[Status and problem of first line eradication of H. pylori infection].

This year eradication of H. pylori was applied for not only peptic ulcer but also chronic gastritis on National insurance system. However recently decrease in first line eradication rate of H. pylori using PPI/AC regimen. Certainly eradication rate after 2000 decreased in intention to treat (ITT) and per protocol(PP) compared to that before 2000. This tendency was induced by increase in CAM-resistant H. pylori. But after 2007 eradication rate decreased only in ITT, eradication rate didn't decrease in PP. That tendency was induced by bad compliance and evaluation of the eradication.

Fluoroquinolone resistance in Helicobacter pylori: role of mutations at position 87 and 91 of GyrA on the level of resistance and identification of a resistance conferring mutation in GyrB.

BACKGROUND AND AIMS: Fluoroquinolone-containing regimens have been suggested as an alternate to standard triple therapy for the treatment of Helicobacter pylori infections. To determine the relationship between fluoroquinolone resistance and mutations of GyrA and GyrB in H. pylori, we exchanged the mutations at positions 87 and 91 of GyrA among fluoroquinolone-resistant clinical isolates. GyrB of a strain with no mutations in GyrA was also analyzed to identify mechanisms of resistance to norfloxacin. MATERIALS & METHODS: Natural transformation was performed using the amplified fragment of the gyrA and gyrB gene as donor DNA. The amino acid sequences of GyrA and GyrB were determined by DNA sequencing of the gyrA and gyrB genes. RESULTS: Norfloxacin-resistant strains which had mutations at position 87 and 91 became susceptible when the mutations were converted to the wild type. When the mutation from Asp to Asn at position 91 was exchanged to the mutation from Asn to Lys at position 87, the MIC to levofloxacin, gatifloxacin, and sitafloxacin increased. Norfloxacin-resistant strain TS132 with no mutations in GyrA but had a mutation at position 463 in GyrB. Transformants obtained by natural transformation using gyrB DNA of TS132 had a mutation at position 463 of GyrB and revealed resistant to norfloxacin and levofloxacin. CONCLUSION: Mutation from Asn to Lys at position 87 of GyrA confers higher resistance to levofloxacin and gatifloxacin than does mutation from Asp to Asn at position 91. We propose that mutation at position 463 in GyrB as a novel mechanism of fluoroquinolone resistance in H. pylori.

Effect of pretreatment with Lactobacillus gasseri OLL2716 on first-line Helicobacter pylori eradication therapy.

BACKGROUND AND AIM: Helicobacter pylori eradication clearly decreases peptic ulcer recurrence rates. H. pylori eradication is achieved in 70-90% of cases, but treatment failures due to poor patient compliance and resistant organisms do occur. Lactobacillus gasseri can suppress both clarithromycin-susceptible and -resistant strains of H. pylori in vitro. The aim of this study was to determine the effect of pretreatment with L. gasseri- containing yogurt on H. pylori eradication. We conducted a randomized, controlled clinical trial in patients with H. pylori infection. METHODS: A total of 229 patients were randomized into either a 1-week triple therapy of rabeprazole (10 mg bid), amoxicillin (750 mg bid), and clarithromycin (200 mg bid) or triple therapy plus L. gasseri-containing yogurt. In the yogurt-plus-triple therapy groups, yogurt containing L. gasseri OLL2716 (112 g) was given twice daily for 4 weeks (3 weeks pretreatment and also 1 week during eradication therapy). Clarithromycin resistance was determined by the detection of a mutation in 23S rRNA using nested polymerase chain reaction and the direct sequencing of DNA from pretreatment feces. H. pylori eradication was diagnosed based on the urea breath test and a stool antigen test after 8 weeks of eradication. RESULTS: The status of H. pylori susceptibility to clarithromycin was successively determined in 188 out of 229 samples. The rate of infection with clarithromycin-resistant strains of H. pylori was 27.1%. Overall eradication (intention to treat/per protocol) was 69.3/74.5% for the triple-only group, and 82.6/85.6% for the yogurt-plus-triple group (P = 0.018/P = 0.041). Eradication of primary clarithromycin-resistant strains tended to be higher for yogurt-plus-triple therapy than triple-only therapy (38.5 vs 28.0%, respectively, P = 0.458). CONCLUSION: This study confirmed that the major cause of treatment failure is resistance to clarithromycin. A 4-week treatment with L. gasseri-containing yogurt improves the efficacy of triple therapy in patients with H. pylori infection.

