Materiały źródłowe

• #1 Vulvovaginitis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2188931-overview

  Vulvovaginal candidiasis can be an acute, chronic, recurrent, or persistent condition that can involve the vulva, vagina, and adjacent crural areas. The specific causative agent belongs to the genus Candida. These organisms are found in almost all humans and many animals. An estimated 10-50% of reproductive-aged American women are considered opportunistic carriers. […] The species C albicans is identified approximately 85-90% of the time. However, an increased frequency of other Candida species, such as C glabrata, C tropicalis, and C krusei, has been reported. The emergence of these other Candida species may possibly be due to widespread use of over-the-counter drugs, long-term use of suppressive azoles, and the use of frequent short courses of antifungal drugs. […] Any host factor that affects the vaginal environment or vaginal secretions can play a role in the initiation of Candida vulvovaginitis. Pregnancy is one of the most common predisposing factors. Studies have demonstrated that up to one third of pregnant women worldwide on any day can be affected. The high levels of reproductive hormones and an increase in the vaginal environments glycogen content create a favorable environment for Candida species, providing an abundant source of carbon for candidal growth, germination, and adherence.

• #2 Vaginal Candidiasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459317/

  Candidal vulvovaginitis occurs when Candida species superficially penetrate the mucosal lining of the vagina and cause an inflammatory response. The dominant inflammatory cells are typically polymorphonuclear cells and macrophages. The inflammatory response results in copious thick discharge and vaginal irritation, excoriations, dysuria, itching, burning, dyspareunia, or swelling.[8] […] Candidal vulvovaginitis is caused by inflammatory changes in the vaginal and vulvar epithelium secondary to infection with Candida species, most commonly Candida albicans. However, Candida is part of the normal flora in many women, identified in 10% of asymptomatic women.[2] Therefore, candidal vulvovaginitis requires both the presence of Candida in the vagina and associated symptoms (eg, irritation, itching, dysuria, or inflammation).[3]

• #3 Vaginal Candidiasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459317/

  Candidal vulvovaginitis occurs when Candida species superficially penetrate the mucosal lining of the vagina and cause an inflammatory response. The dominant inflammatory cells are typically polymorphonuclear cells and macrophages. The inflammatory response results in copious thick discharge and vaginal irritation, excoriations, dysuria, itching, burning, dyspareunia, or swelling.[8] […] Candidal vulvovaginitis is caused by inflammatory changes in the vaginal and vulvar epithelium secondary to infection with Candida species, most commonly Candida albicans. However, Candida is part of the normal flora in many women, identified in 10% of asymptomatic women.[2] Therefore, candidal vulvovaginitis requires both the presence of Candida in the vagina and associated symptoms (eg, irritation, itching, dysuria, or inflammation).[3]

• #4 Best Probiotics For Vaginal Health: Top Probiotics To Treat

  https://www.globenewswire.com/news-release/2025/05/02/3073441/0/en/Best-Probiotics-For-Vaginal-Health-Top-Probiotics-To-Treat-Bacterial-Vaginosis-BV-pH-Balance-WOLFSON-BRANDS-UK-LIMITED.html

  The vaginal microbiome refers to the diverse population of microorganisms, predominantly bacteria, that inhabit the vaginal canal. A healthy vaginal microbiome is typically dominated by Lactobacillus species, which help protect against infections by producing lactic acid. This acid maintains the vaginal environment at an acidic pH (around 3.8 to 4.5), making it inhospitable to many harmful bacteria and yeast. […] When the balance shifts and harmful organisms like Gardnerella vaginalis or Candida albicans become dominant, it can result in conditions such as bacterial vaginosis or yeast infections. […] Maintaining a healthy vaginal microbiome is not only important for preventing discomfort and infection, but it also plays a role in fertility and pregnancy outcomes. An imbalanced microbiome has been linked to complications such as preterm birth and infertility.

