Helicobacter Pylori Research Paper

The causes of campylobacter are undercooked meats. The food source of campylobacter are raw poultry. You can prevent yourself and others from receiving campylobacter by thoroughly cooking raw food, using a thermometer to be sure that the internal temperature reaches the necessary degree. One fact that you may not know about campylobacter is that the campylobacter species is spiral shaped.

Helicobacter pylori (H. pylori) is a human pathogen that is responsible for ulcers and stomach inflammation. The organism had been researched by several scientists around the world since 1875; however none of them was successfully culture it. Until 1982, Dr. Barry Marshall and Dr. Robin Warren succeeded in observing the colonies, and thus became the first scientists to discover this bacterium. By self-testing, Dr. Marshall drank a liquid that contained H. pylori culture. A few days later, he got sick with many symptoms such as vomiting and nausea. After ten days, by undergoing endoscopy, he was able to confirm the role of H. pylori in causing gastritis. Then he and Dr. Warren also demonstrated the effect of

Commonly prescribed antibiotics used to treat H. pylori infection include amoxicillin (Amoxil, Trimox), clarithromycin (Biaxin), metronidazole (Flagyl), and tetracycline (Sumycin). This combination of medicines is taken for 10 to 14 days. It is important for patients to take the full course of medications exactly as directed. An improvement in symptoms does not necessarily mean that H. pylori bacteria are no longer present (O'Connor, Vaira, Gisbert, & O'Morain, 2014).

In the past it was believed that gastric ulcers were caused by life style modifiable risk factors. The biggest culprit now is Helicobacter pylori (H. pylori). H. Pyloris is a bacterium commonly found in the gut. The bacteria breaks down the lining of the stomach. Then the stomach acid further breaks down the lining which causes the ulcer. This is the reason, unless contraindicated, most patient receives either a Histamine-2 Receptor Antagonist or a proton pump inhibitor in the hospital. The GI symptoms that are present with gastric ulcers would decrease the appetite of the patient. Therefore the patient would encounter a digestion problem.

Helicobacter pylori is an important human pathogen that chronically infects the gastric and duodenal mucosa (1). It affects approximately 50% of the population worldwide, and is associated with multiple gastric pathologies, including gastritis, peptic ulcer disease (PUD), gastric cancer (GC) and mucosa-associated lymphoid tissue (MALT) lymphoma (2). While the majority of individuals infected with H. pylori are asymptomatic, essentially all develop chronic inflammation (3). Among infected individuals, approximately 10% develop PUD, 1-3% progresses to GC and 0.1% develop MALT lymphoma (3). Clinical outcomes of long-term infection vary, as disease severity is thought to be related to a combination of host genetics, environmental factors, and genetic heterogeneity of H. pylori (2). Helicobacter pylori exhibits a much greater genetic diversity than most bacteria, and this is often attributed to the differences in prevalence and expression of bacterial virulence factors that may impact the outcome of gastric disease (4). Several virulence genes related to the risk of gastric disease have been identified, including cagA, cagE, vacA, iceA, and babA2 (2). A large number of studies have shown that VacA producing H. pylori strains are related to more severe clinical outcomes, although the genetic mechanism(s) underlying this observed associations is not yet

Over half of human stomachs in the world are colonized by H. pylori. This bacterium is the culprit for almost 80% of all gastric adenocarcinoma cases and upwards of 90% of all duodenal peptic ulcer cases making it the second most common bacterial infection worldwide (6). Those colonized with H. pylori have a two to six times increased risk of forming gastric cancer or ulcers. Because of this, H. pylori has since been classified as a class I carcinogen. There are currently two completely sequenced genomes of H. pylori (strain 26695 and strain J99) which have been revolutionary in the research and understanding of its genetic diversity and pathogenic mechanisms. H. pylori are gram-negative, spiral shaped, adorned with three to five polar

Campylobacter -like organisms can produce an enterocolitis/proctocolitis syndrome in homosexual males, who are at increased risk for Helicobacter cinaedi and Helicobacter fennelliae infections. C jejuni infections may also produce serious bacteremic conditions in individuals with AIDS. Most reported bacteremias have been due to Campylobacter fetus fetus infection. Campylobacter lari, which is found in healthy seagulls, has also been reported to produce mild recurrent diarrhea in children.Campylobacter upsaliensis may cause diarrhea or bacteremia, while Campylobacter

