Research Paper Helicobacter Pylori

Helicobacter pylori Previously named Campylobacter pyloridis, is a Gram-negative, microaerophilic bacterium give in the jump out. Microbiology (B1325) look into Paper Detailed Introduction Helicobacter pylori ar a species of epsilon proteo bacterium which colonizes the harsh surroundings of the human stomach. Its name refers to both its spiral shape (Helicobacter) and the bea of the dismantle stomach which it habitually colonizes the gateway (pylorus) between the stomach and small gut (Meyers, 2007).This bacterium is thought to be put forward within up to 50% of the human population and has been linked to the development of a material body of divers(prenominal) medical conditions (Chalmers et al. 2004). This report will provide information about the denudation of H. pylori as well as its morphological characteristics, taxonomic information, biochemical/ metabolous characteristics, chemotherapeutic methods of control/ manipulation/ obliteration, immunological responses, pathological information, and epidemiology information. Morphological Characteristics Helicobacter pylori are a spiral-shaped, Gram-negative rod just about 0. x 3. 0 micrometers in size. It is catalase-positive being which has 4-6 cover flagella attached to one pole which allow for motility. It lives in the human stomach and duodenum. H. pylori possess five major outer membrane protein (OMP) families. The largest family includes known and putative adhesions. The other four families include porins, iron transporters, flagellum-associated proteins and proteins of unknown quantity function. Like other typical Gram-negative bacteria, the outer membrane of H. pylori consists of phospholipids and lipopolysaccharide (LPS).The O antigen of LPS whitethorn be fucosylated and mimic Lewis blood group antigens found on the stomachic epithelium. The outer membrane also contains cholesterol gluco facial expressions, which are found in few other bacteria. H. pylori has four to six lophotric hous flagella all stomachal and enterohepatic Helicobacter species are highly motile collect to flagella. The characteristic sheathed flagella filaments of Helicobacter are composed of two copolymerized flagellants, FlaA and FlaB. 1(From Wikipedia, the free encyclopedia). Taxonomic Information Helicobacter pylori are a gram-negative, spiral-shaped organism associated with gastrointestinal disease in universe.It has a worldwide prevalence, with approximately 50% of the worlds population befouled. Before the first isolation and documentation of this organism from the human stomach in 1982, it was assumed that the human stomach was a sterile environment be stimulate of the high levels of acid, which would exclude it as an ecologic street corner for any organism. This bacterium is the human-adapted Helicobacter primarily found in the gastric mucous membrane and areas of gastric metaplasia in the duodenum and occasionally in Meckels diverticulum and the rectum. It has been cultured rarely from feces, blood, and saliva.It female genital organ be detected by polymerase chain reaction (PCR) in dental consonant plaque and feces. In the last mentioned instances, the viability of the bacteria is in question. H. pylori also drive home been found in nonhuman primates and cats. H. pylori detection in animals is non common and could be due to human contact with animals. To date, no environmental reservoir has been shown. 2(http//www. gastro. theclinics. com/article/S0889-8553(05)70135-7/abstract) Biochemical/Metabolic Characteristics The genus Helicobacter was created in 1989 with H. pylori as the part species. Since then the genus has expanded to include about 18 species.Some species were reclassified from Campylobacter, unless to the highest degree were rude(a)ly discovered microorganisms from gastric or intestinal sites in mammalian host animals. The essential property of almost all helicobacter is the bearing of sheathed flagella. Most species possess stron g ureolytic ability, particularly those associated with gastric mucosa, and exhibit wide diversity in cell morphology with respect to cell length, number and location of flagella, and presence of periplasmic fibrils. H. pylori earn a global distri entirelyion and infect human gastric mucosa exclusively but there is any(prenominal) evidence for transmission in cats.Genomes of isolates from unalike individuals are unusual in their diversity in gene order and sequences within individual genes. H. heilmannii1 is other gastric spiral shaped organism less frequently infecting humans but commonly found in cat and dog gastric tissue. H. felis is important in the mouse model of infection. A sphere of conventional phenotypic tests as well as almost new PCR based assays are available for identifying isolates of Helicobacter from clinical specimens. 11( http//bmb. oxfordjournals. org/content/54/1/17. full. pdf) Chemotherapeutic Methods of Control, Treatment, and EradicationTreatment If you are found to have Helicobacter pylori infection, you may wish to have antibiotic treatment of some kind. Treatment of Helicobacter pylori is usually simple nifty for hospital ward. However, occasional patients need repeated endoscopies, biopsies, breath tests and several courses of treatment with different antibiotic combinations. After treatment of H. pylori, it is necessary to repeat one of these tests to throw if the germ has been killed or eradicated for good. Only breath tests or endoscopy with biopsy can be used to prove that the bacterium has been eradicated.The blood tests *(serology) is not suitable to reminder H. pylori eradication because antibodies to H. pylori may remain positive for months or even geezerhood after successfully killing the H. pylori. 