binding elections of certain bacteria. VI. Pathogenesis E. historical are frequently found in the human colon in persons without symptoms of disease. The ameba’s must adhere using a critical surface protein (or election) to specific receptors on host cells containing dislocates residues (I. E. M Gal-galena).

In experimental models, attachment to cells is inhibited by adding calaboose. Attachment is also inhibited by intestinal mucus, which suggests that disruption of the mucus layer may be a critical event in the pathogenesis of embassies. Damage to host cells requires intimate cell-to-cell contact and takes place in three steps: (1) receptor-mediated attachment to the mammalian target via the Gal-galena binding election; (2) contact-dependent killing, probably by insertion of pore-forming proteins (embargoes) into the host cell membrane; and (3) ingestion of the killed host cell by the mamba.

Although certain strains of E. historical produce an intervention, it is not yet clear whether intervention production correlates with virulence. Phagocyte cells do not control amoebic infection in immune hosts: pathogenic strains of ameba’s actually kill interruption and non-activated macrophages. The situation is different in immune hosts, in whom the most important line of defense appears to be cell-mediated immunity (which was suggested by he finding that ameba’s can be killed in vitro by activated macrophages).

Furthermore, persons given steroids (which suppress cell-mediated immunity) tend to have disseminated infection despite high titters of antibodies. Thus, circulating antibodies may not play a critical role in protection against amoebic infection. Ameba’s are known to produce a cytosine proteins that digests secretors GA, Gig, and other proteins involved in the humeral immune response. Gig is one of the 5 basic class of antibodies which is a heavy chain constant region defined as a, a dimmer of 2 monomer units (antigen valence of 4).

It is solely responsible for mucosa immunity – actively secreted across mucosa epithelium into the lining fluid; it will neutralize the antigen (statically hinder the interaction of toxin, bacteria and virus) and may also serve as posing (any various of proteins as antibodies or complement that bind to foreign particles and cells like bacteria making them more susceptible to the action of phagocytes. On the other hand, Gig is also one of the 5 basic class of antibodies which is a heavy chain constant region defined as D, an antigenic material monomer with valence of 2.

It is responsible for the systemic body lids, circulatory and interstitial fluids in naturalization of antigen by secreted antibody. It also postpones antigenic material which promotes association of the antigenic material with phagocyte membranes that activates a phagocyte’s killing mechanism. VI’. Incubation Period The incubation period of intestinal embassies can vary, ranging from a few days to months or years but is generally 1 to 4 weeks. With proper treatment, the infection can be controlled, usually without long-term effects. Most individuals recover fully within 2 to 4 weeks after beginning treatment.

Without treatment, however, mortality can be high. Serious medical complications can develop into life-threatening conditions. Although rare, lung or brain infection can result in chronic disease. VIII. Period of Communicability The protozoan has a simple life cycle with two forms: the actively growing, vegetative trophies and the dormant but highly resistant cyst Patients with diarrhea pose only a minor threat of transmission because they excrete the actively growing yet labile trapezoids; this form of the parasite is easily destroyed by drying in the environment and, if ingested, by acid in the stomach.

Conversely, asymptomatic carriers excrete the durable cyst form of the parasite, which survives well in the environment and remains intact through the stomach. Asymptomatic carriers thus represent the greatest danger Of transmission. When ameba’s are in balance with their host, they do not cause symptoms but are excreted as cysts, thus ensuring their transmissible. IX. Mode of Transmission E. historical is transmitted from person to person through the fecal-oral route.

The only requirement for transmission is that contaminated feces of the carrier be ingested with food or water. Both cysts and trapezoids are sometimes present in the feces. Cysts are usually found in firm stool, whereas trapezoids are found in loose stool. Sexual transmission (anal-oral or oral-genital) is also important, particularly among homosexual men. Occasionally trapezoids might be transmitted during sexual intercourse. X. Reservoir Humans are the only known reservoir. XSL. Prognosis Drug treatment can cure embassies within a few weeks.