Characterization of enterococcus strains contained in probiotic products.

Probiotics are additives containing live microbes that beneficially affect a host by improving the properties of the host intestinal microflora. Recently, advances in medical treatments have led to increased numbers of immunocompromised patients; some patients contract opportunistic infections of Enterococcus species, which are considered non-pathogenic bacteria. To evaluate the safety of probiotics containing Enterococcus strains, we isolated Enterococcus from six probiotic products and compared the pathogenic genes and antimicrobial susceptibility of the probiotic strains to those of clinical isolates. Our study showed that all Enterococcus strains contained in probiotic products were E. faecium, and no vancomycin-resistant strains were found. In addition, no pathogenic genes, such as ace, agg, gelE, cylM, cylB, cylA, cpd, cob, ccf, efaA(fs), efaA(fm), esp(fs), or esp(fm), were found in the probiotic strains. Pulsed-field gel electrophoresis (PFGE) analysis showed obvious genetic differences between the probiotic strains and the clinical isolates. The data suggested that the probiotic Enterococcus strains were not transmitted to hospitalized patients. Therefore, our results strongly suggest that probiotic products are unlikely agents for causing opportunistic infections.

Augmentation of gene expression and production of promatrix metalloproteinase 2 by Propionibacterium acnes-derived factors in hamster sebocytes and dermal fibroblasts: a possible mechanism for acne scarring.

Aberrant extracellular matrix (ECM) remodeling in sebaceous glands and pilosebaceous units in the skin is associated with scar formation under acne conditions. To investigate the involvement of Propionibacterium acnes (P. acnes), a Gram-positive anaerobic microbial species, in ECM remodeling in sebaceous glands and pilosebaceous units, we examined the effects of P. acnes culture media, formalin-fixed P. acnes, and peptidoglycan (PGN) from Gram-positive bacteria walls on the production of promatrix metalloproteinase 2 (proMMP-2)/progelatinase A in hamster sebocytes and dermal fibroblasts. When hamster sebocytes (1.8×10(5) cells) and dermal fibroblasts (1×10(5) cells) were treated with P. acnes culture media and formalin-fixed P. acnes (corresponding to 1×10(6) and 1×10(7) bacterial cells), the production of proMMP-2 was augmented. In addition, PGN (5-50 µg/ml) dose-dependently augmented the production of proMMP-2 in both cells. Furthermore, the PGN (50 µg/ml)-augmented proMMP-2 production was resulted from an increase of its transcript. In contrast, there were no changes in cell proliferative activity in either the P. acnes or PGN-treated sebocytes and dermal fibroblasts, indicating that the augmented proMMP-2 production was not due to an increase in cell numbers. Therefore, these results provide novel evidence that PGN transcriptionally up-regulates the production of proMMP-2 in hamster sebocytes and dermal fibroblasts. Given an increase in the quantity of Gram-positive bacteria, including P. acnes in acne lesions, the aberrant ECM degradation may progress in sebaceous glands and pilosebaceous units, which is associated with acne scar formation.

Fluoroquinolone efflux by the plasmid-mediated multidrug efflux pump QacB variant QacBIII in Staphylococcus aureus.

