scholarly journals 979. Getting Candid with Candida auris: Evaluation of Isolates at SBH Health System

2021 ◽  
Vol 8 (Supplement_1) ◽  
pp. S580-S581
Author(s):  
Debra M Willner ◽  
Bismarck Bisono-Garcia ◽  
Judith Berger ◽  
Judith Berger ◽  
Victoria Bengualid ◽  
...  

Abstract Background Candida auris is a multidrug resistant yeast that was originally isolated in the external ear of a patient in Japan in 2009. Since then, it has rapidly spread throughout the world. C. auris is inherently a multidrug resistant organism, making echinocandins the drugs of choice. C. auris was first isolated in SBH in a wound culture in 2018, and it has become a major health concern. Our objectives were to evaluate our clinical C. auris isolates, identify potential risk factors for infection, and assess our susceptibilities to determine the most appropriate treatment option. Methods This was a retrospective chart review of all clinical isolates of C. auris from July 2018 – April 2021. Data collection included location prior to admission, SBH hospitalization within 90 days, hospital vs community acquired, new vs recurrent, specimen type, susceptibilities, and lines at the time of culture. Results A total of 121 clinical isolates were evaluated from 74 patients. Although initially clinical isolates were rare, prevalence increased in subsequent years, with 97 clinical isolates identified in 2020. Isolates were identified in various specimen types, with the majority in urine, respiratory samples, or blood cultures. 64% of the isolates were hospital onset. Among patients who tested positive for C. auris colonization through surveillance testing, 22% proceeded to develop clinical infections. Most of the patients with positive blood cultures had either one or multiple IV access points, which may be a risk factor for candidemia. All isolates were resistant to fluconazole, 87% were susceptible to amphotericin B, and susceptibility to echinocandins ranged from 98-99%. Susceptibilities Susceptibilities for the Candida auris clinical isolates received from the NYS Department of Health Specimen Type IV Access in Positive Blood Cultures Access points that were present at the time of candidemia Conclusion Candida auris is a persistent fungus that is highly contagious that has been increasing in prevalence. Infection control measures remain the most proven method to decrease the development of clinical infections. Our study has some limitations, such as the retrospective design, the lack of a control group, lack of clinical outcomes, and limited surveillance testing capabilities. C. auris remains a major cause of concern for nosocomial infections, particularly in patients with various indwelling catheters. Our susceptibilities confirmed echinocandins as the class of choice for treatment of C. auris infections. Disclosures Judith Berger, MD, Nothing to disclose

2020 ◽  
Vol 16 ◽  
pp. 117693432093626
Author(s):  
Iván Darío Ocampo-Ibáñez ◽  
Yamil Liscano ◽  
Sandra Patricia Rivera-Sánchez ◽  
José Oñate-Garzón ◽  
Ashley Dayan Lugo-Guevara ◽  
...  

Infections caused by multidrug-resistant (MDR) Pseudomonas aeruginosa and Klebsiella pneumoniae are a serious worldwide public health concern due to the ineffectiveness of empirical antibiotic therapy. Therefore, research and the development of new antibiotic alternatives are urgently needed to control these bacteria. The use of cationic antimicrobial peptides (CAMPs) is a promising candidate alternative therapeutic strategy to antibiotics because they exhibit antibacterial activity against both antibiotic susceptible and MDR strains. In this study, we aimed to investigate the in vitro antibacterial effect of a short synthetic CAMP derived from the ΔM2 analog of Cec D-like (CAMP-CecD) against clinical isolates of K pneumoniae (n = 30) and P aeruginosa (n = 30), as well as its hemolytic activity. Minimal inhibitory concentrations (MICs) and minimal bactericidal concentrations (MBCs) of CAMP-CecD against wild-type and MDR strains were determined by the broth microdilution test. In addition, an in silico molecular dynamic simulation was performed to predict the interaction between CAMP-CecD and membrane models of K pneumoniae and P aeruginosa. The results revealed a bactericidal effect of CAMP-CecD against both wild-type and resistant strains, but MDR P aeruginosa showed higher susceptibility to this peptide with MIC values between 32 and >256 μg/mL. CAMP-CecD showed higher stability in the P aeruginosa membrane model compared with the K pneumoniae model due to the greater number of noncovalent interactions with phospholipid 1-Palmitoyl-2-oleyl-sn-glycero-3-(phospho-rac-(1-glycerol)) (POPG). This may be related to the boosted effectiveness of the peptide against P aeruginosa clinical isolates. Given the antibacterial activity of CAMP-CecD against wild-type and MDR clinical isolates of P aeruginosa and K pneumoniae and its nonhemolytic effects on human erythrocytes, CAMP-CecD may be a promising alternative to conventional antibiotics.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S291-S292
Author(s):  
Nkuchia M M’ikanatha ◽  
Kelly E Kline ◽  
Sameh W Boktor ◽  
Xin Yin ◽  
Lisa Dettinger ◽  
...  

