Candida Auris: Review on worldwide spread, seems prone to antifungal and disinfectant therapies

 Corresponding author: Vaishnavi V Khairnar Copyright © 2025 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution Liscense 4.0. Candida Auris: Review on worldwide spread, seems prone to antifungal and disinfectant therapies Vaishnavi V Khairnar 1, *, Yogesh S Wankhede 2 and Amol R Patil 1 1 Department of Pharmaceutical Chemistry, Srujan Foundations, G. D. Burkule Institute of Research and Education in Pharmaceutical Sciences, Cidco Nashik Maharashtra, India. 2 Department of Pharmaceutical Chemistry, METs Institute of D Pharmacy, Adgaon Nashik Maharashtra, India. World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 Publication history: Received on 07 December 2024; revised on 23 January 2025; accepted on 26 January 2025 Article DOI: https://doi.org/10.30574/wjbphs.2025.21.1.0072 Abstract In recent years, C. auris has become a leading source of invasive fungal diseases, with outbreaks occurring across all continents. This fungus infection poses a severe hazard to healthcare, with outbreaks primarily affecting older patients with comorbidities and high fatality rates. Controlling epidemics has been challenging because to poor detection, fast spread, and resistance to environmental cleaning methods. C. auris is currently the major cause, or one of the leading causes of invasive fungal infections in many healthcare facilities, primarily due to its potential may exhibit or acquire resistance to many types of antifungal medications and due to their Ability to persevere in healthcare circumstances. Timely diagnosis by swift and reliable identification. techniques and dedication in infection control procedures can assist to limit the spread of C. auris, and prevent and manage epidemics Keywords: Candida Auris; Antimicrobial Resistance; Environmental Conditions; Treatments; Hospital Outbreaks 1. Introduction Infections caused by fungi are being growing in prominence as a global crisis to human health. Fungal infections affect approximately 1.7 billion individuals globally, with the majority of cases being superficial infections of the skin and mucosa [1]. Candida species are the most common cause of nosocomial fungal infections and the fourth greatest cause of hospital-acquired illnesses [2]. Annually, there are around 400,000 bloodstream infections caused by Candida species worldwide, with death rates surpassing 40%. Candida albicans is one of the most often seen Candida species, but nonalbicans species such Candida tropicalis, Candida parapsilosis, and Candida glabrata have become more common in recent decades due to confined antifungal medication choices [3,4]. Candida Auris, an unfamiliar species of the Candida/Clavispora category, was first identified in a female patient's ear discharge in Japan in 2009 [5]. Considering the fact that the initial isolate of Candida Auris was identified more than a decade ago, there is still a worldwide screening strategy insufficient, as well as in underdeveloped countries, and there is an urgent need for effective therapy against this multidrug-resistant bacteria [8.7]. Indeed, C. auris has been detected in over 35 countries, with the majority of cases attributed to healthcare-associated person-to-person transmission [8]. C. auris has a high rate of transmission due to its capacity to colonize skin and other body locations and survive for weeks on abiotic surfaces and equipment [9]. The main concerns of C. auris infection include the high prevalence of antifungal treatment resistance [10], the ease of transmission among healthcare staff and patients in hospitals, and misidentification. The difficulty in correctly identifying C. auris strains, which are often misidentified as other pathogens, as well as inadequate diagnostic tools in many countries, leads to misidentification and incorrect therapy, resulting in multidrug resistance [11-14]. World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 548 C. auris has been linked to several types of malignant microbial infections. The most of documented data on patient infections and outcomes is derived from India, although there have also been reports from small numbers of patients in South Korea, Venezuela, South Africa, the United Kingdom, the United States, Colombia, and Canada. Invasive C. auris infection has been strongly linked to candidemia, including incidents related with CVC usage, as well as pericarditis, respiratory tract and urinary tract infections. C. auris infection is typically found in severely sick patients having surgical operations in intensive care units. Patients with significant underlying medical disorders, such as hematological malignancies or immunosuppressive diseases, are typically eligible for treatment. A study described a case of C. auris infection from a donor after lung transplant. Yeast was found in bronchoalveolar lavage samples before and after implantation, but was originally misinterpreted by biochemical and molecular tests.