W Witte
Robert Koch Institute
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European Journal of Clinical Microbiology & Infectious Diseases | 2005
Ingo Klare; C. Konstabel; S. Mueller-Bertling; Guido Werner; Birgit Strommenger; C. Kettlitz; S. Borgmann; B. Schulte; D. Jonas; A. Serr; A. M. Fahr; U. Eigner; W Witte
The incidence of vancomycin-resistant Enterococcus faecium isolation was low (≤5%) in German hospitals before 2003. Within the second half of 2003 and the first half of 2004, however, increasing frequencies of up to 14% were noticed in several hospitals in southwestern Germany. This increase was attributed mainly to the occurrence and spread of epidemic-virulent ampicillin/vancomycin-resistant, vanA- and vanB-positive E. faecium clones, most of which exhibited the virulence factors enterococcal surface protein (esp) and bacteriocin activity and some which exhibited hyaluronidase (hyl). E. faecium possessing hyaluronidase was initially found in U.S. hospitals and recently detected in several European hospitals and, subsequently, in German hospitals as well. Ampicillin/vancomycin-resistant E. faecium clones originating mainly from southwestern German hospitals were characterized by multilocus sequence typing since different sequence types (STs) belonging to the clonal complex-17 are currently disseminated worldwide. Multilocus sequence typing revealed that, in 1998 and 1999, ampicillin/vancomycin-resistant E. faecium clone ST-117 was prevalent in various German hospitals, while in 2003 and 2004, clone ST-203 dominated in several hospitals located in southwestern Germany. Both sequence types display single-locus variants of ST-78, which was frequently recorded in various Italian hospitals between 2000 and 2003, and all of these STs belong to the clonal complex-17. Expression of linezolid resistance was observed in ampicillin/glycopeptide-resistant E. faecium strains (VanA type) from two tertiary hospitals in southwestern Germany due to mutations in domain V of the 23S rDNA (G2576T). While in one hospital the resistance emerged during linezolid therapy, in the other hospital resistance was caused by transfer of an identical linezolid/ampicillin/glycopeptide-resistant E. faecium strain. In conclusion, it is very important to monitor the occurrence of epidemic-virulent clonal complex-17 strains of E. faecium to prevent their spread in hospitals, especially if they are resistant to glycopeptides and linezolid.
European Journal of Clinical Microbiology & Infectious Diseases | 2005
J. Maier; H. Melzl; Udo Reischl; I. Drubel; W Witte; Norbert Lehn; Hans-Jörg Linde
Until recently, Panton–Valentine leukocidin (PVL)-positive methicillin-resistant Staphylococcus aureus (MRSA) strains were considered to be rare in Germany [1, 2]. However, data collected retrospectively (122 cases in the period 1995–2003) and prospectively (127 cases in 2004) for the geographical region of southeast Bavaria indicate that PVL-positive MRSA might be more common than previously acknowledged [3]. In the study presented here, we evaluated 122 patients in whom PVL-positive MRSA was detected in 2004. Nineteen of these patients had either traveled to (or originated from) foreign countries (predominantly in the Middle East) prior to the onset of symptoms or they belonged to a family originating from a Mediterranean country. The emergence of PVL-positive MRSA has been noted worldwide in patients without common risk factors for nosocomial multidrug-resistant pathogens [4, 5]. Patients typically present with a history of multiple recurrent deepseated abscesses, often without an obvious point of entry [6]. Necrotizing pneumonia may also occur. In many cases, carrier status or infections are recorded in close contacts of the index case, such as family members, sexual contacts, fellow military recruits, contact-sport participants, or prison inmates. In the laboratory, PVL-positive MRSA can be distinguished from nosocomial MRSA negative for PVL by a number of phenotypic and genotypic characteristics. Oxacillin resistance is caused by the mecA gene as part of a specific mec-type IV or -type II staphylococcal cassette chromosome [7]. In contrast to