Abstract Background Antimicrobial resistance (AMR) in foodborne pathogens of animal origin, including nontyphoidal Salmonella (NTS), is a public health concern. Pennsylvania conducts integrated surveillance for AMR in NTS from human and animal sources in collaboration with the FDA and CDC National Antimicrobial Resistant Monitoring System (NARMS). Methods We reviewed pulsed-field gel electrophoresis (PFGE), antimicrobial susceptibility (SST) and whole-genome sequencing (WGS) data for isolates from animal and food sources, including 96 NTS from 2,520 meat samples (poultry, ground beef and pork chops) purchased during 2015–2017 from randomly selected retail outlets in Pennsylvania. SST to 15 antimicrobial agents was done on 109 NTS clinical isolates that had similar PFGE patterns to meat isolates. SST and WGS were used to characterize all isolates from meat and two clinical isolates from 2017. Results 28 (29.2%) and 17 (17.7%) NTS isolated from meat sources were resistant to ≥3 and ≥5 antibiotics classes, respectively. Resistance to ceftriaxone rose from 12% (3/25) in 2015 to 27% (10/37) in 2016 and resistance to amoxicillin/clavulanate also increased. Plasmid-mediated bla CMY-2 β-lactam resistance genes that hydrolyze extended-spectrum cephalosporins (ESC) increased from 12% in 2015 (3/25) to 18.9% (7/37) in 2016. Four blaCTX-M-65 genes that confer resistance to extended-spectrum β-lactamases (ESBLs) were identified in 2016 (n = 3) and 2017. Of the 109 clinical isolates, 25.7% demonstrated resistance to ≥3 and 11% to ≥5 antibiotics classes, respectively. No clinical isolates were resistant to ceftriaxone in 2015, 12.5% (6/48) and 24.3% (9/37) were resistant in 2016 and 2017, respectively. Resistance to amoxicillin/clavulanate was demonstrated in 8.3% (4/48) of isolates in 2016 (figure). Two clinical isolates carried blaCTX-M-65 ESB Ls genes and were resistant to eight antimicrobial agents (ACSSuTCxNalCot. Phenotype). Conclusion NTS (≥25%) from animal and human sources were multidrug-resistant and harbored CMY-2 and CTX-M-65 genes. Dissemination of genes that confer resistance to ESBLs and ESCs in NTS undermines recommended treatment for severe infections and underscores the need for One-Health surveillance and antimicrobial stewardship efforts. Disclosures All authors: No reported disclosures.


mSystems ◽  
2019 ◽  
Vol 4 (4) ◽  
Author(s):  
Daniel Zamith-Miranda ◽  
Heino M. Heyman ◽  
Levi G. Cleare ◽  
Sneha P. Couvillion ◽  
Geremy C. Clair ◽  
...  

