ABSTRACT
BACKGROUND: Antibiotic resistance of bacterial pathogens is an emerging problem worldwide. To combat multidrug resistant organisms (MRDOs) networks of care providers have been established in all states in Germany. The HICARE-network, a project to combat MRDOs, founded by the Federal Ministry of Education and Research, has published data from 2010 of a voluntary, German-wide, multicenter point-prevalence survey in 2011 conducted in collaboration with the German Society of Hospital Hygiene. The aim of the present survey was the re-evaluation of the situation in 2012. METHOD: The survey was conducted as a voluntary, anonymous, point-prevalence in May 2012 using routine data of microbiological diagnostics of the hospitals. As in the former survey of 2010 it was differentiated between primary, secondary and tertiary care hospitals and only data from intensive care units, surgical and medical wards were collected. Based on the survey form used in 2010, an updated version was used including more pathogens and corrected issues observed in the former survey. Methicillin-resistant Staphylococcus aureus (MRSA) (total as well as separated in hospital-acquired (HA), community-acquired (CA) and lifestock-associated (LA) MRSA), vancomycin resistant Staphylococcus aureus (VRSA/GRSA), vancomycin resistant Enterococcus faecalis resp. Enterococcus faecium (VR-E. faecalis resp. VR-E. faecium), extended-spectrum-beta-lactamase-building (ESBL) E. coli (ESBL-EC) and Klebsiella pneumoniae (ESBL-KP), multiresistant Acinetobacter spp. (MAB), multiresistant Pseudomonas spp. (MRP), carbapenemase-producing Enterobacteriaceae (CRE) as well as Clostridium difficile (CD) infections and severe infections requiring ICU-treatment were included in the survey along with additional data on screening strategy, the equipment with infection control staff and possible confounders. RESULTS: Out of 1,550 hospitals asked to participate, 62 returned data (4%). Data from 56 hospitals including primary (26), secondary (20) and tertiary (10) care hospitals were analyzable (3.6%). The most frequently reported organisms were MRSA 1.53% [CI95: 1.32-1.75], followed by CDAD 1.30% [CI95: 1.11-1.50], ESBL-EC 0.97% [CI95: 0.80-1.14], and ESBL-KP 0.27% [CI95: 0.18-0.36], regardless of the level of care. Prevalence of MRDOs depended on the level of care and on the type of ward, as expected. Overall prevalence was highest on intensive care wards, and prevalences were remarkably high on medical wards compared to surgical wards. All tertiary care providers employed their own infection control nurse, while only ~70% of the secondary and primary care hospitals did. Surprisingly, in two of the ten participating tertiary care providers neither an internal nor an external infection control doctor was available. DISCUSSION: With more than 13,000 patients in 56 hospitals distributed all over Germany, the survey included more than three times as many patients as the first survey and therefore not only adds valuable information about the epidemiology of emerging nosocomial pathogens, but also helps to raise awareness of the problem of antibacterial resistance in Germany. The prevalences reported seem to be comparable to the results of the former survey and of other surveys published. Some hospitals reported to have no infection control personnel available at all. This statement is in line with another survey published in this issue.
ABSTRACT
Increased gastric production of interleukin 8 and tumor necrosis factor alpha (TNF-alpha) has been implicated in the pathogenesis of Helicobacter pylori-associated gastroduodenal disease. In the present study we used a mouse model to demonstrate whether loss of the tumor necrosis factor receptor 1 (TNF-R1) function leads to differences in gastric inflammation or the systemic immune response in H. pylori infection. Six different clinical isolates of H. pylori (three cytotoxin-positive and three cytotoxin-negative strains) were adapted to C57BL/6 mice. TNF-R1-deficient (TNF-R1(-/-)) mice (n = 19) and isogenetic controls (n = 24) were infected and sacrificed after 4 weeks of infection. Inflammation of the stomach and the humoral immune response to H. pylori were evaluated by histological, immunohistochemical, and serological methods. There was no detectable difference in the grade or activity of gastritis in TNF-R1(-/-) mice when they were compared with wild-type mice, but the number of lymphoid aggregates was slightly reduced in the gastric mucosa of TNF-R1(-/-) mice. Interestingly, total immunoglobulin G (IgG), as well as IgG1, IgG2b, and IgG3, H. pylori-specific antibody titers were significantly higher in wild-type mice. As revealed by immunoblot analysis, the difference in reactivity against H. pylori antigens was not based on a failure to recognize single H. pylori antigens in TNF-R1(-/-) mice. We therefore suggest that TNF-R1-mediated TNF-alpha signals might support a systemic humoral immune response against H. pylori and that the gastric inflammatory response to H. pylori infection seems to be independent of TNF-R1-mediated signals.
