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: H. pyloriis the major cause of chronic gastritis, and a risk factor for peptic ulcer and gastric cancer.: To investigate the effect of probiotic supplementation on the tolerance and efficacy ofH. pylorieradication treatment in a randomized, double-blind, placebo-controlled trial.: A total of 338 volunteers were screened forH. pyloriinfection. The eligibility criteria were met by 47 subjects whoseH. pyloriinfection was verified at the outset and re-evaluated after the treatment by the13C-urea breath test and by enzyme immunoassay serology. The subjects were randomized to receive probiotic therapy (Lactobacillus rhamnosusGG,L. rhamnosusLC705,Bifidobacterium breveBb99 andPropionibacterium freudenreichiissp.shermaniiJS) or a placebo duringH. pylorieradication and for 3 weeks following the treatment, and recorded their daily symptoms in a standardized diary.: When the frequencies of new or aggravated symptoms were evaluated, no significant differences were found between the two groups for individual symptoms. However, the probiotic group showed less treatment-related symptoms as measured by the total symptom score change (P = 0.038) throughout theH. pylorieradication therapy in contrast to the placebo group. TheH. pylorieradication rate was non-significantly higher in the group receiving probiotic therapy (91% vs. 79%,P = 0.42). In this group the recovery of probiotic bacteria in the faeces increased significantly (P < 0.001).: In this pilot study, probiotic supplementation did not diminish significantly the frequency of new or aggravated symptoms duringH. pylorieradication. However, our data suggest an improved tolerance to the eradication treatment when total symptom severity was taken into account. Furthermore, the results show that probiotic bacteria are able to survive in the gastrointestinal tract despite the intensive antimicrobial therapy. [ABSTRACT FROM AUTHOR]

To determine the efficacy of threeHelicobacter pylorieradication regimens and factors affecting the eradication results in Finland.A total of 342H. pylori-positive adult patients from primary health care referred for gastroscopy at 23 centres in different parts of Finland were randomized to receive either (i) lansoprazole 30 mg b.d., amoxicillin 1 g b.d. and metronidazole 400 mg t.d.s. (LAM), (ii) lansoprazole 30 mg b.d., amoxicillin 1 g b.d. and clarithromycin 500 mg b.d. (LAC), or (iii) ranitidine bismuth citrate 400 mg b.d., metronidazole 400 mg t.d.s. and tetracycline 500 mg q.d.s. (RMT). A13C-urea breath test was performed 4 weeks after therapy.The eradication result could be assessed in 329 cases. Intention-to-treat cure rates of LAM, LAC, and RMT were 78, 91 and 81%. The difference was significant between LAM and LAC (P = 0.01) and between LAC and RMT (P = 0.04). The eradication rates in cases with metronidazole-susceptible vs. -resistant isolates were for LAM 93% vs. 53% (P = 0.00001), for LAC 95% vs. 84%, and for RMT 91% vs. 67% (P = 0.002). Previous antibiotic use, smoking, and coffee drinking reduced the efficacy of therapy.In unselected patients in primary health care, LAC was the most effective first-line eradication. [ABSTRACT FROM AUTHOR]

Aim: To systematically determine Helicobacter pylon primary antimicrobial resistance in Finland and the associated demographic and clinical features. Methods: A total of 342 adult patients referred for gastroscopy at 23 centres in different parts of Finland and positive for the rapid biopsy urease test were recruited. Clinical and demographic data were collected via a structured questionnaire. Patients with positive H. pylon culture and successful antibiotic sensitivity determination by the E-test method (n = 292) were included in the present analysis. Results: The study population consisted of 134 men and 158 women, mean age 56 years (95% CI, 55-58 years). Resistance to metronidazole was 38% (110 of 292) and to clarithromycin 2% (seven of 292). Resistance to metronidazole was higher in women than in men (48% vs. 25%, P < 0.001).Previous use of antibiotics for gynaecological infections predicted metronidazole resistance (P = 0.01), and previous use of antibiotics for respiratory (P = 0.02) and dental infections (P = 0.02) the clarithromycin resistance. We observed no major geographical variations in metronidazole resistance. Conclusions: The primary metronidazole resistance of H. pylon was 38% and was common in women previously treated for gynaecological infections. Primary clarithromycin resistance was uncommon (2%) and may associate with previous dental and respiratory infections. [ABSTRACT FROM AUTHOR]

