Archive for May 18, 2010

Clostridium difficile is not associated with outbreaks of viral gastroenteritis in the elderly in the Netherlands

European Journal of Clinical Microbiology & Infectious Diseases March 2010 V.29 N.6 p.677 – 682

S. Svraka1 , E. Kuijper2, E. Duizer1, D. Bakker2 and M. Koopmans1, 3

(1)  Laboratory for Infectious Diseases and Perinatal Screening, Center for Infectious Disease Control, National Institute for Public Health and the Environment, P.O. Box 1, 3720 BA Bilthoven, The Netherlands

(2)  Department of Medical Microbiology, Leiden University Medical Center, Leiden, The Netherlands

(3)  Erasmus Medical Center, Rotterdam, The Netherlands


The coincidental increase in norovirus outbreaks and Clostridium difficile infection (CDI) raised the question of whether these events could be related, e.g. by enhancing spread by diarrhoeal disease outbreaks. Therefore, we studied the prevalence of C. difficile in outbreaks of viral gastroenteritis in nursing homes for the elderly and characterised enzyme immunoassay (EIA)-positive stool samples. Stool samples from nursing home residents (n = 752) in 137 outbreaks of viral aetiology were investigated by EIA for the presence of C. difficile toxins. Positive samples were further tested by a cell neutralisation cytotoxicity test, a second EIA and culture. Cultured isolates were tested for the presence of toxin genes, the production of toxins and characterised by 16S rRNA polymerase chain reaction (PCR) and sequencing. Twenty-four samples (3.2%) tested positive in the EIA. Of these 24 positive samples, only two were positive by cytotoxicity and three by a second EIA. Bacterial culture of 21 available stool samples yielded a toxinogenic C. difficile PCR ribotype 001 in one patient sample only. In conclusion, we found no evidence in this retrospective study for an association between viral gastroenteritis outbreaks and C. difficile. The high rate of false-positive EIA samples emphasises the need for second confirmation tests to diagnose CDI.



May 18, 2010 at 4:40 pm Leave a comment

Performance of rapid influenza testing in hospitalized children

European Journal of Clinical Microbiology & Infectious Diseases March 2010 V.29 N.6 p.683 – 688

F. Stripeli1 , Z. Sakkou1, N. Papadopoulos1, V. Georgiou1, P. Gratsia1, I. Christodoulou1 and M. Tsolia1

(1)  P&A Kyriakou Children’s Hospital, Athens, Greece


Influenza infection is associated with high hospitalization rates among young children. Rapid diagnosis of influenza infection is particularly useful in order to prevent nosocomial infection and allows for the timely initiation of antiviral treatment. We evaluated the performance of a rapid influenza test in hospitalized children during the influenza season. All children (aged 6 months to 14 years) hospitalized with fever and/or respiratory symptoms, admitted during the 2005 influenza season, participated in the study. A multiplex reverse transcriptase polymerase chain reaction (RT-PCR), able to identify IFV-A H1N1, H3N2, and IFV-B subtypes, was performed on nasopharyngeal aspirates. The nasal swab was tested with a lateral-flow immunoassay (QuickVue Influenza Test). The performance of the rapid test was compared with the results of PCR. Influenza infection was diagnosed by PCR in 41/217 (19%) patients. Infection with influenza A virus (H3N2) was diagnosed in all cases. The performance of the QuickVue Influenza Test was estimated as follows: sensitivity 67.5%, specificity 96%, positive predictive value 79%, and negative predictive value 93%. The sensitivity of the test was higher in infants aged 6–12 months, in those with short duration of symptoms, and in the peak phase of the epidemic. The QuickVue Influenza Test is useful and reasonably accurate to detect influenza infection in hospitalized children during the influenza season. Infection with influenza virus is unlikely if the test is negative. A positive result suggests that infection is probable if influenza virus circulates in the community.


May 18, 2010 at 4:38 pm Leave a comment

Skin bacteria after chlorhexidine exposure—is there a difference in response to human β-Defensin-3?