ABSTRACT Candida auris is a recently described pathogenic fungus that is causing invasive outbreaks on all continents. The fungus is of high concern given the numbers of multidrug-resistant strains that have been isolated in distinct sites across the globe. The fact that its diagnosis is still problematic suggests that the spreading of the pathogen remains underestimated. Notably, the molecular mechanisms of virulence and antifungal resistance employed by this new species are largely unknown. In the present work, we compared two clinical isolates of C. auris with distinct drug susceptibility profiles and a Candida albicans reference strain using a multi-omics approach. Our results show that, despite the distinct drug resistance profile, both C. auris isolates appear to be very similar, albeit with a few notable differences. However, compared to C. albicans both C. auris isolates have major differences regarding their carbon utilization and downstream lipid and protein content, suggesting a multifactorial mechanism of drug resistance. The molecular profile displayed by C. auris helps to explain the antifungal resistance and virulence phenotypes of this new emerging pathogen. IMPORTANCE Candida auris was first described in Japan in 2009 and has now been the cause of significant outbreaks across the globe. The high number of isolates that are resistant to one or more antifungals, as well as the high mortality rates from patients with bloodstream infections, has attracted the attention of the medical mycology, infectious disease, and public health communities to this pathogenic fungus. In the current work, we performed a broad multi-omics approach on two clinical isolates isolated in New York, the most affected area in the United States and found that the omic profile of C. auris differs significantly from C. albicans. In addition to our insights into C. auris carbon utilization and lipid and protein content, we believe that the availability of these data will enhance our ability to combat this rapidly emerging pathogenic yeast.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Michael A. Olu-Taiwo ◽  
Japheth A. Opintan ◽  
Francis Samuel Codjoe ◽  
Akua Obeng Forson

Metallo-beta-lactamase-producing Acinetobacter spp. is a major challenge for therapeutic treatment of nosocomial infections. This study is aimed at determining the prevalence of MBL-producing Acinetobacter spp. among 87 clinical isolates of Acinetobacter spp. from the Korle-Bu Teaching Hospital, Accra, between August 2014 and July 2015. Acinetobacter spp. was identified by standard bacteriological method, and resistance to different antibiotics was assessed with the Kirby–Bauer disc diffusion method. Meropenem-resistant Acinetobacter isolates were screened for enzyme activity using the modified Hodge test (MHT) and combined disc test (CDT). Additionally, multiplex PCR was used to determine MBL genes presence (blaVIM,blaIMP, and blaNDM). All Acinetobacter isolates showed high resistance to cefotaxime (90.8%), ceftazidime (75.9%), cotrimoxazole (70.1%), ciprofloxacin (64.4%), gentamicin (72.4%), levofloxacin (67.8%), and meropenem (59.8%). A total of 54 (62.1%) of Acinetobacter isolates were multidrug-resistant. Out of 52 (59.8%) meropenem-resistant Acinetobacter, 3 (5.8%) were carbapenemase producers by MHT, whilst, 23 (44.2%) were CDT positive. There was no significant difference between the resistance pattern of amikacin, ceftazidime, cotrimoxazole, ciprofloxacin, and meropenem amongst CDT-positive and CDT-negative isolates (p>0.05). A total of 7/87 (8.1%) CDT-positive Acinetobacter isolates harboured blaNDM; of these, 4 (57.1%) were from wound swabs, urine (n=2) (28.6%), and ear swab (n=1) (14.3%). The study revealed that less than 9% of Acinetobacter spp. contained blaNDM encoding genes. Strict antibiotics usage plan and infection control measures are required to prevent the spread of these resistance genes.