[15]. As in Table 1. Table 1 Candida Auris Infection cases by disease type reported in the literature Sr. No Location of Isolation Number of cases 1 Candidema 291 2 Central Venous Catheter Tip 2 3 CNS 1 4 ENT 21 5 Respiratory Tract 18 6 Urogenital System 17 7 Abdominal 13 8 Surgical Wounds on Skin and Soft Tissues 12 9 Bone 2 2. Climate changes The changing climate has a significant influence on malignant fungal infections. Pathogenic fungus, unlike humans, adapt fast and become more virulent as temperatures rise. Changes in fungal disease epidemiology have led to the creation of novel diseases, such as Candida Auris, which can tolerate high temperatures and adapt to human bodies. [16-18] Most fungal organisms cannot survive at human temperatures (36.5-37.5˚C and up to 40˚C during fever), preventing them from colonizing and causing diseases. Unlike similar Candida species, C. auris may thrive at high temperatures (>40˚C) [19-21]. An investigation analyzing the temperature resistance of C. auris to other Candida species indicated that climate change, notably global warming, may have influenced the pathogen's capacity to thrive at high temperatures [22]. C. auris, unlike other Candida species, can withstand higher salt concentrations (>10% NaCl, wt/vol) [19-21]. C. auris responds to high salt concentrations by forming pseudo hyphae-like morphologies, which may be adaptive under stressful conditions [19-21]. Thermotolerance and osmotolerance are properties that may contribute to C. auris' endurance and existence on biotic and abiotic surfaces for long periods of time [23-25]. Fungal pathogens can adapt to one environmental threat, making them more resilient to future challenges. This observation applies to a variety of human-induced factors that contribute to climate change. Fungal melanin protects against extreme temperature and pH stress, heavy metals, and radioactive isotopes, allowing some fungal taxa to thrive in metal-polluted areas, acidic environments, and radioactive wastelands following nuclear disasters.[26]. The presence of agricultural and industrial contaminants in rivers, lakes, and tap water significantly increases the chance of developing fungal illnesses. Contamination in water bodies and supply systems has been linked to increased proliferation and variety of fungus, including pathogenic species. Polluting substances like nitrates and iron can provide a favorable pH and nutritional environment for fungal development.[27] Contamination in freshwater can lead to microbial infections and threaten health care systems, even in developed countries.[28-30] World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 549 Figure 1 Climate change effect in the emergence of Candida Auris Rapid urbanization impacts both environmental change and microbiological ecosystems in different ways. Increased urban population density, along with industrial and biological variables like diminished vegetation cover, leads to elevated air and soil temperatures, as well as streams warming.[31]. Heat islands in urban areas set evolutionary pressure on microorganisms, resulting in increased fungal stress adaptability compared to rural isolates from neighboring locations.[32] Climate change impacts both fungal adaptability and host vulnerability to pathogenic fungus. UV radiation exposure has been related to negative effects on human immunity, including T-cell polarization, increased production of inhibitory cytokines, and altered complement activation.[33]. 