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Available online at ajdhs.com 

Asian Journal of Dental and Health Sciences 
Open Access to Pharmaceutical and Medical Research 

Copyright  © 2022 The  Author(s): This is an open-access article distributed under the terms of the CC BY-NC 4.0 
which permits unrestricted use, distribution, and reproduction in any medium for non-commercial use provided the 

original author and source are credited 

 

 

 

An Update on the Recent Emergence of Candida auris 

Monika Jain1, Anushree Jain1, Basant Khare1, Deepak Kumar Jain2, Rubeena Khan1, Dolly Jain*1 

1 Adina College of Pharmacy, ADINA Campus Rd, Lahdara, Sagar, MP, 470001 

2 Sun Institute of Pharmaceutical Education & Research (SIPER), Bhatpura Road, Lahar, Bhind, MP, 477445  

Article Info: 
_________________________________________ 
Article History: 

Received 10 Jan 2022      
Reviewed 26 Feb 2022 
Accepted 05 March 2022 
Published 15 March 2022 

_________________________________________ 
Cite this article as:  

Jain M, Jain A, Khare B, Jain DK, Khan R, Jain D, An 
Update on the Recent Emergence of Candida auris, 
Asian Journal of Dental and Health Sciences. 2022; 
2(1):14-19 

DOI: http://dx.doi.org/10.22270/ajdhs.v2i1.11                                  

_________________________________________ 

*Address for Correspondence:   

Dolly Jain, Adina College of Pharmacy, ADINA 
Campus Rd, Lahdara, Sagar, MP, 470001 

Abstract 
___________________________________________________________________________________________________________________ 

The incidence of invasive fungal infections (IFI) caused by unusual pathogens is on the rise, partly 
driven by the increased population of immunocompromised patients. The emerging multidrug-
resistant yeast pathogen Candida auris (C. auris) has been a source of concern as an agent of 
healthcare-associated infections. C. auris is emerging multidrug-resistant yeast that causes serious 
invasive infections with high mortality. It was first discovered in 2009, and since then, individual 
cases or outbreaks have been reported from over 20 countries on five continents. Controlling C. auris 
is challenging for several reasons: (1) it is resistant to multiple classes of antifungals, (2) it can be 
misidentified as other yeasts by commonly available Identification methods, and (3) because of its 
ability to colonize patients perhaps indefinitely and persist in the healthcare environment, it can 
spread between patients in healthcare settings. The transmissibility and high levels of antifungal 
resistance that are characteristic of C. auris set it apart from most other Candida species. A robust 
response that involves the laboratory, clinicians, and public health agencies is needed to identify and 
treat infections and prevent transmission. This review highlights epidemiology, pathogenesis, 
microbiological characteristics, clinical presentation, diagnostic challenges and treatment options of C. 
auris infections. Infection prevention measures to prevent spread of C. auris and special measures 
during an outbreak situation have also been reviewed. Rapid emergence of hospital onset C. auris is 
worrisome. Early diagnosis of C. auris is essential for better outcomes and the implementation of 
infection prevention measures. Lack of widespread awareness, absence of general availability of 
diagnostic testing methods, and limited options for treatment of C. auris infections make it a difficult-
to-treat pathogen. Further studies are needed for better understanding of this emerging pathogen. 

Keywords: Fungal infection, Candida, C. auris, Candidemia, Bloodstream infection 

Email: dollyjain.btpc@gmail.com 

Introduction 

Candida species commonly colonizes the human mucosal and 
skin surfaces with potential to cause infections. Disruption in 
host immunity increases the risk for development of 
opportunistic infections from Candida. Candidemia is 
recognized as the fourth most common cause of nosocomial 
bloodstream infections in the United States (US) associated 
with high morbidity and mortality rates (30%-40%)1. Candida 
auris is emerging multidrug-resistant yeast that can cause 
invasive infections, is associated with high mortality, and can 
spread in healthcare settings. This yeast was first described in 
2009 and has since been reported in over 20 countries on five 
continents. C. auris poses a global health threat for several 
reasons:  

1. Multidrug resistance is common, and a few isolates are 
resistant to all three of the main classes of antifungal drugs, 
severely limiting treatment options2. 