2011 ◽  
Vol 55 (7) ◽  
pp. 3345-3356 ◽  
Author(s):  
Kelli L. Palmer ◽  
Anu Daniel ◽  
Crystal Hardy ◽  
Jared Silverman ◽  
Michael S. Gilmore

ABSTRACTThe emergence of multidrug-resistant enterococci as a leading cause of hospital-acquired infection is an important public health concern. Little is known about the genetic mechanisms by which enterococci adapt to strong selective pressures, including the use of antibiotics. The lipopeptide antibiotic daptomycin is approved to treat Gram-positive bacterial infections, including those caused by enterococci. Since its introduction, resistance to daptomycin by strains ofEnterococcus faecalisandEnterococcus faeciumhas been reported but is still rare. We evolved daptomycin-resistant strains of the multidrug-resistantE. faecalisstrain V583. Based on the availability of a fully closed genome sequence for V583, we used whole-genome resequencing to identify the mutations that became fixed over short time scales (∼2 weeks) upon serial passage in the presence of daptomycin. By comparison of the genome sequences of the three adapted strains to that of parental V583, we identified seven candidate daptomycin resistance genes and three different mutational paths to daptomycin resistance inE. faecalis. Mutations in one of the seven candidate genes (EF0631), encoding a putative cardiolipin synthase, were found in each of the adaptedE. faecalisV583 strains as well as in daptomycin-resistantE. faecalisandE. faeciumclinical isolates. Alleles of EF0631 from daptomycin-resistant strains are dominant intransand confer daptomycin resistance upon a susceptible host. These results demonstrate a mechanism of enterococcal daptomycin resistance that is genetically distinct from that occurring in staphylococci and indicate that enterococci possessing alternate EF0631 alleles are selected for during daptomycin therapy. However, our analysis ofE. faecalisclinical isolates indicates that resistance pathways independent from mutant forms of EF0631 also exist.


Author(s):  
Jeffrey M. Rybak ◽  
José F. Muñoz ◽  
Katherine S. Barker ◽  
Josie E. Parker ◽  
Brooke D. Esquivel ◽  
...  

ABSTRACTCandida auris has emerged as a multidrug-resistant pathogen of great clinical concern. Approximately 90% of clinical C. auris isolates are resistant to fluconazole, the most commonly prescribed antifungal agent, yet it remains unknown what mechanisms underpin this fluconazole resistance. To identify novel mechanisms contributing to fluconazole resistance in C. auris, the fluconazole-susceptible C. auris clinical isolate AR0387 was passaged in media supplemented with fluconazole to generate derivative strains which had acquired increased fluconazole resistance in vitro. Comparative analysis of comprehensive sterol profiles, [3H]-fluconazole uptake, sequencing of C. auris genes homologous to genes known to contribute to fluconazole resistance in other species of Candida, and the relative expression of C. auris ERG11, CDR1, and MDR1 were performed. All fluconazole-evolved derivative strains were found to have acquired mutations in the zinc-cluster transcription factor-encoding gene, TAC1B, and a corresponding increase in CDR1 expression relative to the parental clinical isolate, AR0387. Mutations in TAC1B were also identified in a set of 304 globally distributed C. auris clinical isolates representing each of the four major clades. Introduction of the most common mutation found among fluconazole-resistant clinical isolates of C. auris into the fluconazole-susceptible isolate AR0387, was confirmed to increase fluconazole resistance by 8-fold, and the correction of the same mutation in a fluconazole-resistant isolate, AR0390, decreased fluconazole MIC by 16-fold. Taken together, these data demonstrate that C. auris can rapidly acquire resistance to fluconazole in-vitro, and that mutations in TAC1B significantly contribute to clinical fluconazole resistance.IMPORTANCECandida auris is an emerging multidrug-resistant pathogen of global concern, known to be responsible for outbreaks on six continents and commonly resistant to antifungals. While the vast majority of clinical C. auris isolates are highly resistant to fluconazole, an essential part of the available antifungal arsenal, very little is known about the mechanisms contributing to resistance. In this work, we show that mutations in the transcription factor TAC1B significantly contribute to clinical fluconazole resistance. These studies demonstrate that mutations in TAC1B can arise rapidly in vitro upon exposure to fluconazole, and that a multitude of resistance-associated TAC1B mutations are present among the majority of fluconazole-resistant C. auris isolates from a global collection and appear specific to a subset of lineages or clades. Thus, identification of this novel genetic determinant of resistance significantly adds to the understanding of clinical antifungal resistance in C. auris.


mBio ◽  
2020 ◽  
Vol 11 (3) ◽  
Author(s):  
Jeffrey M. Rybak ◽  
José F. Muñoz ◽  
Katherine S. Barker ◽  
Josie E. Parker ◽  
Brooke D. Esquivel ◽  
...  

