H Pylori Infection Case Study

Tetracyclines and erythromycin are the most commonly used oral antimicrobials. In many cases, long-term treatment is needed to maintain remission. The long-term use of antimicrobials is not well tolerated, however, because of side-effects, including gastrointestinal intolerance,

Helicobacter Pylori is a disease, which if untreated can cause ulcers. My disease [Helicobacter Pylori]. This is a disease in the stomach that causes severe stomach pain. I needed tough hope to conquer my painful story of Helicobacter Pylori.

Helicobacter pylori, also known as H. pylori, is a spiral bacterium that lives inside the human stomach. H. pylori likes the acidic environment that the stomach provides and evidence has linked it to a variety of minor gastrointestinal illnesses. H. pylori causes inflammation in the lining of the stomach and is involved in 90% of stomach and intestinal ulcers. H. pylori also has an apparent cause to the development of adenocarcinoma, a common stomach cancer. J. Robin Warren first detected H. pylori in the stomachs of ulcer patients in 1979. Warren then isolated the microbe in a culture and tested it effects by swallowing some of the inoculum. A short-term case of gastritis (inflammation of the lining of the

Hello Kelli, I enjoyed reading your post. You made some good points. I just want to add to what your mention about H. pylori being treated with two varieties of antibiotics the patient may also be given proton pump inhibitor, histamine receptor blocker, and protectants to help relieve pain. I think it is interesting o how the breath test is performed and thanks for sharing that information because it very helpful. It is also important that patient doesn’t eat or drink anything for a least 6 hours before the breath or stomach biopsy is performed. Other than those small adjustments that I wanted to add, I think you did a wonderful job.

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.

One common cause of gastritis is H. Pylori. H. Pylori is a bacteria found worldwide, but especially in developing countries, where up to 10% of children and 80% of adults are likely to have had an H. pylori infection. However, patient usually are without any symptoms (Pilotto & Franceschi, 2014). The human host is the only known reservoir. Transmission occurs by person-to-person contact, by both fecal-oral and oral-oral routes therefore, infection is most likely acquired in childhood (Go,2003).

Prior to the isolation of Helicobacter pylori (H. pylori} by Robin Warren and Barry Marshall in 1982, it was theorized that peptic ulceration, an ailment first described in 1857 by William Brinton, stemmed from poor diet, tobacco use, and stress due to the failure to definitively identify a causative agent as well as the belief that the inhospitable environment within the human stomach resulted in its sterility (Tanenbaum 2005). Because physicians were ignorant to the existence of H. pylori, individuals suffering from peptic ulcerations underwent ineffective treatments for over a century. The successful isolation of H. pylori and identification of its role in gastric diseases earned Warren and Marshall a joint Nobel Prize in Physiology or Medicine in 2005 (The Nobel Prize 2005). Despite the passage of thirty-two years, modern medicine has been unable to definitively eradicate H. pylori, but research continues in hopes of developing a more permanent cure as well as effective methods of preventing initial peptic ulceration, as occurrence is linked to an increased risk of developing gastric carcinomas.

First, the risk of uncomplicated peptic ulcer linked to acute or chronic use of NSAIDS and/or aspirin. Secondly, the efficacy of anti-secretory treatment with the use of PPI or H2blockers on these drug induced ulcers (Pilotto, et al., 2004) The brief literature review provided context and support for the study, along with gaps from previous studies, such as the efficacy of concomitantly use of anti-ulcers and aspirin to prevent GI injuries in a short term period (Pilotto, et al., 2004). I could not find any procedures used to protect the participants during the

Most of the T cells in the gastric mucosa differentiate into Th1 cytokines, the others become anergic. Anergy of T cells may be brought about by the interaction of T cells with the gastric epithelial cells that express B7-H1. B7-H1 is a costimulatory molecule that increases during H. pylori infection. In gastric epithelial cells the development of Treg cells from naïve T cells is brought about by exposure to H. pylori via induction of BH-71. This suggests that H. pylori might utilise the epithelium to promote the development of Treg cells which play a vital role in suppressing effector T cells. Because of this the existence on Treg cells in H. pylori infection may diminish the adaptive immune

