Helicobacter Pylori

faecalis has a low pathogenicity (scilo), it is a virulent, opportunistic pathogen to be reckoned with and is thought of as a super-bug. This is not only due to its ability to resist a variety of antibiotics, but also its ability to travel and employ biofilm formations. It can grow and adapt in many different environments. It can thrive in a wide range of temperatures and has disregard whether salt or oxygen are present, or whether the pH is basic or acidic. Its resilience on inanimate objects makes it a perfect candidate for transmission to occur within the hospital environment from hand to instrument, but it can also be spread via hand-to-hand contact and from food contamination (Public Health Agency of

into ammonia, and thus neutralizing the surrounding acidic environment. Also, H. pylori contains "hydrogenase" enzyme, which can oxidize molecules hydrogen being produced by other gastric bacteria, in order to produce energy. Some other enzymes that can be utilized by H. pylori are "oxidase" and "catalase", which are also used to test for the presence of this organism. It can also form "biofilm" on the gastric mucosa epithelium, which results in its ability to resist against many antimicrobials. From spiral form, it is able to convert into "coccoid form" - one of its advantage which helps in its survival and epidemic potential [5].

pylori. However, the second option omeprazole 20 mg twice daily, clarithromycin 500 mg twice daily and amoxicillin 500 mg twice daily, is better for the patient based on cost because it is less expensive and the patient has concerns about medication with less copay.

H. pylori is a narrow, curved, Gram-negative rod with polar flagella. It grows slowly in a microaerophilic atmosphere in a manner similar to Campylobacter. The bacteria have only recently be identified as the causative agent to gastric ulcers, a condition long believed to be the result of stress and lifestyle habits.

When found in the pyloric antrum H. pylori causes duodenal ulcers and when in the corpus, or body of the stomach, H. pylori can cause gastric ulcers and gastric carcinoma (“Helicobacter pylori,” Wikipedia). Helicobacter pylori can be detected by a blood test, urea breath test, stool antigen test, and/or stomach biopsy done during an endoscopy (“Helicobacter Pylori Tests”). When treating Helicobacter pylori, patients will typically be given three medications (“Helicobacter pylori,” Wikipedia). The use of the three medications is called triple therapy (“Helicobacter pylori,” Wikipedia). One example of a triple therapy used to treat H. pylori is the use of Omeprazole, a proton pump inhibitor, along with clarithromycin and amoxicillin, antibiotics (“Helicobacter pylori,” Wikipedia). However, a patient may be given substitute proton pump inhibitors, such as pantoprazole or rabeprazole, if they are allergic to omeprazole (“Helicobacter pylori,” Wikipedia). Substitute antibiotics may also be prescribed if the patient is allergic to amoxicillin, such as, metronidazole (“Helicobacter pylori,” Wikipedia). Through research, triple therapies have been found to have better results in curing H. pylori than monotherapies or dual therapies (Fuccio et al. 746-747). The triple therapy must be taken for at least seven days and in some cases up to 14 days (“Helicobacter pylori,” Wikipedia). Eating yogurt that contains Lactobacillus and Bifidobacterium has also been shown to increase the rate at which H. pylori is cured (“Helicobacter pylori,”

pylori appears to be humans, but it has also been isolated from non-human primates, domestic cats, pigs, sheep, and, more recently, the housefly. However, non-human primates are unlikely to be a significant route of transmission to humans, since there is limited contact between the two species, and there has been little evidence to suggest that domestic cats, pigs, or houseflies serve as vectors for H. pylori infection. Sheep, on the other hand, remain a possible source of transmission which warrants further investigation. While not yet confirmed, the most likely route of H. pylori transmission for the general population is from person to person through oral-oral, via saliva, dental plaque, and vomit, or through fecal-oral routes. Iatrogenic infection remains the only proven route of transmission of H. pylori, due to the difficulty of completely disinfecting an endoscope, but is unlikely to be the main route of transmission. Waterborne transmission of H. pylori may also be possible as H. pylori can live and remain infectious in milk and tap water for several days, especially in less-developed parts of the world where water is not treated

