Biomedical subjects

H Wisplinghoff

Publications and source records attributed to H Wisplinghoff.

7 recordsLinked to original sources

PubMed2003

Clonal spread of methicillin-resistant Staphylococcus aureus in a large geographic area of the United States.

Methicillin resistance in Staphylococcus aureus has rapidly increased over the last two decades. This increase is paralleled by the emergence of unique multi-resistant MRSA clones. In Brazil, Argentina, Uruguay, Portugal and Czech Republic a specific MRSA clone is widely spread, the so-called Brazilian epidemic clone. Another epidemic clone, the Iberian clone, is disseminated in Spain, Portugal, Belgium, Scotland, Italy, Germany and New York. Thus, a large number of hospital-acquired infections have been caused by specific MRSA clones. Using different molecular techniques for MRSA typing, we verified that two unique epidemic clones are spread over large geographic area in the US. In addition, we showed that a previously described MRSA clone type, the New York clone (I::A:A), is widely spread beyond the New York frontiers.

Cloning, Molecular↗

PubMed2001

Systemic inflammatory response syndrome in adult patients with nosocomial bloodstream infection due to Staphylococcus aureus.

To determine the impact of methicillin resistance on clinical course and outcome, we evaluated nosocomial bloodstream infections (BSIs) due to Staphylococcus aureus that were diagnosed in 82 adult patients at the Medical College of Virginia Hospitals from December 1995 through May 1997. Patients with BSI due to methicillin-resistant S. aureus were compared with patients with BSI due to methicillin-susceptible S. aureus; the groups did not differ with regard to inflammatory response or outcome. Mortality was predicted by systemic inflammatory response and Acute Physiology and Chronic Health Evaluation II score but did not correlate with bacterial resistance to methicillin.

APACHE↗

PubMed2000

Nosocomial bloodstream infections caused by Acinetobacter species in United States hospitals: clinical features, molecular epidemiology, and antimicrobial susceptibility.

We examined the clinical and epidemiological features of nosocomial bloodstream infections (BSIs) caused by Acinetobacter species and observed from 1 March 1995 through 28 February 1998 at 49 United States hospitals (SCOPE National Surveillance Program). Acinetobacter species were found in 24 hospitals (49%) and accounted for 1.5% of all nosocomial BSIs reported. One hundred twenty-nine isolates were identified either as A. baumannii (n=111) or other Acinetobacter species (n=18). Patients with A. baumannii BSI, compared with patients with nosocomial BSI caused by other gram-negative pathogens, were more frequently observed in the intensive care unit (69% vs. 47%, respectively; P<.001; odds ratio [OR] 2.4; 95% confidence interval [CI] 1.6-3.7) and were more frequently receiving mechanical ventilation (58% vs. 30%, respectively; P<.001; OR 3.2; 95% CI 2.1-4.8). Crude mortality in patients with A. baumannii BSI was 32%. Molecular relatedness of strains was studied by use of polymerase chain reaction-based fingerprinting. Clonal spread of a single strain occurred in 5 hospitals. Interhospital spread of epidemic A. baumannii strains was not observed. The most active antimicrobial agents against A. baumannii (90% minimum inhibitory concentration values) were imipenem (1 mg/L; 100% of isolates susceptible), amikacin (8 mg/L; 96%), tobramycin (4 mg/L; 92%), and doxycycline (4 mg/L; 91%). Thirty percent of isolates were resistant to > or =4 classes of antimicrobials and were considered to be multidrug resistant.

Acinetobacter↗

PubMed2000

Comparative activities of ciprofloxacin, clinafloxacin, gatifloxacin, gemifloxacin, levofloxacin, moxifloxacin, and trovafloxacin against epidemiologically defined Acinetobacter baumannii strains.

In vitro activities of seven fluoroquinolones against 140 clinical Acinetobacter baumannii isolates representing 138 different strain types were determined. The rank order of activity was clinafloxacin > gatifloxacin > levofloxacin > trovafloxacin > gemifloxacin = moxifloxacin > ciprofloxacin. The 31 outbreak-related A. baumannii strains were significantly more resistant than were 109 sporadic strains.

Acinetobacter↗

PubMed1999

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Journal Article↗

PubMed1999

Risk factors for nosocomial bloodstream infections due to Acinetobacter baumannii: a case-control study of adult burn patients.

Risk factors for Acinetobacter baumannii bloodstream infection (BSI) were studied in patients with severe thermal injury in a burn intensive care unit where A. baumannii was endemic. Of 367 patients hospitalized for severe thermal injury during the study period, 29 patients with nosocomial A. baumannii BSI were identified (attack rate, 7.9%). Cases were compared with 58 matched controls without A. baumannii BSI. The overall mortality rate was 31% among cases and 14% among controls; only two deaths (7%) were considered directly related to A. baumannii BSI. Molecular typing of A. baumannii blood isolates by means of randomly amplified polymorphic DNA analysis and pulsed-field gel electrophoresis revealed the presence of three different strain types. Multivariate analysis showed that female gender (P = .027), total body surface area burn of > 50% (P = .016), prior nosocomial colonization with A. baumannii at a distant site (P = .0002), and use of hydrotherapy (P = .037) were independently associated with the acquisition of A. baumannii BSI in burn patients. These data underscore the need for effective infection control measures for this emerging nosocomial problem.

Acinetobacter↗

PubMed1999

Molecular relationships and antimicrobial susceptibilities of viridans group streptococci isolated from blood of neutropenic cancer patients.

From January 1995 to May 1998, 57 episodes of bacteremia due to viridans group streptococci were identified in 50 febrile neutropenic patients with hematologic malignancies. Four patients experienced two separate episodes of streptococcal bacteremia, and one patient had four separate episodes of streptococcal bacteremia. Strains were identified to species level as Streptococcus mitis (n = 37), Streptococcus oralis (n = 19), and Streptococcus salivarius (n = 1). Epidemiologic relatedness of these strains was studied by using PCR-based fingerprinting with M13 and ERIC-2 primers and pulsed-field gel electrophoresis with restriction enzyme SmaI. All strains that were isolated from different patients exhibited unique fingerprint patterns, thus suggesting that viridans group streptococcal bacteremia usually derives from an endogenous source. Cross-transmission of strains between patients could not be established. Four S. mitis isolates recovered during four separate bacteremic episodes in a single patient had identical fingerprint patterns. Susceptibility testing was carried out by broth microdilution technique according to National Committee for Clinical Laboratory Standards guidelines. The MICs at which 90% of the isolates are inhibited were (in milligrams per liter) as follows: 0. 5 (penicillin), 0.5 (amoxicillin), 0.25 (cefotaxime), 2 (chloramphenicol), 4 (erythromycin), 0.5 (clindamycin), >/=32 (tetracycline), >/=32 (trimethoprim-sulfamethoxazole), 4 (ciprofloxacin), 0.5 (sparfloxacin), 0.5 (vancomycin), 0.25 (teicoplanin), and 1 (quinupristin-dalfopristin). High-level penicillin resistance (MIC, >/=4 mg/liter) was found in one isolate only, but intermediate penicillin resistance was noted in 11 isolates (19%). Resistance rates to other drugs were as follows: 7% (amoxicillin), 4% (cefotaxime), 4% (chloramphenicol), 32% (erythromycin), 9% (clindamycin), 39% (tetracycline), 68% (trimethoprim-sulfamethoxazole), 23% (ciprofloxacin), 0% (sparfloxacin), 0% (vancomycin), 0% (teicoplanin), and 0% (quinupristin-dalfopristin).

Adolescent↗