scholarly journals Helicobacter pylori cag pathogenicity island genotype diversity within the gastric niche of a single host

2007 ◽  
Vol 56 (5) ◽  
pp. 664-669 ◽  
Author(s):  
Mario José Matteo ◽  
Gabriela Granados ◽  
Cecilia Valeria Pérez ◽  
Martín Olmos ◽  
Cristian Sanchez ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Presentation ◽  
Random Amplified Polymorphic Dna ◽  
Positive Culture ◽  
Pathogenicity Island ◽  
Empty Site ◽  
Multiple Biopsies ◽  
Single Host ◽  
Dna Pcr ◽  
Positive Half

cag pathogenicity island (PAI) integrity was investigated in isolates from multiple biopsies recovered from 40 patients in an attempt to determine the co-existence of a varying cagPAI-positive to cagPAI-negative ratio in a single host. Six biopsies were obtained from each patient during the same endoscopic session. cagPAI analysis included amplification of seven loci (cagA, cagE, cagG, cagM, cagT, HP0527 and HP0524) and the left end of cagII (LEC). Absence of the island was confirmed by empty-site PCR. lspA-glmM RFLP and random amplified polymorphic DNA PCR were used for strain delineation. The number of biopsies with Helicobacter pylori-positive culture ranged from three to six per patient and a total of 218 isolates were recovered. Mixed infection was only found in two patients. Nearly one-third of the 40 patients harboured isolates with an intact cagPAI in all niches, another third of the isolates were empty-site-positive in all niches, whilst the remaining third of the isolates had a disrupted cagPAI in all or at least one of the niches. Co-existence of variants of the same strain with different cagPAI genotypes was observed in one-quarter of patients. The variations in cagPAI genotype included co-existence of: diverse cagPAI deletions in different niches, variants with intact and with partially deleted islands, variants with empty-site-positive and with partially deleted cagPAIs, and variants with an intact cagPAI and with empty-site-positive. Half of the patients with different cagPAI genotypes harboured an intact cagPAI in at least one niche. Co-existence of diverse genotypes of putative virulence factors in a single host must be considered when drawing a correlation with clinical presentation.

scholarly journals Implication of the Structure of the Helicobacter pylori cag Pathogenicity Island in Induction of Interleukin-8 Secretion

2001 ◽  
Vol 69 (3) ◽  
pp. 1625-1629 ◽  
Author(s):  
C. Audibert ◽  
C. Burucoa ◽  
B. Janvier ◽  
J. L. Fauchère
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Presentation ◽  
Blot Hybridization ◽  
Pathogenicity Island ◽  
Interleukin 8 ◽  
Middle Region ◽  
Dot Blot ◽  
Long Distance ◽  
H Pylori

ABSTRACT Helicobacter pylori virulence is associated with the presence of the cag pathogenicity island (PAI). Thecag PAI is involved in the ability to induce interleukin-8 (IL-8) secretion by human cells, which is implicated in the inflammatory response of the gastric mucosa to H. pyloriinfection. The aim of this study was to determine whether the genetic structure of the cag PAI is conserved and whether it is linked to IL-8 induction ability. Detection of specific markers (cagA, picB, cag13-cag14, virD4, and IS605) by PCR and dot blot hybridization and long-distance PCR determination of the presence of cagI, cagII, and the middle region of thecag PAI were performed on 153 strains isolated from adults suffering from ulcers (n = 79) or gastritis (n = 74). IL-8 induction ability was evaluated by coculture of the strains with HEp-2 cells. Eighty-three strains (54.3%) had an entire cag PAI, 12 strains (7.8%) had thecag PAI split in two, 49 strains (32%) had nocag PAI, and 9 strains exhibited other structural combinations. The presence of an entire cag PAI was statistically correlated with the presence of IS605(P = 0.006) and the ability to induce IL-8 secretion but not with clinical presentation of the infection. The structure of the cag PAI appears to be rather conserved and is related to the proinflammatory power of a strain. The existence of strains inducing IL-8 secretion regardless of the cag PAI structure suggests that this region is not the only requirement for IL-8 secretion.

scholarly journals Genetic Analysis of Helicobacter pylori Strain Populations Colonizing the Stomach at Different Times Postinfection

2007 ◽  
Vol 189 (10) ◽  
pp. 3834-3845 ◽  
Author(s):  
Nina R. Salama ◽  
Gerardo Gonzalez-Valencia ◽  
Brooke Deatherage ◽  
Francisco Aviles-Jimenez ◽  
John C. Atherton ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Genetic Divergence ◽  
Random Amplified Polymorphic Dna ◽  
Genetic Exchange ◽  
Comparative Genomic ◽  
New Host ◽  
Genetic Changes ◽  
Individual Host ◽  
Single Host ◽  
The One

