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This article, published in the journal Endoscopy, discusses the accuracy of a gastric juice-based molecular antibiotic susceptibility testing (AST) for Helicobacter pylori (H. pylori) infection. The study evaluated the use of the medical device Endofaster in combination with upper gastrointestinal endoscopy to assess the presence of H. pylori and determine antibiotic resistance to clarithromycin and levofloxacin. The results showed a high level of concordance between the molecular AST and conventional phenotypic AST, indicating that the molecular AST is a valid tool for selecting tailored eradication regimens for H. pylori infection. [Extracted from the article]

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The knowledge on prevalence rates of yeasts and moulds in patients with cystic fibrosis (CF) in Germany is scarce. The aim of this report is to give an overview of the diversity and epidemiology of fungal species in CF patients. Over a 5-year period, all fungal isolates cultured from microbiological specimen from CF patients were recorded. Beside standard bacteriological culture media two fungal media were used for cultivation. Species were identified by microscopy, biochemical profiling, MALDI-TOF analysis or DNA sequencing methods. In sum, 25,975 clinical samples from CF patients were analyzed. About 75% of CF patients were colonized by yeasts, mainly Candida albicans (38%) and Candida dubliniensis (12%). In 35% of the patients Aspergillus spp. (Aspergillus fumigatus: 29%) were detected, followed by Exophiala dermatitidis and Scedosporium/Lomentospora complex isolates (4% each). Data for other fungal species are shown. Over a 5-year period, the epidemiology of fungal species detected in CF patientswas relatively constant. Clinical microbiology laboratories should carefully monitor samples from CF patients for newly occurring fungal pathogens. [ABSTRACT FROM AUTHOR]

We investigated to which extent bacterial and fungal donor organ contamination (DOC) caused posttransplant nosocomial infections (NI) in solid organ transplant (Tx) recipients. Between January 2002 to December 2003 (lung and heart Tx) and October 2003 to September 2004 (liver Tx), NIs were determined according to modified CDC criteria for NIs for all transplantations performed at Hannover Medical School. Organisms of the same species cultured from donor organs and infected transplantees were genotyped if available. Out of 282 solid organ recipients (140 lung-Tx, 16 heart-lung-Tx, 51 heart-Tx, 75 liver-Tx), 150 recipients (53.2%) received contaminated donor organs. Incidences of NIs were 33.7% in lung, 68.8% in heart-lung, 21.6% in heart, and 28% in liver recipients. In 11 out of 282 transplantees (3.9%, CI 95% 2.0-6.9%) organisms of NIs and of contamination of the donor organ were of the same species. Even if assuming five missing pairs of organisms as genetically identical, incidences of DOC-related posttransplant infections were only between 1.3% (CI95% 0.0; 7.2) in liver-Tx and 18.8% (CI95% 4; 45.6) in heart-lung Tx, and DOC related mortality was 0.4% (CI95% 0.0;1.9). Despite high DOC rates, posttransplant infections due to DOC were rare under the condition of adequate preoperative antibiotic prophylaxis and aseptic organ retrievement. [ABSTRACT FROM AUTHOR]

We investigated to which extent bacterial and fungal donor organ contamination (DOC) caused posttransplant nosocomial infections (NI) in solid organ transplant (Tx) recipients. Between January 2002 to December 2003 (lung and heart Tx) and October 2003 to September 2004 (liver Tx), NIs were determined according to modified CDC criteria for NIs for all transplantations performed at Hannover Medical School. Organisms of the same species cultured from donor organs and infected transplantees were genotyped if available. Out of 282 solid organ recipients (140 lung-Tx, 16 heart-lung-Tx, 51 heart-Tx, 75 liver-Tx), 150 recipients (53.2%) received contaminated donor organs. Incidences of NIs were 33.7% in lung, 68.8% in heart-lung, 21.6% in heart, and 28% in liver recipients. In 11 out of 282 transplantees (3.9%, CI 95% 2.0–6.9%) organisms of NIs and of contamination of the donor organ were of the same species. Even if assuming five missing pairs of organisms as genetically identical, incidences of DOC-related posttransplant infections were only between 1.3% (CI95% 0.0; 7.2) in liver-Tx and 18.8% (CI95% 4; 45.6) in heart-lung Tx, and DOC related mortality was 0.4% (CI95% 0.0;1.9). Despite high DOC rates, posttransplant infections due to DOC were rare under the condition of adequate preoperative antibiotic prophylaxis and aseptic organ retrievement. [ABSTRACT FROM AUTHOR]