3 (http//www. helico. com/? q=TreatmentForHelicobacterPylori) Eradication Prolonging the treatment period is a possible stpacegy for improving H. pylori eradication rates. Several studies have been print that tes ted this approach, including this paper by Calvet et al. These authors canvass the value of extending PPI-based ternary therapy from 7 to 10 days and found no additional benefit for patients with peptic ulcerations.There was, however, a significant benefit for nonulcer dyspepsia patients (an increase from 66% to 77% in the intention-to-treat analysis and from 73% to 91% in the per-protocol analysis). The authors concluded that the treatment period should be extended from 7 to 10 days for patients with nonulcer dyspepsia. As most eradication therapy, however, is given to patients with uninvestigated dyspepsia, it is not unreasonable to argue that daylong therapy should be given to all subjects. Distinguishing between patients with ulcer and nonulcer dyspepsia is hence rather academic and impractical.The most obvious one is that existing PPI-based triple therapy regimens are not perfect. In the community at large, up to 30% of patients might fail this therapy. If clinicians presc ribe triple therapy it should therefore be order for longer than 7 days. This runs the assay of decreased patient compliance, more side effects and a greater cost, but ultimately it boils down to local anaesthetic and national guidelines, which vary from one country to another. Alternatively, clinicians might consider some of the newer eradication approaches, such as use of fluoroquinolone-based therapy or sequential treatment.The latter comprises quadruple therapy over a 10-day period, starting with a PPI plus amoxicillin (1,000 mg twice daily) for the first 5 days, followed by PPI plus clarithromycin (500 mg twice daily) and tinidazole (500 mg twice daily) for another 5 days. Intention-to-treat analysis eradication rates of 97%, 92%, and 94% have been reported in children, larges and elderly patients, respectively. Ultimately, clinicians should still strive towards a frequently simpler eradication strategy, but this will require investment in novel antibiotic find or a sepa rate understanding of the pathogenesis of H. ylori. Either way, there is much to be gained from continued interest in this little organism. 4(http//www. medscape. com/viewarticle/525100_2) Immunological Responses lifelong Helicobacter pylori infection and its associated gastric lighting underlie peptic ulceration and gastric carcinogenesis. The immune and inflammatory responses to H. pylori are doubly responsible gastric inflammation is the main mediator of pathology, and the immune and inflammatory response is ineffective, allowing lifelong bacterial persistence.However, despite inducing gastric inflammation, most infections do not cause disease, and bacterial, host and environmental factors determine individual disease risk. Although H. pylori avoid galore(postnominal) native immune receptors, specific virulence factors (including those encoded on the cag pathogenicity island) stimulate innate immunity to increase gastric inflammation and increase disease risk. An acquired T he lper 1 response up regulates local immune effectors. The tip to which environmental factors (including parasite infection), host factors and H. ylori itself influence T-helper differentiation and regulatory T-cell responses body controversial. Finally, effective vaccines have still not been developed a better understanding of the immune response to H. pylori may help. 5(http//www. ncbi. nlm. nih. gov/pubmed/17382275) Pathological Information Until the baring of Helicobacter in 1982, ulcers were thought to be caused by stress. Now it is known that ulcers, in addition to gastritis, are caused by a bacterial infection of H. pylori. though relatively easy to treat with antibiotics, H. ylori can be a risk factor for gastric crabby person if it becomes a long-term infection 6 ( give tongue to by D. J. Kelly, 2004. The University of Sheffield). The bodys natural defenses cannot combat H. pylori because white and killer T cells cannot easily receive by the stomach lining. The defense cells eventually die, spilling their superoxide radicals on stomach lining cells, on which H. pylori can feed6 (Stated by Helicobacter Foundation, 2004). Epidemiology Information The frequency of H pylori infection in the United States may be linked to race. discolour persons account for 29% of cases, and Hispanic persons account for 60% of cases.Internationally, H pylori are a ubiquitous organism. At least 50% of all mess are infected, but an film determination is not available, mostly because exact data are not available from developing countries. H pylori may be detected in approximately 90% of individuals with peptic ulcer disease however, less than 15% of infected persons may have this disease. The mortality rate related to H pylori infection is not precisely known, but it seems to be minimal (i. e. , approximately 2-4% of all infected people). Mortality is due to the complications of the infection, uch as gastric ulcer perforation or MALTomas of the GI tract. Otherwise, th e morbidity of H pylori infection can be very high. 7(http//emedicine. medscape. com/article/176938-overviewa0199) The pathogenetic role of H pylori may differ depending on geography and race. White persons are infected with H pylori less frequently than persons of other racial groups. The prevalence rate is approximately 20% in white persons, 54% in African American persons, and 60% in Hispanic persons. No sex supposition is known however, females have a higher incidence of reinfection (5-8%) than males.H pylori infection may be acquired at any age. According to some epidemiologic studies, this infection is acquired most frequently during childhood. Children and females have a higher incidence of reinfection (5-8%) than adult males. 