ArticleInfection and immunity2014
Candida glabrata intra-abdominal candidiasis is characterized by persistence within the peritoneal cavity and abscesses.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.FEMS yeast research · 2025Review
- Pharmacokinetic and pharmacodynamic considerations for antifungal therapy optimisation in the treatment of intra-abdominal candidiasis.Critical care (London, England) · 2023Review
- Pre-exposure toVirulence · 2020Article
- Article
- The Quiet and Underappreciated Rise of Drug-Resistant Invasive Fungal Pathogens.Journal of fungi (Basel, Switzerland) · 2020Review
- Candida albicans Impacts Staphylococcus aureus Alpha-Toxin Production via Extracellular Alkalinization.mSphere · 2019Article
- Article
- NovelEmerging microbes & infections · 2019Article
- Autophagy-Inducing Factor Atg1 Is Required for Virulence in the Pathogenic FungusFrontiers in microbiology · 2019Article
- Treatment of Invasive Candidiasis: A Narrative Review.Journal of fungi (Basel, Switzerland) · 2018Review
- Echinocandin resistance among Candida isolates at an academic medical centre 2005-15: analysis of trends and outcomes.The Journal of antimicrobial chemotherapy · 2018Article
- Dectin-1 plays an important role in host defense against systemic Candida glabrata infection.Virulence · 2017Article
- Specific Human and Candida Cellular Interactions Lead to Controlled or Persistent Infection Outcomes during Granuloma-Like Formation.Infection and immunity · 2017Article
- Morphology-Independent Virulence of Candida Species during Polymicrobial Intra-abdominal Infections with Staphylococcus aureus.Infection and immunity · 2016Article
- Intra-Abdominal Candidiasis: The Importance of Early Source Control and Antifungal Treatment.PloS one · 2016Article
- Echinocandin Resistance in Candida.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015Article
- Review
- Mechanisms of echinocandin antifungal drug resistance.Annals of the New York Academy of Sciences · 2015Review
- Abdominal candidiasis is a hidden reservoir of echinocandin resistance.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of Candida glabrata infections is poorly understood. We studied the pathogenesis of intra-abdominal candidiasis (IAC) in mice that were infected intraperitoneally with C. glabrata and sterile feces. C. glabrata BG2 (5 × 10(8) CFU) caused a 100% mortality rate. Sublethal inocula of BG2 (1 × 10(8) or 1 × 10(7) CFU) caused peritonitis that progressed to abscesses. Three clinical C. glabrata strains (5 × 10(8) CFU) caused 80 to 100% mortality rates, while a fourth (strain 346) caused a 29% mortality rate. Following sublethal inocula (1 × 10(7) CFU), the intra-abscess burdens of virulent strain 356 were ∼1 log greater than those of strain 346. A C. glabrata Δplb1-2 mutant (phospholipase B genes disrupted) killed mice as well as BG2 did. When sublethal inocula were used, however, the Δplb1-2 mutant was associated with more rapid abscess resolution and lower intra-abscess burdens; these findings were reversed by PLB1 and PLB2 reinsertion. The Δplb1-2 mutant was also more susceptible than BG2 to killing by human neutrophils in vitro. BG2 and the Δplb1-2 mutant were indistinguishable during hematogenously disseminated candidiasis. C. albicans SC5314 was more virulent than C. glabrata BG2 during IAC, causing a 100% mortality rate following a challenge with 5 × 10(7) CFU. In contrast, a sublethal inoculum (1 × 10(7) CFU) of BG2 caused less neutrophil infiltration and greater burdens in peritoneal fluid than SC5314 did and abscesses that persisted longer and contained greater burdens. In conclusion, a mouse model of C. glabrata IAC mimics disease in humans and distinguishes the relative virulence of clinical and gene disruption strains. C. glabrata differed from C. albicans during IAC by being less lethal and eliciting dampened neutrophil responses but resulting in more persistent peritonitis and abscesses.
Indexed as
Identifiers
What 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.