2. C. auris is commonly misidentified in clinical laboratories. 
Unless laboratories are aware of possible misidentification 
and have the ability to perform further evaluation, cases of C. 
auris could go undetected. 

3. C. auris can be transmitted between patients in healthcare 
settings and cause healthcare-associated outbreaks. C. auris 
can colonize patients, especially on the skin, perhaps 

indefinitely, and persist for weeks in the healthcare 
environment. The lack of decolonization methods and 
suboptimal efficacy of some commonly used hospital 
environmental disinfectants compounds the challenge of 
controlling its spread. 

The genus Candida comprises an array of phenotypically 
similar yet genetically highly divergent yeasts. C. auris differs 
markedly from common pathogenic Candida species like 
Candida albicans and Candida glabrata. In healthcare settings, 
C. auris behaves more like transmissible bacterial multidrug-
resistant organisms (MDROs), such as methicillin-resistant 
Staphylococcus aureus (MRSA) and carbapenem-resistant 
Enterobacteriacea (CRE), than other Candida species. Unlike 
other Candida infections, which are generally thought to result 
from autoinfection from host flora, C. auris can be transmitted 
between patients. Unlike for most other Candida species, for 
which transmission-based precautions are generally not 
required, C. auris requires implementation of specific infection 
control measures, much like those used for control of MRSA 
and CRE. With itsmultidrug resistance, transmissibility and 
severe outcomes, C. auris has all the makings of a superbug. 
Control of C. auris requires better understanding of the 
organism itself, vigilance and accurate identification, 
appropriate treatment and infection control measures, and a 
coordinated public health response. We review the emergence 
of C. auris, examining the global advent, biology, challenges of 

                       Open Access                                                                                                                                                                                                             Review Article                                           

http://jddtonline.info/
http://dx.doi.org/10.22270/ajdhs.v2i1.11


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identification, multidrug resistance, clinical manifestations, 
treatment, risk factors for infection, transmission, and control 
of C. auris. 

Epidemiology 

Incidence and prevalence 

The incidence of Candida infections and causative Candida 
species has varied with time and across geographic locations. 
Until recently, the most common isolated species during 
nosocomial fungemia has been C. albicans, however with 
changing epidemiology, non-C. albicans has emerged as the 
predominant species in many countries1. Candida glabrata is 
recognized as the most common cause of candidemia in the US 
while C. parapsilosis, C. tropicalis and C. krusei are common in 
other parts of the world1. The true incidence of C. auris 
fungemia and its global prevalence are poorly understood. 
This uncertainty is related to failure of conventional diagnostic 
methods to accurately identify C. auris and lack of global 
availability of diagnostic methods for its rapid identification3. 
Few centers with diagnostic capabilities have estimated 
incidence and prevalence of C. auris fungemia at their 
healthcare facilities. Prevalence of C. auris was rare prior to 
2009 according to the investigation conducted on a pool of 
uncommon Candida species included in the international 
antifungal surveillance program (SENTRY). Of the 15,271 
isolates reviewed from 4 continents between2004-2015, only 
four isolates were identified as C. auris4. However, since 2009 
there has been a rapid and global emergence of C. auris. 
According to a single center study in Sub-Saharan Africa from 
September 2010-June2013, candidemia attributed to 39% of 
nosocomial infections. During the study period, C. haemulonii, 
later reidentified as C. auris, was the most common cause of 
hospital-onset fungemia (38%) followed by C. albicans (27%)5. 
Another study in multiple hospital systems in South Africa 
highlighted the prevalence of C. auris-related candidemia to be 
0.3%6. Unfortunately, both these studies did not provide 
specific data on study period and total number of candidemia 
cases identified to understand the true impact of C. auris. A 
tertiary medical center in South America reported C. auris as 
the 6th most common cause of bloodstream infection in the 
hospital between March 2012-July 20137. An 18-month 
prospective study in Indian ICUs reported 1400 candidemia 
cases. Candida auris was identified as the 5th most common 
cause of ICU-onset candidemia, discovered in 19 of 27 ICUs, 
with prevalence of 5.3% (n=74) 8. A random one-year 
screening for C. auris in patients admitted at a cardiothoracic 
center in London identified prevalence rateof 0.04% (1/2246 
screened patients)9. Overall, the prevalence of C. auris, 
predominantly nosocomial-onset, is rising globally. 