• #5 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  Candida albicans, along with other closely related Candida species, are the primary causative agents of vulvovaginal candidiasis (VVC) a multifactorial infectious disease of the lower female reproductive tract resulting in pathologic inflammation. […] While VVC is non-lethal, its high global incidence and profound negative impact on quality-of-life necessitates further understanding of the host and fungal factors that drive disease pathogenesis. […] Common disease symptoms include vaginal itching, burning, pain and redness. […] However, symptomatic infection can result from exuberant mucosal inflammation that is caused primarily by fungal overgrowth in the vagina and subsequent epithelial invasion and production of virulence effectors. […] The capacity to transition between these morphologies is the primary virulence attribute of C. albicans, as strains unable to undergo this switch are severely attenuated in pathogenicity or colonization.

• #6 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  This review provides an overview of the current knowledge regarding the pathogenic mechanisms underlying VVC/RVVC, with particular emphasis on the key role played by host innate immunity, vaginal dysbiosis and Candida-related virulence factors. […] The adhesion of C. albicans to the vaginal mucosal surface is essential for its persistence in the host either as a commensal or pathogenic microorganism. This is a complex, dynamic, multifactorial process involving an intimate association between components of the fungal cell wall and epithelial surface proteins. VECs are continuously exposed to C. albicans, as this fungus is the main component of the healthy vaginal mycobiota. Interestingly, it has been demonstrated that VECs are able to discriminate between commensal and pathogenic forms of C. albicans. Moreover, the host innate immune response is dependent on both Candida morphotype and fungal load. Indeed, in healthy women, VECs are able to tolerate C. albicans yeast and low filamentous fungal burden. However, in the presence of a massive load of hyphae, VECs become susceptible to the fungus and trigger an intense inflammatory response.

• #7

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The pathogenicity in VVC seems to be an interplay between vaginal microbiome dysbiosis followed by the vaginal epithelium invasion by Candida, colonization, and immune escape. […] The virulence feature of Candida include polymorphism, surface expression of adhesins, hydrolytic enzymes for invasion, immune evasion, biofilm formation which altogether support its colonization and sustenance. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane. […] The presence of secreted aspartyl proteinases (SAP) in vaginal secretions of women with symptomatic vaginitis caused by pathogenic Candida spp. suggest key role of these enzymes in virulence. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane.

• #8 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  The initial interaction between the fungus and the vaginal epithelium is mediated by passive forces, i.e., van der Waals forces and hydrophobic interactions. Subsequently, the adhesion is strengthened and stabilized by the binding of the fungal adhesins with specific surface epithelial cell receptors and host extracellular matrix components. […] Once Candida has adhered to the vaginal mucosa, the dimorphic transition from the yeast to the hyphal form results in the expression of additional adhesins associated with the hyphal morphotypes, namely, Als3p, Hwp1p (hyphal wall protein 1) and Ssa1p. These proteins reinforce the adhesion of the fungus to epithelial cells by interacting with E-cadherin, a key component of intercellular junctions, and with a heterodimeric receptor complex composed of epidermal growth factor receptor (EGFR) and Her2 (EGFR/Her2).

• #9 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #10 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #11 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #12 Vaginal yeast infection – Wikipedia

  https://en.wikipedia.org/wiki/Vaginal_yeast_infection

  Vaginal yeast infections are due to excessive growth of Candida. […] The causes of excessive Candida growth are not well understood, but some predisposing factors have been identified. […] There is some support for the theory that RVVC results from an especially intense inflammatory reaction to colonization. Candida antigens can be presented to antigen-presenting cells, which may trigger cytokine production and activate lymphocytes and neutrophils that then cause inflammation and edema. […] PRA1 gene (pH-regulated antigen) is strongly up-regulated during vaginal infections, which correlates with inflammation.

• #13

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The pathogenicity in VVC seems to be an interplay between vaginal microbiome dysbiosis followed by the vaginal epithelium invasion by Candida, colonization, and immune escape. […] The virulence feature of Candida include polymorphism, surface expression of adhesins, hydrolytic enzymes for invasion, immune evasion, biofilm formation which altogether support its colonization and sustenance. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane. […] The presence of secreted aspartyl proteinases (SAP) in vaginal secretions of women with symptomatic vaginitis caused by pathogenic Candida spp. suggest key role of these enzymes in virulence. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane.

