Introduction: Clinicians are increasingly challenged by patients with refractory vulvovaginal candidiasis (VVC) caused by azole-resistant Candida species. Fluconazole resistant C.albicans is a grow...

Current treatment options for vulvovaginal candidiasis caused by azole-resistant Candida species.

The human fungal pathogen Candida albicans is the major etiological agent of vulvovaginal candidiasis (VVC) Despite this fact, other non-albicans Candida (NAC) species have frequently been reported, as well Despite their presence in the vaginal environment, little is known about their capacities to elicit immune responses classically associated with C albicans-mediated immunopathology, including neutrophil recruitment and proinflammatory cytokine signaling Therefore, using a combination of in vitro and in vivo approaches, we undertook a comparative analysis to determine whether a representative panel of NAC species could colonize, induce immunopathological markers, or cause damage at the vaginal mucosa Using a murine model of VVC, C albicans was found to induce robust immunopathology (neutrophils and interleukin 1β [IL-1β]) and elicit mucosal damage However, all the NAC species tested (including C dubliniensis, C tropicalis, C parapsilosis, C krusei, C glabrata, and C auris) induced significantly less damage and neutrophil recruitment than C albicans, despite achieving similar early colonization levels These results largely correlated with a notable lack of ability by the NAC species (including C dubliniensis and C tropicalis) to form hyphae both in vitro and in vivo Furthermore, both C dubliniensis and C tropicalis induced significantly less expression of the ECE1 gene encoding candidalysin, a key fungal virulence determinant driving VVC immunopathology In order to determine the relative capacities of these species to elicit inflammasome-dependent IL-1β release, both wild-type and NLRP3-/- THP-1 cells were challenged in vitro While most species tested elicited only modest amounts of IL-1β, challenge with C albicans led to significantly elevated levels that were largely NLRP3 dependent Collectively, our findings demonstrate that although NAC species are increasingly reported as causative agents of VVC, C albicans appears to be exceedingly vaginopathogenic, exhibiting robust immunopathology, hypha formation, and candidalysin expression Thus, this study provides mechanistic insight into why C albicans is overwhelmingly the major pathogen reported during VVC

Comparative Analysis of the Capacity of the Candida Species To Elicit Vaginal Immunopathology

Vulvovaginal candidiasis (VVC) is a common infection of the genital tract affecting millions of women worldwide. Data on epidemiological trends of VVC in Greece are scarce. This study was undertaken to evaluate the prevalence of VVC among symptomatic women in Crete, Greece, identify the Candida species involved and determine their susceptibility to antifungals. Over a 6-year period (2012-2017), 10 256 symptomatic women with vaginitis were evaluated. Isolation of yeasts was performed on Sabouraud dextrose agar with chloramphenicol, and the isolates were identified using the API 20 C AUX and/or the Vitek 2 YST card. Susceptibility of the isolates to amphotericin, fluconazole, voriconazole and flucytosine was determined by the Vitek 2 automated system. The results were interpreted according to Clinical and Laboratory Standards criteria. Vaginal swab cultures of 1217 (11.9%) women yielded Candida species. Recurrent VVC was documented in 62 (5.1%) of them. Candida albicans was the most frequently isolated species (75.6%), followed by Candida glabrata (13.6%). Overall, resistance rates to amphotericin B, fluconazole, voriconazole and flucytosine were 0.2%, 6.6%, 1.4% and 2.1%, respectively. Fluconazole resistance of C. albicans significantly increased in the second period of the study (2015-2017) (P = 0.031). This study demonstrated that VVC is a common infection among women in our region, with C. albicans being the predominant species involved. Although resistance to antifungals was infrequent, resistance to fluconazole among C. albicans isolates was found to significantly increase with time. Continued surveillance of changes in species distribution and susceptibility to antifungals are necessary to guide treatment.

Epidemiology and antifungal susceptibility patterns of Candida isolates from Greek women with vulvovaginal candidiasis

Background and purpose Candida albicans (C. albicans) is an opportunistic fungus that can colonize women's mucosal epithelial cell surfaces, causing vulvovaginitis in specific circumstances. The major genes contributing to drug resistance in C. albicans are the candida drug resistance (CDR) and multi drug resistance (MDR) genes. The purpose of this study was to evaluate the CDR-2 and MDR-1 gene expression patterns in C. albicans strains isolated from patients with recurrent vulvovaginal candidiasis. Materials and methods In this study, 40 isolates of fluconazole-resistant C. albicans were cultured on Sabouraud dextrose agar. These isolates were collected from women with vulvovaginitis who were referred to a clinic in Tehran, Iran, and transferred to a mycology laboratory. Then, RNA was extracted from the isolates using phenol-chloroform and glass beads, and the complementary DNA (cDNA) was synthetized. To detect the semi-quantitative expression of CDR-2 and MDR-1 genes, the reverse transcriptase-PCR (RT-PCR) technique was performed using specific primers. Results Our findings indicated that of the 40 C. albicans isolates, 35 (87.5%) strains were positive for mRNA of the CDR-2 gene, 32 (80%) strains expressed mRNA of the MDR-1 gene, and 30 (75%) strains were confirmed to express mRNA of both the CDR-2 and MDR-1 genes simultaneously using the RT-PCR assay. Conclusion According to the obtained results, the expression rates of CDR-2 and MDR-1 genes were high in fluconazole-resistant C. albicans isolates, which can cause treatments to fail and result in chronic infections. Inhibiting these important genes using novel or natural agents can help with the treatment of chronic and recurrent vaginitis.

http://cmm.mazums.ac.ir/article_90344_6fbbb3c39d0e8cd13ba68dd74fd872c9.pdf

Overexpression of MDR-1 and CDR-2 genes in fluconazole resistance of Candida albicans isolated from patients with vulvovaginal candidiasis.

