Two severe cases of Vibrio vulnificus wound infection with secondary septicemia occurred during 1 week in August 2003 on the German island of Usedom in the southwestern Baltic Sea. In both cases, pre-existing wounds were inoculated by wading in contaminated sea water. One of the patients died from septic multiorgan failure. To the best of our knowledge, this is the first fatality due to a V. vulnificus infection to have occurred in Germany. Microbiological analysis revealed high concentrations of V. vulnificus in sea water along the coastline, following a period when water temperature exceeded 20°C for more than 2 weeks.

Over 15 months, 60 patients at a German University Hospital became infected or colonized by a multiresistant Pseudomonas aeruginosa strain, which was isolated from tracheal secretions, blood, urine, venous catheters, ascites and several wounds. Most patients had undergone invasive treatment (surgery, cancer therapy). The genetic relationship of the isolates was investigated by pulsed field gel electrophoresis. The isolates were resistant to beta-lactam antibiotics, including carbapenems and aztreonam, to aminoglycosides and quinolones. The only in vitro susceptibility was to polymyxin B. Extensive sampling was carried out to identify contaminated medical devices, surfaces or media (water, food). Samples were taken from doctors and nursing staff and various treatment procedures were observed for several weeks. The handling of respirators, resuscitation tubes, urine bottles, and bedpans resulted in the contamination of the patients' environment, although most devices were cleaned and disinfected with automatic washer/disinfectors. Several wash basins on the intensive care unit were contaminated, but none of the drinking water samples showed any growth of P. aeruginosa. We recommend the strict use of gloves and strict application of alcoholic hand disinfectants immediately after discarding the gloves. The chain of infection ceased after strict cohort isolation and the subsequent introduction of the specific hygiene regime.

The aim of this study was to analyze methicillin-resistant Staphylococcus aureus strains isolated during a 1-year period by means of pulsed-field gel electrophoresis, resistance phenotyping and determination of biochemical features. Eight different resistance phenotypes with the predominant resistance type Pen Oxa Cip (penicillin, oxacillin, ciprofloxacin) were observed. None of the strains tested exhibited decreased susceptibility to vancomycin, but two strains were resistant to mupirocin. Genetic relatedness of methicillin-resistant Staphylococcus aureus isolates could be shown for two outbreaks, one of which was caused by a clone with an epidemic potential concerning duration of colonization/infection of patients and dissemination of the strains in the hospital.

Multiply-resistant Pseudomonas aeruginosa were first detected in north-eastern Germany at the end of 1996; since then they have been isolated predominantly from patients in intensive care units. Colonization/infection, especially of the respiratory tract, has been demonstrated in 80 patients, with strains resistant to beta-lactams, carbapenems, aminoglycosides and quinolones. Amikacin showed in-vitro synergy with cefepime, ceftazidime or piperacillin/tazobactam. Horizontal transfer of strains was followed by PFGE and identical strains were detected in the environment, but the source of infection was not established. Rigorous infection control and restricted clinical use of carbapenems limited further dissemination of this outbreak.

Hunsicker, Andreas; Kullich, W.; Weissenhofer, W.; Lorenz, D.; Petermann, J.; Klöting, I.; Panzig, B. Author Information

Pediatric PulmonologyVolume 23, Issue 5 p. 389-391 Letter to the Editor Multiple brain abscesses in al 25-year-old patient with cystic fibrosis, successfully treated with an anti-pseudomonas plus anti-mycobacterial antibiotic regimen S.K.W. Wiersbitzky, Corresponding Author S.K.W. Wiersbitzky Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanyDepartment of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorR. Bruns, R. Bruns Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorE.-H. Ballke, E.-H. Ballke Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorR.-D. Stenger, R.-D. Stenger Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorH. Wiersbitzky, H. Wiersbitzky Unit of Pediatric Roentgenology Center of Radiology Greifswald, GermanySearch for more papers by this authorG. Kallwellis, G. Kallwellis Unit of Pediatric Roentgenology Center of Radiology Greifswald, GermanySearch for more papers by this authorB. Panzig, B. Panzig Department of Microbiology, Ernst-Moritz-Arndt University, Greifswald, GermanySearch for more papers by this authorR. Mentel, R. Mentel Department of Microbiology, Ernst-Moritz-Arndt University, Greifswald, GermanySearch for more papers by this author S.K.W. Wiersbitzky, Corresponding Author S.K.W. Wiersbitzky Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanyDepartment of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorR. Bruns, R. Bruns Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorE.-H. Ballke, E.-H. Ballke Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorR.-D. Stenger, R.-D. Stenger Department of Pediatrics, Center for Children and Youth, University Hospital Greifswald, GermanySearch for more papers by this authorH. Wiersbitzky, H. Wiersbitzky Unit of Pediatric Roentgenology Center of Radiology Greifswald, GermanySearch for more papers by this authorG. Kallwellis, G. Kallwellis Unit of Pediatric Roentgenology Center of Radiology Greifswald, GermanySearch for more papers by this authorB. Panzig, B. Panzig Department of Microbiology, Ernst-Moritz-Arndt University, Greifswald, GermanySearch for more papers by this authorR. Mentel, R. Mentel Department of Microbiology, Ernst-Moritz-Arndt University, Greifswald, GermanySearch for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1099-0496(199705)23:5<389::AID-PPUL13>3.0.CO;2-1Citations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume23, Issue5May 1997Pages 389-391 RelatedInformation