Background: There are few data on the natural course of Helicobacter pylori -related atrophic gastritis. Aim: To investigate the effect of H. pylori eradication on advanced atrophic gastritis in the corpus. Methods: Twenty-two elderly men with H. pylori infection and moderate or severe atrophic corpus gastritis formed the study population. These men were under endoscopic surveillance because of the presence of indefinite or definite dysplastic gastric lesions in addition to atrophic corpus gastritis. The men were gastroscopically and bioptically examined four times before they received H. pylori eradication therapy (mean follow-up time, 7.5 years), and once again 2.5 years after eradication therapy. Serum levels of pepsinogen I and H. pylori antibodies were analysed at baseline, immediately before and 2.5 years after eradication therapy. Results: During the 7.5-year period prior to eradication therapy, no significant changes were observed in the mean atrophy and intestinal metaplasia scores or in the mean serum level of pepsinogen I. However, a significant improvement occurred in the mean histological scores of inflammation (from 2.2 to 0.5), atrophy (from 2.2 to 1.2) and intestinal metaplasia (from 1.6 to 1.1) in the corpus mucosa after H. pylori eradication. In addition, the mean serum level of pepsinogen I increased from 16.3 to 25.7 μg/L (P =0.0071, Wilcoxon signed rank test) after eradication therapy. Conclusions: The results suggest that advanced atrophic corpus gastritis (and intestinal metaplasia) improves and may even heal after the eradication of H. pylori. [ABSTRACT FROM AUTHOR]

Background: Long-term Helicobacter pylori infection increases the risk of gastric malignancies. Since the symptoms for H. pylori gastritis, as well as for several malignancies, may be nonexisting or highly unspecific, even H. pylori-positive subjects with underlying malignancies may receive eradication therapy. The aim was to assess the incidence of gastrointestinal and various other malignancies in individuals after eradication therapy for H. pylori infection., Materials and Methods: A cohort of 217,554 subjects (120,344 women and 97,210 men), who had purchased specific combinations of drugs for H. pylori eradication therapy in 1994-2004, was identified by the Finnish National Prescription Registry and followed for cancer incidence until the end of 2008 (1.89 million person-years at risk)., Results: A total of 22,398 malignancies were identified in the cohort. In both genders, for the first 6 months after drug prescription, the standardized incidence ratios (SIRs) were between 5 and 32 for gastric, colorectal, and pancreatic cancers, and 2 and 3 for several other malignancies. Although later on the SIRs of most malignancies fell rapidly, those of gastric noncardia and lung cancers remained elevated up to 5 years of follow-up. The only SIRs below unity were seen in men for gastric cancers (cardia 0.61, 95% CI: 0.37-0.95; intestinal noncardia 0.74, 95% CI: 0.56-0.97) during the post-therapy period covering years 5-15., Conclusion: Incidence levels significantly above the population rates were detected for many malignancies. Although eradication of H. pylori may have a long-lasting protective effect against gastric cancer, H. pylori therapy may postpone the detection of malignancies possibly underlying unspecific gastrointestinal symptoms. Therefore, it should be emphasized that the diagnostic work-up for malignancies should not be stopped in case of detection and treatment of H. pylori infection., (© 2023 The Authors. Helicobacter published by John Wiley & Sons Ltd.)