Isolation of C. auris 

Candida auris has been isolated from multiple body sites. First 
isolation of C. auris was from the external ear canal of a 70-
year-old woman in Japan10. A multicenter surveillance study in 
Korea (2004-2006) reported 15 specimens isolated from the 
ears of patients with chronic otitis media as closely related C. 
haemulonii species by sequence analysis, later re-identified as 
C. auris11. Vaginal sample from a young woman in India 
identified C. auris as cause of vulvovaginitis12. Candida auris 
has been described as the cause of fatal pericarditis in an 
Indian patient with end stage liver disease13. First three cases 
of bloodstream infection from C. auris were reported from 
South Korea in 200914. A fatal case of donor-derived C. auris 
infection was reported in a 71-year old lung transplant 
recipient in the US in 201715. Currently, C. auris fungemia has 
been reported nearly from all continents except Australia and 
Antarctica. As awareness of C. auris has grown, novel isolates 
and previously unidentified Candida isolates are increasingly 
being recognized as C. auris. According to the Center for 

Diseases control and prevention (CDC) in the United States, 86 
isolates of C. auris have been identified in the US from 
infectious and non-infectious sources, mostly emerging from 
the east coast. 

Biology and morphology 

The closest relatives of C. auris are C. ruelliae, C. 
pseudohaemulonii, Candida duobushaemulonii, Candida 
vulturna, C. heveicola, Candida konsanensis, Candida 
chanthaburiensis, C. haemulonii, and Candida haemulonis var. 
vulnera16. C. auris is an ovoid to elongate budding yeast, which 
seldom forms rudimentary pseudohyphae and typically 
appears as pink, but sometimes white or red, colonies on 
CHROMagar Candida or CAN2 chromogenic medium. This 
organism has a high tolerance for salinity and heat. Its unique 
ability to grow at temperatures up to 42◦C16-20 and to grow in 
high salt conditions may help to distinguish C. auris from other 
Candida species and aid laboratory isolation19. However, none 
of the phenotypic characteristics of C. auris are sufficient 
evidence for definitive identification. Sequencing, mass 
spectrometry, or a VITEK 2 version 8.01 are needed to 
accurately distinguish C. auris from closely related Candida 
species. Some strains of C. auris have been reported to form 
aggregations in culture, which may allow the organism to 
resist penetration by detergents, ultraviolet light, or other 
cleaning methods21. C. auris also forms biofilms, which provide 
a mechanism of adherence to surfaces. However, these 
biofilms are significantly thinner and less complex than those 
of C. albicans, primarily due to the rarity of pseudohyphae. C. 
auris may therefore have reduced ability to attach to surfaces 
like catheter material as compared to species that can form 
more robust biofilms22. In animal models, C. auris exhibits 
similar or slightly less virulence as C. albicans and Candida 
tropicalis and greater virulence than the closely related 
species C. haemulonii23,24. Its ability to form biofilms, produce 
phospholipase and proteinase, and secrete aspartic proteases 
as well as the presence of oligopeptide transporters and 
mannosyl transferases may explain some of the virulence seen 
with C. auris, though some of these characteristics have varied 
by strain25. Aggregate-forming strains may be less virulent 
than strains without cell aggregations. Despite these advances 
in our understanding of C. auris, much remains unknown 
about its cell biology and virulence characteristics. 

