During 1981-1993, 229 episodes of bacteraemia due to beta-haemolytic streptococci of groups A, B, C and G were diagnosed in the County of Northern Jutland, Denmark. The annual rates for bacteraemia were quite constant during the 13-year period for each streptococcal group. Group A streptococcal (GAS) bacteraemia was the most frequent, comprising 1.4% of all bacteraemias. The incidence of GAS bacteraemia was 1.8/100,000/year in children 60 years old. With the notable exception of group B streptococcal (GBS) bacteraemia in neonates, beta-haemolytic streptococci of groups B, C (GCS) and G (GGS) were isolated mostly from elderly patients. Except for GBS bacteraemia in neonates, approximately one-third of the bacteraemias in each group was nosocomially acquired. Predisposing factors included operative procedures in GAS and GCS bacteraemia, and diabetes mellitus in GBS bacteraemia. The skin was the most common primary focus in GAC, GCC and GGS bacteraemias, whereas the urinary tract was the commonest focus in GBS bacteraemia in adults. The mortality rates in GAS, GCS, GGS, and adult GBS bacteraemia were 23%, 16%, 17% and 19%, respectively. Of the 23 fatal cases of GAS bacteraemia, 57% died within 24 h after blood cultures had been obtained.
14-Year Survey in a Swedish County Reveals a Pronounced Increase in Bloodstream Infections (BSI). Comorbidity - An Independent Risk Factor for Both BSI and Mortality.
we assessed the incidence, risk factors and outcome of BSI over a 14-year period (2000-2013) in a Swedish county.
retrospective cohort study on culture confirmed BSI among patients in the county of Östergötland, Sweden, with approximately 440,000 inhabitants. A BSI was defined as either community-onset BSI (CO-BSI) or hospital-acquired BSI (HA-BSI).
of a total of 11,480 BSIs, 67% were CO-BSI and 33% HA-BSI. The incidence of BSI increased by 64% from 945 to 1,546 per 100,000 hospital admissions per year during the study period. The most prominent increase, 83% was observed within the CO-BSI cohort whilst HA-BSI increased by 32%. Prescriptions of antibiotics in outpatient care decreased with 24% from 422 to 322 prescriptions dispensed/1,000 inhabitants/year, whereas antibiotics prescribed in hospital increased by 67% (from 424 to 709 DDD per 1,000 days of care). The overall 30-day mortality for HA-BSIs was 17.2%, compared to 10.6% for CO-BSIs, with an average yearly increase per 100,000 hospital admissions of 2 and 5% respectively. The proportion of patients with one or more comorbidities, increased from 20.8 to 55.3%. In multivariate analyses, risk factors for mortality within 30 days were: HA-BSI (2.22); two or more comorbidities (1.89); single comorbidity (1.56); CO-BSI (1.21); male (1.05); and high age (1.04).
this survey revealed an alarming increase in the incidence of BSI over the 14-year study period. Interventions to decrease BSI in general should be considered together with robust antibiotic stewardship programmes to avoid both over- and underuse of antibiotics.
Notes
Cites: Infect Control Hosp Epidemiol. 2009 Nov;30(11):1036-4419780675
Cites: Am J Infect Control. 2016 Feb;44(2):167-7226577629
Between November 1 and 22, 1985, an outbreak of acute, nonbacterial gastroenteritis occurred in a 600-bed hospital in Toronto, Ontario, Canada. Illness in 635 of 2,379 (27%) staff was characterized by fatigue, nausea, diarrhea, and vomiting and had a median duration of 24-48 hours. The finding of virus-like particles measuring 25-30 nm in six stool specimens and low rates of seroresponse to Norwalk virus (3/39) and Snow Mountain agent (1/6) suggest that a Norwalk-like virus was responsible for the outbreak. The outbreak was of abrupt onset and high incidence, affecting 79 people in a single day. No common food or water exposure could be identified. The attack rate was greatest (69%) for staff who had worked in the Emergency Room. Of 100 patients and their companions who visited the Emergency Room on November 11-12 for unrelated problems, 33 (33%) developed gastroenteritis 24-48 hours after their visit, versus 0 of 18 who visited the Emergency Room on November 8 (p less than 0.001). An analysis of housekeepers who worked at least once during the period from November 9-13, which included those who became ill during the period of November 9-14, showed that the risk of becoming ill was four times greater for those who visited or walked through the Emergency Room than for those who did not (p = 0.028). These data are consistent with the possibility of the airborne spread of a virus.
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.
To report a multi-institution outbreak caused by a single strain of methicillin-resistant Staphylococcus aureus (MRSA).
Between September 19 and November 20, 1996 an index case and five secondary cases of nosocomial MRSA occurred on a 26 bed adult plastic surgery/burn unit (PSBU) at a tertiary care teaching hospital. Between November 11 and December 23, 1996, six additional cases were identified at a community hospital. One of the community hospital cases was transferred from the PSBU. All strains were identical by pulsed-field gel electrophoresis. MRSA may have contributed to skin graft breakdown in one case, and delayed wound healing in others. Patients required 2 to 226 isolation days.