ABSTRACT Genetic diversity of the human gastric pathogen Helicobacter pylori in an individual host has been observed; whether this diversity represents diversification of a founding strain or a mixed infection with distinct strain populations is not clear. To examine this issue, we analyzed multiple single-colony isolates from two to four separate stomach biopsies of eight adult and four pediatric patients from a high-incidence Mexican population. Eleven of the 12 patients contained isolates with identical random amplified polymorphic DNA, amplified fragment length polymorphism, and vacA allele molecular footprints, whereas a single adult patient had two distinct profiles. Comparative genomic hybridization using whole-genome microarrays (array CGH) revealed variation in 24 to 67 genes in isolates from patients with similar molecular footprints. The one patient with distinct profiles contained two strain populations differing at 113 gene loci, including the cag pathogenicity island virulence genes. The two strain populations in this single host had different spatial distributions in the stomach and exhibited very limited genetic exchange. The total genetic divergence and pairwise genetic divergence between isolates from adults and isolates from children were not statistically different. We also analyzed isolates obtained 15 and 90 days after experimental infection of humans and found no evidence of genetic divergence, indicating that transmission to a new host does not induce rapid genetic changes in the bacterial population in the human stomach. Our data suggest that humans are infected with a population of closely related strains that vary at a small number of gene loci, that this population of strains may already be present when an infection is acquired, and that even during superinfection genetic exchange among distinct strains is rare.

scholarly journals Helicobacter pylori oipA, vacA and dupA genetic diversity in individual hosts

2010 ◽  
Vol 59 (1) ◽  
pp. 89-95 ◽  
Author(s):  
Mario José Matteo ◽  
Rita Inés Armitano ◽  
Gabriela Granados ◽  
Andrés Dario Wonaga ◽  
Christian Sánches ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Helicobacter Pylori ◽  
Sequence Analysis ◽  
Dna Sequence ◽  
Mixed Infection ◽  
Chronic Infection ◽  
Multiple Biopsies ◽  
Single Host ◽  
Expression Status

Helicobacter pylori putative virulence factors can undergo a continuously evolving mechanism as an approach to bacterial adaptation to the host changing environment during chronic infection. oipA, vacA and dupA genetic diversity among isolates from multiple biopsies (niches) from the antrum and corpus of 40 patients was investigated. A set of 229 isolates was examined. Direct DNA sequence analysis of amplified fragments was used to study oipA ‘on/off’ expression status as well as the presence of C or T insertion in jhp0917 that originates a continuous (jhp0917–jhp0918) dupA gene. vacA alleles were identified by multiplex PCR. Different inter-niches oipA CT repeat patterns were observed in nine patients; in six of these, ‘on’ and ‘off’ mixed patterns were found. In three of these nine patients, different vacA alleles were also observed in a single host. Inter-niche dupA differences involved the absence and presence of jhp0917 and/or jhp0918 or mutations in dupA, including those that may originate a non-functional gene, and they were also present in two patients with mixed oipA CT patterns and in another seven patients. Evidence of mixed infection was observed in two patients only. In conclusion, oipA and dupA genes showed similar inter-niche variability, occurring in approximately 1/4 patients. Conversely, vacA allele microevolution seemed to be a less common event, occurring in approximately 1/10 patients, probably due to the mechanism that this gene evolves ‘in vivo’.

Clinical presentation in relation to diversity within the Helicobacter pylori cag pathogenicity island

2002 ◽  
Vol 97 (9) ◽  
pp. 2231-2238 ◽  
Author(s):  
Ping-I. Hsu ◽  
Il-ran Hwang ◽  
Diana Cittelly ◽  
Kwok-Hung Lai ◽  
Hala M.T. El-Zimaity ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Presentation ◽  
Pathogenicity Island ◽  
Cag Pathogenicity Island

scholarly journals The organization of Helicobacter pylori cag-pathogenicity island (cagPAI) genes in multiracial population with histopathological changes of gastric mucosa

2019 ◽  
Author(s):  
Alfizah Hanafiah ◽  
Shaza Azlin Razak ◽  
Hui-min Neoh ◽  
Noraziah Mohamad Zin ◽  
Bruno S. Lopes
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Pathogenicity Island ◽  
Type Iv Secretion ◽  
Virulence Determinants ◽  
Gastric Diseases ◽  
Cag Pathogenicity Island ◽  
Type Iv ◽  
Inflammatory Score ◽  
H Pylori

Abstract Background: Helicobacter pylori is a Gram-negative bacillus that colonises only the mucus layer of the human stomach and is implicated in gastric diseases. Virulent H. pylori harbouring cag-pathogenicity island (cagPAI) which encodes genes for type IV secretion system (T4SS) and CagA protein is one of the major virulence determinants involved in disease development. We examined the entire cagPAI genes in 95 H. pylori isolates from a multiracial population and examined the intactness of cagPAI region with histopathological scores of the gastric mucosa. Results: 95.8% of H. pylori isolates were cagPAI-positive with 23.2% having an intact cagPAI, whereas 72.6% had a partial/rearranged cagPAI. In our study, cag2 and cag4 were found to be significantly higher in H. pylori isolated from Malays, whereas cag4 was predominant in Chinese isolates. We also detected cag24 in significantly high proportion in isolates from the Malays and the Indians compared to the Chinese isolates. The intactness of cagPAI region showed an association with histopathological scores of the gastric mucosa. Significant association was observed between H. pylori harbouring partial cagPAI and higher density of H. pylori and neutrophil activity, whereas strains which lacked cagPAI was associated with higher inflammatory score. Conclusions: The screening of the entire cagPAI genes provides an accurate overview of the cagPAI organisation in H. pylori isolates in a multiracial population. The genotypes of H. pylori strains with various cagPAI rearrangement associated with patients’ ethnicities and histopathological scores might contribute to the pathogenesis of H. pylori infection in a multi-ethnic population.

