2
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Mouse Strains Differ in Their Susceptibility to Poststroke Infections

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective: Severe infections, in particular pneumonia, have a major impact on the clinical management and outcome of stroke patients. In a mouse model we have recently demonstrated that stroke induces immunodepression which can result in life-threatening infections. Here, we investigated whether the susceptibility to infections after stroke is strain dependent. Methods and Results: Mice from 129SV, C57/B6, and Balb/C strains were subjected to experimental stroke by filament occlusion of the middle cerebral artery (MCAO) for 60 min. Infarct volumes were measured 3 days after MCAO. Microbiological assessment was based on cultures of bronchoalveolar lavage (BAL), lung tissue and blood of animals obtained 3 days after stroke. Three days after stroke 129SV mice did not only develop bacterial chest infection, but also had a strongly increased susceptibility to bacteremia. In contrast, C57BL/6 and Balb/C mice acquired bacterial lung infections only. In addition, bacterial load in BAL was significantly higher in 129SV mice than in the other mice strains. These differences in susceptibility to infection did not correlate with infarct volumes. Conclusions: Stroke-associated pneumonia developed in three commonly used mouse strains while severity of infections differed between strains. Since infections affect outcome, monitoring of infections is highly relevant for the interpretation of results in experimental stroke research.

          Related collections

          Most cited references 12

          • Record: found
          • Abstract: found
          • Article: not found

          Predictors of in-hospital mortality and attributable risks of death after ischemic stroke: the German Stroke Registers Study Group.

          There is a lack of information about factors associated with in-hospital death and the impact of neurological complications on early outcome for patients with stroke treated in community settings. We investigated predictors for in-hospital mortality and attributable risks of death after ischemic stroke in a pooled analysis of large German stroke registers. Stroke patients admitted to hospitals cooperating within the German Stroke Registers Study Group (ADSR) between January 1, 2000, and December 31, 2000, were analyzed. The ADSR is a network of regional stroke registers, combining data from 104 academic and community hospitals throughout Germany. The impact of patients' demographic and clinical characteristics, their comorbid conditions, and the treating hospital expertise in stroke care on in-hospital mortality was analyzed using Cox regression analysis. Attributable risks of death for medical and neurological complications were calculated. A total of 13 440 ischemic stroke patients were included. Overall in-hospital mortality was 4.9%. In women, higher age (P<.001), severity of stroke defined by number of neurological deficits (P<.001), and atrial fibrillation (hazard ratio [HR], 1.3; 95% confidence interval [CI], 1.0-1.6) were independent predictors for in-hospital death. In men, diabetes (HR, 1.3; 95% CI, 1.0-1.8) and previous stroke (HR 1.4; 95% CI, 1.0-1.9) had a significant negative impact on early outcome in addition to the factors identified for women. The complication with the highest attributable risk proportion was increased intracranial pressure, accounting for 94% (95% CI, 93.9%-94.1%) of deaths among patients with this complication. Pneumonia was the complication with the highest attributable proportion of death in the entire stroke population, accounting for 31.2% (95% CI, 30.9%-31.5%) of all deaths. More than 50% of all in-hospital deaths were caused by serious medical or neurological complications (54.4%; 95% CI, 54.3%-54.5%). Substantial differences were found in the impact of comorbid conditions on early outcome for men and women. Programs aiming at an improvement in short-term outcome after stroke should focus especially on a reduction of pneumonia and an early treatment of increased intracranial pressure.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Reduced brain edema and infarction volume in mice lacking the neuronal isoform of nitric oxide synthase after transient MCA occlusion.

            Infarct volume and edema were assessed after transient focal ischemia in mice lacking neuronal nitric oxide synthase (NOS) gene expression. With use of an 8-0 coated monofilament, the middle cerebral artery (MCA) of mutant (n = 32) and wild-type mice [SV-129 (n = 31), C57Black/6 (n = 18)] were occluded for 3 h and reperfused for up to 24 h. Regional CBF (rCBF), neurological deficits, water content, and infarct volume were examined in all three strains. rCBF, blood pressure, and heart rate did not differ between groups when measured for 1 h after reperfusion. Neurological deficits were less severe in mutant mice after MCA occlusion. Brain water content at 3 h after reperfusion and infarct volume at 24 h after reperfusion were greater in wild-type mice. These data indicate that genetic deletion of neuronal NOS confers resistance to focal ischemic injury in a reperfusion model. The findings agree with previous studies showing that tissue injury is less extensive after both permanent MCA occlusion and global ischemia in mice lacking neuronal NOS gene expression. Hence, NO may play a pivotal role in the pathogenesis of ischemic brain damage.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Fever and infection early after ischemic stroke.

              Previous studies showed that elevated body temperature early after ischemic stroke is associated with severe neurological deficit and a poor outcome. The aim of this study was to analyse the prevalence and putative etiology of febrile body temperature (>/=38.0 degrees C) early after stroke and to investigate the association between body temperature, stroke severity and outcome. We investigated 119 consecutive patients who were admitted within 24 h after ischemic stroke. Patients were examined for infection before ischemia using a standardized questionnaire and received daily clinical examination after stroke. In case of fever, standardized radiological and microbiological examinations were performed. Fever within 48 h after stroke was observed in 30 (25.2%) patients. The probable cause of fever was infective or chemical aspiration pneumonia (n=12), other respiratory tract infection (n=7), urinary tract infection (n=4), viral infections (n=3) or insufficiently defined (n=5). (One patient had two potential causes of fever.) In thirteen of these patients, infection was most probably acquired before stroke. Fever newly developed more often during day 1 to 2 than day 3 to 7 after stroke (P=0.016). Fever was associated with a more severe deficit on admission independent from age, vascular diseases and risk factors (odds ratio 9.6; 95% confidence interval 3.1-29). Fever is a frequent complication early after stroke and in the majority of cases, it can be explained by infection or chemical aspiration pneumonia. In about half of the infected patients, infection was most probably acquired before stroke. Fever was associated with a more severe neurological deficit on admission.
                Bookmark

                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                2006
                August 2006
                08 August 2006
                : 13
                : 1
                : 13-18
                Affiliations
                Departments of a Neurology, b Experimental Neurology and c Pediatric Pneumology and Immunology and d Institute of Medical Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany
                Article
                92109 Neuroimmunomodulation 2006;13:13–18
                10.1159/000092109
                16612133
                © 2006 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, References: 22, Pages: 6
                Categories
                Original Paper

                Comments

                Comment on this article