3. Biology Figure 2 a: C. auris Cell under Microscope. b: Developed colonies of the fungi in Chromogenic Agar Candida medium World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 550 • Cell Biology: C. auris develops pink to beige colonies on chromogenic agar Candida medium and grows well at 42°C, but growth is inconsistent at higher temperatures and does not occur in the presence of 0.01% cycloheximide. It produces oval or elongated yeast cells that might appear alone, in pairs, or in clusters. Importantly, no hyphal or pseudohyphal variants have been identified. [34] • Morphological Transitions: C. auris, like other pathological Candida species, displays a variety of morphological phenotypes[35-38], while the regulatory mechanisms and significance of each morphology in C. auris remain unclear. Many C. auris isolates occur as single-celled yeast. However, certain natural C. auris isolates can produce huge clusters of pseudohyphal-like cells, with mother and daughter cells still connected [39-40]. In the Galleria mellonella infection model, aggregating cells are less virulent than non-aggregating cells, while being more resistant to antifungal drugs [41]. Pseudohyphal-like clusters in C. auris may indicate problem in cell division. Recent research found that genotoxic stressors induced DNA damage and disrupted replication forks in C. auris, leading to pseudohyphal development [42]. • Microorganisms often exploit morphological plasticity to adapt quickly to environmental changes [43,44]. Under specific environmental circumstances, both bacterial and fungal species can undergo morphological changes. Pathogenic Candida species, including C. albicans and C. tropicalis, can undergo a variety of morphological changes [45,46]. They can flip between cell types on their own or in response to environmental signals. C. albicans and C. tropicalis, for example, have well-studied morphological changes such as the yeast-hyphal transition and the white-opaque flip. Morphological flexibility in these species is crucial for disease and mating [45,46]. • Phenotypic shift occurs within colonies. Growing C. auris colonies on CHROMagar allows for morphological changes between pink, white, and dark purple phenotypes [47]. • Filamentation: Pathogenic Candida species rely on filamentous (hyphal or pseudohyphal) cell development to invade host tissues. The shift from yeast to filamentous growth forms of C. albicans has been extensively studied. Initially, it was thought that C. auris could only create pseudohyphae and not real hyphae. Recent research suggests that C. auris isolates can generate genuine hyphae under certain conditions. • Development of biofilms: Biofilms are organized microbial communities that grow on both abiotic and biotic surfaces and are embedded in an extracellular matrix [48]. C. auris has been shown to create biofilms on surfaces, however these biofilms are weaker than those produced by C. albicans [36]. C. auris biofilm cells, like C. albicans biofilm cells, are more resistant to antifungal drugs than free-floating planktonic cells. C. auris biofilms have a role in the virulence, antifungal resistance, and survival of C. auris in the environment and host, albeit their relevance is unclear compared to other Candida species. Future research should focus on developing treatment techniques that target C. auris biofilms in both patients and the environment. 4. Rise and widespread within years 4.1. The development of Candida Auris as major pathogen Whereas C. auris was initially identified in 2009, retroactive investigations of culture collections have revealed other C. auris isolates that were previously mistaken as C. haemulonii, including a bloodstream strain collected in 1996 [51,52]. C. auris is phylogenetically similar to other members of the C. haemulonii complex [53,54]. C. auris is extremely clonal, although whole genome sequencing analysis have discovered five different clades separated by thousands of singlenucleotide polymorphisms [54-56]. There are five geographically distinct clades: South Asian (Clade I), East Asian (Clade II), African (Clade III), South American (Clade IV), and Iranian (Clade V). Clade I, III, and IV isolates usually produce invasive infections and outbreaks, but Clade II isolates have a preference for the ear, which is uncommon among other isolates [58]. The Clade V isolate was originally discovered in a case of otomycoses [57,59]. C. auris strains differ in their resistance to fluconazole and susceptibility to other antibiotics, including echinocandins and amphotericin B. Many isolates are multidrug-resistant [40,71,73,89,95]. Several C. auris clades developed on various continents almost concurrently. World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 551 Figure 3 A map showing the key clades of C. auris's global distribution 4.2. C. auris alongside Covid-19 Research suggests that individuals with severe COVID-19 infection in the early stages of the pandemic are more likely to develop bacterial and fungal illnesses [65-66]. The COVID-19 pandemic may have led to increased spread of C. auris. This might be due to strain on the global healthcare system and inadequate infection prevention and control measures. The pandemic