Plasmids that carry the multidrug efflux genes qacA and qacB are widely distributed in methicillin-resistant Staphylococcus aureus (MRSA). Although the QacA and QacB proteins are similar to each other, their respective substrate specificities may differ. We investigated the variability and structure-function relationships of QacA and QacB in MRSA isolates. The amino acid sequences of 7 QacA and 25 QacB proteins showed that QacB was present in three variants, designated QacBII, QacBIII, and QacBIV, that were different from the prototypic QacB variant encoded by plasmid pSK23, which was named QacBI, while QacA was present in two variants. When cloned and expressed in S. aureus, the strain carrying qacBIII exhibited higher susceptibility to dyes and decreased susceptibility to norfloxacin and ciprofloxacin compared to strains carrying the other QacB variants. Site-directed mutagenesis experiments revealed that the residue at position 320 in QacB plays an important role in the resistance phenotypes to dyes and fluoroquinolones. Furthermore, the accumulation of norfloxacin and ciprofloxacin in the strain carrying qacBIII was significantly decreased. Our data demonstrate that the plasmid-mediated multidrug efflux pump QacB variant QacBIII confers the capability for fluoroquinolone efflux on S. aureus.

Analysis of clarithromycin resistance and CagA status in Helicobacter pylori by use of feces from children in Thailand.

The clarithromycin resistance and CagA status of Helicobacter pylori in Thai children were investigated using fecal samples. Of the 284 samples, H. pylori was detected in 120 samples, and the clarithromycin resistance rate was 29.2%. The cagA gene was detected in 59 samples, and only 6.8% of these samples contained the East Asian CagA type.

Isolation and identification of a potent antimalarial and antibacterial polyacetylene from Bidens pilosa.

Diseases caused by malaria parasites and pathogenic bacteria were thought to be on the brink of eradication in the 1950-1960s, but they have once again become a serious threat to mankind as a result of the appearance of multidrug resistant strains. The spread of these multidrug resistant organisms has prompted a worldwide search for new classes of effective antimalarial and antibacterial drugs. Natural products have been recognized as highly important candidates for this purpose. Our attention has focused on the herbal plant Bidens pilosa, a weed common throughout the world, as one of the target plants in the search for new active compounds, owing to its empirical use in the treatment of infectious diseases and to pharmaco-chemical studies of its crude extract. We report the isolation of two new compounds of B. pilosa, the linear polyacetylenic diol 1 and its glucoside 2 which have previously been isolated from different plants. Compound 1 exhibited highly potent antimalarial and antibacterial properties in vitro as well as potent antimalarial activity by way of intravenous injection in vivo, thereby representing a promising new class of drugs potentially effective in the treatment of malarial and bacterial diseases. We suspect that discovery of these compounds in B. pilosa in appreciable quantity is because the Fijian tradition of using the fresh plant for extraction rather than the Asian tradition of using dried plants (1 is unstable in the dried state) was followed.

Development of effective antimicrobial cocktails to prevent bacterial contamination of allograft tissues under low temperature conditions.

OBJECTIVES: Prevention of bacterial transmission in recipient patients via allograft decontamination with an antimicrobial cocktail consisting of cefmetazole (cefoxitin), vancomycin, lincomycin and polymyxin B is an important procedure commonly practised in tissue banks. However, some allografts are lost due to the failure of decontamination under low temperature conditions. Here, we aimed to develop new antimicrobial cocktails that exert a high bactericidal activity at 4°C. METHODS: Bacterial species used in this study were selected as major causative pathogens of allograft tissue contamination. The efficacy of the combination of 2 antimicrobial agents was determined by the checkerboard titration method. The bactericidal effects of the new antimicrobial cocktails were evaluated under the same conditions as those used for the storage and preservation of allograft tissues. RESULTS: Among the selected antimicrobial agents, daptomycin exhibited the highest bactericidal activity against methicillin-resistant Staphylococcus aureus under low temperature conditions. The combination of daptomycin + gentamicin and daptomycin + levofloxacin showed a synergistic or additive effect against various bacterial species. The antimicrobial cocktail containing 200 µg/ml of daptomycin, gentamicin and levofloxacin could eradicate ≤104 colony-forming units/ml of methicillin-resistant S. aureus and Enterococcus faecalis, which exhibit a low susceptibility to antimicrobial agents at 4°C for 24 h. CONCLUSIONS: We have developed a new formula for an antimicrobial cocktail to effectively and sufficiently prevent bacterial contamination of allograft tissues under low temperature conditions in vitro.