• #14

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The infection of VVC is extremely distressful with itchy, burning, and wet sensation. […] The presence of Lactobacillus keeps the vagina healthy as well as checks the pathogenic trait of Candida, and hence monitoring this microbiome forms the basis of recommending probiotics-based therapy for VVC. […] The interaction between Lactobacillus and Candida in the vaginal region is facilitated via the secretion of metabolic products by Lactobacillus that either directly regulate the virulence traits of Candida or activate the immune response for extending protection. […] Any dysbiosis in this control system results in the development of Candida mediated disease state in the vaginal area. […] The vaginal region has varying amounts of short-chain aliphatic organic acids, lactic acid (LA), and acetic acid (AA), depending upon the dominant Lactobacillus species.

• #15 Best Probiotics For Vaginal Health: Top Probiotics To Treat

  https://www.globenewswire.com/news-release/2025/05/02/3073441/0/en/Best-Probiotics-For-Vaginal-Health-Top-Probiotics-To-Treat-Bacterial-Vaginosis-BV-pH-Balance-WOLFSON-BRANDS-UK-LIMITED.html

  The vaginal microbiome refers to the diverse population of microorganisms, predominantly bacteria, that inhabit the vaginal canal. A healthy vaginal microbiome is typically dominated by Lactobacillus species, which help protect against infections by producing lactic acid. This acid maintains the vaginal environment at an acidic pH (around 3.8 to 4.5), making it inhospitable to many harmful bacteria and yeast. […] When the balance shifts and harmful organisms like Gardnerella vaginalis or Candida albicans become dominant, it can result in conditions such as bacterial vaginosis or yeast infections. […] Maintaining a healthy vaginal microbiome is not only important for preventing discomfort and infection, but it also plays a role in fertility and pregnancy outcomes. An imbalanced microbiome has been linked to complications such as preterm birth and infertility.

• #16

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  In the era of globalization, the concept of world health needs to be practiced where a significant consideration should be given to women health. Of many issues, the most common and under-rated is vulvovaginal candidiasis (VVC); a superficial to invasive mucosal infection of lower reproductive tract in women, primarily caused by commensal yeast Candida. […] The present review aimed to highlight the problem and concerns of women related to VVC, covering all aspects of disease development, host response, conventional drug failure, and possibilities of formulating phytomolecule based VVC therapy. […] Any dysbiosis in vaginal microbiome disturbs the harmony between residing microbes and leads to commencement of VVC. Lactobacillus is key care-taker microbe that keeps check on over growth of Candida by various means. However, Candida have evolved numerous virulence traits to overcome the governance of Lactobacillus as well as host immune system.

• #17 Vulvovaginitis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2188931-overview

  Furthermore, the acidity of the pregnant vaginal flora can suppress the growth of other microorganisms that are naturally inhibitory to Candida. Although the initial attachment of the organism occurs more readily at high pH values (6-7), the germ tube formation and the development of mycelia are favored by a low vaginal pH ( 5). […] Disorders associated with an altered immune response, such as acquired immunodeficiency syndrome (AIDS) and diabetes mellitus, also predispose women to Candida vulvovaginitis. […] Antimicrobials are thought to predispose a patient to Candida by reducing the number of protective resident vaginal bacteria. The most common offenders are broad-spectrum agents such as tetracycline, cephalosporins, and ampicillin-like agents. […] Recurrent vulvovaginal candidiasis has also been associated with a decreased in vivo concentration of mannose binding lectin (MBL) and an increased concentration of interleukin-4 (IL-4). Studies have shown that the prevalence of a variant MLB gene is higher in women with recurrent vulvovaginal candidiasis than in controls without candidiasis. Furthermore, IL-4 blocks the anti-Candida response mediated by macrophages; thus, elevation of IL-4 levels results in the inhibition of local defense mechanisms.

