Increasing the reliability of fully automated surveillance for central line–associated bloodstream infections

OBJECTIVETo increase reliability of the algorithm used in our fully automated electronic surveillance system by adding rules to better identify bloodstream infections secondary to other hospital-acquired infections.METHODSIntensive care unit (ICU) patients with positive blood cultures were reviewed. Central line–associated bloodstream infection (CLABSI) determinations were based on 2 sources: routine surveillance by infection preventionists, and fully automated surveillance. Discrepancies between the 2 sources were evaluated to determine root causes. Secondary infection sites were identified in most discrepant cases. New rules to identify secondary sites were added to the algorithm and applied to this ICU population and a non-ICU population. Sensitivity, specificity, predictive values, and kappa were calculated for the new models.RESULTSOf 643 positive ICU blood cultures reviewed, 68 (10.6%) were identified as central line–associated bloodstream infections by fully automated electronic surveillance, whereas 38 (5.9%) were confirmed by routine surveillance. New rules were tested to identify organisms as central line–associated bloodstream infections if they did not meet one, or a combination of, the following: (I) matching organisms (by genus and species) cultured from any other site; (II) any organisms cultured from sterile site; (III) any organisms cultured from skin/wound; (IV) any organisms cultured from respiratory tract. The best-fit model included new rules I and II when applied to positive blood cultures in an ICU population. However, they didn’t improve performance of the algorithm when applied to positive blood cultures in a non-ICU population.CONCLUSIONElectronic surveillance system algorithms may need adjustment for specific populations.Infect. Control Hosp. Epidemiol. 2015;36(12):1396–1400</jats:sec

Quantitative systematic review of the effects of non‐pharmacological interventions on reducing apathy in persons with dementia

AimTo review the quantitative evidence concerning the effects of non‐pharmacological interventions on reducing apathy in persons with dementia.BackgroundApathy, a prevalent behavioural symptom among persons with Alzheimer Disease, is defined as a disorder of motivation with deficits in behavioural, emotional and cognitive domains and is associated with serious social and physical obstacles. Non‐pharmacological interventions show promise as symptom control modalities among persons with dementia.DesignQuantitative systematic review.Data sourcesCINAHL, PubMed, PSYCHinfo and Cochrane Trials databases were searched for published English language research inclusive through December 2014, with no early year limiters set.Review methodsComprehensive searches yielded 16 international randomized controlled trials or quasi‐experimental studies based on inclusion criteria and a rigorous quality appraisal process.ResultsA narrative summary analysis revealed that non‐pharmacological interventions for apathy varied substantially and lacked specificity, conceptual clarity and were methodologically heterogeneous. Select interventions demonstrated effectiveness, but lacked systematic long‐term follow‐up. Limitations include publication bias and lack of a meta‐analytic approach due to the methodological heterogeneity of included studies.ConclusionStudy results demonstrate promise for the use of non‐pharmacological interventions, particularly music‐based interventions, in reducing apathy levels in individuals with dementia. Intervening to reduce apathy may have a positive clinical impact and healthcare providers should be encouraged to incorporate positive sources of interest and intellectual stimulation into care. However, future research is needed to examine the aetiologic mechanism and predictors of apathy, to improve evidence‐based interventions and specificity and to optimize dosage and timing of non‐pharmacological interventions across the disease trajectory.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134246/1/jan13026_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134246/2/jan13026.pd

Inhibition of Salmonella Typhimurium by medium chain fatty acids in an in vitro simulation of the porcine caecum

To lower the contamination of pork meat with Salmonella, feed additives such as medium chain fatty acids (MCFA\u27s) can be applied at the primary production level. An in vitro continuous culture system, simulating the porcine caecum, was developed for investigating the effect of MCFAs on the pig intestinal microbial community. The system was monitored by plating on selective media, 16S rDNA PCR denaturing gradient gel electrophoresis (PCR-DGGE) and HPLC analysis of fermentation products. In a simulation of the porcine caecum without MCFA treatment, with Salmonella Typhimurium added after stabilization of the microbial community, the strain could establish itself at a stable population size of about 5 log cfu/ml. The effect of selected MCFAs was observed from all monitored parameters and depended on chain length and concentration applied. At a dose of 15 mM, caproate and caprinate did not show any pronounced effect, while a clear Salmonella inhibiting effect (3 log units reduction) was found for caprylate. Doubling the caprylate dose did not result in enhanced Salmonella inhibition

Provably scale-covariant networks from oriented quasi quadrature measures in cascade

This article presents a continuous model for hierarchical networks based on a combination of mathematically derived models of receptive fields and biologically inspired computations. Based on a functional model of complex cells in terms of an oriented quasi quadrature combination of first- and second-order directional Gaussian derivatives, we couple such primitive computations in cascade over combinatorial expansions over image orientations. Scale-space properties of the computational primitives are analysed and it is shown that the resulting representation allows for provable scale and rotation covariance. A prototype application to texture analysis is developed and it is demonstrated that a simplified mean-reduced representation of the resulting QuasiQuadNet leads to promising experimental results on three texture datasets.Comment: 12 pages, 3 figures, 1 tabl

Reversible thrombocytopenia during hibernation originates from storage and release of platelets in liver sinusoids

Immobility is a risk factor for thrombosis due to low blood flow, which may result in activation of the coagulation system, recruitment of platelets and clot formation. Nevertheless, hibernating animals-who endure lengthy periods of immobility-do not show signs of thrombosis throughout or after hibernation. One of the adaptations of hemostasis in hibernators consists of a rapidly reversible reduction of the number of circulating platelets during torpor, i.e., the hibernation phase with reduction of metabolic rate, low blood flow and immobility. It is unknown whether these platelet dynamics in hibernating hamsters originate from storage and release, as suggested for ground squirrel, or from breakdown and de novo synthesis. A reduction in detaching forces due to low blood flow can induce reversible adhesion of platelets to the vessel wall, which is called margination. Here, we hypothesized that storage-and-release by margination to the vessel wall induces reversible thrombocytopenia in torpor. Therefore, we transfused labeled platelets in hibernating Syrian hamster (Mesocricetus auratus) and platelets were analyzed using flow cytometry and electron microscopy. The half-life of labeled platelets was extended from 20 to 30 h in hibernating animals compared to non-hibernating control hamsters. More than 90% of labeled platelets were cleared from the circulation during torpor, followed by emergence during arousal which supports storage-and-release to govern thrombocytopenia in torpor. Furthermore, the low number of immature platelets, plasma level of interleukin-1α and normal numbers of megakaryocytes in bone marrow make platelet synthesis or megakaryocyte rupture via interleukin-1α unlikely to account for the recovery of platelet counts upon arousal. Finally, using large-scale electron microscopy we revealed platelets to accumulate in liver sinusoids, but not in spleen or lung, during torpor. These results thus demonstrate that platelet dynamics in hibernation are caused by storage and release of platelets, most likely by margination to the vessel wall in liver sinusoids. Translating the molecular mechanisms that govern platelet retention in the liver, may be of major relevance for hemostatic management in (accidental) hypothermia and for the development of novel anti-thrombotic strategies