Unlike Canada albicans, which is known to colonize mucosal surfaces in the human body, Candida parapsilosis is encountered in multiple environments [1]. This organism has true virulence factors including biofilm formation and enzymes that help it to enter the bloodstream and cause infections [2].

For many years C. parapsilosis was associated with outbreaks in neonates [3], but the number of reports of C. parapsilosis outbreaks have increased in the last two decades and these outbreaks are no longer limited to a specific patient population. In a PubMed search using the terms “C. parapsilosis” plus “outbreaks,” reports gradually increased from 19 in 2000 to 64 in 2020. In one report, Kuhn et al. collected C. parapsilosis isolates from April to October 2001 in a US hospital and noted that these isolates were genetically related and from an environmental origin [4]. The authors observed invasiveness and adherence that was not reported by others and that total parenteral nutrition solutions can promote adhesion, growth, and biofilm formation in C. parapsilosis isolates [4].

A rise in the number of reports of fluconazole-resistant C. parapsilosis has also been observed. A PubMed search using key words “C. parapsilosis” plus “fluconazole resistance” retrieved only 8 publications in 2000 but 70 in 2020. Fluconazole resistance is driven by the use of this agent. In a study by Arastehfar et al., the authors noted that fluconazole resistance in C. parapsilosis increased in a Turkish hospital after 2015 when a 3-fold increase in use of fluconazole for treatment or prophylaxis was documented [5]. The fluconazole resistance mechanisms included alterations or increased expression of the target of azoles, Erg11, and/or the overexpression of efflux systems CDR1 and MDR1 [6].

In a study by our group evaluating the fluconazole-nonsusceptible C. parapsilosis isolates collected during 2016–2017 in 60 hospitals located in 25 countries worldwide, we observed that most isolates carried the substitution Y132F in Erg11 alone or with other resistance mechanisms [7]. Isolates harboring this alteration were mainly detected in Italy, but also in France, Korea, and the US. Similar findings were concomitantly or later reported in multiple Italian regions [8,9], Brazil [10], Mexico [11], Greece [12], Spain [13], and Turkey [5].

In this study, we expanded our knowledge of the dissemination of fluconazole-resistant C. parapsilosis isolates by investigating isolates that were collected from invasive candidiasis and submitted to the SENTRY Antifungal Surveillance Program from 2018 to 2021. We compared this new data to our prior results from 2016 and 2017 [7]. Utilizing isolates from this previous study [7] we developed a PCR assay for the rapid detection of the Y132F Erg11 alteration in C. parapsilosis. This assay was used to screen all fluconazole-nonsusceptible C. parapsilosis isolates collected from 2018 to 2021 for the presence of this common fluconazole resistance mechanism. All nonsusceptible isolates were chosen for screening (including susceptible dose-dependent) over strictly resistant isolates to capture prevalence of this resistance mechanism in all isolates with reduced fluconazole susceptibility.