In contrast to the other Nordic countries Sweden has long had a favourable position as regards meningococcal disease. In the last 10 year period the annual incidence has been only about one case per 100,000 inhabitants. The treatment once the cause is confirmed is conventional and no different from that in the other Nordic countries but varies somewhat in the event of unknown etiology. Cortisone therapy also seems to be more frequent in treatment of meningitis. Two strategies for antibiotic prophylaxis are used in Sweden.
We aim to investigate the prevalence, putative virulence factors and antimicrobial resistance of mesophilic Aeromonas isolated from ready-to-eat (RTE) seafood available on the Norwegian market, and to assess the potential risks by consuming RTE seafood to consumers.
The prevalence of mesophilic Aeromonas in 148 RTE seafood was investigated and the highest prevalence was found in retail sushi (17%), followed by oysters (10%), fresh salmon loins (10%) and scallops (4%). Among 43 Aeromonas isolates, 75% of them were identified as A. media, 23% as A. salmonicida and 2% as A. bestiarum based on partial gryB gene sequencing. Aeromonas isolates were potentially pathogenic due to the presence of four virulence genes: alt (73%), hylA (22%), aerA (17%) and act (6%). In addition, all isolates were resistant to ampicillin and erythromycin. Most of the isolates (98%) were multidrug resistant.
The occurrence of potentially pathogenic and multidrug-resistant Aeromonas strains in RTE seafood implies a potential risk to consumers. Our finding suggests that RTE seafood could be a potential vehicle for the transfer of virulent and multidrug-resistant Aeromonas.
To our knowledge, this is the first study to report multiple antibiotic resistance in Aeromonas associated with RTE seafood in Norway.
Ampicillin-resistant enterococci (ARE) have recently emerged as clinical pathogens in Sweden. Between 1991 and 1995 the incidence of ARE among enterococcal isolates at Uppsala University Hospital increased from 0.5% to 8.1%. Shedding of ARE from infected cases and risk factors for infection with ARE were studied during a period of 7 months for 38 ARE cases and 38 controls with ampicillin-susceptible enterococci. ARE cases had longer mean duration of hospitalization than controls (29 d vs. 15 d; p = 0.002). In univariate analysis other risk factors for infection with ARE were found to be prior therapy with > 2 antimicrobials (odds ratio [OR] 3.3; 95% confidence interval [CI] 1.2-9.5), > 4 weeks of antimicrobial therapy (OR 6.9; CI 1.8-28.3) and cephalosporin therapy (OR 9.1; CI 2.6-33.7). Fourteen of 26 skin carriers of ARE were found to be shedding ARE to the environment, compared to 2 of 12 non-skin carriers (p = 0.03). Pulsed-field gel electrophoresis suggested multifocal origin of the majority of the infecting ARE strains. Non-recognized fecal colonization and silent spread of ARE among many patients and over a prolonged time period is suggested to be the main explanation for the increase of ARE infections in our hospital. Infection control measures focusing on protecting patients at high risk for ARE infections and further efforts to optimize antimicrobial use are proposed.
The prevalence of ampicillin-resistance was assessed among a total of 2766 strains of H. influenzae isolated from lower respiratory tract secretions, middle ear secretions, spinal fluid specimens, and blood cultures from children 0-15 years of age tested in two separate counties in Denmark during the period from 1986 to May, 1993. All strains were tested for susceptibility to ampicillin with disc or tablet diffusion technique and strains were examined for beta-lactamase production with a chromogenic cephalosporinase test. In the county of Northern Jutland the rate of beta-lactamase production in non-encapsulated H. influenzae was 2.5% in 1986 rising to 9.3% in 1993. The rate of beta-lactamase production in H. influenzae type b was 4.1% without any rise. In the county of Copenhagen the rate of beta-lactamase production in non-encapsulated H. influenzae rose from 6.3% in 1986 to 10.6% in 1992. In 1993 a further increase to 20.7% was noticed. This year the number of specimens sent to the laboratory and the number of H. influenzae isolated were lower compared to previous years. Thus a different selection of patients may explain the increase in the rate of beta-lactamase production in 1993. The rate of beta-lactamase production in H. influenzae type b was 8.5%. No strains were resistant to ampicillin in diffusion test other than the beta-lactamase producers.