The management of peptic ulcer disease and its complications remain a challenge. In addition, non-steroidal anti-inflammatory drugs (NSAIDs), low-dose aspirin, smoking, excessive alcohol use, emotional stress and psychosocial factors are increasingly important causes of ulcers and their complications even in H. pylori-negative patients. Other rare causes of peptic ulcer disease in the absence of H. pylori, NSAIDs, and aspirin also

Acute infection can give an upper gastrointestinal illness with nausea and pain; vomiting and fever may be present also. The acute symptoms may last for less than 1 week or as long as 2 weeks. Once colonized the H pylori infection persists for years and perhaps decades or even a lifetime. About 90% of patients with duodenal ulcers and 50–80% of those with gastric ulcers have H pylori infection. H pylori also may have a role in gastric carcinoma and lymphoma [51].

Helicobacter Pylori or H. Pylori is a type of bacteria that invades the body and infects the digestive tract. It was discovered around 1983 by Warren, a biologist and Marshall, a clinician. It is named because of the spiral shape that allows the bacterium to burrow itself deep within the mucosal layer of the stomach wall. This penetration of the stomach lining enables to the bacteria to protect itself against immune cells that would recognize the organism as an invader. In order to survive the natural acidity of the stomach and its contents H. Pylori secretes an enzyme called urease. Although this enzyme helps protect the H. Pylori bacterium against the acidity of the stomach, it does not provide any protection for the depressions or holes in the stomach wall caused by the bacteria. This damage to the stomach wall can lead to ulcers that may bleed, cause other infections, or keep food from passing through the digestive tract. If these ulcers are left untreated, they can more severe diagnoses such as GERD, gastric cancer or gastric mucosa-associated lymphoid tissue lymphoma if left untreated.

In the system of the gastrointestinal tract, there are some conditions that can affect quality of life and is common. One of these conditions is called peptic ulcer disease (PUD) or also known as H. Pylori (Helicobacter pylori), which is the bacteria associated with PUD that causes the infection that leads to PUD. Almost two thirds of the world is affected with this infection, unbeknownst to the host (Moscou, page 421). This infection is introduced in the body through contaminated sources of food or water. It also can be transmitted through person to person contact by kissing. Once ingested, buffers are released and the bacteria is able to survive despite the acidic conditions of the stomach. Most people do not produce symptoms of the infection, however, there are some that may experience irritation and tissue damage from overproduction of gastric acids and peptic ulcers. Duodenal ulcers, which form in the upper region of the small intestines, are more common in younger people. Peptic ulcers tend to be more common with age as they are more likely to be infected. This disease is treatable and obliteration of the H. pylori results in ulcer cure and prevention of recurrences (Zoorob, page 243)

Esophageal reflux, irritable bowel syndrome, heartburn, constipation and flatulence can be signs of helicobacter pylori.

Antibiotic resistance is the main factor accounting for unsuccessful eradication of Helicobactor pylori (H. pylori). Being knowledgeable of the regional resistance rates of H. pylori isolates can regulate not only the empiric antibiotic therapy but also lead to second line treatment and rescue regiments. At present, the most common treatment is empiric eradication, thus, global regional regiment therapies should be based upon regional in-vitro antibiotic resistance rates. This approach is crucial in successfully treating the individual patient. However, in regions where antibiotic susceptibility testing is unavailable, epidemiological data for secondary H. pylori resistance are essential for the rational use of antibiotics following several treatment failures in. Primary H. pylori resistance to clarithromycin is generally less prevalent worldwide than H. pylori resistance to metronidazole. Secondary resistance that develops in vivo in previously susceptible organisms has been documented in cases of therapeutic failures. All antibiotics used to treat H. pylori are also widely employed to treat other bacterial infections, therefore, pretreatment exposure of H. pylori to inadequate levels of these drugs as well as the use of inadequate regional antibiotics, is associated with secondary resistance. Herein, we review regional resistance rates of H. pylori isolates to clarithromycin, metronidazole and