Status of Helicobacter pylori cag pathogenicity island ( cag PAI) integrity and significance of its individual genes

2018 ◽  
Vol 59 ◽  
pp. 167-171 ◽  
Author(s):  
Rumyana Markovska ◽  
Lyudmila Boyanova ◽  
Daniel Yordanov ◽  
Petya Stankova ◽  
Galina Gergova ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Pathogenicity Island ◽  
Cag Pathogenicity Island ◽  
Cag Pai

scholarly journals Genetic basis for clarithromycin resistance among isolates of Mycobacterium chelonae and Mycobacterium abscessus.

1996 ◽  
Vol 40 (7) ◽  
pp. 1676-1681 ◽  
Author(s):  
R J Wallace ◽  
A Meier ◽  
B A Brown ◽  
Y Zhang ◽  
P Sander ◽  
...  
Keyword(s):  
Point Mutation ◽  
Random Amplified Polymorphic Dna ◽  
Mycobacterium Abscessus ◽  
Single Step ◽  
23S Rrna ◽  
Mycobacterium Chelonae ◽  
Clarithromycin Resistance ◽  
Gene Coding ◽  
Disseminated Disease ◽  
Dna Pcr

Resistance to clarithromycin among isolates of Mycobacterium chelonae and M. abscessus was observed in 18 of 800 (2.3%) patients tested between 1990 and 1995. Patients whose isolates were resistant had either disseminated disease or chronic lung disease, and the resistant isolates were recovered after clarithromycin monotherapy. Sequencing of the gene coding for the 23S rRNA peptidyltransferase region revealed a point mutation involving adenine at position 2058 (38%) or adenine at position 2059 (62%) in 20 of 20 relapse isolates from the first 13 patients identified. By pulsed-field gel electrophoresis or random amplified polymorphic DNA PCR, initial and relapse isolates were shown to have identical DNA patterns. M. chelonae and M. abscessus isolates were found to have only a single chromosomal copy of the rRNA operon, thus making them susceptible to single-step mutations. Thus, clarithromycin resistance in these species of rapidly growing mycobacteria relates to a point mutation in the gene coding for 23S rRNA and occurs in limited clinical situations, but was identified in almost 5% of isolates tested in 1995.

scholarly journals Mucormycosis of the hard palate masquerading as carcinoma

2012 ◽  
Vol 2 (1) ◽  
pp. 28 ◽  
Author(s):  
Bhari Sharanesha Manjunatha ◽  
Nagarajappa Das ◽  
Rakesh V. Sutariya ◽  
Tanveer Ahmed
Keyword(s):  
Clinical Presentation ◽  
Fungal Infections ◽  
Survival Rates ◽  
Positive Culture ◽  
Staining Technique ◽  
Necrotic Bone ◽  
Chronic Ulcers ◽  
Hematoxylin And Eosin ◽  
Clinical Differential Diagnosis ◽  
Hematoxylin And Eosin Stain

A growing number of medically compromised patients are encountered by dentists in their practices. Opportunistic fungal infections such as mucormycosis usually occur in immunocompromised patients but can infect healthy individuals as well. Mucormycosis is an acute opportunistic, uncommon, frequently fatal fungal infection, caused by a saprophytic fungus that belongs to the class of phycomycetes. Among the clinical differential diagnosis we can consider squamous cell carcinoma. Such cases present as chronic ulcers with raised margins causing exposure of underlying bone. There is a close histopathological resemblance between mucormycosis and aspergillosis. Microscopically, aspergillosis has septate branching hyphae, which can be distinguished from mucormycotic hyphae by a smaller width and prominent acute angulations of branching hyphae. A definitive diagnosis of mucormycosis can be made by tissue biopsy that identifies the characteristic hyphae, by positive culture or both. The culture of diseased tissue may be negative and histopathologic examination is essential for early diagnosis. Mucormycosis was long regarded as a fatal infection with poor prognosis. However with early medical and surgical management survival rates are now thought to exceed 80%. In the present case, the fungus was identified by hematoxylin and eosin stain and confirmed by Grocott’s silver methenamine special staining technique. Removal of the necrotic bone, which acted as a nidus of infection, was done. Post-operatively patient was advised an obturator to prevent oronasal regurgitation. Since mucormycosis occurs infrequently, it may pose a diagnostic and therapeutic dilemma for those who are not familiar with its clinical presentation.

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