The GroES homolog of Helicobacter pylori confers protective immunity against mucosal infection in mice.

Helicobacter pylori is an important etiologic agent of gastroduodenal disease. In common with other organisms, H. pylori bacteria express heat shock proteins that share homologies with the GroES-GroEL class of proteins from Escherichia coli. We have assessed the heat shock proteins of H. pylori as potential protective antigens in a murine model of gastric Helicobacter infection. Orogastric immunization of mice with recombinant H. pylori GroES- and GroEL-like proteins protected 80% (n = 20) and 70% (n = 10) of animals, respectively, from a challenge dose of 10(4) Helicobacter felis bacteria (compared to control mice, P = 0.0042 and P = 0.0904, respectively). All mice (n = 19) that were immunized with a dual antigen preparation, consisting of H. pylori GroES-like protein and the B subunit of H. pylori urease, were protected against infection. This represented a level of protection equivalent to that provided by a sonicated Helicobacter extract (P = 0.955). Antibodies directed against the recombinant H. pylori antigens were predominantly of the IgG1 class, suggesting that a type 2 T-helper cell response was involved in protection. This work reports a protein belonging to the GroES class of heat shock proteins that was shown to induce protective immunity. In conclusion, GroES-like and urease B-subunit proteins have been identified as potential components of a future H. pylori subunit vaccine.

Identification and characterization of periplasmic proteins implicated in the adaptation of Helicobacter pylori to the human gastric niche