Risk factors 

Candida auris is a hospital-acquired pathogen causing 
infection in certain high-risk patient populations. The 
predisposing risk factors for C. auris infection are similar to 
other candidal species. Patients with immunocompromising 
diseases (diabetes mellitus, malignancy, chronic kidney 
disease, neutropenia), concomitant bacteremia, broad- 
spectrum antibacterial or antifungal therapy in prior 90 days, 
surgery within 90 days, presence of central venous catheters 
or urinary catheters, stay in intensive care unit (ICU) and total 
parenteral nutrition (TPN) administration confer increased 
risk for acquiring C. auris26-28. Till date, only one case-control 
study has been performed to determine specific risk factors 
predisposing to C. auris candidemia8. The study was conducted 
in the ICUs in India comparing C. auris (n=74) and non-auris 
(n=1087) fungemia cases. The multivariate analysis showed 
patients with respiratory illness, vascular surgery, antifungal 
exposure in prior 30-days and low APACHE II score on 
admission had higher likelihood to develop ICU-onset C. auris 
fungemia. 

Multidrug resistance 

C. auris is a highly concerning pathogen because it can be 
resistant to multiple antifungal drugs, with some isolates 
resistant to all three major antifungal classes (azoles, 



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polyenes, and echinocandins). The Clinical and Laboratory 
Standards Institute (CLSI) and the European Committee for 
Antimicrobial Susceptibility Testing (EUCAST) have not 
established clinical susceptibility minimum inhibitory 
concentration (MIC) breakpoints for C. auris. In the interim, 
CDC has proposed the following tentative breakpoints, 
conservatively based on those established for other species: 
≥32 for fluconazole, ≥2 for amphotericin B (or ≥1.5 if using 
Etest), ≥4 for anidulafungin and micafungin, and ≥2 for 
caspofungin29. In a collection of 54 isolates from India, 
Pakistan, South Africa, and Venezuela, 93% of isolates were 
resistant to fluconazole, 35% were resistant to amphotericin 
B, and 7% were resistant to echinocandins using the following 
breakpoints: ≥32 for fluconazole, ≥2 for amphotericin B, and 
≥8 for echinocandins. Forty-one percent of isolates were 
resistant to at least two drug classes and two isolates were 
pan-resistant. 

In the largest study of C. auris resistance, on 350 isolates from 
India, 90% of isolates were resistant to fluconazole by the 
tentative breakpoints described above, 2% to anidulafungin, 
2% to micafungin, and 8% to amphotericin B. In the United 
States, about 90% of isolates have been resistant to 
fluconazole, 30% have been resistant to amphotericin B, and 
5% have been resistant to echinocandins29. Public Health 
England has reported that all UK isolates have been resistant 
to fluconazole, approximately 20% have been resistant to 
amphotericin B, and about 10% have been resistant to 
echinocandins30. Taking data from around the world into 
account, C. auris has been generally resistant to fluconazole, 
and a substantial portion of isolates has been resistant to 
amphotericin B and echinocandins Most other species of 
Candida identified in clinical specimens exhibit high in vitro 
susceptibility to antifungal drugs. One of the other drug-
resistant Candida of high concern has been C. glabrata, in 
which approximately 10% of isolates in the United States 
exhibit fluconazole resistance and 0–10% exhibit 
echinocandin resistance31,32. In comparison, the level of drug 
resistance observed in C. auris is unprecedented. Molecular 
mechanisms underlying this resistance are currently under 
investigation. Twelve Erg11 mutations, which have been found 
in fluconazole-resistant but not wild-type C. albicans, have 
been found in C. auris33.Three of these mutations have been 
directly linked to drug resistance in C. albicans, suggesting that 
they contribute to the resistance observed in C. auris as well34. 
Efflux pump activity contributes to azole resistance in other 
Candida species and may contribute to resistance in C. auris, 
though the extent of this contribution is unknown. None of 
these mechanisms alone can account for the high levels of 
resistance seen in C. auris, so multiple mechanisms are likely 
involved. Elevated echinocandin MICs are likely the result of 
FKS mutations observed in C. auris isolates, such as the S639F 
mutation observed in isolates from India33.These mutations 
correspond to known mutations in other Candida species, 
which have been directly linked to echinocandin resistance35. 
Finally, while resistance to amphotericin B is rare in the most 
common Candida species, it is observed in approximately 30% 
of US isolates of C. auris. Though unconfirmed at this time, it is 
suspected that this is likely due to a reduction in ergosterol 
content in the cellular membrane-specifically a mutation in a 
gene involved in ergosterol biosynthesis36. 