A hand held shower and stretcher for showering in the hydrotherapy room of the PSBU were culture positive for the outbreak strain, and the presumed means of transmission. Replacement of stretcher showering with bedside sterile burn wound compresses terminated the outbreak. The PSBU was closed to new admissions and transfers out for 11 days during the investigation. Seven of 12 patients had effective decolonization therapy.
Environmental contamination is a potential source of nosocomial MRSA transmission on a burn unit. Notification among institutions and community care providers of shared patients infected or colonized with an antimicrobial resistant microorganism is necessary.
The aim of the present investigation was the study of the epidemic process of hospital candidiasis. The study was carried out from October 1991 to May 1992 in a hematological ward of one of the hospitals of St.-Petersburg on 9 patients with generalized forms of candidiasis: in 4 of them the disease was caused by C. albicans and 5--by C. parapsilosis. Intestinal dysfunction as one of the first manifestations of candidosepsis caused by C. albicans, the isolation of C. albicans from feces, ulcero-necrotic colitis (established by postmortem examination), as well as the incapacity of these patients of immune response (in 2 serologically examined patients the titer of antibodies to fungi of the genus Candida was found to be lower than the diagnostic titer), were indicative of the dissemination of fungi from the gastrointestinal tract. The cases of fungemia caused by C. parapsilosis were due to the fungal contamination of vascular catheters in these patients. This infective agent was also isolated from washings obtained from the hands of nurses carrying out treatment and from medical rubber gloves. Moreover, some violations in the rules of the preparation of disinfecting solutions and the treatment of the hands of the personnel were established.
BACKGROUND: Pseudomonas aeruginosa is an opportunistic bacterium that can cause severe infection in susceptible patients. During the winter of 2001-2002, we investigated an outbreak of P. aeruginosa infection among patients in several hospitals across Norway. METHODS: A nationwide outbreak investigation was performed with case finding, questionnaires, and product sampling. All available clinical and environmental P. aeruginosa strains were genotyped. Detailed information was collected from patients with the outbreak strain or with any P. aeruginosa in blood or cerebrospinal fluid samples. To identify risk factors, we conducted a case-control study among patients with P. aeruginosa isolated from blood or cerebrospinal fluid samples during October 2001-December 2002. Case patients were patients infected with the outbreak genotype, and control subjects were patients infected with other genotypes. RESULTS: A total of 231 patients from 24 hospitals were identified as having the outbreak strain; 39 of these patients had positive blood culture results. Seventy-one patients (31%) died while hospitalized; all of the patients who died had severe underlying disease. Among 39 case patients and 159 control subjects, use of the moist mouth swab (adjusted odds ratio, 5.3; 95% confidence interval, 2.0-13.6) and receipt of mechanical ventilation (adjusted odds ratio, 6.4; 95% confidence interval, 2.3-17.2) were associated with infection due to the outbreak strain. Genotypically identical strains of P. aeruginosa were identified in 76 mouth swabs from 12 different batches and from the production line. CONCLUSIONS: Contamination of mouth swabs during production caused the largest-ever outbreak of P. aeruginosa infection in Norway. Susceptible patient groups should use only documented quality-controlled, high-level-disinfected products and items in the oropharynx.
Division of Infectious Diseases, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. marcus_e@telia.com
Pseudomonas aeruginosa is 1 of the bacteria most adaptive to anti-bacterial treatment. Previous studies have shown nosocomial spread and transmission of clonal strains of P. aeruginosa in European hospitals. In this study we investigated antibiotic susceptibility and clonality in 101 P. aeruginosa isolates from 88 patients admitted to 8 Swedish ICUs during 2002. We also compared phenotypes and genotypes of P. aeruginosa and carried out cluster analysis to determine if phenotypic data can be used for surveillance of clonal spread. All isolates were collected on clinical indication as part of the NPRS II study in Sweden and were subjected to AFLP analysis for genotyping. 68 isolates with unique genotypes were found. Phenotyping was performed using MIC values for 5 anti-pseudomonal agents. Almost 6% of the isolates were multi-drug resistant (MDR), and this figure rose to almost 8% when intermediate isolates were also included. We found probable clonal spread in 9 cases, but none of them was found to be an MDR strain. Phenotypical cluster analysis produced 40 clusters. Comparing partitions did not demonstrate any significant concordance between the typing methods. The conclusion of our study is that cross-transmission and clonal spread of MDR P. aeruginosa does not present a clinical problem in Swedish ICUs, but probable cross-transmission of non-MDR clones indicate a need for improved hygiene routines bedside. The phenotype clusters were not concordant with genotype clusters, and genotyping is still recommended for epidemiological tracking.