may have made it difficult to discover new instances [56]. During the peak of the pandemic, outbreaks of C. auris among extremely sick COVID-19 patients were only recorded in certain countries, including Italy and the USA [68]. During the pandemic, an epidemiological investigation in the UAE indicated an increase in COVID-19 and C. auris coinfection in hospitals with overburdened intensive care units [70]. Patients with major comorbidities received broadspectrum antibiotics and immunosuppressive treatments. Additionally, they used urine and intravenous catheters [71]. An epidemic of C. auris was discovered in an ICU with COVID-19 patients in India. The mortality rate was high. Infection onset occurred 3-8 weeks after hospitalization. The majority of patients had central venous and urine catheters, required mechanical breathing, and had underlying chronic illnesses such diabetes and hypertension [72]. During the pandemic, Spain and Italy saw a rise in C. auris and multidrug-resistant organism infections, including nosocomial outbreaks in COVID-19 patients admitted to critical care units [72-74]. 5. Common commercial antifungals and candida auris treatment failure: Candida Auris, a multidrug-resistant species, causes substantial morbidity and death in immunocompromised persons globally [74]. C. auris has several critical properties, including easy dissemination in the environment, rapid transit among hospitalized patients [75,76], and resistance to standard disinfectants in healthcare settings [77]. C. auris is a potentially aggressive and worldwide developing disease, posing issues for infection control due to limited microbiological diagnostic tools and significant levels of antifungal resistance [78-81]. There are few antifungal medicines available for treating C. auris infections. In clinics, three types of antifungals (azoles, polyenes, and echinocandins) are often used to treat infected individuals [82]. Antifungal drugs significantly affect the development of C. auris in both planktonic and sessile states. C. auris can develop biofilms on medical surfaces in immunocompromised patients, as well as bio-surfaces [83,84]. The type and phenotypic characteristics of the isolates are significantly related [85]. Biofilms can lead to antifungal resistance and chronic infections in this species [86]. Antifungal resistance in C. auris is largely attributed to its biofilm characteristic [87]. 5.1. Mechanisms of molecular resistance The majority of clinical C. auris isolates are resistant to key antifungal classes (azoles, polyenes, or echinocandins), including multi-drug resistance (MDR) to more than two classes [13]. Research has focused on the molecular processes World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 552 of resistance development, leading to limited treatment options [13,89]. Accurate detection and identification of the C. auris pathogen is crucial for successful therapy [90,91]. Setting MICs for antifungals against C. auris strains has been requested, as increased MICs are a serious issue [92]. Monitoring antifungal resistance in various locations is crucial, as is implementing effective treatment recommendations [93]. 5.2. Azole Resistance Mechanisms Azole resistance in C. auris is acquired through various mechanisms, including overexpression of efflux pumps such as ATP-binding cassette (ABC) and major facilitator superfamily (MFS) transporters, which are known to cause deliberate multidrug resistance [94,95]. The C. auris genome includes three Mrr1 homologs and two Tac1 homologs. Mutations in the zinc cluster transcription factors Mrr1 and Tac1 lead to C. auris' intrinsic flu resistance [96]. 5.3. Echinocandin Resistance Mechanisms Echinocandins are the primary treatment for C. auris infections and seldom acquire resistance [13,97]. Resistance to echinocandins is often linked to mutations in the FKS1 gene, which encodes the enzyme (1,3)-β-D-glucan synthase. These mutations reduce the enzyme's affinity for the drug [98]. Sequencing 38 C. auris strains revealed an S639F amino acid alteration linked to pan-echinocandin resistance [99]. This mutation aligns with C. albicans FKS1's HS1 region [100]. 5.4. Flucytosine resistance mechanisms (5-fluorocytosine) Flucytosine, a nucleoside analog, prevents nucleic acid synthesis. Because this antifungal chemical is less often used than other medications, the mechanism of resistance is less understood, and less research have been conducted to determine C. auris resistance to this treatment. Mutations in the FUR1 gene have been linked to flucytosine resistance in non-Candida Auris Candida [101], whereas mutations in the FCY2 and FCY1 genes may also cause resistance to 5fluorocytosine [102]. In resistant C. auris, a previously unknown missense mutation in the FUR1 gene resulted in an F211I amino acid substitution. Further research is needed to determine the underlying processes for the resistance to flucytosine tested in Candida Auris strain.