The purpose of our study was to establish a standardized reproducible animal model of intraperitoneal sepsis, induced by E. coli endotoxinaemia in LEW.1W rats, in order to investigate early immunoserological responses with a view to identifying a mediator-based evaluation system for such sepsis. In the pilot phase of this study we evaluate some mediators like endotoxin, phospholipase A2 and neopterin (biopterin) as possible markers for the outcome, i.e., the prognosis of a peritonitis infection.

Treatment of long-term artificially ventilated patients is often complicated by nosocomial infections. The infection that occurs with the highest frequency during intensive care treatment is pneumonia (22-63%). Ninety per cent of nosocomial infections of intensive care patients are endogenous infections caused by mainly gram-negative aerobic microorganisms that have colonized in the gastrointestinal tract. Selective decontamination of the intestine provides a method that prevents nosocomial infections. In a prospective study 13 patients whose oropharynx and gastrointestinal tract had been decontaminated (SDD) were compared to 17 patients in a control group. In a third group twelve patients were decontaminated in the gastrointestinal tract (SGD) only, and in a fourth group 16 patients were decontaminated in the oropharynx (SMD) only. Trachea, oropharynx and faeces of the patients belonging to the control group (KG) were colonized to almost 100% with gram-negative bacteria. Only 10% of the patients of the SDD and SMD groups showed gram-negative bacteria located in the trachea and oropharynx after one week of decontamination. No gram-negative aerobic bacteria were present after seven days in the faeces of the patients of the SDD and SGD groups. There was no difference with regard to the trachea and oropharynx between the control group and the SGD group. The gram-negative aerobic intestinal flora was not affected by the selective mouth decontamination. The average rate of pneumonia occurrence within the 15-day observation period was 28.2% for the control group, 14% for the SGD group, and 9.6% for the SDD group, and 4.1% for the SMD group. Decontamination of the oropharynx of patients is essential in order to successfully prevent pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)

A previously described cold adapted (ca) attenuated virus, K/25, derived from parent strain A/Krasnodar/101/59 (H2N2), was further modified by 35 additional passages in chick embryos at suboptimal temperature. The virus obtained had retained a distinct ts and ca phenotype and some other markers of attenuation but differed from formerly isolated ca variants by its higher genetic stability connected with an increased growth capacity in chick embryos.

Human influenza virus A/Krasnodar/101/59 (H2N2) was passaged in chick fibroblast cultures in the presence of trypsin at suboptimal temperature. The virus which underwent 16 passages at 28 degrees C possessed cold-adapted (ca) and temperature sensitive (ts) phenotypes and formed larger plaques at the optimal temperature (33 degrees C). Its reproduction in the lungs of hamsters was decreased as evidenced by approximately 2.5 log10 lower titres; only one of 9 virus isolates from the lungs of hamsters acquired the ts +/- phenotype, although it had retained a ca phenotype. Recombination of this variant with ts mutants of fowl plague virus (FPV) revealed a ts mutation only in gene 4 of this variant coding for haemagglutinin (HA). The virus which had had 25 passages at 28 degrees C possessed the same properties as the previous variant, but all eight virus isolates from the lungs of hamsters retained the ts phenotype; the genome of this variant contained ts mutations in genes 1, 3, 4, 5 and 6. The mutation found in gene 8 was not a ts mutation. The virus, which underwent 25 passages at 28 degrees C and additional 15 passages at 27 degrees C, formed large plaques and alike to the previous variants it possessed the ca and ts phenotypes; however, its reproduction in the lungs of hamsters was decreased by 4.0 log10 and occurred in the lungs only of 4 out 16 infected animals. This variant contained ts mutations in genes 1, 3, 4, 5, 6 and 7 and a non-ts mutation in gene 8.

Forty-Four sera of patients with confirmed influenza-A infection were titrated in parallel with and without 2-mercaptoethanic treatment against influenza-A by means of passive haemagglutination. Reduction of titre by at least two levels was detectable in 21 cases. Gradient centrifugation was additionally undertaken of 23 patient sera and three serum samples obtained from intact probands who had produced a titre against influenza-A in passive haemagglutination. Antibody against influenza-A was present in both the IgM and IgG fractions of the patients' serum samples. Yet, in the three control sera of intact probands antibody against influenza-A was recordable only from the IgG fraction. IgM antibody could not be detected by 2-mercaptoethanoic treatment alone unless the 7s-antibody portion in a given serum sample was smaller than the 19s-antibody portion.