Campylobacter jejuni and Campylobacter coli are important bacterial enteropathogens. Poultry is the best-known reservoir for Campylobacter infection but natural bodies of water have also been shown to be important pathways for transmission. Campylobacter can survive in cold water but most of the studies have focused on C. jejuni only. In this paper, we take a closer look at the biology and water survival strategies of C. coli. Eight C. coli isolates cultivated from raw (incoming) surface water at water plants in Sweden were characterized using whole-genome sequencing and phenotypical assays. Phylogenetic analysis assigned the Swedish water isolates to clades 2 and 3, known to include C. coli of environmental origin. In addition, 53 earlier published sequences of C. coli clade 2 and 3 from environmental waters were included for in silico analyses. Generally, clade 2 isolates had larger genomes, which included a functional tricarballylate utilization locus, while clade 3 isolates contained different genes involved in oxidative stress as well as putative virulence factors. The Swedish water isolates of clade 2 formed large, blurry bacterial colonies on agar, whereas clade 3 colonies were smaller. All Swedish isolates were motile, but clade 3 isolates formed larger motility zones on soft agar, and none of these isolates produced biofilm. Although water survival varied between the analyzed isolates, there were hardly any clade-specific significant differences. Our results highlight the diversity of C. coli in general, and show differences in metabolic capabilities and ways to handle oxidative stress between clade 2 and 3 water isolates., (© 2018 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.)

Background: Helicobacter pylori is the primary cause of gastritis and peptic ulceration in humans. In a minority of patients with upper gastrointestinal symptoms, long tightly coiled spiral bacteria, provisionally named "Helicobacter heilmannii," are observed in gastric biopsies. These bacteria are extremely fastidious and only one previous study has succeeded in obtaining an isolate in vitro., Materials and Methods: We used two different selective media to isolate "H. heilmannii" from the gastric mucosa of a Finnish patient presenting with severe dyspeptic symptoms. The isolates were characterized by testing for urease and catalase activity, by using light and electron microscopy, and by sequencing of the partial 16S rRNA and ureAB genes. Single-enzyme amplified fragment length polymorphism (sAFLP) was used to analyze the genetic diversity among the isolates., Results: We obtained 15 isolates from different gastric biopsies prior and three after unsuccessful treatment of the patient. The isolates were identified as Helicobacter bizzozeronii. Eradication therapy was unsuccessful most probably due to high level of resistance to metronidazole. Persistent colonization by the same H. bizzozeronii clone was confirmed by sAFLP, however, small differences between the profiles suggested long-term colonization of the patient., Conclusions: Helicobacter bizzozeronii remains the only "H. heilmannii" species isolated from human gastric mucosa although it has been an infrequent observation among "H. heilmannii"-infected patients in PCR-based screening studies. The relevance of H. bizzozeronii and other potentially zoonotic gastric Helicobacter spp. in human disease remains to be determined.

Background: To accelerate the decline of Helicobacter pylori infection, and to study the significance of the possible risk factors for H. pylori infection in Finland, we started a voluntary H. pylori"screen-treat-retest-and-retreat" program for all young adults at primary health care in Vammala, Finland after a pilot study in 1994 including 504 subjects aged 15-75., Materials and Methods: A total of 3326 aged 15-40 in 1996, and 716 aged 15 and 584 aged 45 in 1997-2000 were screened for H. pylori using serology. Helicobacter pylori positive were treated, cure was verified by serology., Results: The eradication rates were 93.8%, 82.2%, and 77.6% per protocol in pilot study in 1994, in subjects invited in 1996 and 1997-2000, respectively. Helicobacter pylori seroprevalence rates were calculated to have decreased from 36% to 14% in pilot study, from 12% to 4% among subjects invited in 1996, from 3% to 2% among subjects aged 15 and from 27% to 12% among subjects aged 45 in 1997-2000. An epidemiologic questionnaire in 1996 revealed that crowding in the childhood household, low education of the mother, current smoking and alcohol consumption, unfavorable housing conditions, and sick leaves due to dyspepsia were independently associated with H. pylori infection., Conclusions: This intervention with high participation rates resulted in a significant decline in calculated H. pylori seroprevalence rates. Although the low prevalence of H. pylori infection may limit the cost efficiency of the program, the intervention is expected to reduce the burden of H. pylori-associated diseases.

