Tracing the Evolutionary History and Global Expansion of Candida auris Using Population Genomic Analyses
In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of...
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| Published in | mBio Vol. 11; no. 2; pp. e03364 - 19 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Microbiology
28.04.2020
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | In less than a decade,
C. auris
has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other
Candida
species,
C. auris
is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new
C. auris
introductions. Through a global collaboration, we assessed genome evolution of isolates of
C. auris
from 19 countries. Here, we described estimated timing of the expansion of each
C. auris
clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology.
Candida auris
has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description,
C. auris
has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304
C. auris
isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure.
C. auris
isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in
ERG11
as the most widespread mutation associated with azole resistance and S639P in
FKS1
for echinocandin resistance. Copy number variants in
ERG11
predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in
C. auris
.
IMPORTANCE
In less than a decade,
C. auris
has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other
Candida
species,
C. auris
is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new
C. auris
introductions. Through a global collaboration, we assessed genome evolution of isolates of
C. auris
from 19 countries. Here, we described estimated timing of the expansion of each
C. auris
clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. |
|---|---|
| AbstractList | Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, C. auris has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 C. auris isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. C. auris isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in ERG11 as the most widespread mutation associated with azole resistance and S639P in FKS1 for echinocandin resistance. Copy number variants in ERG11 predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in C. aurisIMPORTANCE In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new C. auris introductions. Through a global collaboration, we assessed genome evolution of isolates of C. auris from 19 countries. Here, we described estimated timing of the expansion of each C. auris clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology.Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, C. auris has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 C. auris isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. C. auris isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in ERG11 as the most widespread mutation associated with azole resistance and S639P in FKS1 for echinocandin resistance. Copy number variants in ERG11 predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in C. aurisIMPORTANCE In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new C. auris introductions. Through a global collaboration, we assessed genome evolution of isolates of C. auris from 19 countries. Here, we described estimated timing of the expansion of each C. auris clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new C. auris introductions. Through a global collaboration, we assessed genome evolution of isolates of C. auris from 19 countries. Here, we described estimated timing of the expansion of each C. auris clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, C. auris has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 C. auris isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. C. auris isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in ERG11 as the most widespread mutation associated with azole resistance and S639P in FKS1 for echinocandin resistance. Copy number variants in ERG11 predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in C. auris . IMPORTANCE In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new C. auris introductions. Through a global collaboration, we assessed genome evolution of isolates of C. auris from 19 countries. Here, we described estimated timing of the expansion of each C. auris clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in as the most widespread mutation associated with azole resistance and S639P in for echinocandin resistance. Copy number variants in predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in In less than a decade, has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other species, is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new introductions. Through a global collaboration, we assessed genome evolution of isolates of from 19 countries. Here, we described estimated timing of the expansion of each clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. ABSTRACT Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, C. auris has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 C. auris isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. C. auris isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in ERG11 as the most widespread mutation associated with azole resistance and S639P in FKS1 for echinocandin resistance. Copy number variants in ERG11 predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in C. auris. IMPORTANCE In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new C. auris introductions. Through a global collaboration, we assessed genome evolution of isolates of C. auris from 19 countries. Here, we described estimated timing of the expansion of each C. auris clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, C. auris has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 C. auris isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. C. auris isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in ERG11 as the most widespread mutation associated with azole resistance and S639P in FKS1 for echinocandin resistance. Copy number variants in ERG11 predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in C. auris. In less than a decade, C. auris has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive candidiasis. In contrast to other Candida species, C. auris is unique in its ability to spread via nosocomial transmission and its high rates of drug resistance. As part of the public health response, whole-genome sequencing has played a major role in characterizing transmission dynamics and detecting new C. auris introductions. Through a global collaboration, we assessed genome evolution of isolates of C. auris from 19 countries. Here, we described estimated timing of the expansion of each C. auris clade and of fluconazole resistance, characterized discrete phylogeographic population structure of each clade, and compared genome data to sensitivity measurements to describe how antifungal resistance mechanisms vary across the population. These efforts are critical for a sustained, robust public health response that effectively utilizes molecular epidemiology. Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India, Pakistan, South Africa, and Venezuela revealed four populations (clades I, II, III, and IV) corresponding to these geographic regions. Since this description, C. auris has been reported in more than 30 additional countries. To trace this global emergence, we compared the genomes of 304 C. auris isolates from 19 countries on six continents. We found that four predominant clades persist across wide geographic locations. We observed phylogeographic mixing in most clades; clade IV, with isolates mainly from South America, demonstrated the strongest phylogeographic substructure. C. auris isolates from two clades with opposite mating types were detected contemporaneously in a single health care facility in Kenya. We estimated a Bayesian molecular clock phylogeny and dated the origin of each clade within the last 360 years; outbreak-causing clusters from clades I, III, and IV originated 36 to 38 years ago. We observed high rates of antifungal resistance in clade I, including four isolates resistant to all three major classes of antifungals. Mutations that contribute to resistance varied between the clades, with Y132F in ERG11 as the most widespread mutation associated with azole resistance and S639P in FKS1 for echinocandin resistance. Copy number variants in ERG11 predominantly appeared in clade III and were associated with fluconazole resistance. These results provide a global context for the phylogeography, population structure, and mechanisms associated with antifungal resistance in C. auris . |
| Author | Kurzai, Oliver Martin, Ronny Berkow, Elizabeth L. Litvintseva, Anastasia P. Heath, Christopher H. Althawadi, Sahar Escandón, Patricia Araúz, Ana Belén Desnos-Ollivier, Marie Cuomo, Christina A. Li, Xiao Alanio, Alexandre Gardam, Dianne Adam, Rodney Alastruey-Izquierdo, Ana Gade, Lalitha Bharat, Amrita Forsberg, Kaitlin Gunturu, Revathi Welsh, Rory M. Calvo, Belinda Muñoz, José F. Ben-Ami, Ronen Chow, Nancy A. Lockhart, Shawn R. |
| Author_xml | – sequence: 1 givenname: Nancy A. surname: Chow fullname: Chow, Nancy A. organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 2 givenname: José F. orcidid: 0000-0003-4987-7957 surname: Muñoz fullname: Muñoz, José F. organization: Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA – sequence: 3 givenname: Lalitha surname: Gade fullname: Gade, Lalitha organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 4 givenname: Elizabeth L. surname: Berkow fullname: Berkow, Elizabeth L. organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 5 givenname: Xiao surname: Li fullname: Li, Xiao organization: Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA – sequence: 6 givenname: Rory M. surname: Welsh fullname: Welsh, Rory M. organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 7 givenname: Kaitlin surname: Forsberg fullname: Forsberg, Kaitlin organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 8 givenname: Shawn R. surname: Lockhart fullname: Lockhart, Shawn R. organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 9 givenname: Rodney surname: Adam fullname: Adam, Rodney organization: Department of Pathology, Aga Khan University Hospital, Nairobi, Kenya – sequence: 10 givenname: Alexandre orcidid: 0000-0001-9726-3082 surname: Alanio fullname: Alanio, Alexandre organization: Institut Pasteur, Molecular Mycology Unit, CNRS UMR2000, National Reference Center for Invasive Mycoses and Antifungals (NRCMA), Paris, France, Laboratoire de Parasitologie-Mycologie, Hôpital Saint-Louis, Groupe Hospitalier Lariboisière, Saint-Louis, Fernand Widal, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France, Université