7(http//emedicine. medscape. com/article/176938-overviewa0199) Cultural Characteristics Approximately two-thirds of the worlds population is infected with H. pylori. In the United States, H. pylori are more prevalent among older adults, African America ns, Hispanics, and dispirit socioeconomic groups. It is not known how H. ylori are transmitted or why some patients become symptomatic while others do not. The bacteria are most likely spread from person to person through fecal-oral or oral-oral routes. Possible environmental reservoirs include contaminated water sources. iatrogenic spread through contaminated endoscopes has been documented but can be prevented by proper cleaning of equipment. 8(Centers for disease and control prevention) Case meditate 1 Title Correlation of Helicobacter pylori and gastric carcinoma. Authors Khanna, AK, Seth, P, Nath, G, Dixit, V K, Kumar, M complete Date 26-Jan-2002Citation Khanna AK, Seth P, Nath G, Dixit VK, Kumar M. Correlation of Helicobacter pylori and gastric carcinoma. Journal of Postgraduate Medicine. 2002 Jan-Mar 48(1) 27-8 words Eng. Type Journal word Abstract BACKGROUND Difference of purview about the prevalence of H. pylori association with gastric cancer exists in the literature. AIMS To rent the correlation of Helicobacter pylori (H. pylori) to gastric carcinoma. METHODS 50 proved cases of gastric cancer were studied by fast urease test, culture, histopathology and ELISA test for H. pylori IgG.RESULTS 68% of cases of gastric cancer were found to be positive for H. pylori infection as compared to 74% of heavy controls. CONCLUSIONS The prevalence rate of H. pylori infection in our patients of gastric cancer was lower than in the control population though statistically not significant, suggesting that H. pylori may not be responsible for gastric carcinogenesis in this population. Source URI http//www. jpgmonline. com URI http//imsear. hellis. org/ time lag/123456789/116058 engage * Adult * Case-Control Studies * Enzyme-Linked Immunosorbent Assay * Female Helicobacter Infections complications * Helicobacter pylori isolation & shade * existence * Male * Middle Aged * Prevalence 9(http//imsear. hellis. org/ pass over/123456789/116058Stomach Neoplasms microb iology) Case write up 2 Title Helicobacter pylori in dental plaque of children and their family members. Authors Gill, H H, Shankaran, K, Desai, H G Issue Date 1-Sep-1994 Citation Gill HH, Shankaran K, Desai HG. Helicobacter pylori in dental plaque of children and their family members. Journal of the Association of Physicians of India. 1994 Sep 42(9) 719, 721 Language Eng.Type Journal Article Abstract A prospective study was undertaken to determine the presence of Helicobacter pylori in the dental plaque of children and their family members. 22 children (age range 2-12 years males 16) admitted to the pediatric ward for various disorders and 17 healthy family members (age range 7-40 years males 9) of 13 of these children were screened for presence of Helicobacter pylori in the dental plaque by the rapid urease test. H. pylori were detected in dental plaque of 82% (18/22) children and 88% (15/17) of family members.In 85% (28/33) of the positive cases the rapid urease test was positiv e within 1 hour. Our observations indicate that Helicobacter pylori are present in the dental plaque of majority of children and their family members. Source URI http//www. japi. org URI http//imsear. hellis. org/clutch/123456789/95238 MeSH * Child * Child, Preschool * Dental Plaque microbiology * Family Health * Female * Helicobacter pylori isolation & purification * Humans * Male * Prospective Studies Appears in Collections Journal of the Association of Physicians of India 10(http//imsear. ellis. org/handle/123456789/95238) Conclusion The author covered morphological characteristics, taxonomic information, biochemical/metabolic characteristics, chemotherapeutic methods of control/treatment/eradication, immunological responses, pathological information, and epidemiology in this paper. The whelm conclusion is that it is critical to survival of the human race that hygiene and procreation will be the best possible steps to overcome an change magnitude body of bacteria in our world. References 1. From Wikipedia, the free encyclopedia 2. http//www. gastro. theclinics. om/article/S0889-8553(05)70135-7/abstract) 3. http//www. helico. com/? q=TreatmentForHelicobacterPylori 4. http//www. medscape. com/viewarticle/525100_2 5. http//www. ncbi. nlm. nih. gov/pubmed/17382275 6. Stated by D. J. Kelly, 2004. The University of Sheffield 7. http//emedicine. medscape. com/article/176938-overviewa0199 8. Centers for disease and control prevention 9. http//imsear. hellis. org/handle/123456789/116058Stomach Neoplasms microbiology 10. http//imsear. hellis. org/handle/123456789/95238 11. http//bmb. oxfordjournals. org/content/54/1/17. full. pdf