Helicobacter pylori �� un batterio Gram-negativo in grado di colonizzare la mucosa gastrica umana e persistere per l'intero arco della vita dell'ospite. E' associato a patologie gastrointestinali, quali gastrite cronica, ulcere gastriche e duodenali, adenocarcinomi e linfomi gastrici. Si tratta di uno dei patogeni pi�� diffusi, presente in circa met�� della popolazione mondiale, e il solo che si �� adattato a vivere nell'ambiente ostile dello stomaco umano. Molteplici sono i fattori di virulenza che permettono al batterio la colonizzazione della nicchia gastrica e contribuiscono, anche attraverso l' induzione di una risposta infiammatoria, a profonde modificazioni dell' omeostasi gastrica. Queste ultime si associano, ad esempio, all'iperproduzione di fattori proinfiammatori, ad alterazioni sia della regolazione della secrezione acida gastrica sia del ciclo cellulare e della morte cellulare programmata (apoptosi) delle cellule epiteliali gastriche, a disordini nel metabolismo del ferro e a carenze di elementi essenziali. Studi sulla diversit�� genetica di H. pylori osservata in ceppi isolati da varie regioni del mondo, dimostrano che tale batterio ha avuto una coevoluzione col genere umano attraverso la storia, ed �� verosimile che H. pylori sia stato un costituente del microbiota gastrico per almeno 50.000 anni. Scopo della tesi �� stato quello di identificare e caratterizzare proteine importanti per la colonizzazione e l'adattamento di H. pylori alla nicchia gastrica. In particolare gli sforzi si sono concentrati su due proteine periplasmatiche, la prima coinvolta nella difesa antiossidante (l'enzima catalasi-like, HP0485), e la seconda nel trasporto di nutrienti presenti nell'ambiente dello stomaco all'interno della cellula (la componente solubile di un ABC transporter, HP0298). La strategia utilizzata prevede un'analisi bioinformatica preliminare, l'ottenimento del gene per amplificazione, mediante PCR, dal genoma dell'organismo, la costruzione di un vettore per il clonaggio, l'espressione eterologa in E. coli e la successiva purificazione. La proteina cos�� ottenuta viene caratterizzata mediante diverse tecniche, quali spettroscopia UV, dicroismo circolare, gel filtrazione analitica, spettrometria di massa. Il capitolo 1 contiene un'introduzione generale sul batterio, il capitolo 2 e il capitolo 3 descrivono gli studi relativi alle due proteine e sono entrambi suddivisi in un abstract iniziale, un'introduzione, la presentazione dei risultati, la discussione di questi ultimi, i materiali e i metodi utilizzati. La catalasi-like (HP0485) �� una proteina periplasmatica con struttura monomerica, appartenente ad una famiglia di enzimi a funzione per la maggior parte sconosciuta, ma evolutivamente correlati alla ben nota catalasi, attore fondamentale nella difesa di H. pylori, grazie alla sua azione specifica di rimozione dell'acqua ossigenata. HP0485, pur conservando il fold catalasico e il legame al cofattore eme, non pu�� compiere la reazione di dismutazione dell'acqua ossigenata; possiede invece un'attivit�� perossidasica ad ampio spettro, essendo in grado di accoppiare la riduzione del perossido di idrogeno all'ossidazione di diversi substrati. Come la catalasi, lavora ad alte concentrazioni di aqua ossigenata e non arriva a saturazione a concentrazioni molto elevate di questo substrato (200 mM); la velocit�� di reazione catalizzata rimane lineare anche a questi valori, aspetto che la differenzia dalle perossidasi che vengono in genere inattivate da concentrazioni di perossido di idrogeno superiori a 10-50 mM. Queste caratteristiche di versatilit�� e robustezza suggeriscono che la catalasi-like abbia un ruolo di scavenger dell'acqua ossigenata e probabilmente anche un'altra funzione connessa al suo secondo substrato, ossia l'ossidazione di composti nello spazio periplasmatico cellulare. Oltre alla caratterizzazione dell'attivit�� �� descritta anche la presenza di un ponte disolfuro, conservato nelle catalasi-like periplasmatiche, con un ruolo nell'assemblaggio dell'eme per ottenere un enzima attivo e funzionale. La proteina periplasmatica HP0298, componente di un sistema di trasporto ABC, �� classificata come trasportatore di dipeptidi e appartiene a una famiglia di proteine in grado di legare diversi substrati, tra cui di- e oligopeptidi, nichel, eme, glutatione. Bench�� tutte associate a trasportatori di membrana batterici, queste proteine presentano un dominio di legame al substrato che risulta essere conservato nei domini extracellulari di recettori specifici di mammifero e uomo. Un esempio sono i recettori ionotropici e metabotropici del sistema nervoso. Per caratterizzare questa proteina �� stato messo a punto un protocollo di ligand-fishing accoppiato alla spettrometria di massa. La proteina purificata, avente un tag di istidine, �� stata incubata con un estratto cellulare di H. pylori per poter interagire con il suo substrato specifico all'interno dell'ambiente naturale in cui avviene il legame. Il complesso proteina-ligando �� stato poi purificato per cromatografia di affinit�� e analizzato mediante HPLC-MS. L'identificazione dei picchi differenziali tra campioni con la proteina e 5 campioni di controllo ha portato alla caratterizzazione di pentapeptidi particolarmente ricchi in aminoacidi idrofobici e con almeno un residuo carico negativamente. Considerando che H. pylori necessita di alcuni aminoacidi essenziali, per la maggior parte idrofobici, e che lo stomaco umano �� particolarmente ricco di peptidi prodotti dalla digestione delle proteine introdotte con il cibo, il ruolo fisiologico di HP0298 potrebbe essere l'internalizzazione di peptidi, con caratteristiche specifiche di lunghezza e composizione, che sono naturalmente presenti nella nicchia gastrica.