Clinical manifestations 

Similar to other Candida species, C. auris can cause severe 
invasive infections or colonize patients without infection. C. 
auris has been isolated from normally sterile body sites, 
including blood, bone, and cerebrospinal fluid, indicating 
invasive infection. Infections may be severe, and persistently 
positive blood cultures for >5 days or recurrent candidemia in 
those with C. auris candidemia have been reported. C. auris 

candidemia is associated with mortality rates of about 30–
60%, depending on the setting . Other clinical sources found in 
the course of routine patient care have been bile fluid, the ear, 
jejuna biopsy, ocular secretion, peritoneal fluid, pleural fluid, 
the respiratory tract, urine, vaginal fluid, and wounds; some of 
these represent sites of colonization rather than infection. 
Patients can also be asymptomatically colonized with C. auris 
on the skin, nares, and other body sites37-39. 

Diagnosis 

The under-recognition and delay in accurate diagnosis of C. 
auris species has been attributed to its misidentification by 
commercial biochemical methods (manual and automated). 
The conventional commercial diagnostic yeast identification 
systems such as Vitek 2, BD Phoenix and API20 are not able to 
identify or frequently misidentify C. auris isolates as one of the 
closely related Candida species C. haemulonii, C. famata, C. 
catenulata, C. sake and Rhodotorula glutinis40. 

Molecular testing 

Investigators have relied upon molecular methods to facilitate 
accurate identification of C. auris species. One of the most 
common methods described in multiple research studies and 
case reports was genomic DNA extraction from the 
misidentified Candida species followed by DNA amplification 
and sequencing of the internal transcribed spacers (ITS) and 
D1/D2 regions of the ribosomal DNA. These sequences were 
re-identified based on 98%-100% homology with C. auris 
isolate using GenBank Basic Local Alignment Search Tool 
(BLAST) from national center for biotechnology information 
(NCBI) database18,41. The ITS sequencing was also beneficial to 
define genomic diversity between C. auris and closely related 
Candida isolates differentiating them into separate clades with 
bootstrap value of 99%18,42. Rapid, efficient and successful 
identification of C. auris isolates was shown using MSVITEK 
and Bruker MicroFlex Matrix-assisted laser desorption 
ionization time of flight mass spectrometry (MALDI-TOF) 
identification system43. However, caution is advised while 
using MALDI-TOF as not all devices include C. auris in the 
reference database44. During laboratory identification and 
validation of CDC panel containing C. auris, incorporation of 
research-use-only library containing C. auris resulted in 
accurate identification of C. auris isolates by both MALDI-TOF 
systems45. Polymerase chain reaction (PCR) and real-time PCR 
assays have been developed targeting rDNA region nucleotide 
sequences specific for C. auris. The assays showed rapid and 
accurate identification of C. auris similar to DNA sequencing 
results46. The US CDC has provided guidance to healthcare 
facilities to suspect C. auris based on detection of misidentified 
Candida species by standard testing method and for accurate 
identification of C. auris using diagnostic methods such as 
MALDI-TOF with updated database and DNA sequencing. 
Laboratories located in the US without capability to identify 
suspected Candida isolates have an option to send samples to 
the CDC using state public health laboratories for further 
characterization. 