ABSTRACT Candida auris has emerged as a multidrug-resistant pathogen of great clinical concern. Approximately 90% of clinical C. auris isolates are resistant to fluconazole, the most commonly prescribed antifungal agent, and yet it remains unknown what mechanisms underpin this fluconazole resistance. To identify novel mechanisms contributing to fluconazole resistance in C. auris, fluconazole-susceptible C. auris clinical isolate AR0387 was passaged in media supplemented with fluconazole to generate derivative strains which had acquired increased fluconazole resistance in vitro. Comparative analyses of comprehensive sterol profiles, [3H]fluconazole uptake, sequencing of C. auris genes homologous to genes known to contribute to fluconazole resistance in other species of Candida, and relative expression levels of C. auris ERG11, CDR1, and MDR1 were performed. All fluconazole-evolved derivative strains were found to have acquired mutations in the zinc-cluster transcription factor-encoding gene TAC1B and to show a corresponding increase in CDR1 expression relative to the parental clinical isolate, AR0387. Mutations in TAC1B were also identified in a set of 304 globally distributed C. auris clinical isolates representing each of the four major clades. Introduction of the most common mutation found among fluconazole-resistant clinical isolates of C. auris into fluconazole-susceptible isolate AR0387 was confirmed to increase fluconazole resistance by 8-fold, and the correction of the same mutation in a fluconazole-resistant isolate, AR0390, decreased fluconazole MIC by 16-fold. Taken together, these data demonstrate that C. auris can rapidly acquire resistance to fluconazole in vitro and that mutations in TAC1B significantly contribute to clinical fluconazole resistance. IMPORTANCE Candida auris is an emerging multidrug-resistant pathogen of global concern, known to be responsible for outbreaks on six continents and to be commonly resistant to antifungals. While the vast majority of clinical C. auris isolates are highly resistant to fluconazole, an essential part of the available antifungal arsenal, very little is known about the mechanisms contributing to resistance. In this work, we show that mutations in the transcription factor TAC1B significantly contribute to clinical fluconazole resistance. These studies demonstrated that mutations in TAC1B can arise rapidly in vitro upon exposure to fluconazole and that a multitude of resistance-associated TAC1B mutations are present among the majority of fluconazole-resistant C. auris isolates from a global collection and appear specific to a subset of lineages or clades. Thus, identification of this novel genetic determinant of resistance significantly adds to the understanding of clinical antifungal resistance in C. auris.


2019 ◽  
Vol 63 (4) ◽  
Author(s):  
Jeffrey M. Rybak ◽  
Laura A. Doorley ◽  
Andrew T. Nishimoto ◽  
Katherine S. Barker ◽  
Glen E. Palmer ◽  
...  

ABSTRACT Candida auris has rapidly emerged as a health care-associated and multidrug-resistant pathogen of global concern. In this work, we examined the relative expression of the four C. auris genes with the highest degree of homology to Candida albicans CDR1 and MDR1 among three triazole-resistant clinical isolates as compared to the triazole-susceptible genome reference clinical isolate. We subsequently utilized a novel Cas9-mediated system for genetic manipulations to delete C. auris CDR1 and MDR1 in both a triazole-resistant clinical isolate and a susceptible reference strain and observed that MICs for all clinically available triazoles decreased as much as 128-fold in the CDR1 deletion strains. The findings of this work reveal for the first time that C. auris CDR1 and MDR1 are more highly expressed among triazole-resistant clinical isolates of C. auris and that the overexpression of CDR1 is a significant contributor to clinical triazole resistance.