interdum works by capitalizing on its external structure. A. interdum uses its spiral- like shape to embed itself within the stomach lining and alter the acidic conditions of the stomach. Unlike H. pylori , which generally increases the acidity of the stomach by releasing gastric acid secretion, A. interdum works to lower the pH level. It has been found that gastrin, a hormone synthesized by G cells, is a proton pump inhibitor that controls the acidity of the stomach. In A. interdum, Gastrin is coded to slightly decrease the acidity of the stomach in the presence of H. pylori. Without the acidic conditions, H. pylori will die, therefore it will not be able to inflame the stomach lining. This creates optimal conditions for A. interdum. Reducing of inflammation is made possible as A. interdum penetrates the stomach lining and releases amino acids, which quickly causes re-growth of villi. As soon as the villi sense nutrients to be absorbed they begin to react. Once embedded in the stomach lining, A. interdum stay for approximately two weeks where it continues to grow adjacent to the villi. It is important to note that A. interdum grows at a rate three times as fast so it is always taller than the villi. A patient can then return to eating a regular diet, including gluten-containing foods, because A. interdum feeds on the amino acids in gluten and aids with the digestive process. After two weeks the bacteria detaches from the stomach lining and is processed through the rest

H. pylori thrives in the acidic environment of the stomach and the finding that this bacteria contributed to the condition was remarkable news and led to the standard practice of treating peptic ulcers with antibiotics. As a result, the rate of H. pylori-induced ulcers has dropped by more than 50 percent. (Ackerman, 2012)

Answer: I used emedicine to reference more statistical history on H. pylori and its common applications in relation to the ulcer bug currently. Using the same data that was gathered from the study referenced on D2L the protocols for treatment have vastly improved over the last couple years. I thought about the long term effect that antibiotic treatment of this bacteria and how the bacteria itself “burrows” itself into the stomach mucosa thus causing the ulceration. The article I read also mentioned that this specific bacteria is also responsible for inflammation in the duodenum (part of the small intestine). In summation there also is a higher risk for stomach cancer and lymphoma also associated with this bug.

Prevalence of duodenal and gastric ulcers in patients with liver cirrhosis increases as the disease progress[11] and this prevalence becomes higher in decompensated cirrhosis than in compensated cirrhosis [12]. Currently, PPIs are the mainstay treatment option of peptic ulcers in the

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

An example of a flagellated bacterium is the ulcer-causing Helicobacter pylori, which uses multiple flagella to propel itself through the mucus lining to reach the stomach

Torpy, J. M., Lynm, C., & Golub, R. M. (2012). Peptic ulcer disease. JAMA, 307(12), 1329.

The mucosal epithelial cells are affected by these toxins through receptor mediated endocytosis which set off a series of events that eventually leads to cell death.6 Toxins A and B also cause the host cells to secrete cytokines, including interleukin-8 which creates acute neutrophilic inflammatory infiltrate which is one of the characterising factors of C. difficile.6 C. difficile can also cause a build-up of dead mucosal cells, pus, and bacteria in the large intestine to create pseudomembranous colitis (PMC) covers the intestinal wall which affects the fluid reabsorption and contributes to the vast amount of diarrhea, and dehydration.3 In the last decade C. difficile infections have increased dramatically, one of the reasons could be

A peptic ulcer can be defined as an “excavation that forms in the mucosal wall of the stomach, in the pylorus, in the duodenum, or in the esophagus” (Brunner, Suddarth and Smeltzer, 2008). According to Fromm, (2009) Helobactor pylori is a gram-negative bacteria that is the cause of most peptic ulcer disease and is considered a primary risk factor in the development of gastic cancer (pg. 394). Other causes include stress, and excessive secrtion of Hydrochloric acid in the stomach. Transmission of H. pylori according to Gurney, Carvalho, Gonzalez, Galaviz & Sonstein (2014) states there is strong research supporting that H. pylori can be spread person to person through direct contact with saliva, vomit, or fecal matter (pg. 393). H. Pylori is more prevalent in crowded areas without reliable access to clean water. Other risk factors include poor hygiene, smoking, and close living conditions with someone who is infected with H. pylori. Symptoms of an ulcer include a burning sensation in the stomach and esophagus, vomiting, diarrhea or constipation and bleeding. Treatment of Peptic Ulcer Disease includes antibiotics to eradicate H. pylori bacteria; proton pump inhibitors are used to treat NSAID-induced ulcers and other ulcers not associated with the bacterial infection, smoking cessation and dietary modifications. Surgical management is recommended for ulcers that fail to heal after 12-16 months of treatments and the procedures include pyloroplasy, anrectomy or vagotomy.