However, because medication cannot keep you from getting infected again, repeat episodes of embassies may occur if you continue to live in or travel to areas where amoebas are found. Among children in developing countries, especially infants and those younger than 5, gastrointestinal embassies can be fatal. Worldwide, embassies is the third most common cause of death from parasitic infections. XII- Signs and Symptoms Most people with this infection do not have symptoms. If symptoms occur, they are seen 7 to 28 days after being exposed to the parasite. Symptoms could be characterized as mild or severe.

Mild symptoms include abdominal pains, diarrhea (passage of 3-8 semi- formed stools per day; passage of soft stools with mucus and occasional load), fatigue, excessive gas -? flatulence, rectal pain while having a bowel movement – tenseness, unintentional weight loss. Severe symptoms include abdominal tenderness, bloody stools (passage of liquid stools with streaks of blood; passage of 10-20 stools per day), fever, nausea and vomiting. Signs seen on oscilloscope include colonic mucosa arrhythmia (redness of the inner surface of the colon), ulcers, bleeding. XIII.

Complications Peritonitis (the inflammation of the peritoneum which is the thin membrane that lines the abdominal wall) as a result of perforation has been reported in connection with severe amoebic infection. Gastrointestinal amoebas is usually associated with liver infection, causing abscesses and/or enlargement. The abscess appears as a slowly enlarging liver mass and will cause noticeable pain. Jaundice may also occur due to blockage of the bile. Pleural, pulmonary, and pericardia infection results from metastasis spread from the liver, but can also manifest in other parts of the viscera or give rise to a brain abscess.

However, these complications are uncommon. XIV. Treatment Treatment depends on the severity of infection. Usually, intermediation is the drug of choice because it is converted to its active form by the yardage:foregoing crustaceans or POOR (major metabolic pathway in anaerobic bacteria and protozoa to generate AT P) which attacks the DNA that produces strand breakage. It is highly effective against the trophies form of the amoeba. It is to be given by mouth for 10 days. Intermediation is generally contraindicated in the first trimester of pregnancy.

Since intermediation is less efficient at killing ameba’s (mamba cysts) within the intestinal lumen, a second drug like pyromaniac, deadline or disunion is used to eradicate the alumina forms and can also be used to treat asymptomatic carriers of pathogenic strains. Intermediation and prominence should not be given at the same time because diarrhea is a common side effect of prominence and may impair assessment of the patient’s response to therapy. Medicines to stop diarrhea are usually not prescribed because they can make the condition worse.

If the patient is vomiting, he may need medications through a vein (intravenously) until he can take them by mouth. After treatment, the stool should be rechecked to make sure that the infection has been cleared. W. Prevention and Control Measures 1 . Symptomatic cases should be excluded from food handling and from direct are of hospitalized and institutionalized patients until completion of antimicrobial therapy. 2. Patients must be advised of the importance and effectiveness of washing hands with soap and water after defecation and before preparing, serving or eating food. . Because of the risk of shedding infectious cysts, people diagnosed with embassies should be counseled to refrain from recreational water venues until after their course of alumina therapy has been completed and any diarrhea they might have been experiencing has stopped. 4. Patients with embassies should be counseled on voiding sexual practices that may permit fecal-oral transmission. 5. Contracts should have adequate stool examinations performed and be treated only if results are positive. 6.

Symptomatic contacts should be assessed by a physician. 7. Contacts should be educated on transmission and preventive measures. 8. Protection of public water supplies from fecal contamination. Sand filtration of water removes nearly all cysts and diatomaceous earth filter remove them completely. Chlorination of water generally practiced in municipal water treatment does not always kill cysts. 9. Small quantities of water are best reared with prescribed concentrations of iodine, either as liquid or water purification tablets.

Cite this of Amebiasis disease

of Amebiasis disease. (2018, May 31). Retrieved from https://graduateway.com/a-description-of-amebiasis/

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