Mutations in penicillin-binding proteins 1, 2 and 3 are responsible for amoxicillin resistance in Helicobacter pylori.

OBJECTIVES: To elucidate the relationship between the mutations of penicillin-binding protein (PBP)1, PBP2 and PBP3 and amoxicillin resistance in Helicobacter pylori. METHODS: The mutations detected only in clinical amoxicillin-resistant strains were determined by comparison of the deduced amino acid sequences of PBP1(HP0597), PBP2(HP1556) and PBP3(HP1565) encoded by the pbp1, ftsI and pbp2 genes, respectively, in 13 clinical H. pylori strains and three ATCC strains. The contribution of the mutations in PBPs was analysed by the natural transformation of the amoxicillin-susceptible strain ATCC 700392 with various combinations of the pbp1, ftsI and pbp2 genes from the amoxicillin-resistant strain TH743 (MIC of amoxicillin: 8 mg/L). RESULTS: We initially identified six, four and two mutations of PBP1, PBP2 and PBP3, respectively, which were detected only in amoxicillin-resistant strains. By the natural transformation of an amoxicillin-susceptible strain ATCC 700392, we found that mutations in PBP1 and PBP3 conferred higher resistance to amoxicillin than mutations in PBP1 and PBP2, or mutations only in PBP1. Furthermore, mutations in PBP1, PBP2 and PBP3 conferred a 256-fold higher amoxicillin resistance when compared with ATCC 700392. CONCLUSIONS: Multiple mutations in PBP2 and PBP3, in addition to mutations in PBP1, confer higher amoxicillin resistance in H. pylori.

Characterization of the pTZ2162 encoding multidrug efflux gene qacB from Staphylococcus aureus.

The plasmid-borne multidrug efflux gene qacB is widely distributed in methicillin-resistant Staphylococcus aureus (MRSA). We analyzed the complete nucleotide sequence of the plasmid pTZ2162 (35.4 kb) encoding qacB. The plasmid pTZ2162 contains 47 ORFs and four copies of IS257 (designated IS257A to D). The 24.7-kb region of pTZ2162, which excluding the region flanked by IS257A and IS257D, is 99.9% identical to pN315 carried by MRSA N315. However, the repA-like region of pTZ2162 was divided into two ORFs, ORF46 and ORF47. Functional analysis with the pUC19-based vector pTZN03 showed that both ORF46 and ORF47 were essential for the replication of pTZ2162 and ORF1 is required for the stable maintenance of pTZ2162 in S. aureus. When pTZ2162 was searched for evidence of mobile elements, an 8-bp duplicated sequence (GATAAAGA) was existed at the left boundary of IS257A and the right boundary of IS257D. Therefore, the 10.7-kb region between IS257A and IS257D in pTZ2162 has the potential to act as a transposon. In addition to qacB, the pTZ2162 transposon-like element contains a novel fosfomycin resistance determinant fosD and an aminoglycoside resistance determinant aacA-aphD. This transposon-like element appears to have translocated into the beta-lactamase gene blaZ. Our data suggest that qacB is transferred between MRSA as a multiple antibiotic resistance transposon.

Molecular epidemiology and antimicrobial susceptibilities of 273 exfoliative toxin-encoding-gene-positive Staphylococcus aureus isolates from patients with impetigo in Japan.

The molecular epidemiology and antimicrobial susceptibilities of 273 Staphylococcus aureus isolates positive for the exfoliative toxin-encoding gene obtained from patients with impetigo in Japan in 2006 were studied. The mecA gene was detected in 74 meticillin-resistant S. aureus (MRSA) and 23 meticillin-susceptible S. aureus (MSSA) isolates. All isolates with the staphylococcal cassette chromosome (SCC) mec were classified into type IV (92.8%, 90/97) or V (7.2%, 7/97). The ET-encoding gene etb was found primarily in strains with mecA (87.7%, 71/81), whilst eta (86.6%, 161/186) was detected mainly in strains without mecA. The chromosomal enterotoxin-encoding gene cluster egc was found in 83.0% of strains with eta, whilst no enterotoxin-encoding gene was detected in strains with only etb. PFGE showed that each strain carrying eta, etb and etd could be classified into distinct groups. The susceptibility profiles of MRSA to antimicrobial agents excluding beta-lactams were similar to those of MSSA. Gentamicin- and clarithromycin-resistant strains were frequently found for both MRSA and MSSA. The aminoglycoside-resistance gene aacA-aphD was detected in 97.3% of MRSA and 85.4% of MSSA. Additionally, the macrolide-resistance gene ermA or ermC was detected in 67.6% of MRSA and 71.4% of MSSA. Therefore, these results suggest that SCCmec types IV or V have spread, particularly in MSSA carrying etb in the community.