Recurrence of Helicobacter pylori infection in adults with intellectual disability

Although Helicobacter pylori infection is very common among particular groups of adults with intellectual disability, the rate of recurrence (reinfection or recrudescence) is unknown in this population. Thirty-six months after successful treatment of H. pylori, 28 adults with intellectual disability were retested using the faecal antigen test. Six (21%) of 28 patients tested positive, giving an approximate yearly recurrence rate of 7%, a rate considerably higher than that in the general popu-lation (

Effects of Helicobacter pylori eradication among adults with intellectual disability

Background Compared to the general population, Helicobacter pylori infection is more common among adults with intellectual disability (ID) and is associated with greater levels of disability, maladaptive behaviour, and institutionalization. Little information exists about the effects of eradication therapy in this group, so we aimed to evaluate: (1) success of a standard H. pylori eradication protocol; (2) frequency of side-effects; and (3) impact of eradication on level of functional ability and maladaptive behaviour. Method A cohort of adults with ID underwent assessment of their levels of function and maladaptive behaviour, medical history, physical examination, and H. pylori testing using serology and faecal antigen tests. Some received standard H. pylori eradication therapy. Twelve months later, participants underwent repeat assessment, were grouped by change in H. pylori status and compared. Results Of 168 participants, 117 (70%) were currently infected with H. pylori at baseline, and 96 (82%) of the 117 were given standard H. pylori eradication therapy. The overall eradication rate was 61% but 31% reported side-effects. Institutional status of the participants, their level of behaviour or function, and number of comorbid medical conditions were not associated with failure of eradication. There were no statistically significant differences in level of behaviour or function, ferritin, or weight between the groups in whom H. pylori was eradicated or stayed positive. Conclusion Adults with ID have lower H. pylori eradication and higher side-effect rates than the general population. Levels of maladaptive behaviour and disability did not improve with eradication and thus greater levels of maladaptive behaviour or disability appear to be risk factors for, rather than consequences of, H. pylori infection.

Stool antigen testing for the diagnosis and confirmation of eradication of Helicobacter pylori infection

No Abstract

Drug delivery strategies for the treatment of Helicobacter pylori infections

Helicobacter pylori is one of the most common pathogenic bacterial infections, colonising an estimated half of all humans. It is associated with the development of serious gastroduodenal disease - including peptic ulcers, gastric lymphoma and acute chronic gastritis. Current recommended regimes are not wholly effective and patient compliance, side-effects and bacterial resistance can be problematic. Drug delivery to the site of residence in the gastric mucosa may improve efficacy of the current and emerging treatments. Gastric retentive delivery systems potentially allow increased penetration of the mucus layer and therefore increased drug concentration at the site of action. Proposed gastric retentive systems for the enhancement of local drug delivery include floating systems, expandable or swellable systems and bioadhesive systems. Generally, problems with these formulations are lack of specificity, limited to mucus turnover or failure to persist in the stomach. Gastric mucoadhesive systems are hailed as a promising technology to address this issue, penetrating the mucus layer and prolonging activity at the mucus-epithelial interface. This review appraises gastroretentive delivery strategies specifically with regard to their application as a delivery system to target Helicobacter. As drug-resistant strains emerge, the development of a vaccine to eradicate and prevent reinfection is an attractive proposition. Proposed prophylactic and therapeutic vaccines have been delivered using a number of mucosal routes using viral and non-viral vectors. The delivery form, inclusion of adjuvants, and delivery regime will influence the immune response generated. �� 2005 Bentham Science Publishers Ltd.

Apoptosis induction in gastric mucous cells in vitro:lesser potency of Helicobacter pylori than Escherichia coli lipopolysaccharide, but positive interaction with ibuprofen

Non-steroidal anti-inflammatory drugs (NSAIDs) cause peptic ulcer disease, but whether they interact with Helicobacter pylori to promote damage is controversial. Moreover, the reported induction of apoptosis in gastric cells by H. pylori lipopolysaccharide (LPS) (10-9 g /ml) contrasts with studies showing low immunological potency of this LPS. Therefore, the effects of LPS from H. pylori NCTC 11637 and Escherichia coli 0111:B4 on apoptosis in a primary culture of guinea-pig gastric mucous cells were investigated in the presence and absence of the NSAID, ibuprofen. Cell loss was estimated by a crystal violet assay, and apoptosis determined from caspase activity and from condensation and fragmentation of nuclei. Exposure to E. coli LPS for 24 h caused cell loss and enhanced apoptotic activity at concentrations ��� 10-9 g/ml, but similar effects were only obtained with H. pylori LPS at concentrations ���10-6 g/ml. Although ibuprofen (250 ��M) caused cell loss and apoptosis, addition of either E. coli or H. pylori LPSs further enhanced these effects. In conclusion, LPS and ibuprofen interact to enhance gastric cell loss and apoptosis. In such interactions, E. coli LPS is more potent than that of H. pylori. The low potency of H. pylori LPS may contribute to a chronic low-grade gastritis that can be enhanced by the use of NSAIDs. �� W. S. Maney & Son Ltd.