MRSA, many PVL-positive MRSA strains isolated in Germany, France or Switzerland are also resistant to fusidic acid (often associated with the far1 gene coding for an efflux mechanism [2, 8]), whereas resistance to other classes of antibiotics is rare. In addition, most strains of PVL-positive MRSA harbor a specific set of pathogenicity factors (e.g., staphylococcal enterotoxin H, bacteriocin bca, and Panton–Valentine leukocidin) [9]. Although the clinical presentation of infection caused by S. aureus might depend on a variety of factors not yet fully understood [10, 11], PVL is likely to play a key role in skin-related infections and necrotizing pneumonia [6]. PVL is a pore-forming toxin causing lysis of granulocytes and macrophages [12, 13]. The presence of PVL genes is demonstrated by PCR testing for lukS/F [6]. In a prospective study starting in January 2004, we collected clinical and epidemiological data from 127 patients with PVL-positive MRSA using a standardized questionnaire in interviews with patients or their physicians. A case was considered community-acquired if, at the time of symptom onset, the patient or close contacts had no connection with a medical institution and none of the following risk factors: open wound, chronic disease, or antibiotic consumption in the preceding 6 months. Otherwise, the case was considered nosocomial. Altogether, 39 community-acquired and 88 nosocomial cases were observed. Of the 88 nosocomial cases, 75 were detected in one single outbreak that was unrelated to all of the other cases, as proven by epidemiological data, a uniform and unique pattern in pulsed-field gel-electrophoresis, and MLST type 22 (data not shown); these cases were excluded from further analysis in this report. In 19 patients acquisition of PVL-positive MRSA was linked to foreign countries through travel or family connections: nine patients had a history of travel and ten patients had family originating from the Mediterranean J. Maier . H. Melzl . U. Reischl . N. Lehn . H. Linde (*) Institut für Medizinische Mikrobiologie und Hygiene, Franz-Josef-Strauss-Allee 11, 93049 Regensburg, Germany e-mail: [email protected] Tel.: +49-941-9446414 Fax: +49-941-9446402
European Journal of Clinical Microbiology & Infectious Diseases | 2002
Sissolak D; Alexandra Geusau; Heinze G; W Witte; Manfred Rotter
Nasal carriage is an important risk factor for Staphylococcus aureus infection, particularly in HIV-infected individuals. In this analytical cross-sectional study, a variety of probable risk factors associated with nasal carriage of Staphylococcus aureus were investigated. HIV-infected patients were examined within a larger cohort of infectious diseases patients. Staphylococcus aureus strains from HIV-infected and non-HIV-infected carriers were identified by molecular biological analysis. One hundred seventy infectious disease patients, 47 of them infected with HIV, were included. All patients were admitted to the University Hospital of Vienna, Austria, between January and July 1999. Independent significant effects on Staphylococcus aureus nasal carriage were found to be HIV status (OR 2.5, 95% CI 1.1–5.6; P=0.0303), history of operation or severe wound within 3 months prior to admission (OR 4.0, 95% CI 1.3–13.0; P=0.0208), presence of an intravenous device within 2 weeks prior to admission (OR 10.8, 95% CI 2.0–59.4; P=0.0065), and intake of antibiotics within 2 weeks prior to hospitalisation (OR 0.2, 95% CI 0.09–0.6; P=0.0016). Molecular analysis of the Staphylococcus aureus strains revealed that the strains in both groups resembled those of healthy nonhospitalized carriers in the community.
Epidemiology and Infection | 1994
W Witte; Christa Cuny; Christine Braulke; Dagmar Heuck
Clonal dissemination of two different MRSA strains, both clumping factor negative, has been observed in Germany for more than a year. Both strains possess the mec-A determinant and each exhibits a characteristic genomic DNA fragment pattern. One strain has spread in the north, the other in the south-west of Germany. Intensive care units are mainly affected by MRSA-infections and probably play a special role in further intra- and inter-hospital spread.