Paris Diderot, Université de Paris, Paris, France – sequence: 11 givenname: Ana orcidid: 0000-0001-8651-4405 surname: Alastruey-Izquierdo fullname: Alastruey-Izquierdo, Ana organization: Mycology Reference Laboratory, National Centre for Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain – sequence: 12 givenname: Sahar surname: Althawadi fullname: Althawadi, Sahar organization: Department of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia – sequence: 13 givenname: Ana Belén surname: Araúz fullname: Araúz, Ana Belén organization: Hospital Santo Tomás, Panama City, Panama – sequence: 14 givenname: Ronen surname: Ben-Ami fullname: Ben-Ami, Ronen organization: Infectious Diseases Unit, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel – sequence: 15 givenname: Amrita surname: Bharat fullname: Bharat, Amrita organization: National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada – sequence: 16 givenname: Belinda surname: Calvo fullname: Calvo, Belinda organization: Department of Infectious Diseases, School of Medicine, Universidad del Zulia, Maracaibo, Venezuela – sequence: 17 givenname: Marie orcidid: 0000-0002-9137-0466 surname: Desnos-Ollivier fullname: Desnos-Ollivier, Marie organization: Institut Pasteur, Molecular Mycology Unit, CNRS UMR2000, National Reference Center for Invasive Mycoses and Antifungals (NRCMA), Paris, France – sequence: 18 givenname: Patricia surname: Escandón fullname: Escandón, Patricia organization: Grupo de Microbiología, Instituto Nacional de Salud, Bogotá, Colombia – sequence: 19 givenname: Dianne surname: Gardam fullname: Gardam, Dianne organization: Department of Microbiology, PathWest Laboratory Medicine FSH Network, Fiona Stanley Hospital, Murdoch, Australia – sequence: 20 givenname: Revathi surname: Gunturu fullname: Gunturu, Revathi organization: Department of Pathology, Aga Khan University Hospital, Nairobi, Kenya – sequence: 21 givenname: Christopher H. orcidid: 0000-0001-7850-6931 surname: Heath fullname: Heath, Christopher H. organization: Department of Microbiology, PathWest Laboratory Medicine FSH Network, Fiona Stanley Hospital, Murdoch, Australia, Department of Infectious Diseases, Fiona Stanley Hospital, Murdoch, Australia, Infectious Diseases, Royal Perth Hospital, Perth, Australia, Faculty of Health & Medical Sciences, University of Western Australia, Crawley, Washington, Australia – sequence: 22 givenname: Oliver orcidid: 0000-0002-7277-2646 surname: Kurzai fullname: Kurzai, Oliver organization: German National Reference Center for Invasive Fungal Infections NRZMyk, Leibniz Institute for Natural Product Research and Infection Biology–Hans-Knöll-Institute, Jena, Germany, Institute for Hygiene and Microbiology, University of Würzburg, Würzburg, Germany – sequence: 23 givenname: Ronny surname: Martin fullname: Martin, Ronny organization: German National Reference Center for Invasive Fungal Infections NRZMyk, Leibniz Institute for Natural Product Research and Infection Biology–Hans-Knöll-Institute, Jena, Germany, Institute for Hygiene and Microbiology, University of Würzburg, Würzburg, Germany – sequence: 24 givenname: Anastasia P. surname: Litvintseva fullname: Litvintseva, Anastasia P. organization: Mycotic Diseases Branch, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Atlanta, Georgia, USA – sequence: 25 givenname: Christina A. orcidid: 0000-0002-5778-960X surname: Cuomo fullname: Cuomo, Christina A. organization: Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32345637$$D View this record in MEDLINE/PubMed https://pasteur.hal.science/pasteur-03243537$$DView record in HAL |
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| Keywords | Candida auris population genetics emerging species genome analysis antifungal resistance |
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| Snippet | In less than a decade,
C. auris
has emerged in health care settings worldwide; this species is capable of colonizing skin and causing outbreaks of invasive... has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from Japan, India,... Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of isolates from... ABSTRACT Candida auris has emerged globally as a multidrug-resistant yeast that can spread via nosocomial transmission. An initial phylogenetic study of... |
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| SubjectTerms | Antifungal Agents Antifungal Agents - pharmacology antifungal resistance Azoles Azoles - pharmacology Biological Evolution Candida Candida - classification Candida - drug effects Candida - genetics Candida - isolation & purification Candida auris Candidiasis, Invasive Candidiasis, Invasive - drug therapy Candidiasis, Invasive - epidemiology Drug Resistance, Fungal Drug Resistance, Fungal - genetics Echinocandins Echinocandins - pharmacology Ecological and Evolutionary Science emerging species Fluconazole Fluconazole - pharmacology Genes, Fungal Genetics, Population Genetics, Population - methods genome analysis Genome, Fungal Humans Life Sciences Metagenomics Microbiology and Parasitology Molecular Epidemiology Mutation Mycology Phylogeny Phylogeography population genetics Whole Genome Sequencing |
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| Title | Tracing the Evolutionary History and Global Expansion of Candida auris Using Population Genomic Analyses |
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