ArticleCurrent infectious disease reports2003
Can Enterococcal Infections Initiate Sepsis Syndrome?
Article in Current infectious disease reports, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Extracellular vesicles derived from Enterococcus faecalis: inflammatory activation does not require internalization.Cell communication and signaling : CCS · 2026Article
- Global prevalence of antibiotic resistance in blood-isolatedInfection and drug resistance · 2019Article
- Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages.Infection and immunity · 2014Article
- Enterococcal leucine-rich repeat-containing protein involved in virulence and host inflammatory response.Infection and immunity · 2007Article
- Clostridium glycolicum bacteremia in a bone marrow transplant patient.Journal of clinical microbiology · 2007Article
- Experimental infection ofOpen veterinary journalArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterococci are the third most common nosocomial bloodstream pathogen and frequently are the causative pathogen(s) of intra-abdominal, genitourinary, surgical wound, endovascular, or other serious infections. In addition to a diverse spectrum of intrinsic and acquired antimicrobial resistance mechanisms, some strains of enterococci exhibit numerous virulence factors that facilitate mucosal adherence, tissue invasiveness, endovascular attachment, and inflammation production. However, the opportunistic nature of enterococcal infection coupled with animal models of experimental enterococcal and mixed infection have caused many to question the independent capacity of this organism to incite severe sepsis or septic shock. Despite evidence suggesting that this organism possesses low intrinsic virulence, observational and interventional trials of enterococcal bacteremia and sepsis strongly support the notion that Enterococcus is capable of promulgating sepsis as a solitary or copathogen with more serious sequelae in the immunocompromised hosts. Monomicrobial enterococcal bacteremia appears to be increasing during the glycopeptide-resistant era, which bolsters the notion that pure enterococcal sepsis is a real entity.
Identifiers
13678566What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.