Biofilm formation on oral implants can cause inflammation of peri-implant tissues, which endangers the long-term success of osseointegrated implants. It has been reported previously that implants revealing signs of peri-implantitis contain subgingival microbiota similar to those of natural teeth with periodontitis. The purpose of the first part of this study was an atraumatic, quantitative investigation of biofilm formation on oral implant abutments; the objective of the second part was to investigate whether Haemophilus actinomycetemcomitans and Porphyromonas gingivalis were present in the crevicular fluid around oral implants. Biofilm formation on 14 healing abutments, inserted for 14 days in 10 patients, was analysed quantitatively by use of secondary-electron and Rutherford-backscattering-detection methods. A 16S rRNA-based polymerase chain reaction detection method was used to detect the presence of H. actinomycetemcomitans and P. gingivalis in the crevicular fluid. For this investigation, samples of sulcus fluid were collected with sterile paper points at four measurement points per abutment. The difference between biofilm coverage of supragingival surfaces (17·5 ± 18·3%) and subgingival surfaces (0·8 ± 1·0%) was statistically significant ( P < 0·05). By use of universal primers, bacteria were found in all the samples taken, although the two periodontal pathogens were not found in any of the samples. The absence of periodontal pathogens from the sulcus fluid during initial bacterial colonization, despite massive supragingival biofilm formation, substantiates the assumption that cellular adherence of peri-implant tissue by means of hemidesmosoma, actin filaments and microvilli reduces the risk of formation of anaerobic subgingival pockets. [ABSTRACT FROM AUTHOR]

Copyright of Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A 34-year-old man with chronic inflammatory joint disease and recurrent fever over 6 years was diagnosed as having Still's disease. Treatment with corticosteroids and azathioprine was ineffective. Therefore, infliximab/methotrexate was started. The patient subsequently developed a wasting disease with rapid weight loss, erythema nodosum, diarrhoea, progressive lymph node enlargement, and a sigmoido-vesical fistula. Histological analysis of several enlarged lymph nodes, the margins of the fistula, and the small bowel established the diagnosis of Whipple's disease (WD). The presence of Tropheryma whipplei (Tw) DNA in the tissues was confirmed by polymerase chain reaction (PCR). Careful re-evaluation of biopsies taken from the ileum and the liver 2 years earlier, which at that time was not judged to be diagnostic for WD, retrospectively showed subtle histological signs of WD and were positive for Tw DNA. In summary, infliximab treatment seems to increase the risk of exacerbation of WD. WD should be carefully ruled out prior to application of tumour necrosis factor-a (TNF-a) blockade. [ABSTRACT FROM AUTHOR]

Chronic myelitis from Whipple's disease of the spinal cord is extremely rare. The differential diagnosis includes chronic inflammatory lesions, viral or bacterial infections, and tumours of the spinal cord. Here we present a 50-year-old man with mild sensory deficits because of a large lesion of the cervical spinal cord who markedly showed improvement during probatory antibiotic therapy. PCR and jejunal biopsy were initially negative and only later confirmed the diagnosis of Whipple's disease. Clinical and neuroradiological criteria are suggested which may be of help in the early diagnosis of spinal Whipple's disease before confirmation by molecular biology or histology. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the performance of three antigenic preparations for serological diagnosis of Helicobacter pylori infection: (i) native antigens from Helicobacter pylori strain N6 or its aflagellated isogenic mutant N6 flbA–, or an acellular extract (antigen AgFA) from a pool of six clinical strains; (ii) recombinant antigens consisting of CagA fused to MS2 polymerase and HspA or recombinant UreA and UreB fused to the maltose-binding protein, and (iii) the preparations provided with two commercial kits, the Cobas Core (Roche Diagnostic Systems, France) and the Pylori Stat (BioWhittaker, Belgium). All preparations were used in an enzyme immunoassay to test 92 sera from dyspeptic patients for whom the status of Helicobacter infection was established. Sensitivities were higher (90 to 100%) for the native antigens and the commercial kits than for the recombinant antigens. Specificities were higher than 90%, except with UreA + UreB (42%). The most useful antigens were those extracted from strains N6 and N6 flbA–. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to evaluate the primary and acquired resistance of H. pylori against clarithromycin, metronidazole, and amoxicillin, and to elucidate the consequential influence on H. pylori eradication. Methods: A total of 195 patients with positive H. pylori status were consecutively included. In 172 patients, H. pylori could be cultured for evaluation of primary antibiotic resistance. Fifty patients received a 2-wk dual therapy with an acid inhibitor and amoxicillin 2,000 mg daily (A), the other 122 patients a 1-wk modified triple therapy with the acid inhibitor clarithromycin 500-1,000 mg daily, and metronidazole 1,000-1,500 mg daily (B: n = 78), or amoxicillin 2,000 mg daily and metronidazole 1,000 mg daily (C: n = 44), respectively. Acid inhibition was conducted with pantoprazole 40 mg b.Ld. (n = 62), omeprazole 20 mg b.Ld. (n = 50), lansoprazole 30 mg b.i.d. (n = 10), or ranitidine 150 mg t.i.d. (n = 50). After therapy, 36 patients remained H. pyloripositive, 20 after dual therapy (A) and 16 after modified triple therapy (B: n = 7, C: n = 9). In 32 of these patients, H. pylori could be recultured for evaluation of acquired resistance (A: n = 18, B: n = 7, C: n = 7). Results: Primary H. pylori resistance to metronidazole was observed in 36 of 172 patients (21%) and to clarithromycin in three of 172 (2%). Acquired resistance was found in six of 14 (43%) and in two of seven (29%), respectively, whereas neither primary nor acquired H. pylori resistance to amoxicillin was noted. Patients infected with metronidazole resistant H. pylori strains were successfully treated in combination with clarithromycin (eight of nine vs 63 of 67 with sensitive strains, NS), but not with amoxicillin (one of eight vs 32 of 34 with sensitive strains, p < 0.0001). In two patients with acquired combined clarithromycin and metronidazole resistance, modified triple therapy failed. Conclusion: The value of modified triple therapy with amoxicillin and... [ABSTRACT FROM AUTHOR]

