Candida guilliermondii complex is characterized by high antifungal resistance but low attributable mortality: a report of 20 cases of candidaemia

Author(s):  
Laura Judith Marcos-Zambrano
2014 ◽  
Vol 58 (8) ◽  
pp. 4565-4572 ◽  
Author(s):  
Laura Judith Marcos-Zambrano ◽  
Pilar Escribano ◽  
Carlos Sánchez ◽  
Patricia Muñoz ◽  
Emilio Bouza ◽  
...  

ABSTRACTAccurate knowledge of fungemia epidemiology requires identification of strains to the molecular level. Various studies have shown that the rate of resistance to fluconazole ranges from 2.5% to 9% inCandidaspp. isolated from blood samples. However, trends in antifungal resistance have received little attention and have been studied only using CLSI M27-A3 methodology. We assessed the fungemia epidemiology in a large tertiary care institution in Madrid, Spain, by identifying isolates to the molecular level and performing antifungal susceptibility testing according to the updated breakpoints of European Committee for Antimicrobial Susceptibility Testing (EUCAST) definitive document (EDef) 7.2. We studied 613 isolates causing 598 episodes of fungemia in 544 patients admitted to our hospital (January 2007 to December 2013). Strains were identified after amplification and sequencing of the ITS1-5.8S-ITS2 region and further tested forin vitrosusceptibility to amphotericin B, fluconazole, posaconazole, voriconazole, micafungin, and anidulafungin. Resistance was defined using EUCAST species-specific breakpoints, and epidemiological cutoff values (ECOFFs) were applied as tentative breakpoints. Most episodes were caused byCandida albicans(46%),Candida parapsilosis(28.7%),Candida glabrata(9.8%), andCandida tropicalis(8%). Molecular identification enabled us to better detect cryptic species ofCandida guilliermondiiandC. parapsilosiscomplexes and episodes of polyfungal fungemia. The overall percentage of fluconazole-resistant isolates was 5%, although it was higher inC. glabrata(8.6%) and non-Candidayeast isolates (47.4%). The rate of resistance to echinocandins was 4.4% and was mainly due to the presence of intrinsically resistant non-Candidaspecies. Resistance mainly affected non-Candidayeasts. The rate of resistance to fluconazole and echinocandins did not change considerably during the study period.


2014 ◽  
Vol 179 (3-4) ◽  
pp. 205-211 ◽  
Author(s):  
Eglė Lastauskienė ◽  
Jolita Čeputytė ◽  
Irutė Girkontaitė ◽  
Auksė Zinkevičienė

Author(s):  
Wouter C. Rottier ◽  
Mette Pinholt ◽  
Akke K. van der Bij ◽  
Magnus Arpi ◽  
Sybrandus N. Blank ◽  
...  

Abstract Objective: To study whether replacement of nosocomial ampicillin-resistant Enterococcus faecium (ARE) clones by vancomycin-resistant E. faecium (VRE), belonging to the same genetic lineages, increases mortality in patients with E. faecium bacteremia, and to evaluate whether any such increase is mediated by a delay in appropriate antibiotic therapy. Design: Retrospective, matched-cohort study. Setting: The study included 20 Dutch and Danish hospitals from 2009 to 2014. Patients: Within the study period, 63 patients with VRE bacteremia (36 Dutch and 27 Danish) were identified and subsequently matched to 234 patients with ARE bacteremia (130 Dutch and 104 Danish) for hospital, ward, length of hospital stay prior to bacteremia, and age. For all patients, 30-day mortality after bacteremia onset was assessed. Methods: The risk ratio (RR) reflecting the impact of vancomycin resistance on 30-day mortality was estimated using Cox regression with further analytic control for confounding factors. Results: The 30-day mortality rates were 27% and 38% for ARE in the Netherlands and Denmark, respectively, and the 30-day mortality rates were 33% and 48% for VRE in these respective countries. The adjusted RR for 30-day mortality for VRE was 1.54 (95% confidence interval, 1.06–2.25). Although appropriate antibiotic therapy was initiated later for VRE than for ARE bacteremia, further analysis did not reveal mediation of the increased mortality risk. Conclusions: Compared to ARE bacteremia, VRE bacteremia was associated with higher 30-day mortality. One explanation for this association would be increased virulence of VRE, although both phenotypes belong to the same well-characterized core genomic lineage. Alternatively, it may be the result of unmeasured confounding.