Infection | 1994
W Witte; Christine Braulke; Dagmar Heuck; Christa Cuny
SummaryTwo outbreaks of nosocomial infections with MRSA, one in a urological unit in connection with transurethral prostatectomy and the other in an orthopaedic clinic with infections after implantation of prosthetic hips, have been analyzed on the basis of typing MRSA by phagepatterns, plasmid profiles and genomic DNA fragment patterns. Main reasons for these outbreaks were obviously mistakes in hospital hygiene and an inappropriate antibiotic prophylaxis (in the first outbreak a quinolone over about 7 days, in the second a third generation cephalosporin). Both outbreaks could be stopped by measures of hospital hygiene including isolated or cohort nursing of affected patients, and change in antibiotic prophylaxis. Intensive care units (ICUs) are more often affected by MRSA than other clinical settings. As described by the example of an outbreak with MRSA in a municipal hospital, ICUs can play a special role in intrahospital spread of MRSA. The recently observed inter-regional clonal interhospital dissemination of MRSA in Germany is mainly due to a transfer of patients between hospitals; prewarning of the hospital of destination and a number of hygiene measures can prevent further spread.ZusammenfassungZwei Ausbrüche von Krankenhausinfektionen mit MRSA, im ersten Fall in einer urologischen Abteilung im Zusammenhang mit transurethraler Prostatectomy, im zweiten Fall in einer orthopädischen Klinik nach Hüftgelenkersatz, wurden auf der Grundlage der Typisierung von MRSA mittels Lysotypie, Plasmidprofilen und Fragmentmustern der genomischen DNS analysiert. Hauptursachen für diese Ausbrüche waren offensichtliche Fehler der Krankenhaushygiene und unpassende Antibiotikaprophylaxe (beim ersten Ausbruch ein Chinolon über 7 Tage, beim zweiten Ausbruch ein Drittgenerations-Cephalosporin). Beide Ausbrüche konnten durch Maßnahmen der Krankenhaushygiene, die eine Isoliertpflege der betroffenen Patienten einschlossen, und durch Änderungen der Antibiotikaprophylaxe beendet werden. Intensivpflegestationen (ICU) werden deutlich häufiger durch Infektionen mit MRSA betroffen als andere klinische Bereiche. Wie am Beispiel eines Ausbruchs mit MRSA in einem städtischen Krankenhaus beschrieben wird, können ICU eine besondere Bedeutung für die weitere Ausbreitung von MRSA in einem Krankenhaus haben. Die gegenwärtig in Deutschland beobachtete überregionale klonale Ausbreitung von MRSA ist vorrangig auf die Verlegung von Patienten zwischen Krankenhäusern zurückzuführen. Eine Vorwarnung in Verbindung mit rechtzeitig getroffenen Hygienemaßnahmen kann die weitere Ausbreitung verhindern.
Infection | 2004
Elke Halle; J. Padberg; S. Rosseau; Ingo Klare; Guido Werner; W Witte
Abstract.Here we report the first German case of necrotizing pancreatitis, peritonitis, and septic shock caused by linezolid-resistant Enterococcus faecium and Enterococcus faecalis.
European Journal of Clinical Microbiology & Infectious Diseases | 1999
C. Windmeier; Christa Cuny; Christine Braulke; Dagmar Heuck; W Witte
1. Lin HJ: Hepatitis G virus. Journal of the International Federation of Clinical Chemistry (1997) 9 :27–30 2. Alter MJ, Gallagher M, Morris TT, Moyer LA, Meeks EL, Krawczynski K, Kim JP, Margolis HS: Acute non-A-E hepatitis in the United States and the role of hepatitis G virus infection. New England Journal of Medicine (1997) 336 :741–746 3. Nakatsuji Y, Shih JW, Tanaka E, Kiyosawa K, Wages J Jr, Kim JP, Alter HJ: Prevalence and disease association of hepatitis G virus infection in Japan. Journal of Viral Hepatitis (1996) 3 :307–316 4. Fiordalisi G, Zanella I, Mantero G, Bettinardi A, Stellini R, Paraninfo G, Cadeo G, Primi D: High prevalence of GB virus C infection in a group of Italian patients with hepatitis of unknown etiology. Journal of Infectious Diseases (1996) 174 :181–183 5. Cheung RC, Keeffe EB, Greenberg HB: Hepatitis G virus: is it a hepatitis virus? Western Journal of Medicine (1997) 167 :23–33 6. Ichimura H, Tamura I, Kurimura O, Koda T, Mizui M, Tsuchie H, Kurimura T: Hepatitis C virus genotypes, reactivity to recombinant immunoblot assay 2 antigens and liver disease. Journal of Medical Virology (1994) 43 :212–215 7. Okamoto H: Genetic heterogeneity of