Estimates of<i>Helicobacter pylori</i>Densities in the Gastric Mucus Layer by PCR, Histologic Examination, and CLOtest

Nowak, Jan A.; Forouzandeh, Bahram; Nowak, Jonathan A.

doi:10.1093/ajcp/108.3.284

Cited by 14 publications

(6 citation statements)

References 5 publications

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“…As most of the clarithromycin resistance is caused by point mutation at 2143 and 2144, the probable spontaneous mutation rate at these sites is calculated to be 4.0 × 10 −9 /cell division. As the number of H pylori is estimated to be 10 7 –10 9 /100 μl gastric mucus,22 23 the total number of bacteria in a stomach may be in the range 10 9 –10 11 , assuming the amount of gastric mucus is limited to 10 ml. In addition to those in the mucus, a similar number of bacteria adhere to the mucosa, therefore the total number would be twice that.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous colonisation of Helicobacter pylori with and without mutations in the 23S rRNA gene in patients with no history of clarithromycin exposure

Matsuoka

Yoshida

Hayakawa

et al. 1999

Gut

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Background-It was recently reported that A to G transition mutations at positions 2143 and 2144 in the 23S rRNA gene are associated with clarithromycin resistance in Helicobacter pylori. Aims-To study the incidence and mechanism of development of clarithromycin resistance by analysing these mutations. Subjects-Eighty two H pylori positive patients who had an endoscopic examination and no history of treatment with macrolide antibiotics. Methods-Clarithromycin resistance was screened for by polymerase chain reaction-restriction fragment length polymorphism of the 23S rRNA gene coupled with antibiotic susceptibility testing. In clinical isolates with mutations or resistance, mutations in individual colonies were analysed by direct sequencing. Results-Of the 79 amplicons (DNA fragments amplified by polymerase chain reaction), Alw26I and MboII digestion disclosed the mutation in four (5%) and one (1%) respectively. However, the Alw26I cleavage was incomplete in two of the four amplicons, as was the MboII cleavage. Individual colony analysis of the isolates with incomplete cleavage patterns showed the presence of both wild type and mutated strains in the 23S rRNA genes. Conclusions-Both clarithromycin sensitive and resistant strains colonised in some patients with no history of exposure to macrolides. The results suggest that resistant strains may not be formed but selected by clarithromycin administration. (Gut 1999;45:503-507)

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Section: Discussionmentioning

confidence: 99%

Simultaneous colonisation of Helicobacter pylori with and without mutations in the 23S rRNA gene in patients with no history of clarithromycin exposure

Matsuoka

Yoshida

Hayakawa

et al. 1999

Gut

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“…For example, the typical response in the murine mode! has been the absence., or more typically the reduction in the number, H. pylori by 2 logn, compared to controls [4,13,18-20|. Quantitative competitive PCR should also be useful to assess H. pylori density in different regions ot the stomach in humans (e.g., in the duodenal bulb) [7][8][9][10]. The requirements for the assay are the same {e.g., identification of an H. pylorispecific target not normally present in gastric contents).…”

Section: Discussionmentioning

confidence: 99%

Quantitation of Helicobacter pylori in the Stomach Using Quantitative Polymerase Chain Reaction Assays

Ozpolat¹

2000

Helicobacter

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“…4). Two pieces of evidence supporting this finite capacity are as follows: the presence of adhesion pedestals induced by H. pylori (19) indicates irreversibility of adhesion, and recent estimates on the size of the adherent population (20), on the order of + 1% of the total mucus population size, and the fact that these sites are most advantageous indicate that a limited number of sites are available.…”

Section: The Modelmentioning

confidence: 98%

“…The initial values chosen must reflect the experimentally estimated population sizes. Since during persistence, H. pylori concentrations range from 10 5 to 10 8 per mm 3 (20,22), and colonization begins with an initial inoculum, we choose a smaller value, on the order of 10 1 to 10 4 per mm 3 ; however, the model gives qualitatively similar results with larger initial values. We begin with no adherent population, and with fractional effector and nutrient populations.…”

Section: The Modelmentioning

confidence: 99%

Dynamics of Helicobacter pylori colonization in relation to the host response

Blaser

Kirschner

1999

Proc. Natl. Acad. Sci. U.S.A.

102

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The dynamics of Helicobacter pylori colonization from its acquisition through the development of steadystate are examined through a mathematical model that includes the host response. The model encompasses both host and microbiological variation. The individual capacity of the host response is shown to be a key model parameter, leading to either transient or persistent colonization, whereas the growth rate of that response has little effect. Analyses of competing strains indicate that each must occupy a specific niche, otherwise exclusion occurs. The model implies that there exists a lower bound on the host response to the indigenous microflora that is consistent with current biological views of H. pylori. Parallel models may be useful in understanding other persistent host-microbial interactions.

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Estimates ofHelicobacter pyloriDensities in the Gastric Mucus Layer by PCR, Histologic Examination, and CLOtest

Cited by 14 publications

References 5 publications

Simultaneous colonisation of Helicobacter pylori with and without mutations in the 23S rRNA gene in patients with no history of clarithromycin exposure

Simultaneous colonisation of Helicobacter pylori with and without mutations in the 23S rRNA gene in patients with no history of clarithromycin exposure

Quantitation of Helicobacter pylori in the Stomach Using Quantitative Polymerase Chain Reaction Assays

Dynamics of Helicobacter pylori colonization in relation to the host response

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