Helicobacter pylori produces polar sheathed flagella, which are believed to be essential for the bacterial colonization of the human gastric mucosa. Here we report on the cloning and genetic characterization of a H. pylori gene encoding the subunit of the flagellar filament, the flagellin. Screening of a genomic library of H. pylori with an originalities probe derived from the N-terminal amino acid sequence of purified flagellin resulted in a recombinant plasmids clone carrying the flagellin-encoding gene flaA on a 9.3 kb 8g/II fragment. The nucleotide sequence of flaA revealed an open reading frame of 1530 nucleotides, encoding a protein with a predicted molecular mass of 53.2 kDa, which is similar in size with the purified flagellin protein in SDS-potyacrylamide gel electrophoresis. Sequence alignment of H. pylori flagellin (FlaA) with other bacterial flagellins demonstrates a high degree of similarity in the amino-terminal and carboxy-terminal regions, including those of the closely related genus Campylobacter (56% overall identity with Campylobacter coli flaA), but little homology in the central domain. Southern hybridizations of chromosomal DNA with flaA-specific probes did not reveal the presence of additional homologous flagellin genes in H. pylori. Sequence analysis of the flaA flanking regions and mapping of the flaA mRNA start site by a primer extension experiment indicated that transcription of the gene is under the control of a (σ28-specific promoter sequence in H. pylori. The region upstream of the flaA promoter is subject to local DNA modification, resulting in the masking of two out of three closely linked Hindlll restriction sites in the chromosome of strain 898-1. Escherichia coli strains harbouring the recombinant plasmids did not produce full-length flagellin and data obtained with FlaA fusion proteins using an E. coli plasmid expression system suggest that a distinct nucleotide sequence in the gene interferes with productive... [ABSTRACT FROM AUTHOR]

We present a 10-year-old girl who had been diagnosed with juvenile idiopathic arthritis 5 years before and who experienced a flare of arthritis affecting one knee while she was off medication for almost 3 years. Seronegative Lyme arthritis had to be diagnosed based on the detection of Borrelia burgdorferi DNA in synovial fluid. No humoral immune response to Borrelia burgdorferi was detectable before, at the time of diagnosis and up to 3 years later. [ABSTRACT FROM AUTHOR]

Motility and chemotaxis are amongst the most important factors of H. pylori pathogenicity and persistence. We reported previously that H. pylori cells are attracted by urea and that urea plays an important role in the chemotactic motility of H. pylori in viscous media (Infect. Immun. 1998, 66:4832-4837). To investigate in more detail mechanisms of H. pylori chemotaxis, we performed functional analyses of tlpA- and tlpC-homologous chemotaxis sensor mutants of H. pylori. Materials and Methods: The coding sequence of chemoreceptors tlpA and tlpC from different H. pylori strains was amplified by PCR and cloned. A kanamycin cassette was inserted into the coding sequences of tlpA and tlpC to generate mutants by gene disruption. Mutants were analyzed using electron microscopy and various motility assays. For swarming assays, bacterial stabs in 0.3% refined agar in brucella broth (supplemented with 3-10% serum) were performed. For the behavioral analyses of the mutants in several different environments, the tracking software (MoveTr32)was used. Chemotaxis capillary assays were performed in 50mM potassium phosphate buffer (pH7.0) using capillaries containing 10 mM solutions of amino acids as described previously. Results: 1) tlpA and tlpC mutants showed less swarming than the wild type strains. 2) tlpA and tlpC mutants displayed similar behavior compared to the wildtype strains in various liquid media. 3) tlpA and tlpC mutants showed less chemotactic activity towards urea than the wild type. 4) tlpA and tlpC mutants showed the same level of chemotaxis to several amino acids as the wildtype strains. [ABSTRACT FROM AUTHOR]