A short course for 10 days post-EVL may be reasonable if we concern for ulcer healing. However, high-dose infusion (e.g., pantoprazole 8 mg/h) and prolonged use in the absence of endoscopic procedures is not supported by the literature and should be discouraged until evidence of benefit becomes available. (8)

Helicobacter pylori is found commonly in the mucosal lining of the stomach and the duodenum without penetrating epithelium because its adaptability to the highly acidic and low pH environment. However, occasional or persistent presence has been suggested, (Figure 2) H.pylori DNA was successfully isolated from other locations in the body, such as atherosclerotic plaques and oral cavity, which is not surely confirmed whether its presence due to true colonization for those sites or due to traveling of H.pylori to distant sites as a result of body pathophysiological mechanism. For instance, the phagocytized H.pylori from stomach being transported on macrophages through blood to the atherosclerotic plaques and oral presence as a result of gastric reflux. Other evidences suggesting the presence of Evidence of H. pylori colonization has also been found in the gallbladder, ears, nose, skin, and even eyes.

Maintained: Lina experienced diarrhea episodes back in November 2016 that was attributed to antibiotic treatment, requiring the need to hold Calcium Citrate X 72 hours and Milk of Magnesium for 10 days which end up being discontinued on 1/4/17. One episode of constipation was reported for lack ok of BM’s from 8/27-8/31, this episode required treatment with a suppository Bisacodyl 10 mg once and MOM 30 ml PO once with good results; she was not symptomatic. No further constipation episodes were reported. Lina is currently not taking any laxatives or stool softeners. Dietary constipation preventive measures includes high fiber, 2 oz. of fruit butter, 2 tbsp. ground flaxseeds at breakfast, 2 oz. of Prune juice per day (before breakfast or after supper), only if needed to relieve constipation, and encourage fluids for hydration that also help prevent constipation.

Identify (3) items related to the medical diagnosis that the RN can include in the teaching plan for this patient?

Omeprazole is time sensitive and will only work for twenty-four hours before it is excreted in the urine. Length of treatment is dependent upon the severity of the ulcers and dosage of omeprazole (Bell et al., 2007; Videla and Andrew, 2009). Histamine type II receptor antagonists are another frequently utilized treatment for gastric ulcers. These products prevent the interaction between histamine and histamine receptors and thus inhibit HCl secretion from parietal cells in the stomach (Bell et al., 2007; Videla et al., 2009). However, there is conflicting data concerning the efficacy of these products to reduce gastric ulcers and the half-life for these products are very short, requiring more frequent dosing (Bell et.al., 2007). Nonsteroidal anti-inflammatory drugs (NSAID’s) are often administered to alleviate any pain associated with gastric ulcers, or other pain throughout the equine body. Unfortunately, NSAID’s have been linked to increased gastric ulcers, contributing to the issue (Bell et al., 2007, Videla and Andrews, 2009).

It is believed that the first report about Campylobacter was back in 1886 by Escherich who observed and described non-culturable corkscrew-shaped bacteria isolated from the colonic contents of infants who had died as a result of “cholera infantum” (Escherich, 1886; Skirrow and Butzler, 2000; King and Adams, 2008; Vandamme et al., 2010). Campylobacter identified for the first time in 1906 by John McFadyean and Stewart Stockman, who reported the presence of large numbers of a peculiar organism in the uterine mucus of a pregnant sheep (Skirrow, 2006; Zilbauer et al., 2008). After this in 1913, McFadyean and Stockman isolate these microorganisms from aborted bovine fetuses and successfully cultured for the first time (McFadyean and Stockman,

The nonpharmalogical treatment of peptic ulcer disease involves eliminating the use of NSAIDs, ceasing smoking, and avoiding foods and beverages that could irritate the ulcer such as spicy foods, caffeine, and alcohol.1 The patient should take non-NSAIDs for the treatment of pain such as acetaminophen. The recommended treatment regimen for patients with NSAID-induced gastric ulcers involves either a proton pump inhibitor, an H2 receptor

The current treatment methods according to the Multinational Association of Supportive Care and Cancer/International Society of Oral Oncology Clinical Practice Guidelines for the Management of Mucositis are very narrow (Gibson, R. J. et al. 2013; Lalla et al. 2014). The only therapeutic agent recommended for chemotherapy- induced gastrointestinal mucositis management is octreotide, once loperamide has failed to stop diarrhoea (Al-Dasooqi et al., 2013, Ginopoulos et al., 1996, Logan et al., 2008, Logan et al., 2009). The anti-inflammatory