• #18 Bacterial Vaginosis and Vulvovaginal Candidiasis Pathophysiologic Interrelationship

  https://www.mdpi.com/2076-2607/12/1/108

  A characteristic consequence of anaerobic proliferation in BV is the increased elaboration of biogenic amines including putrescine, cadaverine, and trimethyl amine oxide responsible for the characteristic malodor observed in women with BV. […] While most attention examining vaginal bacterial yeast interaction has focused on the role of Lactobacillus spp., such interactions likely occur with other bacterial species that are part of BV dysbiosis. […] Lactobacillus dominance is considered essential to a physiologic anti-inflammatory environment. […] Despite the wide prevalence of BV, there remains an unmet need to better understand the immunologic microenvironment accompanying and driving the dysbiotic state and the contribution of the individual BV-associated species to this environment and disease process. […] The important role of RBV as a dominant contributory factor to VVC recurrence in some subpopulations is underappreciated by practitioners but certainly not by patients. […] The association of RBV with fluconazole resistance is similarly unrecognized and worthy of further study.

• #19 Bacterial Vaginosis and Vulvovaginal Candidiasis Pathophysiologic Interrelationship

  https://www.mdpi.com/2076-2607/12/1/108

  The vaginal environment in BV is profoundly proinflammatory, as confirmed in multiple studies. […] The role of vaginal inflammatory mediators in the pathogenesis of BV is largely unknown and is perhaps crucial to the loss of protective Lactobacillus species as well as to explaining clinical BV recurrence and resistance to probiotic therapy. […] Vaginal dysbiosis facilitates Candida colonization. […] Antimicrobial use is widely accepted as a common, if not the most common, trigger of acute VVC. […] The mechanisms by which antibiotics facilitate proliferation of commensal yeast are poorly understood. […] The now unrestrained commensal yeast blastopores in turn proliferate, form hyphae, and release virulent enzymes, which facilitate epithelial cell adherence and invasion of the vaginal epithelial cell barrier.

• #20 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #21 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #22 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #23 Vaginal Candidiasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459317/

  Candidal vulvovaginitis occurs when Candida species superficially penetrate the mucosal lining of the vagina and cause an inflammatory response. The dominant inflammatory cells are typically polymorphonuclear cells and macrophages. The inflammatory response results in copious thick discharge and vaginal irritation, excoriations, dysuria, itching, burning, dyspareunia, or swelling.[8] […] Candidal vulvovaginitis is caused by inflammatory changes in the vaginal and vulvar epithelium secondary to infection with Candida species, most commonly Candida albicans. However, Candida is part of the normal flora in many women, identified in 10% of asymptomatic women.[2] Therefore, candidal vulvovaginitis requires both the presence of Candida in the vagina and associated symptoms (eg, irritation, itching, dysuria, or inflammation).[3]

• #24 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #25 Vaginal Candidiasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459317/

  Candidal vulvovaginitis occurs when Candida species superficially penetrate the mucosal lining of the vagina and cause an inflammatory response. The dominant inflammatory cells are typically polymorphonuclear cells and macrophages. The inflammatory response results in copious thick discharge and vaginal irritation, excoriations, dysuria, itching, burning, dyspareunia, or swelling.[8] […] Candidal vulvovaginitis is caused by inflammatory changes in the vaginal and vulvar epithelium secondary to infection with Candida species, most commonly Candida albicans. However, Candida is part of the normal flora in many women, identified in 10% of asymptomatic women.[2] Therefore, candidal vulvovaginitis requires both the presence of Candida in the vagina and associated symptoms (eg, irritation, itching, dysuria, or inflammation).[3]

• #26 Vulvovaginitis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2188931-overview

  Furthermore, the acidity of the pregnant vaginal flora can suppress the growth of other microorganisms that are naturally inhibitory to Candida. Although the initial attachment of the organism occurs more readily at high pH values (6-7), the germ tube formation and the development of mycelia are favored by a low vaginal pH ( 5). […] Disorders associated with an altered immune response, such as acquired immunodeficiency syndrome (AIDS) and diabetes mellitus, also predispose women to Candida vulvovaginitis. […] Antimicrobials are thought to predispose a patient to Candida by reducing the number of protective resident vaginal bacteria. The most common offenders are broad-spectrum agents such as tetracycline, cephalosporins, and ampicillin-like agents. […] Recurrent vulvovaginal candidiasis has also been associated with a decreased in vivo concentration of mannose binding lectin (MBL) and an increased concentration of interleukin-4 (IL-4). Studies have shown that the prevalence of a variant MLB gene is higher in women with recurrent vulvovaginal candidiasis than in controls without candidiasis. Furthermore, IL-4 blocks the anti-Candida response mediated by macrophages; thus, elevation of IL-4 levels results in the inhibition of local defense mechanisms.