Tailored eradication therapy based on fecal Helicobacter pylori clarithromycin sensitivities.

BACKGROUND AND AIM: Helicobacter pylori (H. pylori) eradication rates using the PPI/AC regimen (proton pump inhibitor + amoxicillin + clarithromycin) are declining. We trialed tailoring eradication regimens according to clarithromycin (CAM) susceptibility. METHODS: The subjects were 70 H. pylori positive adults. They were randomly allocated to a tailored group and a control group. In the tailored group, subjects with CAM-sensitive strains were given PPI/AC eradication therapy, and those with CAM-resistant strains were given PPI/AM (metronidazole instead of clarithromycin) therapy. The control group were all given PPI/AC therapy. CAM sensitivity was measured by collecting fecal specimens, and extracting the DNA. The 23S rRNA domain, associated with CAM susceptibility in H. pylori, was amplified using a nested polymerase chain reaction (PCR), and DNA sequencing was used to detect point mutations at A2143G and A2144G. RESULTS: Eradication rates were 94.3% in the tailored group and 71.4% in the control group. In particular, the eradication rate was 100% for CAM-resistant strains in the tailored group. CONCLUSIONS: In Japan, where CAM-resistant H. pylori strains are expected to continue to increase, tailored eradication therapy according to CAM sensitivity will be of benefit.

A study of the relationship between Helicobacter pylori microbial susceptibility, 13C-urea breath test values.

BACKGROUND/AIMS: Diagnostic methods for Helicobacter pylori (H. pylori) infection can be divided into invasive endoscopic methods and non-invasive methods. A typical and widely used non-invasive method is the 13C urea breath test (UBT). In this study, the possibility of a correlation between pre-treatment UBT values with H. pylori antimicrobial resistance is investigated. METHODOLOGY: The subjects were 119 consecutive patients who attended this hospital for H. pylori testing. Average age was 47.5 +/- 13.2 years, with a male:female ratio of 2.05:1. The diagnosis was gastric ulcer in 43 subjects, duodenal ulcer in 27, gastroduodenal ulcer in 21 and chronic gastritis in 28. Subjects underwent UBT as well as upper gastrointestinal endoscopy (UGITE). The diagnosis of H. pylori infection was examined by the results of culture, histological examination and the rapid urease test (RUT). The mean inhibitory concentration (MIC) was determined for each antimicrobial agent in the bacterial isolates that could be cultured. RESULTS: In this study, the sensitivity and specificity were excellent at 97.0% and 100% with a cut-off point of 3.5 per thousand for UBT respectively. Clarithromycin resistance was more common in the group with high UBT values. No correlation at all was seen between UBT values and metronidazole, sparafloxacin, cefaclor and amoxicillin susceptibility. CONCLUSIONS: It is possible that UBT values also tend to be higher in cases of CAM resistance.

Specific clones of Staphylococcus lugdunensis may be associated with colon carcinoma.