{\it Helicobacter pylori\/}: An infectious consideration when screening patients with complaints of dyspepsia

Historically, abdominal complaints have been generally dealt with palliatively. Seldom were underlying causes given consideration. However, in 1982 (Warren & Marshall, 1983), the identification of the bacterial agent Helicobacter pylori (known hereafter in this paper as H. pylori) as a potential link between gastrointestinal complaints such as gastric and duodenal ulcers, Crohn's Disease, and some forms of gastric cancer has given rise for concern. In 1994, the National Institute for Health recommended that patients with complaints of dyspepsia be studied for the occurrence of H. pylori. This study proposes to study the occurrence of H. pylori in patients who complain with dyspepsia with a relatively non invasive screening technique to be done in an office setting. The study findings were considered signifcant if p $\le$.05. This study indicated that 49% of patients with complaints of dyspepsia were postive for H. pylori infection with p =.000. ^

Avalia����o da atividade anti-Helicobacter pylori e citot��xica in vitro de extratos org��nicos obtidos das folhas de Encholirium spectabile e Syzygium cumini

Helicobacter pylori is a spiral, Gram negative, mobile, and microaerophilic bacteria recognized as a major cause of gastritis, ulcer, gastric cancer, and gastric low grade, B cell, mucosa ��� associated lymphoid tissue (MALT) lymphoma, constituting an important microorganism in medical microbiology. Its importance comes from the difficulty of treatment because the requirement of multiple drugs use, besides the increasing emergence of resistant and multiresistant strains to antibiotics used in th e clinic. In order to expand safe and effective therapeutic options , chemical studies on medicinal plants by obtaining extracts, fractions, isolated compounds or essential oils with some biological activity has been intensified . Given the above, the objective was to evaluate the inhi bitory activity of organic extracts derived from Syzygium cumini and Encholirium spectabile, with antiulcer history, and the essential oil, obtained from S. cumini, against H. pylori (ATCC 43504) by the disk diffusion method, for qualitative evaluation, an d determination of minimum inhibitory concentration (MIC) using the broth microdilution method, for quantitative analysis. Also was evaluated the extracts in vitro toxicity by a hemolytic assay using sheep red blood cells, and VERO and HeLa cells using the MTT assay to analyze cell viability. The extracts of both plant used in antimicrobial assays did not inhibit bacterial growth, however the essential oil of S. cumini (SCFO) proved effective, showing MIC value of 205 ��g/mL (0.024 % dilution of the original oil). In the hemolytic assay, the same oil shows moderate toxicity, by promote 25% hemolysis at 1000 ��g/mL. Regarding the cytotoxicity in cell culture, the SCFO, at 260 ��g/mL, affected the cell viability around 80% of HeLa and 50% of VERO cells. So the oi l obtained from S. cumini leaves has antimicrobial activity against H. pylori and cytotoxicity potential, suggesting a source of new molecule drug candidates, since new stages of toxicity in vitro and in vivo, as well, chemical characterization be evaluate d. Moreover, the development of a prospective drug delivery system can result in a prototype to be used in preclinical tests.