• #27 Yeast infection (vaginal) – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/yeast-infection/symptoms-causes/syc-20378999

  A vaginal yeast infection is a fungal infection. It causes irritation, discharge and itching of the vagina and the vulva. Vaginal yeast infection also is called vaginal candidiasis. […] The fungus Candida albicans causes most vaginal yeast infections. Most often, the vagina has a balance of yeast, including candida, and bacteria. Certain bacteria called lactobacillus work to prevent too much yeast. But some factors can affect the balance. Too much candida or the fungus growing deeper into vaginal cells causes symptoms of a yeast infection. […] Too much yeast can result from: Antibiotic use. Pregnancy. Diabetes that isn’t well-managed. A weakened immune system. Use of birth control pills or hormone therapy that raises levels of the hormone estrogen. […] Candida albicans is the most common type of fungus to cause yeast infections. When other types of candida fungus cause yeast infections, they can be harder to treat.

• #28 Vaginal thrush | Hirslanden Switzerland

  https://www.hirslanden.com/en/international/disease-patterns/vaginal-thrush.html

  Vaginal thrush infections are common. Three out of every four women are affected by them at least once in their lives. They are usually yeast infections. Discharge, itching and burning in the vagina are typical symptoms. Antifungal medication, known as antimycotics, usually heals a vaginal fungal infection without difficulty in a few days. […] The mucous membrane of the vagina is usually well protected against fungal infections. Lactic acid bacteria guarantee an acidic environment in the vaginal mucous membrane. This controls the growth of fungi which are naturally present in the vagina in small amounts. If this natural protective mechanism is affected, this can lead to an infection with marked growth of the fungus. The following factors in particular can facilitate the development of a vaginal fungal infection: Antibiotic treatment, Mechanical irritation through tampons or vaginal diaphragms, Excessive intimate hygiene, Pregnancy, Lack of oestrogen, Disorders of the immune system, diabetes mellitus.

• #29 Vaginal yeast infection | Content for the lay public | Microbiota institute

  https://www.biocodexmicrobiotainstitute.com/en/vaginal-yeast-infection

  Other factors that can increase the risk of infection include corticosteroid use, pregnancy, immunosuppressive diseases, poorly controlled diabetes, oral contraception, and IUD. Many factors have been identified but the mechanisms are not yet fully understood. […] The classic treatment for vaginal yeast infections is antifungal medication administered orally or topically. However, relapses can occur and new therapeutic approaches are currently being evaluated. Recent work suggests that oral or topical probiotics may rebalance the vaginal microbiota and reduce the frequency of relapse.

• #30 Bacterial Vaginosis and Vulvovaginal Candidiasis Pathophysiologic Interrelationship

  https://www.mdpi.com/2076-2607/12/1/108

  Acute symptomatic Candida vulvovaginitis represents a dramatic change triggered by multiple factors but always requiring prior vaginal yeast colonization and characterized by proliferation of yeast blastospores and hyphae formation with expression of multiple fungal virulence factors, and these microbiome changes result in superficial vaginal epithelial surface invasion and consequent vaginal epithelial cell proinflammatory reaction. […] Risk factors for acute VVC include vaginal dysbiosis after antimicrobials, increased estrogen, and uncontrolled diabetes, all superimposed upon genetic susceptibility consisting largely of single nucleotide polymorphisms. […] We still lack a full understanding of yeast virulence factors, vaginal microbiota, and host mucosal immune mechanisms involved in acute vaginal candidiasis.

• #31

  https://www.juno.bio/blogs/learn/is-it-really-a-yeast-infection?srsltid=AfmBOop53UbAn8sAsyhUzjEiLhyN6ijk8hXp4c4RVapFNoJWQ9yOYxo_

  This disruption can be triggered by antibiotics, diabetes, immunosuppressant medicine or changes in hormones. […] In a disrupted vaginal microbiome, protective vaginal bacteria known as Lactobacilli are depleted in number. […] Lactobacilli work to protect you from Candida growing out of control by producing lactic acid which creates an unfavourable environment for this fungus. […] So when this protective lactobacillus microbe population is disrupted, all hell can break loose.

