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The Candida haemulonii species complex and other phylogenetically related species, such as Candida auris, are emerging pathogens. The C. haemulonii complex comprises C. haemulonii, C. haemulonii var. vulnera, and Candida duobushaemulonii species. The correct identification of this fungal complex is clinically and epidemiologically relevant; however, conventional identification methods are currently inadequate. In this study, we report the molecular reidentification of two clinical isolates: isolate 553 that was recovered from a patient with total dystrophic onychomycosis and isolate 77-18 from a patient with mucocutaneous candidiasis. Both patients had diabetes mellitus as baseline disease. These isolates were initially identified as C. haemulonii by the VITEK® 2 system but were later determined to be C. duobushaemulonii based on the amplification and sequencing of a 115-bp fragment of the region of 26S rDNA. The isolates were resistant to fluconazole, and only isolate 553 was resistant to amphotericin B. Patients showed clinical and mycological cure after treatment with itraconazole. The clinical and microbiological data of these two cases of superficial candidiasis caused by C. duobushaemulonii, along with previous reports about infections with the C. haemulonii complex species, suggest that patients with diabetes mellitus are highly susceptible to infection with these fungi. Therefore, for diagnosing candidiasis in patients with diabetes mellitus, yeasts must be identified at the species level, and antifungal susceptibility testing must be carried out for adequate treatment., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Candida species, including C. albicans, are part of the mucosal flora of most healthy women, and inhabit the gastrointestinal and genitourinary tracts. Under favourable conditions, they can colonize the vulvovaginal mucosa, giving rise to symptomatic vulvovaginal candidiasis (VVC). The mechanism by which Candida spp. produces inflammation is unknown. Both, the blastoconidia and the pseudohyphae are capable of destroying the vaginal epithelium by direct invasion. Although the symptoms are not always related to the fungal burden, in general, VVC is associated with a greater number of yeasts and pseudohyphae. Some years ago, C. albicans was the species most frequently involved in the different forms of VVC. However, infections by different species have emerged during the last two decades producing an increase in causative species of VVC such as C. glabrata, C. parapsilosis, C. krusei and C. tropicalis. Candida species are pathogenic organisms that have two forms of development: planktonic and biofilm. A biofilm is defined as a community of microorganisms attached to a surface and encompassed by an extracellular matrix. This form of presentation gives microorganisms greater resistance to antifungal agents. This review, about Candia spp. with a special emphasis on Candida albicans discusses specific areas such as biofilm structure and development, cell morphology and biofilm formation, biofilm-associated gene expression, the cell surface and adherence, the extracellular matrix, biofilm metabolism, and biofilm drug resistance in vulvovaginitis biofilms as an important virulence factor in fungi., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The ability of Candida spp. to form biofilms is crucial for its pathogenicity, and thus, it should be considered an important virulence factor in vulvovaginal candidiasis (VVC) and recurrent VVC (RVVC). Its ability to generate biofilms is multifactorial and is generally believed to depend on the site of infection, species and strain involved, and the microenvironment in which the infection develops. Therefore, both cell surface proteins, such as Hwp1, Als1, and Als2, and the cell wall-related protein, Sun41, play a critical role in the adhesion and virulence of the biofilm. Immunological and pharmacological approaches have identified the NLRP3 inflammasome as a crucial molecular factor contributing to host immunopathology. In this context, we have earlier shown that Candida albicans associated with hyphae-secreted aspartyl proteinases (specifically SAP4-6) contribute to the immunopathology of the disease. Transcriptome profiling has revealed that non-coding transcripts regulate protein synthesis post-transcriptionally, which is important for the growth of Candida spp. Other studies have employed RNA sequencing to identify differences in the 1,245 Candida genes involved in surface and invasive cellular metabolism regulation. In vitro systems allow the simultaneous processing of a large number of samples, making them an ideal screening technique for estimating various physicochemical parameters, testing the activity of antimicrobial agents, and analyzing genes involved in biofilm formation and regulation (in situ) in specific strains. Murine VVC models are used to study C. albicans infection, especially in trials of novel treatments and to understand the cause(s) for resistance to conventional therapeutics. This review on the clinical relevance of Candida biofilms in VVC focuses on important advances in its genomics, transcriptomics, and proteomics. Moreover, recent experiments on the influence of biofilm formation on VVC or RVVC pathogenesis in laboratory animals have been discussed. A clear elucidation of one of the pathogenesis mechanisms employed by Candida biofilms in vulvovaginal candidiasis and its applications in clinical practice represents the most significant contribution of this manuscript. [ABSTRACT FROM AUTHOR]

In recent years, a progressive increase in the incidence of invasive fungal infections (IFIs) caused by Candida glabrata has been observed. The objective of this literature review was to study the epidemiology, drug resistance, and virulence factors associated with the C. glabrata complex. For this purpose, a systematic review (January 2001–February 2021) was conducted on the PubMed, Scielo, and Cochrane search engines with the following terms: "C. glabrata complex (C. glabrata sensu stricto, C. nivariensis, C. bracarensis)" associated with "pathogenicity" or "epidemiology" or "antibiotics resistance" or "virulence factors" with language restrictions of English and Spanish. One hundred and ninety-nine articles were found during the search. Various mechanisms of drug resistance to azoles, polyenes, and echinocandins were found for the C. glabrata complex, depending on the geographical region. Among the mechanisms found are the overexpression of drug transporters, gene mutations that alter thermotolerance, the generation of hypervirulence due to increased adhesion factors, and modifications in vital enzymes that produce cell wall proteins that prevent the activity of drugs designed for its inhibition. In addition, it was observed that the C. glabrata complex has virulence factors such as the production of proteases, phospholipases, and hemolysins, and the formation of biofilms that allows the complex to evade the host immune response and generate fungal resistance. Because of this, the C. glabrata complex possesses a perfect pathogenetic combination for the invasion of the immunocompromised host. [ABSTRACT FROM AUTHOR]