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Background: It is unknown whether rising incidence rates of nosocomial bloodstream infections (BSIs) caused by antibiotic-resistant bacteria (ARB) replace antibiotic-susceptible bacteria (ASB), leaving the total BSI rate unaffected., Methods: We investigated temporal trends in annual incidence densities (events per 100 000 patient-days) of nosocomial BSIs caused by methicillin-resistant Staphylococcus aureus (MRSA), ARB other than MRSA, and ASB in 7 ARB-endemic and 7 ARB-nonendemic hospitals between 1998 and 2007., Results: 33 130 nosocomial BSIs (14% caused by ARB) yielded 36 679 microorganisms. From 1998 to 2007, the MRSA incidence density increased from 0.2 to 0.7 (annual increase, 22%) in ARB-nonendemic hospitals, and from 3.1 to 11.7 (annual increase, 10%) in ARB-endemic hospitals (P = .2), increasing the incidence density difference between ARB-endemic and ARB-nonendemic hospitals from 2.9 to 11.0. The non-MRSA ARB incidence density increased from 2.8 to 4.1 (annual increase, 5%) in ARB-nonendemic hospitals, and from 1.5 to 17.4 (annual increase, 22%) in ARB-endemic hospitals (P < .001), changing the incidence density difference from -1.3 to 13.3. Trends in ASB incidence densities were similar in both groups (P = .7). With annual increases of 3.8% and 5.4% of all nosocomial BSIs in ARB-nonendemic and ARB-endemic hospitals, respectively (P < .001), the overall incidence density difference of 3.8 increased to 24.4., Conclusions: Increased nosocomial BSI rates due to ARB occur in addition to infections caused by ASB, increasing the total burden of disease. Hospitals with high ARB infection rates in 2005 had an excess burden of BSI of 20.6 per 100 000 patient-days in a 10-year period, mainly caused by infections with ARB.

In continuous surveillance of routine samples from five Dutch laboratories, we studied resistance to the antibiotics most commonly prescribed for urinary tract infections (UTI) in The Netherlands, namely norfloxacin, amoxycillin, trimethoprim and nitrofurantoin, from 1989 to 1998 in >90000 Escherichia coli isolates. Resistance to norfloxacin increased from 1.3% in 1989 to 5.8% in 1998. Multiresistance, defined as resistance to norfloxacin and at least two of the other three antibiotics, increased from 0.5% in 1989 to 4. 0% in 1998. Multivariate analysis of the norfloxacin resistance demonstrated that this yearly increase (the odds ratio was 1.0 in 1989, 1.6 in 1992, 2.9 in 1995 and 6.1 in 1998) was independent of other determinants of resistance to norfloxacin, such as age, gender and origin of the isolate. Analysis of strata, classified by year, age and gender, demonstrated an association between prescription of fluoroquinolones (defined daily doses per case of UTI) and resistance to norfloxacin in E. coli (P < 0.001). There was no significant association with the prescription of nitrofuran derivatives (nitrofurantoin) and trimethoprim with or without sulphamethoxazole. The yearly increase of resistance to fluoroquinolones in E. coli from UTI may stem from increased prescription of fluoroquinolones for UTI. Resistance of E. coli to these agents is likely to increase further as fluoroquinolone use increases in future.

An electronic surveillance network for monitoring antibiotic resistance in The Netherlands has been in operation since 1989. Seven public health laboratories participate and the system covers about 25% of all bacteriological determinations in The Netherlands. This paper reports the results of staphylococci isolated in the period 1989-1995. About 0.3% of the Staphylococcus aureus isolates in the study period were resistant to methicillin. This low percentage may be due to the restrictive use of antibiotics and to strict isolation measures aimed at eradicating methicillin-resistant S. aureus. Low frequencies of resistance among methicillin-resistant S. aureus were found for vancomycin (0%), chloramphenicol (11%), cotrimoxazole (11%), mupirocin (3% low-level resistance) and fusidic acid (7%). Twenty-one percent of the coagulase-negative staphylococci were resistant to methicillin. Low frequencies of resistance among these methicillin-resistant coagulase-negative staphylococci were those to vancomycin (0.4%), nitrofurantoin (2%), doxycycline (20%) and amikacin (20%). Coagulase-negative staphylococci from cerebrospinal fluid, blood and skin were less often resistant to quinolones than isolates from respiratory tract, faeces and urine. A significant increase in resistance of coagulase-negative staphylococci to methicillin, erythromycin, gentamicin and ciprofloxacin was observed in the investigated period but the resistance to doxycycline and co-trimoxazole decreased in the last few years. To confirm the determination of methicillin resistance and coagulase production, a PCR method was developed which detects both the mecA and the coagulase gene. The results of the PCR method correlated well with the methicillin MIC as determined by an agar-dilution method.

We cultured Pasteurella multocida from the cerebrospinal fluid (CSF) of a 4-month-old infant who presented with meningitis. The patient had been scratched on the head by a cat. Culture of the cat's claws also yielded P. multocida. The isolates had identical biochemical patterns. Analysis of both strains by random amplification of polymorphic DNA and comparison of these strains with P. multocida strains isolated from other cats showed that the two strains were identical and completely different from the unrelated isolates. Our patient's meningitis most likely resulted from direct inoculation of P. multocida into the CSF.

Endocarditis due to a bacterium of CDC coryneform group ANF-3 developed in the native aortic valve of a patient without predisposing factors other than valvular calcification. A review of the literature indicates that corynebacteria are an increasingly important cause of endocarditis. Problems in identification and treatment remain. Techniques for the culture and quick identification of these organisms and effective regimens for treatment of the infections they cause are needed.

The effects were studied of in-vitro exposure to tissue-type plasminogen activator (t-PA) on endocardial vegetations isolated from rabbits with Streptococcus sanguis endocarditis as well as on Str. sanguis-infected plasma clots. For both vegetations and clots t-PA induced lysis of the infected fibrin matrix, demonstrated by a release of streptococci into the incubation medium and by an increase in the concentration of fibrin degradation products. The clots decreased in weight, whereas only partial lysis of the vegetations was obtained. Addition of plasminogen to the incubation medium did not enhance the effect of t-PA on vegetations. Fibrinolysis by t-PA did not interfere with the antimicrobial action of benzylpenicillin on the bacteria in a fibrin matrix. It is concluded that t-PA can degrade the fibrin matrices of infected endocardial vegetations and plasma clots. Reduction of vegetation size by t-PA may prove to be useful in the treatment of bacterial endocarditis.

The ability of tissue-type plasminogen activator (t-PA) to enhance the effect of antibiotics in the treatment of bacterial endocarditis was studied using plasma clots infected with Staphylococcus epidermidis as a model of infected endocardial vegetations. A concentration-dependent lysis of the infected plasma clots was induced by t-PA, as shown by the decrease in the weight of the clots, a decrease in the amount of incorporated 125I fibrin, as well as the release of staphylococci from the clots into the incubation fluid. The addition of cloxacillin to the incubation medium in various concentrations led to a concentration-dependent decrease of the number of S. epidermidis in the clots. The presence of t-PA did not enhance the antibacterial effect of cloxacillin. It is concluded that the lysis induced by t-PA might enhance the effect of treatment of endocarditis by reducing the size of endocardial vegetations but not by enhancement of the effect of antibiotics on the bacteria embedded in the vegetations.