Mutant ftsI genes in the emergence of penicillin-binding protein-mediated beta-lactam resistance in Haemophilus influenzae in Norway.

The most important mechanism for beta-lactam resistance in beta-lactamase-negative ampicillin-resistant (BLNAR) isolates of Haemophilus influenzae is the alteration of penicillin-binding protein 3 (PBP3) as a result of ftsI gene mutations. The present study aimed to map PBP3 alterations and to determine the correlation to beta-lactam resistance in respiratory tract isolates of H. influenzae in Norway, as well as assess the contribution of clonal spread to the emergence of PBP3-mediated resistance. Twenty-three beta-lactamase negative respiratory tract isolates with resistance to penicillins and 23 susceptible control isolates were examined by determination of beta-lactam MICs, ftsI sequencing and molecular typing by pulsed-field gel electrophoresis (PFGE). Ampicillin MIC ranges in the resistant group and the control group were 1-2 mg/L and 0.125-0.5 mg/L, respectively. All isolates in the resistant group had the PBP3 substitution Asn526-->Lys and were thus categorized as group II low-BLNAR. No control isolate met the genetic BLNAR (gBLNAR) criteria. The PBP3 substitution patterns corresponded well to those observed in previous European studies. Eighty-three percent (19/23) of the resistant isolates belonged to two clones, demonstrating the capability of low-BLNAR strains of clonal dissemination. Combined analysis of ftsI DNA sequences and PFGE patterns revealed distinctly different ftsI alleles in genetically indistinguishable isolates and identical copies of the same ftsI allele in unrelated isolates. A possible explanation of this observation is the recombinational exchange of ftsI alleles. This phenomenon, as well as the possibility of endemic European gBLNAR strains, should be further investigated.

Comparison of PCR detection of mecA with agar dilution and Etest for oxacillin susceptibility testing in clinical isolates of coagulase-negative staphylococci.

Oxacillin-resistant staphylococci are heterogeneous in their expression of resistance to beta-lactam antibiotics. Different recommendations regarding screening methods for routine use have been published. In this study, the susceptibility to oxacillin of 232 coagulase-negative staphylococci (CoNS) was determined by agar dilution, Etest and presence of the mecA gene. When an oxacillin resistance breakpoint of > or = 0.5 mg/L was used, the sensitivity and specificity for agar dilution were 97.6% and 100%, and those for Etest were 100% and 95.4%. The current National Committee for Clinical Laboratory Standards oxacillin breakpoint recommendation will categorise accurately the CoNS species encountered commonly.

Heterogeneity of methicillin-resistant Staphylococcus aureus isolated in Norway.

Our objective was to look for differences in susceptibility patterns between Norwegian and imported methicillin-resistant Staphylococcus aureus (MRSA) strains. All MRSA isolates from the participating hospitals (87 isolates from 81 patients) throughout the period 1994-98 were examined, to study the clonal distribution of MRSA isolated in Norway and to identify any epidemic clones among the isolates. We found that imported isolates were resistant to an average of 5.6 antibiotics, while Norwegian isolates were resistant to an average of 2.6 antibiotics. MRSA isolates imported to Norway are more often multiresistant than domestic isolates. MRSA isolates in Norway show a striking diversity. Epidemic clones are present, but no single clone is predominant.

Borrelia burgdorferi sensu lato and Ehrlichia spp. in Ixodes ticks from southern Norway.

We report the results of a study of the prevalence of Ehrlichia and Borrelia species in 341 questing Ixodes ricinus ticks from two locations in southern Norway. The prevalences of Borrelia burgdorferi sensu lato and Ehrlichia spp. were, respectively, 16 and 11.5% at site 1 and 17 and 6% at site 2. Prevalence and species composition of Borrelia and Ehrlichia varied with location and date of collection. The dominant Borrelia species at both sites was Borrelia afzelii, followed by Borrelia burgdorferi sensu stricto. Borrelia garinii was found in only a single tick. The dominant member of the Ehrlichia group was a recently described Ehrlichia-like organism related to the monocytic ehrlichiae. Variants of Ehrlichia phagocytophila and the agent of human granulocytic ehrlichiosis were also found. The highest prevalences for B. afzelii, B. burgdorferi sensu stricto, and the Ehrlichia-like organism were observed in May. B. afzelii was most prevalent in females, less prevalent in nymphs, and least prevalent in males, while the prevalence of Ehrlichia was highest in nymphs, lower in females, and least in males. Double infections with B. afzelii and B. burgdorferi sensu stricto and with B. afzelii and the Ehrlichia-like organism were significantly overrepresented. Tick densities were highest in May, when densities of more than 200 ticks/100 m2 were observed, and declined during the summer months to densities as low as 20 ticks/100 m2. We conclude that estimates of the prevalence of tick-borne bacteria are sensitive to the choice of date and site for collection of ticks. This is the first study of tick-borne Borrelia and Ehrlichia in Norway and the lowest reported B. garinii prevalence in Northern Europe. The prevalence of the Ehrlichia-like organism is described for the first time in questing ticks.

Vancomycin resistance emerging in a clonal outbreak caused by ampicillin-resistant Enterococcus faecium.

OBJECTIVES: To describe the first nosocomial outbreak of ampicillin-resistant Enterococcus faecium (ARE) in Norway, where a few vancomycin-resistant strains have also been identified. METHODS: All cases of ARE and vancomycin-resistant Enterococcus faecium (VRE) diagnosed by the medical microbiological laboratories in a region inhabited by approximately 1 million people were registered. Isolates obtained during the period 1 January 1995 to 31 December 1996 were characterized by pulsed field-gel electrophoresis and the clinical data were recorded. RESULTS: One hundred and forty-nine patients (64 males, 85 females, mean age 70.5 years) were infected with ARE. Isolates from 115 cases were genomically related to the outbreak strain. Infections included bacteremia (14), wound infections (31), urinary tract infections (97) and other infections (seven). Most had a severe underlying disease and 93% of the patients had received antibiotics for a mean time of 23 days. Twenty-four patients (16.1%) died during hospitalization. Four infections were caused by a vanB-type VRE that was genomically related to the ARE outbreak strain. The prescription rate for vancomycin was low, but an increase in vancomycin use paralleled the appearance of VRE. The highest monthly incidence rate was 2.5 per 1000 patient admissions in July 1996 declining to 0.5 in December 1996. CONCLUSIONS: The first nosocomial outbreak caused by ARE was observed in 1995 in Norway and is still ongoing. One year after the onset, VRE occurred in wards which had a relatively high consumption of vancomycin.