Geographical link 

Geographical clustering of C. auris isolates has been performed 
using genomic and proteomic analysis based on mutilocus 
sequence typing (MLST), MALDI-TOF MS and amplified 
fragment length polymorphism (AFLP) typing42. Among the 
analytic methods, M13 PCR fingerprinting and AFLP is 
recognized as most efficient for strain typing and for 
geographical clustering helpful in epidemiological analysis42. 
The AFLP typing grouped C. auris strains mainly into two 
clusters of Indian and Brazilian origin42. Isolates from South 
African origin were randomly distributed among both clusters. 
C. auris isolates from India, Brazil and South Africa were clonal 



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for the respective country of origin with 99%-100% 
nucleotide sequence similarity. A multicenter study in United 
Kingdom (UK) performed rDNA sequencing of 24 C. auris 
isolates, grouping the C. auris strains into three different 
lineages belonging to India/Malaysia/Kuwait, Japan/Korea 
and South African origin47. Whole genome sequencing (WGS) 
of C. auris isolates showed genome size of 12.5Mb similar to 
other Candida species. The WGS helped establish independent 
emergence of C. auris isolates in different continents as the 
isolates differed by tens of thousands of single nucleotide 
polymorphisms (SNPs) between the geographic locations. The 
isolates from the US seem to be related to those from South 
Asia (<60 SNPs apart) and South America (<150 SNPs apart), 
with no proven direct or indirect travel link48. 

Treatment 

Only three major classes of antifungal drugs are available to 
treat invasive fungal infections. C. auris poses a real treatment 
challenge because of high rates of antifungal drug resistance. 
As reported above, most C. auris isolates are resistant to 
fluconazole, the most widely available antifungal treatment for 
candidiasis. The alternatives, echinocandins and amphotericin 
B, are expensive and are not easily available in countries with 
more limited resources. Amphotericin B is also known for 
causing severe side effects. Although studies have reported 
therapeutic outcomes, no systematic study has assessed 
effectiveness of various antifungals against C. auris infections 
in humans. However, in a mouse model, micafungin wasmore 
efficacious at killing C. auris than fluconazole and 
amphotericin B. An in vitro study examining combinations of 
treatment with echinocandins and azoles found a synergistic 
interaction between micafungin and fluconazole and did not 
find any antagonistic interactions between micafungin or 
caspofungin and fluconazole or voriconazole. Research is also 
being conducted on activity of new drugs like SCY- 078, 
APX001A/APX001and CD101against C. auris, but these 
options are not yet available for clinical use in most settings. 
Based on the most frequent resistance profiles, echinocandins 
are the recommended first-line treatment for most C. auris 
infections in adults. Antifungal susceptibility testing is advised 
to inform treatment and patients should be closely monitored 
for treatment failure. Acquired resistance while on treatment 
is a concern. Echinocandin resistance has developed in 
patients with C. auris infection while receiving echinocandin 
treatment. For neonates and infants under 2 months of age, 
CDC recommends amphotericin B deoxycholate (1 mg/kg 
daily) as the first line treatment, with consideration of 
liposomal amphotericin B (5 mg/kg daily) if unresponsive to 
amphotericin B deoxycholate. Echinocandin treatment in 
neonates and infants less than 2 months of age should only be 
considered in rare circumstances and only after checking that 
the central nervous system has not been affected. Removal of 
catheters and lines and surgical debridement has been used 
alongside antifungal drugs when clinically indicated49-55. 

Conclusion 

Within less than a decade of its discovery, C. auris surpasses all 
Candida species as the most difficult pathogen to identify and 
treat. Poor practice of infection prevention measures and 
stewardship efforts may have led to rapid spread of drug-
resistant C. auris. Lack of widespread awareness and 
recognition of this imminent fungal threat is likely to lead to 
significant consequences. Further research is needed to 
understand the spread of this emerging pathogen and to 
develop better management strategies to combat this 
worrisome infection. 

 

 

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