Staphylococcus lugdunensis produces a tannase with activity that may be associated with the onset of colon carcinoma. To clarify this feature of colon carcinoma-associated S. lugdunensis, we obtained isolates from healthy subjects and patients with colon adenomas and carcinomas and analyzed their genetic backgrounds. In total, 40 S. lugdunensis isolates from 288 rectal swabs collected between 2002 and 2008 were used. These isolates were classified into four groups according to the diseases of the subjects: healthy (n=13), colon carcinoma (n=13), colon adenoma (n=9), and unknown (n=5). The isolates were also classified by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing. In addition, an antimicrobial susceptibility test and detection of resistance genes were performed for all isolates. According to the PFGE analysis, 40 isolates could be classified into five groups. Among the groups, carcinoma and colon adenoma patients were significantly more frequently (40.9%) classified into group D (p<0.05), whereas healthy subjects were more frequently (38.5%) classified into group A. All isolates in group D were typed as ST27, which was clearly different than isolates in the other groups. All isolates were susceptible to the antimicrobial agents tested, including ß-lactams, although seven strains produced ß-lactamase. Our data suggest that a specific clone of S. lugdunensis might be associated with colon carcinoma and colon adenoma. This clone showed high susceptibility to many antimicrobial agents. Therefore, eradication therapy may lead to a decreased risk of colon carcinoma.

Detection of mixed clarithromycin-resistant and -susceptible Helicobacter pylori using nested PCR and direct sequencing of DNA extracted from faeces.

The major cause of chemotherapy failure in patients with chronic gastritis and peptic ulcers caused by Helicobacter pylori is clarithromycin (CAM) resistance due to a mutation in the 23S rRNA gene. This study describes a non-invasive and accurate method for the detection of mixed CAM-resistant and -susceptible H. pylori by sequencing of the H. pylori 23S rRNA gene. Faeces were crushed with beads and the 23S rRNA gene was amplified using a nested PCR on the extracted DNA. Mutation analysis of this gene using this method showed that 20.4 % of patients carried mixed CAM-susceptible (wild type) and -resistant (A2142G or A2143G mutant) H. pylori. Furthermore, it was found that 66.6 % of patients who had been treated unsuccessfully carried one of these mutations in the 23S rRNA gene (including the mixed type), whilst standard culture detected CAM-resistant isolates in only 22.2 % of patients with unsuccessful treatment. These data suggest that, for successful therapy, the diagnosis method described here would more accurately detect CAM-resistant H. pylori, including mixed infections.

Mutations in the 23S rRNA gene of clarithromycin-resistant Helicobacter pylori from Japan.

The 23S rRNA gene in clinical isolates of Helicobacter pylori isolated between 1995 and 2004 from Japan was investigated and the relationship between mutations in this gene and clarithromycin susceptibility was studied. Among nine mutations that have previously been reported to confer clarithromycin resistance, an adenine-->guanine transition at position 2142 (A2142G) or 2143 (A2143G) was detected in all clarithromycin-resistant strains (n=67) but not in any clarithromycin-susceptible strains (n=17). Mutations at positions 2182, 2223, 2244 and 2288 have previously been reported to confer clarithromycin resistance in H. pylori isolates from Bangladesh, China and Brazil. However, these mutations were not associated with clarithromycin resistance in H. pylori isolates from Japan in this study. Other mutations at positions 2115, 2144 and 2711, which have also been reported to confer clarithromycin resistance in H. pylori from Sweden and Italy, were not detected in the strains in this study. Our results suggest that susceptibility to clarithromycin is predicted by detection of mutations at positions 2142 and 2143 of the 23S rRNA gene in H. pylori isolates in Japan.

Antimicrobial susceptibilities and distribution of resistance genes for beta-lactams and macrolides in Streptococcus pneumoniae isolated between 2002 and 2004 in Tokyo.