2020 ◽  
Author(s):  
Wenzhi Huang ◽  
Fu Qiao ◽  
Lin Cai ◽  
Zhiyong Zong ◽  
Wei Zhang

Abstract Background: A number of studies have shown that daily bathing by chlorhexidine (CHG) wipes in ICU can reduce healthcare-associated infections (HAIs) caused by methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococci (VRE). However, the impact of CHG bathing on carbapenem-resistant Acinetobacter baumannii (CRAB), carbapenem-resistant Pseudomonas aeruginosa (CRPA), and carbapenem-resistant Enterobacteriaceae (CRE) is not clear and remains controversial. Methods: A semi-experimental study which employs both pre-controls and a parallel control was conducted. In the intervention period (from July 1 to December 31, 2016), strengthened infection control measures and daily bathing with 2% CHG-impregnated wipes once daily was performed in the ICU. Fifty-seven non-ICU wards with the occurrence of multidrug-resistant organisms (MDRO) infections during the same time period were selected as parallel control group (only CHG bathing was not performed). The net effect of the 2% CHG daily bathing was evaluated by the difference in difference (DID) model.Results: The incidence of HAIs caused by CRPA in ICU was significantly decreased between the intervention and pre-intervention period (2.5, 95% confidence interval (CI) 1.6–3.8 vs. 4.6, 95% CI 3.3–6.3 cases /1,000 patient days, P = 0.02). Similarly, the incidence of HAIs caused by CRAB in intervention group was 19.75% lower than that in pre-intervention group (6.0, 95% CI 4.4–7.6 vs. 7.5, 95% CI 5.7–9.3 cases / 1,000 patient days, P = 0.24). The DID model analysis showed that CHG bathing reduced the incidence of CRAB- and CRPA-caused infections in ICU by 1.56 and 2.15 cases/1,000 patient days, respectively, P <0.01, and bathing of every 38 patients (95% CI, 21–268) and 39 patients (95% CI, 24–110) were able to prevent one case of HAIs of CRAB and CRPA, respectively. However, CHG bathing showed no effect on MRSA, VRE and CRE (P>0.05).Conclusion: Daily bathing with 2% CHG-impregnated wipes can reduce HAIs caused by CRAB and CRPA, while it is not effective for the prevalence of infections caused by MRSA, VRE, and CRE.


2017 ◽  
Author(s):  
Dahryn Trivedi

Klebsiella pneumoniae (K. pneumoniae) is a common nosocomial pathogen causing respiratory tract (pneumoniae) and blood stream infections. Multidrug-resistant (MDR) isolates of K. pneumoniae infections are difficult to treat in patients in health care settings. Aim of the present study was to determine the impact of Mr. Trivedi’s biofield treatment on four MDR clinical lab isolates (LS) of K. pneumoniae (LS 2, LS 6, LS 7, and LS 14). Samples were divided into two groups i.e. control and biofield treated. Control and treated groups were analyzed for antimicrobial susceptibility pattern, minimum inhibitory concentration (MIC), biochemical study and biotype number using MicroScan Walk-Away® system. The analysis was done on day 10 after biofield treatment as compared with control group. Antimicrobial sensitivity assay showed that there was 46.42% alteration in sensitivity of tested antimicrobials in treated group of MDR K. pneumonia isolates. MIC results showed an alteration in 30% of tested antimicrobials out of thirty after biofield treatment in clinical isolates of K. pneumoniae. An increase in antimicrobial sensitivity and decrease in MIC value was reported (in LS 6) in case of piperacillin/tazobactam and piperacillin. Biochemical study showed a 15.15% change in biochemical reactions as compared to control. A significant change in biotype numbers were reported in all four clinical isolates of MDR K. pneumoniae after biofield treatment as compared to control group. On the basis of changed biotype number after biofield treatment, new organism was identified as Enterobacter aerogenes in LS 2 and LS 14. These results suggest that biofield treatment has a significant effect on altering the antimicrobial sensitivity, MIC values, biochemical reactions and biotype number of multidrug-resistant isolates of K. pneumoniae.


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