Prevalence of helicobacter pylori infection in advanced gastric carcinoma

There is substantial evidence that infection with Helicobacter pylori plays a role in the development of gastric cancer and that it is rarely found in gastric biopsy of atrophic gastritis and gastric cancer. On advanced gastric tumors, the bacteria can be lost from the stomach. Aims - To analyze the hypothesis that the prevalence of H.pylori in operated advanced gastric carcinomas and adjacent non-tumor tissues is high, comparing intestinal and diffuse tumors according to Lauren���s classifi cation. Methods - A prospective controlled study enrolled 56 patients from ���Hospital Universit��rio���, Federal University of Rio Grande do Norte, Natal, RN, Brazil, with advanced gastric cancer, treated from February 2000 to March 2003. Immediately after partial gastrectomy, the resected stomach was opened and several mucosal biopsy samples were taken from the gastric tumor and from the adjacent mucosa within 4 cm distance from the tumor margin. Tissue sections were stained with hematoxylin and eosin. Lauren���s classifi cation for gastric cancer was used, to analyse the prevalence of H. pylori in intestinal or diffuse carcinomas assessed by the urease rapid test, IgG by ELISA and Giemsa staining. H. pylori infected patients were treated with omeprazole, clarithromycin and amoxicillin for 7 days. Follow-up endoscopy and serology were performed 6 months after treatment to determine successful eradication of H. pylori in non-tumor tissue. Thereafter, follow-up endoscopies were scheduled annually. Chi-square and MacNemar tests with 0.05 signifi cance were used. Results - Thirty-four tumors (60.7%) were intestinal-type and 22 (39.3%) diffuse type carcinomas. In adjacent non-tumor gastric mucosa, chronic gastritis were found in 53 cases (94.6%) and atrophic mucosa in 36 patients (64.3%). All the patients with atrophic mucosa were H. pylori positive. When examined by Giemsa and urease test, H. pylori positive rate in tumor tissue of intestinal type carcinomas was higher than that in diffuse carcinomas. In tumor tissues, 34 (60.7%) H. pylori-positive in gastric carcinomas were detected by Giemsa method. H. pylori was observed in 30 of 56 cases (53.5%) in tissues 4 cm adjacent to tumors. This difference was not signifi cant. Eradication of H. pylori in non-tumor tissue of gastric remnant led to a complete negativity on the 12th postoperative month. Conclusions - The data confi rmed the hypothesis of a high prevalence of H. pylori in tumor tissue of gastric advanced carcinomas and in adjacent non-tumor mucosa of operated stomachs. The presence of H. pylori was predominant in the intestinal-type carcinoma

Novel inhibitors of the tRNA-dependent amidotransferase of "Helicobacter pylori": Peptides generated by phage display and dipeptide-like compounds

