Purpose of Review <p> This review synthesizes recent evidence on how the vaginal microbiota, especially Lactobacillus species, interacts with opportunistic yeasts of the genera <i>Candida</i> and <i>Nakaseomyces</i> to shape health and disease. It emphasizes the shift from the narrow term <i>Candida</i> vulvovaginitis to the more accurate and clinically meaningful concept of fungal vulvovaginitis.</p> Recent Findings <p>Recent evidence indicates that women presenting with vulvovaginitis exhibit a high prevalence of infectious etiologies, predominantly bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC), occurring either as isolated conditions or as mixed infections, with frequent BV fungal co-infection.Vaginal microbiota imbalances, including intermediate states and loss of dominant lactobacilli, markedly increase infection risk. Microbiome analyses identify <i>Nakaseomyces glabratus</i> as a key pathogen in recurrent fungal vulvovaginitis, linked to shifts in Firmicutes and higher <i>Bifidobacterium</i>. Emerging approaches, such as transplants or probiotics, can restore <i>Lactobacillus</i> dominance without promoting organisms associated with bacterial vaginosis or fungal vulvovaginitis.&#xa0;</p> Summary <p> Fungal vulvovaginitis (FVV), primarily caused by <i>Candida albicans</i> and <i>Nakaseomyces glabratus</i>, is a prevalent gynecological infection associated with vaginal dysbiosis and excessive inflammatory responses. The loss of protective <i>Lactobacillus</i> species, particularly <i>L. crispatus</i> and <i>L. iners</i>, alters vaginal pH and immune balance, favoring fungal overgrowth and recurrence. Risk factors include antibiotic use, diabetes, pregnancy, and immunosuppression. <i>C. albicans</i> exhibits strong invasive capacity through morphogenesis and virulence factors such as adhesins and candidalysin, while <i>N. glabratus</i> persists through biofilm formation, stress resistance, and immune evasion. Conventional antifungal therapies often fail to prevent recurrence, prompting interest in alternative treatments such as vaginal microbiota transplantation (VMT), synthetic bacterial consortia transplantation (SBCT), and <i>Lactobacillus</i>-based probiotics. Restoring microbial equilibrium and regulating immune pathways, including IL-22 and IL-18, may enhance mucosal defense and reduce inflammation, providing a promising approach for managing recurrent fungal vulvovaginitis.</p>

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Vaginal Microbiota Dynamics as a Key Determinant of Pathogenesis in Fungal Vulvovaginitis

  • Alí F. Ruiz-Higareda,
  • Blanca E. Alvarez-Salas,
  • Martín G. García-Juárez,
  • Sergio Alanis-Ríos,
  • Ana Ríos-López,
  • Orlando Flores-Maldonado,
  • Tania Heredia-Torres,
  • Hiram Villanueva-Lozano,
  • Rogelio de J. Treviño-Rangel

摘要

Purpose of Review

This review synthesizes recent evidence on how the vaginal microbiota, especially Lactobacillus species, interacts with opportunistic yeasts of the genera Candida and Nakaseomyces to shape health and disease. It emphasizes the shift from the narrow term Candida vulvovaginitis to the more accurate and clinically meaningful concept of fungal vulvovaginitis.

Recent Findings

Recent evidence indicates that women presenting with vulvovaginitis exhibit a high prevalence of infectious etiologies, predominantly bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC), occurring either as isolated conditions or as mixed infections, with frequent BV fungal co-infection.Vaginal microbiota imbalances, including intermediate states and loss of dominant lactobacilli, markedly increase infection risk. Microbiome analyses identify Nakaseomyces glabratus as a key pathogen in recurrent fungal vulvovaginitis, linked to shifts in Firmicutes and higher Bifidobacterium. Emerging approaches, such as transplants or probiotics, can restore Lactobacillus dominance without promoting organisms associated with bacterial vaginosis or fungal vulvovaginitis. 

Summary

Fungal vulvovaginitis (FVV), primarily caused by Candida albicans and Nakaseomyces glabratus, is a prevalent gynecological infection associated with vaginal dysbiosis and excessive inflammatory responses. The loss of protective Lactobacillus species, particularly L. crispatus and L. iners, alters vaginal pH and immune balance, favoring fungal overgrowth and recurrence. Risk factors include antibiotic use, diabetes, pregnancy, and immunosuppression. C. albicans exhibits strong invasive capacity through morphogenesis and virulence factors such as adhesins and candidalysin, while N. glabratus persists through biofilm formation, stress resistance, and immune evasion. Conventional antifungal therapies often fail to prevent recurrence, prompting interest in alternative treatments such as vaginal microbiota transplantation (VMT), synthetic bacterial consortia transplantation (SBCT), and Lactobacillus-based probiotics. Restoring microbial equilibrium and regulating immune pathways, including IL-22 and IL-18, may enhance mucosal defense and reduce inflammation, providing a promising approach for managing recurrent fungal vulvovaginitis.