Antimicrobial resistance of Helicobacter pylori in Germany, 2015 to 2018.

OBJECTIVES: National and international guidelines recommend empiric first-line treatments of individuals infected with Helicobacter pylori without prior antimicrobial susceptibility testing. For this reason, knowledge of primary resistance to first-line antibiotics such as clarithromycin is essential. We assessed the primary resistance of H. pylori in Germany to key antibiotics by molecular genetic methods and evaluated risk factors for the development of resistance. METHODS: Gastric tissue samples of 1851 yet treatment-naïve H. pylori-positive patients were examined with real-time PCR or PCR and Sanger sequencing for mutations conferring resistance to clarithromycin, levofloxacin and tetracycline. Clinical and epidemiological data were documented and univariable and multivariable logistic regression analyses were conducted. RESULTS: Overall primary resistances were 11.3% (210/1851) to clarithromycin, and 13.4% (201/1497) to levofloxacin; resistance to tetracycline (2.5%, 38/1497) was as low as combined resistance to clarithromycin/levofloxacin (2.6%, 39/1497). Female sex and prior antimicrobial therapies owing to unrelated bacterial infections were risk factors for clarithromycin resistance (adjusted OR (aOR) 2.3, 95% CI 1.6-3.4; and 2.6, 95% CI 1.5-4.5, respectively); older age was associated with levofloxacin resistance (aOR for those ≥65 years compared with those 18-35 years: 6.6, 95% CI 3.1-14.2). CONCLUSIONS: Clarithromycin might still be recommended in first-line eradication therapies in yet untreated patients, but as nearly every tenth patient may carry clarithromycin-resistant H. pylori it may be advisable to rule out resistance ahead of treatment by carrying out susceptibility testing or prescribing an alternative therapy.

[Ultrasound diagnosis of pseudomembranous colitis]. / Sonographische Diagnostik der pseudomembranösen Colitis.

BACKGROUND AND OBJECTIVE: The diagnosis of pseudomembranous colitis (PMC) is based on the history of exposure to antibiotics, characteristic endoscopic findings and on demonstrating the presence of Clostridium difficile toxins in the faeces. This report presents typical sonographic features of PMC. PATIENTS AND METHODS: The sonograms of 13 patients with PMC (7 males, 6 females, median age 70 years, range 55-84 years), were retrospectively analyzed. Patients' histories, clinical findings, the results of colonoscopy including histological findings and microbiological tests were related to the sonographic features of inflammation of the colon. RESULTS: At sonography the wall of the colon was thickened (6-17 mm) in each of the patients, different types of changed wall-architecture were seen. In 85% sonographic signs of colitis were restricted to the left colon, whereas in 15% a pancolitis was diagnosed. Ascites was detected in 38%, the colon contents were visible in 85%, in 77% the lumen was narrowed. Colonoscopy confirmed the diagnosis in six patients, in two patients endoscopy was performed only to control the effect of therapy and in five patients endoscopy was thought to be unnecessary. CONCLUSION: Sonography can supplement history and clinical findings if PMC is suspected. Potentially life-saving therapy can be initiated even if colonoscopy has not been performed and results of microbiological assessment are not yet available. However, the diagnosis of PMC remains to be based on the gold standard of colonoscopy and histological findings.

Degradation of keratan sulphate by beta-N-acetylhexosaminidases A and B.

Enzymic cleavage of beta-N-acetylglucosamine residues of keratan sulphate was studied in vitro by using substrate a [3H]glucosamine-labelled desulphated keratan sulphate with N-acetylglucosamine residues at the non-reducing end. Both lysosomal beta-N-acetylhexosaminidases A and B are proposed to participate in the degradation of keratan sulphate on the basis of the following observations. Homogenates of fibroblasts from patients with Sandhoff disease, but not those from patients with Tay--Sachs disease, were unable to release significant amounts of N-acetyl[3H]glucosamine. On isoelectric focusing of beta-N-acetylhexosaminidase from human liver the peaks of keratan sulphate-degrading activity coincided with the activity towards p-nitrophenyl beta-N-acetylglucosaminide. A monospecific antibody against the human enzyme reacted with both enzyme forms and precipitated the keratan sulphate-degrading activity. Both isoenzymes had the same apparent Km of 4mM, but the B form was approximately twice as active as the A form when compared with the activity towards a chromogenic substrate. Differences were noted in the pH--activity profiles of both isoenzymes. Thermal inactivation of isoenzyme B was less pronounced towards the polymeric substrate than towards the p-nitrophenyl derivative.