Cette th��se pr��sente la d��couverte de nouveaux inhibiteurs de l���amidotransf��rase ARNt-d��pendante (AdT), et r��sume les connaissances r��centes sur la biosynth��se du Gln-ARNtGln et de l���Asn-ARNtAsn par la voie indirecte chez la bact��rie Helicobacter pylori. Dans le cytoplasme des eucaryotes, vingt acides amin��s sont li��s �� leur ARNt correspondant par vingt aminoacyl-ARNt synth��tases (aaRSs). Ces enzymes sont tr��s sp��cifiques, et leur fonction est importante pour le d��codage correct du code g��n��tique. Cependant, la plupart des bact��ries, dont H. pylori, sont d��pourvues d���asparaginyl-ARNt synth��tase et/ou de glutaminyl-ARNt synth��tase. Pour former le Gln-ARNtGln, H. pylori utilise une GluRS noncanonique nomm��e GluRS2 qui glutamyle sp��cifiquement l���ARNtGln ; ensuite, une AdT trim��rique, la GatCAB corrige le Glu-ARNtGln m��sappari�� en le transamidant pour former le Gln-ARNtGln, qui lira correctement les codons glutamine pendant la biosynth��se des prot��ines sur les ribosomes. La formation de l���Asn-ARNtAsn est similaire �� celle du Gln-ARNtGln, et utilise la m��me GatCAB et une AspRS non-discriminatrice. Depuis des ann��es 2000, la GatCAB est consid��r��e comme une cible prometteuse pour le d��veloppement de nouveaux antibiotiques, puisqu���elle est absente du cytoplasme de l�����tre humain, et qu���elle est encod��e dans le g��nome de plusieurs bact��ries pathog��nes. Dans le chapitre 3, nous pr��sentons la d��couverte par la technique du �� phage display �� de peptides cycliques riches en tryptophane et en proline, et qui inhibent l���activit�� de la GatCAB de H. pylori. Les peptides P10 (CMPVWKPDC) et P9 (CSAHNWPNC) inhibent cette enzyme de fa��on comp��titive par rapport au substrat Glu-ARNtGln. Leur constante d���inhibition (Ki) est 126 ��M pour P10, et 392 ��M pour P9. Des mod��les mol��culaires ont montr�� qu���ils lient le site actif de la r��action de transmidation catalys��e par la GatCAB, gr��ce �� la formation d���une interaction ��-�� entre le r��sidu Trp de ces peptides et le r��sidu Tyr81 de la sous-unit�� GatB, comme fait le A76 3���-terminal de l���ARNt. Dans une autre ��tude concernant des petits compos��s contenant un groupe sulfone, et qui mimiquent l���interm��diaire de la r��action de transamidation, nous avons identifi�� des compos��s qui inhibent la GatCAB de H. pylori de fa��on comp��titive par rapport au substrat Glu-ARNtGln. Cinq fois plus petits que les peptides cycliques mentionn��s plus haut, ces compos��s inhibent l���activit�� de la GatCAB avec des Ki de 139 ��M pour le compos�� 7, et de 214 ��M pour le compos�� 4. Ces inhibiteurs de GatCAB pourraient ��tre utiles pour des ��tudes m��canistiques, et pourraient ��tre des mol��cules de base pour le d��veloppement de nouvelles classes d���antibiotiques contre des infections caus��es par H. pylori.

Prevalencia de Helicobacter Pylori mediante determinaci��n serol��gica y factores de riesgo asociados en escolares del cant��n Cuenca, 2003-2004

El estudio tiene el objetivo de determinar la prevalencia de Helicobacter Pylori y factores de riesgo asociados en ni��os en edad escolar del ��rea urbana del cant��n Cuenca. Resultados: la prevalencia de Helicobacter Pylori en escolares del ��rea urbana del cant��n Cuenca fue de 14.3: los factores de riesgo asociados a la infecci��n que reflejaron significancia estad��stica fueron edad RP 1.79. (IC 1.10-2.87, P o.41); anafalbetismo de los padres RP 2.49, (ICI. 23-5. 03. P 0.017); no practicar el lavado de manos RP 63.40, (IC 15.71-255.84, P 0.000); no lavar los alimentos RP 9.88, (IC 5,43-17.97, P 0.000); compartir la cama RP 2.23, (IC 1,33-3.73, P 0.00); no disponer de servicio higi��nico RP 5.11, (IC 3.01-8.66, P 0.000) y no consumir agua potable RP 4.79, (IC 2.96-7.74, P 0.000). Tambi��n se encontr�� asociaci��n con dolor abdominal recurrente RP 3.48, (IC 2.03-5.96, P 0.0000) Los factores de riesgo que no se asociaron a infecci��n fueron g��nero RP 1.36, (IC 0.82-2.24, P 0.224) y ocupaci��n manual de los padres RP 1.21, (IC 0.54-2.68, P 0.626). Los signos y s��ntomas que no estuvieron asociados con la presencia de Helicobacter Pylori fueron na��sea y v��mito RP 0.87, (IC 0.13-5.56, P 0.886); sensaci��n de llenura RP 1.70, (IC 0.87-3.30, P 0.127) y pirosis RP 2.24, (IC 0.95-5.27, P 0.083). Conclusiones: 1. La prevalencia de Helicobacter Pylori en escolares del ��rea urbana del cant��n Cuenca 2003-2004 fue 14.3. 2. La prevalencia de Helicobacter Pylori es directamente proporcional con la edad. 3. La falta de aplicaci��n de las normas b��sicas de higiene incrementa el riesgo de infecci��n. 4. Las condiciones sanitarias desfavorables son un determinante para la mayor prevalencia de infecci��n. 5. En la mayor��a de escolares, la infecci��n no curs�� con sintomatolog��a cl��nica. 6. Dolor abdominal recurrente fue la manifestaci��n cl��nica m��s importante en ni��os sintom��ticos infectados