Antimicrobial susceptibilities of 205 Streptococcus pneumoniae strains isolated between 2002 and 2004 in Japan were examined and the distribution of genes for resistance to penicillins and macrolides were investigated by polymerase chain reaction. The molecular epidemiology of 92 randomly selected isolates was also examined by pulsed-field gel electrophoresis (PFGE). The numbers of S. pneumoniae isolates resistant to benzylpenicillin, clarithromycin and tetracycline were, respectively, 39 (19%), 111 (54%) and 155 (76%), and the numbers increased annually. All isolates were susceptible to amoxicillin, fluoroquinolones, vancomycin and linezolid. Analysis of mutations in the genes for penicillin-binding protein showed that 92% of isolates had mutations in pbp1a, pbp2b and/or pbp2x. Susceptibility to benzylpenicillin decreased with increasing number of mutated pbp genes. The macrolide resistance genes ermB and mefA were found in 99 (48%) and 76 (37%) isolates, respectively. The presence of ermB was associated with high-level resistance to macrolides, and the percentage of isolates with ermB increased annually. The presence of mefA also increased with increasing number of mutated pbp genes. Although the 92 isolates belonged to 74 PFGE types, three groups with an 80% similarity in their PFGE patterns were found at high frequency. Two of the three groups contained no isolates susceptible to penicillin and/or tetracycline, and their percentages increased annually. Our results suggest that the number of S. pneumoniae isolates with reduced susceptibility due to accumulation of resistance genes has been increasing.

Association of tannase-producing Staphylococcus lugdunensis with colon cancer and characterization of a novel tannase gene.

BACKGROUND: The relationship between Streptococcus (St.) bovis endocarditis and colon cancer is well known. In St. bovis, the biotype I strain (formerly, St. gallolyticus) produces tannase that degrades tannins. The aim of this study was to investigate the association of tannase-producing bacteria with colon cancer, and to identify the major tannase-producing bacteria and the gene involved. METHODS: Tannase-producing bacteria were isolated in tannic acid-treated selective agar medium from feces and rectal swabs of 357 patients who underwent colon endoscopy from 1999 to 2004. RESULTS: Tannase-producing bacteria were isolated more frequently from the colon cancer group (24.3%) than from the adenoma or normal groups (14.4%; P < 0.05). S. gallolyticus, Staphylococcus (S.) lugdunensis, Lactobacillus (L.) plantarum, and L. pentosus were all identified as tannase-producing bacteria. Of these, S. lugdunensis was significantly isolated from the advanced-stage cancer group (22.2%; P < 0.001) more than from the early-stage cancer (8.6%) or adenoma (4.9%) groups. The gene (tanA) for tannase in S. lugdunensis was cloned and sequenced. The tanA gene was associated with all S. lugdunensis but not with other bacteria by Southern blotting and polymerase chain reaction. CONCLUSIONS: Tannase-producing S. lugdunensis is associated with advanced-stage colon cancer, and the tanA gene is a useful marker for the detection of S. lugdunensis.

Efficacy of low-dose proton pump inhibitor (PPI) in the eradication of Helicobacter pylori following combination PPI/AC therapy in Japan.

BACKGROUND/AIMS: In Japan, eradication regimens consisting of a proton pump inhibitor (PPI) + amoxicillin (AMPC) + clarithromycin (CAM) (PPI/AC) for 1 week have been conducted. In the present study, we assessed the eradication rates following treatment with low doses of various PPIs. METHODOLOGY: 135 patients were divided randomly into one of three 7-day regimens: (i) omeprazole (OPZ) 20 mg/day + AMPC 1500 mg/day + CAM 600 mg/day (OAC); (ii) lansoprazole (LPZ) 30 mg + AMPC 1500 mg/day + CAM 600 mg/day (LAC); and (iii) rabeprazole (RPZ) 10mg/day + AMPC 1500 mg/ day + CAM 600 mg/day (RAC). The genetic polymorphism of CYP2C19 was also examined. RESULTS: The eradication rates according to the treatment regimen were as follows: 69.9% (31/45) for OAC, 62.2% (28/45) for LAC, and 71.1% (32/45) for RPZ. No significant differences were found among the regimens. Moreover, eradication rates, according to CYP2C19 phenotype (homozygous extensive metabolizer (EM), heterozygous EM, and poor metabolizer) were: 68.6% (35/51), 77.4% (41/53), and 82.4% (14/17), respectively. CONCLUSIONS: In PPI/AC therapy, the eradication rate for each low-dose PPI was 60-70%, which is low. Based on previous reports, it is considered that doses greater than 40 mg/day OPZ, 60 mg/day LPZ, and 20 mg/day RPZ are required.