hepatitis C virus. Intervirology (1994) 37 :68–76 8. Egawa K, Yukawa T, Arakawa S, Nakao H, Inoue T, Tanaka T, Tsuda F, Okamoto H, Miyakawa Y, Mayumi M: Infection with GB virus C in leprous patients in Japan. Journal of Medical Virology (1996) 49 :110–114 9. Manolakopoulos S, Morris A, Davies E, Brown D, Hajat S, Dusheiko G: Influence of GB virus C viremia on the clinical, virological and histological features of early hepatitis C related disease. Journal of Hepatology (1998) 28 :173–178 10. Guilera M, Sáiz JC, López-Lobrador FX, Olmedo E, Ampurdanés S, Forns X, Bruix J, Parés A, Sánchez-Tapias JM, Jiménez de Anta MT, Rodés J: Hepatitis G virus infection in chronic liver disease. Gut (1998) 42 :107–111
Infection | 2002
M. Wächtler; D. Eichenlaub; E. Strobel; Ute Koch; W. Doering; M. Overbeck; W Witte
Infective native valve endocarditis caused by Staphylococcus aureus accounts for approximately 35% of cases in patients without intravenous drug abuse and for 61% of cases in intravenous drug abusers [1]. While coagulase-negative staphylococci are the most commonly isolated organisms in prosthetic valve endocarditis, only 5% of cases of native valve endocarditis are due to these pathogens [2]. The species Staphylococcus lugdunensis was described for the first time in 1988 [3]. This organism differs from other coagulase-negative staphylocci in that it tends to cause a more virulent form of infective endocarditis, characterized by an acute onset and destructive clinical course with a high mortality rate similar to that of S. aureus endocarditis [4]. An analysis of the 22 cases reported in the English language literature until 1997 revealed severe sequelae of S. lugdunensis endocarditis: Seven of eight patients who received only antibiotic treatment died and five of 14 patients with antibiotic treatment and operative valve replacement did not survive. 15 of these 22 patients developed severe cardiac complications such as heart insufficiency, perforation or destruction of valve, rupture of chordae tendineae or myocardial abscess [5]. A previously healthy 22-year-old woman became acutely ill 8 days before admission with fever and fatigue. One week prior to the onset of symptoms, she had returned from a 3-week beach holiday in Bali. Further medical history was negative except for rhinitis atopica. Physical examination revealed a patient in good general health with a core temperature of 39.3 °C, heart rate 110/min and blood pressure 140/60 mmHg. A loud pansystolic murmur was heard at the apex. Peripheral signs of bacterial endocarditis were not detected. Transthoracic and transesophageal echocardiography identified a peduncular vegetation, measuring 1.5 0.8 cm, on the anterior leaflet of the mitral valve (Figure 1) with mild regurgitation. Left ventricular diameters and pump function were normal and all other valves showed no evidence of vegetations. Flow in the pulmonary veins was normal. Five days later regurgitation was increased and could be traced back to the pulmonary veins. C-reactive protein was 131 mg/l, the erythrocyte sedimentation rate was 95 mm in the first hour and hemoglobin 11.8 g/dl. 1-, 2and -globulins were slightly elevated in serum protein electrophoresis (5.9, 11.2 and 12.9 rel.%, respectively). Leukocyte count and the other values of clinical chemistry were within the normal range. Infection Correspondence
European Journal of Clinical Microbiology & Infectious Diseases | 2001
B. Kreft; S. Eckstein; A. Kahl; U. Frei; W Witte; M. Trautmann
Abstract.Few data exist regarding the clonal identity of Staphylococcus aureus (SA) that colonises the nostrils and causes exit-site infections in peritoneal dialysis patients. Nasal and exit-site swabs were taken monthly from 41 patients undergoing peritoneal dialysis, and a genetic analysis of SA isolates was performed by pulsed-field-gel electrophoresis. When SA was identified at the exit-site, the clonal identity of nasal and exit-site isolates was demonstrated. In 50% of the SA carriers, nasal isolates were genetically constant over time; in the other 50% a change of colonising SA strains was observed. The risk of exit-site infection was identical in both groups.
Eurosurveillance | 2009
Mardjan Arvand; Hauri Am; Zaiss Nh; W Witte; Gudrun Bettge-Weller