Helicobacter pylori en patolog��a gastroduodenal detecci��n por cultivo y tratamiento doble acortado

Estudio cl��nico descriptivo con una muestra de 100 pacientes con s��ntomas digestvos y sometidos a endoscop��a, para obtener muestras de biopsia g��strica y realizar cultivo de Helico-bacter Pylori, prueba de la ureasa y tinci��n de Gram, 59 pacientes resultaron H. Pylori positivo al cultivo, siendo asignados al azar en dos grupos de tratamiento. El primer grupo recibi�� cimetidina a una dosis de 800 mgs. tres veces al d��a por un per��odo acortado de 7 d��as (grupo tratado). El segundo grupo (grupo control) recibi�� cimetidina a la dosis de 800 mgs. diarios durante un mes. A las 4 semanas posteriores al tratamiento se realiz�� control endosc��pico e histopatol��gico excluy��ndose del estudio 23 pacientes que no se sometieron al control. De los 36 pacientes objeto del estudio se obtuvo los siguients resultados: se erradic�� el H. Pylori en el 71.43del grupo tratado y en el 40del grupo control p 0.05. Los s��ntomas en los dos grupos no presentaron diferencias significativas. Hubo mejor��a endosc��pica e histopatol��gica en el grupo tratado con diferencia significativa (p menor que 0.001) en comparaci��n con el grupo control. Se realiza comparaciones con series citadas en la literatura y se realizan las recomendaciones pertinentes

Prevalencia de Helicobacter Pylori por ant��geno fecal y factores de riesgo en la poblaci��n del cant��n Cuenca.A��o 2003

El conocimiento de la prevalencia del helicobacter en la poblaci��n y los factores de riesgo para controlar la enfermedad son importantes, para su control y erradicaci��n. Conocer la prevalencia de la bacteria en la poblaci��n, urbana y rural de la ciudad de Cuenca; y determinar si hay factores de riesgo que favorezcan la propagaci��n de la infecci��n. La prevalencia del Helicobacter en la ciudad de Cuenca - Ecuador, es de 44.9 por ciento, no hay diferencia estad��sticamente significativas entre los habitantes del sector urbano 48.3 por ciento y rural 41.6 por ciento, las variables: residencia, [RP; 0.86] g��nero, actividad manual, [RP; 0.98 IC: 0.82-1.24] ingesta de agua potable, [RP; 0.99 IC: 0.68-1.48], no se relacionan con la presencia del ant��geno de Helicobacter en materia fecal, por lo que no constituyen un factor de riesgo para contraer la infecci��n, la viariable edad, correlaciona positivamente con la prevalencia de la infecci��n. 1.- La prevalencia del Helicobacter Pylori en el cant��n Cuenca-Ecuador, en el a��o 2003, es del 44.9 por ciento que le ubica como una zona de prevalencia intermedia, menor a la esperada en un pa��s en v��as de desarrollo. 2.- No hay diferencias entre habitar en zona urbana y rural para prevalencia del Helicobacter Pylori 4.- La mayor parte de infecci��n por Helicobacter Pylori, se adquiere en la infancia 5.- Las variables g��nero, ingesta de agua potable, ocupaci��n manual, no son factores de riesgo para contraer la infecci��n