Antifungal resistance to Candida pathogens increases morbidity and mortality of immunosuppressive patients, an emerging crisis worldwide. Understanding the Candida prevalence and antifungal susceptibility pattern is necessary to control and treat candidiasis. We aimed to systematically analyse the susceptibility profiles of Candida species published in the last ten years (December 2011 to December 2021) from mainland China. The studies were collected from PubMed, Google Scholar, and Science Direct search engines. Out of 89 included studies, a total of 44,716 Candida isolates were collected, mainly comprising C. albicans (49.36%), C. tropicalis (21.89%), C. parapsilosis (13.92%), and C. glabrata (11.37%). The lowest susceptibility was detected for azole group; fluconazole susceptibilities against C. parapsilosis, C. albicans, C. glabrata, C. tropicalis, C. guilliermondii, C. pelliculosa, and C. auris were 93.25%, 91.6%, 79.4%, 77.95%, 76%, 50%, and 0% respectively. Amphotericin B and anidulafungin were the most susceptible drugs for all Candida species. Resistance to azole was mainly linked with mutations in ERG11, ERG3, ERG4, MRR1-2, MSH-2, and PDR-1 genes. Mutation in FKS-1 and FKS-2 in C. auris and C. glabrata causing resistance to echinocandins was stated in two studies. Gaps in the studies' characteristics were detected, such as 79.77%, 47.19 %, 26.97%, 7.86%, and 4.49% studies did not mention the mortality rates, age, gender, breakpoint reference guidelines, and fungal identification method, respectively. The current study demonstrates the overall antifungal susceptibility pattern of Candida species, gaps in surveillance studies and risk-reduction strategies that could be supportive in candidiasis therapy and for the researchers in their future studies. 

Distribution and antifungal susceptibility pattern of Candida species from mainland China: A systematic analysis

The histone H2B ubiquitination regulator Wac is essential for plasma cell differentiation

Pseudomonas aeruginosa is one of the leading nosocomial pathogens that causes both severe acute and chronic infections. The strong capacity of P. aeruginosa to form biofilms can dramatically increase its antibiotic resistance and lead to treatment failure. The biofilm resident bacterial cells display distinct gene expression profiles and phenotypes compared to their free-living counterparts. Elucidating the genetic determinants of biofilm formation is crucial for the development of antibiofilm drugs. In this study, a high-throughput transposon-insertion site sequencing (Tn-seq) approach was employed to identify novel P. aeruginosa biofilm genetic determinants. When analyzing the novel biofilm regulatory genes, we found that the cell division factor ZapE (PA4438) controls the P. aeruginosa pqs quorum sensing system. The ∆zapE mutant lost fitness against the wild-type PAO1 strain in biofilms and its production of 2-heptyl-3-hydroxy-4(1H)-quinolone (PQS) had been reduced. Further biochemical analysis showed that ZapE interacts with PqsH, which encodes the synthase that converts 2-heptyl-4-quinolone (HHQ) to PQS. In addition, site-directed mutagenesis of the ATPase active site of ZapE (K72A) abolished the positive regulation of ZapE on PQS signaling. As ZapE is highly conserved among the Pseudomonas group, our study suggests that it is a potential drug target for the control of Pseudomonas infections. 

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/mlf2.12059

Cell division factor ZapE regulates
 Pseudomonas aeruginosa
 biofilm formation by impacting the
 pqs
 quorum sensing system

The increasing incidence of vulvovaginal candidiasis (VVC) and the emergence of fluconazole resistance are an indisputable fact. However, little information is available regarding the correlation between fluconazole resistance in vaginal Candida albicans and the expression of drug efflux pump genes. In this study, we investigated the species distribution, fluconazole susceptibility profiles and the mechanisms of fluconazole resistance in Candida strains. In total, 785 clinical Candida isolates were collected from patients with VVC. C. albicans was the most frequently isolated species(n = 529) followed by C. glabrata (n = 164) and C. krusei (n = 57). Of all Candida isolates, 4.7% were resistant to fluconazole. We randomly selected 18 fluconazole resistant isolates of C. albicans to evaluate the expression of CDR1, CDR2, MDR1 and FLU1 genes. Compared with fluconazole-susceptible C. albicans isolates, CDR1 gene expression displayed 3.16-fold relative increase, which was statistically significant. CDR2, MDR1 and FLU1 overexpression was observed in several fluconazole-resistant C. albicans isolates, but statistical significance was not achieved. These results demonstrate a high frequency of non-albicans species (32.6%); however, C. albicans is the most common Candida species implicated in vaginitis, and this strain displays considerable fluconazole resistance. Meanwhile, our study further indicates that fluconazole resistance in C. albicans may correlate with CDR1 gene overexpression.

Vulvovaginal candidiasis: species distribution, fluconazole resistance and drug efflux pump gene overexpression.

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The histone H2B ubiquitination regulator Wac is essential for plasma cell differentiation

Cell division factor ZapE regulates Pseudomonas aeruginosa biofilm formation by impacting the pqs quorum sensing system

Vulvovaginal candidiasis: species distribution, fluconazole resistance and drug efflux pump gene overexpression.