A pseudo-outbreak due to Acinetobacter species (GIM-1) contamination of the pneumatic transport system of a Large University Hospital.

OBJECTIVE: To establish the source and contamination routes resulting in positive clinical and surveillance microbiological cultures with carbapenem-resistant, GIM-1 metallo-ß-lactamase-positive Acinetobacter pitii and Acinetobacter radioresistens from 21 patients in 8 departments. DESIGN: Retrospective, descriptive study. SETTING: A 1,300-bed tertiary care academic medical facility consisting of 90 buildings linked by a pneumatic transport system (PTS). METHODS: Microbiological workup of the cluster strains included matrix-assisted laser desorption/ionization time-of-flight species identification, phenotypic carbapenemase tests, polymerase chain reaction-based genotyping of carbapenemase, and pulsed-field gel electrophoresis. Outbreak management procedures were employed according to institutional regulations. RESULTS: The rarity of GIM-1 Acinetobacter species in the hospital and region, the lack of epidemiological links between patients, and the fact that in some patients the apparent colonization was clearly nonnosocomial prompted the suspicion of a pseudo-outbreak. Numerous environmental cultures were positive for GIM-1-positive Acinetobacter (including archived sample requisition forms, PTS capsules, cultures from line-diverter and dispenser stations, and sterilized transport capsules following PTS delivery). Moreover, it was observed that condensation fluid from subterranean PTS tubing resulted in water entry in PTS capsules, possibly conferring specimen contamination. After extensive system disinfection, environmental surveys of the PTS were negative, and no further positive patient specimens were encountered. CONCLUSIONS: This is the first report of a PTS-associated pseudo-outbreak. The large number of falsely positive patient-related specimens in conjunction with the potential hazard of airborne and contact spread of multidrug-resistant microorganisms (in this case, GIM-1 carbapenem-resistant Acinetobacter species) underscores the need for implementation of infection control-based monitoring and operating procedures in a hospital PTS.

Methicillin-resistant Staphylococcus aureus in Saarland, Germany: a statewide admission prevalence screening study.

BACKGROUND: The screening of hospital admission patients for methicillin resistant Staphylococcus aureus (MRSA) is of undisputed value in controlling and reducing the overall MRSA burden; yet, a concerted parallel universal screening intervention throughout all hospitals of an entire German Federal State has not yet been performed. METHODOLOGY/PRINCIPAL FINDINGS: During a four-week period, all 24 acute care hospitals of the State of Saarland participated in admission prevalence screening. Overall, 436/20,027 screened patients revealed MRSA carrier status (prevalence, 2.2/100 patients) with geriatrics and intensive care departments associated with highest prevalence (7.6/100 and 6.3/100, respectively). Risk factor analysis among 17,975 admission patients yielded MRSA history (OR, 4.3; CI95 2.7-6.8), a skin condition (OR, 3.2; CI95 2.1-5.0), and/or an indwelling catheter (OR, 2.2; CI95 1.4-3.5) among the leading risks. Hierarchical risk factor ascertainment of the six risk factors associated with highest odd's ratios would require 31% of patients to be laboratory screened to allow for detection of 67% of all MRSA positive admission patients in the State. CONCLUSIONS/SIGNIFICANCE: State-wide admission prevalence screening in conjunction with risk factor ascertainment yields important information on the distribution of the MRSA burden for hospitals, and allows for data-based decisions on local or institutional MRSA screening policies considering risk factor prevalence and expected MRSA identification rates.

Expression of amyotrophic lateral sclerosis-linked SOD1 mutant increases the neurotoxic potential of microglia via TLR2.

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease, in which activated microglia overexpressing ALS-linked SOD1 mutants (mSOD1) are known to contribute to neuronal death. However, it is unclear how mSOD1 expression affects micoglial activation and subsequently damages neurons. In this study, we created mSOD1-overexpressing BV-2 microglial cell lines. Following TLR2, but not TLR4 stimulation, we observed that overexpression of human SOD1 G93A, L8Q, or G10V mutant, as compared with the wild-type SOD1 or a mock control, significantly enhanced microglial secretion of a neurotoxic cytokine, tumor necrosis factor-alpha (TNF-alpha), which was dependent on the NADPH-oxidase-mediated increased generation of reactive oxygen species (ROS). In further experiments, we demonstrated that mSOD1 expression regulated TNF-alpha secretion at a post-transcriptional level and involved ROS-sensitive TNF-alpha-converting enzymes, e.g. ADAM10 and -17, which shed TNF-alpha from its membrane-anchored precursor. Together with a recent report that the function of SOD1, as a self-regulating redox sensor in NADPH oxidase-dependent ROS production, is lost due to its genetic mutations, we conclude that mSOD1 expression in ALS facilitates microglial neurotoxic inflammatory responses via TLR2, which is mediated by an uncontrolled ROS generation. The link, between mSOD1, innate immunity and NADPH oxidase, offers new opportunities in ALS therapies.