2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
G Arzilli ◽  
G Scardina ◽  
V Casigliani ◽  
M Moi ◽  
E Lucenteforte ◽  
...  

Abstract Background Antimicrobial-resistant Gram-negative bacteria (AMR-GNB) have emerged as important health care-associated pathogens. Infections with AMR-GNB are associated with high patient morbidity and attributable mortality. Colonization is a prerequisite for infection, however the extent to which colonized patients develop infection is unclear. This systematic review explored the risk of developing infection during hospitalisation among AMR-GNB faecal carriers. Also, we investigated the acquisition rate for AMR-GNB colonization among patients not colonized at admission. Methods We searched on PubMed, Scopus and Cochrane databases for studies published from 2010 up to April 2019. We included studies reporting on hospitalised patients ≥18 years old in high-income countries (excluding long-term care facilities). Results Out of 9496 articles, 55 studies fulfilled our inclusion criteria. Forty-two studies reported data from EU/EEA, 6 from USA and 7 from other regions. Almost all studies (n = 45) were conducted in university hospitals. Most studies (n = 41;74.5%) were performed in high-risk wards (ICU, haematology, burn units and transplant units). Out of 55 studies, 8 examined AMR-GNB, 27 Enterobacteriaceae, while the others investigated specific pathogens: Klebsiella spp. (n = 11), E. Coli (n = 2), A. Baumannii (n = 3) and P. Aeruginosa (n = 4). The rate of AMR-GNB carriage acquisition was 10.5% (n = 40 studies; 95% CI:8.2-13.1). The risk of progression to infection among patients colonized at hospital admission was 13.9% (n = 15; 5.4-24.9), while the infection rate in patients who acquired carriage during hospitalization was 23.0% (n = 7; 5.9-45.2). Patients with an undefined time of colonization presented an infection rate of 16.9% (n = 13; 11.2-23.4). Considering these three populations as a whole, the risk of developing infection was 16.0% (11.0-21.0). Conclusions Our results suggest that risk of progression to infection in AMR-GNB colonized patients in hospital setting is high. Key messages The aim of our study was to estimate the risk of progression to infection, during hospital stay, in patients colonized by AMR-GNB at hospital admission in high-income countries. Our results suggest that faecal colonization with AMR-GNB poses a 16.0% risk of subsequent AMR-GNB infection. This risk in higher (23.0%) in patients who acquired colonization during hospitalisation.


Author(s):  
Jay J. Xu ◽  
Jarvis T. Chen ◽  
Thomas R. Belin ◽  
Ronald S. Brookmeyer ◽  
Marc A. Suchard ◽  
...  

The coronavirus disease 2019 (COVID-19) epidemic in the United States has disproportionately impacted communities of color across the country. Focusing on COVID-19-attributable mortality, we expand upon a national comparative analysis of years of potential life lost (YPLL) attributable to COVID-19 by race/ethnicity (Bassett et al., 2020), estimating percentages of total YPLL for non-Hispanic Whites, non-Hispanic Blacks, Hispanics, non-Hispanic Asians, and non-Hispanic American Indian or Alaska Natives, contrasting them with their respective percent population shares, as well as age-adjusted YPLL rate ratios—anchoring comparisons to non-Hispanic Whites—in each of 45 states and the District of Columbia using data from the National Center for Health Statistics as of 30 December 2020. Using a novel Monte Carlo simulation procedure to perform estimation, our results reveal substantial racial/ethnic disparities in COVID-19-attributable YPLL across states, with a prevailing pattern of non-Hispanic Blacks and Hispanics experiencing disproportionately high and non-Hispanic Whites experiencing disproportionately low COVID-19-attributable YPLL. Furthermore, estimated disparities are generally more pronounced when measuring mortality in terms of YPLL compared to death counts, reflecting the greater intensity of the disparities at younger ages. We also find substantial state-to-state variability in the magnitudes of the estimated racial/ethnic disparities, suggesting that they are driven in large part by social determinants of health whose degree of association with race/ethnicity varies by state.


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