Aim: The persistence of chronic inflammation in gastric mucosa and elevated Helicobacter pylori antibodies after successful eradication therapy are common findings in clinical practice. We studied their possible association with each other and disappearance in long-term follow up, as well as their possible connection with gastric atrophy., Patients and Methods: The study population consisted of 108 dyspeptic patients with successful eradication therapy median 6.4 years earlier. The patients underwent gastroscopy, and biopsies from antrum and corpus were evaluated by an experienced pathologist. Serum samples collected from 77 patients were studied for H. pylori antibodies, parietal cell antibodies, as well as for pepsinogen I, pepsinogen II, and gastrin-17 levels., Results: The prevalence of chronic gastric inflammation and elevated H. pylori antibodies after successful eradication therapy decreased by time, but still after 5 years, 17 of 51 (33%) subjects had elevated H. pylori antibodies and 14 of 68 (21%) had a mild inactive chronic inflammation in gastric mucosa. In patients with and without chronic inflammation in gastric mucosa, elevated H. pylori antibodies were detected in three of 10 (30%) and 14 of 41 (34%), elevated parietal cell antibodies in one of 10 (10%) and six of 41 (15%), low pepsinogen I in one of 10 (10%) and none of 41, and elevated gastrin-17 in three of 10 (30%) and six of 41 (15%), respectively., Conclusion: More than 5 years after successful H. pylori eradication therapy, mild persistent chronic inflammation may occur in gastric mucosa in up to one-fifth and elevated H. pylori antibodies even in one-third of patients, although these two are independent phenomena.

We report here the case of a 58-year-old asymptomatic male smoker who had a gastroscopy performed in 1990 because of a low serum pepsinogen I level (16 microg/l). The patient had severe atrophic corpus gastritis and elevated Helicobacter pylori antibody titers, but no histologic evidence of the bacteria. Additionally, a hiatal hernia without esophagitis was seen. He was followed up endoscopically because of the atypical changes (indefinite for dysplasia) in addition to atrophic gastritis in some of the gastric biopsy samples. During the follow-up period, H. pylori antibody titers declined to normal levels without eradication therapy, and atrophic gastritis healed. The patient developed first erosive esophagitis, and, 5 years later, a 3-cm-long Barrett's esophagus was detected.

Background: Specific antibodies against Helicobacter were enriched from the colostra of hyperimmunized cows. Efficacies of colostral control preparation and immune preparation containing specific antibodies against Helicobacter felis were studied in the prevention and treatment of experimental H. felis infection in mice., Materials and Methods: H. felis-infected mice were given either immune or control preparation with or without complement or amoxicillin orally in four different trials. H. felis status was assessed on the basis of bacterial stainings, gastric histology and serum antibodies., Results: Immune, but not control preparation, prevented H. felis infection (p > 0.01), the efficacy being dependent on the presence of specific antibodies. In the trial on infected Balb/c mice treatment with immune preparation (p = 0.029) but not control preparation decreased the colonization of gastric antrum by H. felis. In the further trials with infected SJL-mice, treatments with colostral preparations did not decrease colonization. Amoxicillin treatment decreased the colonization with trend-setting significance (p = 0.056; infected mice as controls), whereas amoxicillin combined with immune preparation had a significant effect (p < 0.0005)., Conclusions: Specific colostral antibodies were useful in the prevention of Helicobacter infection in a mouse model. The results of the treatment trials were controversial but a similar colostral immune preparation against H. pylori could be effective and useful in preventing infections in humans and during antibiotic treatment.

Numerous studies are still published on diagnostic tests for Helicobacter pylori, essentially for noninvasive tests. The urea breath test is applied in different types of patients, and there are attempts to have quicker and simpler protocols. Stool tests using monoclonal antibodies are now evaluated while serology is still a subject of interest. The progress in PCR (multiplex PCR, real-time PCR) has also stimulated the research in this area of invasive tests, in order to get insight into virulence factors, macrolide susceptibility and to detect H. pylori in nonconventional specimens.