[103]. 5.5. Polyene Resistance Mechanisms The processes behind polyene resistance in C. auris are poorly known. Whole-genome sequencing of resistant isolates revealed four unique non-synonymous mutations that are likely linked to AmB resistance. Overexpression of mutant ERG genes causes a drop in ergosterol concentration in the cellular membrane [13, 97] [98]. Mutations were found in genes related to C. albicans' FLO8 transcription factor and a membrane transporter [99]. Table 2 Antifungal drugs are often employed to treat C. auris infections, and resistance mechanisms have been documented Antifungal Drugs Used Mechanism of Action Resistance Mechanism Azoles Inhibit the activity of lanosterol 14-αdemethylase enzyme; prevent converting lanosterol to ergosterol, leading to damaging integrity of cell membrane. Overexpression of ATP-binding cassette (ABC) and major facilitator superfamily (MFS) transporters. ERG11 point mutation: Y132F and K143R. Mutation in zinc cluster transcription factors Mrr1 and Tac1. Polyenes Bind ergosterol molecules in the cytoplasmic membrane; disturb the permeability of cell membrane by formation of pores, causing oxidative damage. Induction of genes associated with sterol biosynthetic process including ERG1, ERG2, ERG6, and ERG13. SNPs in different genomic loci related to increased resistance. Echinocandins Inhibit β-(1,3)-D-glucan synthase enzyme, leading to defective cell wall formation. Hot-spot mutation in FKS1 gene associated with S639Y, S639P, and S639Y regions and FKS2. Flucytosine Inhibit the nucleic acid synthesis (DNA and RNA) of fungi. Mutation of FUR1 gene, specifically missense mutation of FUR1 causing F211I amino acid substituted in the FUR1 gene in one flucytosineresistant isolate. Mutations in the FCY2, FCY1 genes World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 553 6. Novel treatments and combination therapies To prevent C. auris infections, novel therapies, medicines, and technologies are being evaluated urgently. One of the potential ways appears to be synergistic interactions between chemicals and antifungals. Researchers are exploring novel chemicals with anti-fungal properties to combat C. auris growth, both in vitro and in vivo. APX001A, a new inhibitor of the fungal protein Gwt1 (glycosylphosphatidylinositol-anchored wall transfer protein 1), has been tested against C. auris. In vitro and in an immunocompromised mouse model with disseminated infection, APX001A demonstrated effective antifungal efficacy with lower MIC50 and MIC90 than anidulafungin [100]. New antimicrobial peptides may be more effective than chemical antimicrobials in combating multidrug-resistant species due to their decreased risk of causing resistance [102]. Probiotic yeasts have been shown in clinical studies to effectively inhibit the growth of Candida spp., including C. albicans, Candida tropicalis, C. glabrata, Candida parapsilosis, Candida krusei, and C. auris. S. cerevisiae var. boulardii is the only commercially available probiotic yeast that may lower pathogen pathogenicity by blocking Candida spp. adherence and morphological transition, making it a prospective treatment alternative. [103] Evidence suggests that administering micafungin and AmB together may have therapeutic utility against C. auris and may be a good alternative to flucytosine [104,105], which can be hazardous to some patient populations with bone marrow disorders or to expectant mothers [106,107,108]. Currently, screening focuses on compounds with inhibitory effects, such as sulfamethoxazole, which exhibits strong synergistic interactions with Vcz and itraconazole in vitro [109]. Lopinavir inhibits HIV protease, but when combined with itraconazole, it has a synergistic impact against C. auris [110]. This drug sensitized C. albicans, C. tropicalis, C. krusei, and C. parapsilosis to azoles, most likely via altering efflux pump activity [111]. A previous study found synergistic interactions between suloctidil (a sulfur-containing aminoalcohol vasodilator) and Vcz, as well as ebselen (a synthetic organoselenium molecule) and anidulafungin [112]. Aprepitant, a medication used to alleviate nausea and vomiting, can also improve the antifungal activity of azoles against C. aureus by chemosensitizing [113]. The authors found that aprepitant/itraconazole interfered with metal ion homeostasis, resulting in reduced detoxifying capabilities of reactive oxygen species. [114] Figure 4 Novel Alternative Therapies Candida biofilms on indwelling catheters are difficult to treat. Antimicrobial lock treatment is a non-invasive method for removing persistent cells from a catheter.