{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T01:52:30Z","timestamp":1793757150614,"version":"4.6.1"},"reference-count":24,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2006,9,26]],"date-time":"2006-09-26T00:00:00Z","timestamp":1159228800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/www.springer.com\/tdm"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Infect Dis"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Enterococci are the third leading cause of nosocomial bloodstream infection (BSI). Vancomycin resistant enterococci are common and provide treatment challenges; however questions remain about VRE's pathogenicity and its direct clinical impact. This study analyzed the inflammatory response of Enterococcal BSI, contrasting infections from vancomycin-resistant and vancomycin-susceptible isolates.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed a historical cohort study on 50 adults with enterococcal BSI to evaluate the associated systemic inflammatory response syndrome (SIRS) and mortality. We examined SIRS scores 2 days prior through 14 days after the first positive blood culture. Vancomycin resistant (n = 17) and susceptible infections (n = 33) were compared. Variables significant in univariate analysis were entered into a logistic regression model to determine the affect on mortality.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>60% of BSI were caused by<jats:italic>E. faecalis<\/jats:italic>and 34% by<jats:italic>E. faecium<\/jats:italic>. 34% of the isolates were vancomycin resistant. Mean APACHE II (A2) score on the day of BSI was 16. Appropriate antimicrobials were begun within 24 hours in 52%. Septic shock occurred in 62% and severe sepsis in an additional 18%. Incidence of organ failure was as follows: respiratory 42%, renal 48%, hematologic 44%, hepatic 26%. Crude mortality was 48%. Progression to septic shock was associated with death (OR 14.9, p &lt; .001). There was no difference in A2 scores on days -2, -1 and 0 between the VRE and VSE groups. Maximal SIR (severe sepsis, septic shock or death) was seen on day 2 for VSE BSI vs. day 8 for VRE. No significant difference was noted in the incidence of organ failure, 7-day or overall mortality between the two groups. Univariate analysis revealed that AP2&gt;18 at BSI onset, and respiratory, cardiovascular, renal, hematologic and hepatic failure were associated with death, but time to appropriate therapy &gt;24 hours, age, and infection due to VRE were not. Multivariate analysis revealed that hematologic (OR 8.4, p = .025) and cardiovascular failure (OR 7.5, p = 032) independently predicted death.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In patients with enterococcal BSI, (1) the incidence of septic shock and organ failure is high, (2) patients with VRE BSI are not more acutely ill prior to infection than those with VSE BSI, and (3) the development of hematologic or cardiovascular failure independently predicts death.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1471-2334-6-145","type":"journal-article","created":{"date-parts":[[2006,9,26]],"date-time":"2006-09-26T18:25:13Z","timestamp":1159295113000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Systemic inflammatory response syndrome in adult patients with nosocomial bloodstream infections due to enterococci"],"prefix":"10.1186","volume":"6","author":[{"given":"Katharine","family":"Bar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hilmar","family":"Wisplinghoff","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard P","family":"Wenzel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gonzalo ML","family":"Bearman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael B","family":"Edmond","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2006,9,26]]},"reference":[{"key":"409_CR1","doi-asserted-by":"publisher","first-page":"309","DOI":"10.1086\/421946","volume":"39","author":"H Wisplinghoff","year":"2004","unstructured":"Wisplinghoff H, Bischoff T, Tallant S, Seifert H, Wenzel RP, Edmond MB: Nosocomial bloodstream infections in US hospitals: Analysis of 24,179 cases from a prospective nationwide surveillance study. 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