European Journal of Clinical Microbiology & Infectious Diseases March 2010 V.29 N.6 p.623 – 632

M. Reichel1, 2 , A. Heisig2, P. Heisig2 and G. Kampf1, 3

(1)  BODE Chemie GmbH, Scientific Affairs, Melanchthonstr. 27, 22525 Hamburg, Germany

(2)  Department of Pharmaceutical Biology and Microbiology, Institute of Pharmacy, University of Hamburg, Bundesstr. 45, 20146 Hamburg, Germany

(3)  Institute for Hygiene and Environmental Medicine, Ernst-Moritz-Arndt University, Walther-Rathenau-Str. 49a, 17487 Greifswald, Germany


We investigated whether exposure to sub-lethal concentrations of chlorhexidine digluconate (CHG) changed the response of five Staphylococcus spp. to human β-Defensin-3 (hBD-3). The change in response for each strain was determined in vitro with time–kill experiments in suspension by comparing the mean log10 reduction caused by hBD-3 at 1.5 and 3 h in exposed and non-exposed bacteria. The identity of staphylococcal species was verified by DNA sequence homology in the gyrA genes in comparison with reference strains. Baseline sub-lethal concentrations allowing visible bacterial growth were between 0.0625 and 0.25 μg/ml. Sub-lethal CHG concentrations increased within 3 days in two isolates. For S. capitis 19/2, CHG-exposed cells were less susceptible to 0.5 μg/ml hBD-3 (log10 reduction 0.78 versus 2.06 at 1.5 h; p < 0.001; t-test). For S. aureus, however, CHG-exposed cells were more susceptible to 1 μg/ml hBD-3. The observed changes between CHG-exposed and non-exposed cells did not indicate a general trend in response to hBD-3. Overall, we found no consistent evidence that 3 days of exposure to CHG changed the response of five Staphylococcus spp. to hBD-3. The use of CHG for skin antisepsis is, based on our data, unlikely to change the natural defence activity of hBD-3.


May 18, 2010 at 4:37 pm Leave a comment

Antibody responses in patients with invasive Staphylococcus aureus infections

European Journal of Clinical Microbiology & Infectious Diseases April 2010 V.29 N.6 p.715 – 725

G. Jacobsson1 , P. Colque-Navarro2, E. Gustafsson2, 3, R. Andersson4 and R. Möllby2

(1)  Department of Infectious Diseases, Skaraborg Hospital, 541 85 Skövde, Sweden

(2)  Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institute, Stockholm, Sweden

(3)  School of Life Sciences, University of Skövde, Skövde, Sweden

(4)  Research and Development Centre, Skaraborg Hospital, Skövde, Sweden


Correlation between antibody response and clinical outcome in Staphylococcus aureus bacteremia has yielded conflicting results. Immunization schedules have failed in clinical trials. Is the humoral response toward S. aureus of protective nature? A prospective study was performed in patients with invasive S. aureus (ISA) infections during the period 2003–2005. The antibody levels were determined at the beginning and at the end of treatment and one month later (n = 96, n = 71, and n = 51, respectively). As controls, 115 healthy individuals were used. A quantitative enzyme-linked immunosorbent assay (ELISA) against eight purified antigens was performed. Bacterial isolates were grouped as to the production of alpha-toxin, agr type, and pulsed-field gel electrophoresis (PFGE) type. Large variations were seen in the antibody levels. The levels in the second sample were the highest. A correlation between agr group, PFGE group, alpha-toxin production, and initial antibody levels was observed. Patients with fatal outcome displayed lower initial antibody levels to all antigens and significantly so in regard to teichoic acid, lipase, enterotoxin A, and scalded skin syndrome toxin. In episodes with complicated bacteremia, initial significantly low levels to teichoic acid and lipase were registered. Low initial antibody levels against several antigens were associated with increased mortality and complicated bacteremia in invasive S. aureus infections. Bacterial properties, strain, and toxin production affected the antibody response.


May 18, 2010 at 4:35 pm Leave a comment


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