[115] Sumiyoshi and colleagues picked this technique. Caspofungin in low ionic solutions significantly reduced candidal biofilms, including resistant C. auris, in the catheter-lock treatment model [116]. New antifungal agents have also been investigated. PC945, a triazole, outperformed posaconazole, Vcz, and Flu as an inhibitor of C. auris isolates. T-2307, an arylamidine, effectively inhibits fungal mitochondrial membrane potential and has been tested against Candida species in vitro and in vivo, as well as C. auris [108]. In relation to novel and alternative World Journal of Biology Pharmacy and Health Sciences, 2025, 21(01), 547-560 554 treatments , it was discovered that C. auris was surprisingly susceptible to translation inhibition by a class of compounds called rocaglates, which are naturally occurring products found in Meliaceae plants. These compounds activated a program that leads to cell death, and as a result, they demonstrated fungicidal activity against this yeast [109]. Another option is to irradiate photoactive dyes with a light source of the proper wavelength, resulting in the generation of reactive oxygen species, which is known as photodynamic treatment. Combining methylene blue with a light-emitting diode decreased the survivability of C. auris, both planktonic and biofilm. Finally, a pulsed-xenon UV transportable device successfully decreased the colony forming unit survival of C. auris .UV-C radiation was explored as a potential method of room disinfection. The greatest results for C. auris death were achieved after 30 minutes of UV-C exposure at 2 metres. C. auris may survive on surfaces for up to two weeks [114]. 7. Conclusion 7.1. Questions and perspectives on the future C. auris represents a new public global health hazard. C. auris is closely related to other pathogenic Candida species, but has distinct characteristics in biology, genetics, epidemiology, antifungal resistance, virulence, host adaptability, and transmission. At the moment, therapy options that are new or unconventional include photodynamic therapy, innovative triazoles (like PC945), and natural compounds (such rocaglates). Antimicrobial stewardship initiatives can improve patient outcomes, minimize antibiotic side effects, and decrease antimicrobial resistance. New diagnostic technologies have improved patient care and infection control, minimizing the risk of C. auris spread. To effectively prevent and treat C. auris, a collaborative effort among clinicians, laboratories, and healthcare institutes is necessary. The emergence and biology of C. auris remain largely unknown, despite the fact that it has recently attracted a great deal of scientific research. What are the original habitats for C. auris? How did genetically diverse isolates arise globally simultaneously? How did multidrug resistance develop in C. auris? What allows C. auris to survive in clinical settings for extended periods of time? Is C. auris capable of sexual or parasexual reproduction, and if so, how did it become a pathogen? More study is needed to address these concerns. We need to investigate the biology and genetics of antifungal resistance and pathogenicity in C. auris. Developing speedy and effective detection methods for C. auris can aid in identifying infections and distinguishing it from other Candida species. We will create disinfection techniques to effectively remove C. auris from surfaces, preventing future outbreaks. To tackle infections caused by C. auris and other fungal diseases, new and safe antifungals and treatment regimens with various pharmacological targets are needed. Compliance with ethical standards Disclosure of conflict of interest No conflict of interest to be disclosed. References [1] Brown GD, Denning DW, Gow NA, Levitz SM, Netea MG, White TC. Hidden killers: human fungal infections. Sci Transl Med. 2012; 4(165):165rv13. https://doi.org/10.1126/scitranslmed.3004404 PMID: 23253612. [2] Wisplinghoff H, Bischoff T, Tallent SM, Seifert H, Wenzel RP, Edmond MB. Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Clin Infect Dis. 2004; 39(3):309–317. 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