• #32 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Vulvovaginal candidiasis (VVC), which is primarily caused by Candida albicans, is an infection that affects up to 75% of all reproductive-age women worldwide. Recurrent VVC (RVVC) is defined as >3 episodes per year and affects nearly 8% of women globally. At mucosal sites of the vagina, a delicate and complex balance exists between Candida spp., host immunity and local microbial communities. In fact, both immune response and microbiota composition play a central role in counteracting overgrowth of the fungus and maintaining homeostasis in the host. If this balance is perturbed, the conditions may favor C. albicans overgrowth and the yeast-to-hyphal transition, predisposing the host to VVC. […] Understanding the host- and fungus-related factors that drive VVC pathogenesis is of paramount importance for the development of adequate therapeutic interventions to combat this common genital infection. This review focuses on the latest advances in the pathogenic mechanisms implicated in the onset of VVC and also discusses novel potential strategies, with a special focus on the use of probiotics and vaginal microbiota transplantation in the treatment and/or prevention of recurrent VVC.

• #33 Candida vulvovaginitis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Candida_vulvovaginitis_pathophysiology

  Several virulence factors of Candida are implicated in vulvovaginitis, but the process of transition from asymptomatic vaginal colonization to symptomatic vulvovaginitis is poorly understood. […] Candida vulvovaginitis is a microbial disease and not all patients with detectable pathogen are symptomatic. Multiple risk factors and the imbalance in the protective vaginal defenses predispose patients to develop active disease. […] Candida vaginal infections are more common in the reproductive age group because of the high concentration of estrogen as it increases the amount of glycogen in the vagina providing a carbon source for Candida organisms to colonize. It also increases the adherence of Candida to the vaginal epithelial cells. […] The initial step of infection is colonization and symptoms appear with the invasion of the blastospores or pseudohyphae of the vaginal wall. […] The understanding of the transition from asymptomatic vaginal colonization with Candida to symptomatic vulvovaginitis is not clear.

• #34 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  This review provides an overview of the current knowledge regarding the pathogenic mechanisms underlying VVC/RVVC, with particular emphasis on the key role played by host innate immunity, vaginal dysbiosis and Candida-related virulence factors. […] The adhesion of C. albicans to the vaginal mucosal surface is essential for its persistence in the host either as a commensal or pathogenic microorganism. This is a complex, dynamic, multifactorial process involving an intimate association between components of the fungal cell wall and epithelial surface proteins. VECs are continuously exposed to C. albicans, as this fungus is the main component of the healthy vaginal mycobiota. Interestingly, it has been demonstrated that VECs are able to discriminate between commensal and pathogenic forms of C. albicans. Moreover, the host innate immune response is dependent on both Candida morphotype and fungal load. Indeed, in healthy women, VECs are able to tolerate C. albicans yeast and low filamentous fungal burden. However, in the presence of a massive load of hyphae, VECs become susceptible to the fungus and trigger an intense inflammatory response.

• #35 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. […] It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. […] These exciting new studies highlight the immunopathological response as a crucial element of vaginitis pathogenesis. […] C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen.

• #36 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. […] It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. […] These exciting new studies highlight the immunopathological response as a crucial element of vaginitis pathogenesis. […] C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen.

• #37 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  These initial signals, coupled with secondary amplification of immune effectors by recruited PMNs, contribute to symptomatic infection and characteristic immunopathology. […] Cumulatively, these studies confirm an important role for the morphogenetic response in vaginitis immunopathology. […] Vaginitis is a complex disease, requiring a perfect storm scenario to initiate infection. Estrogen production, microbiota disruption, pH modification, fungal virulence factor expression, and exuberant innate immune activity must synchronize to culminate in symptomatic infection. […] Current research has elucidated a major paradigm shift in the philosophy of Candida vaginitis pathogenesis, highlighting the role of the host innate immune response in disease immunopathology.

• #38 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  This review provides an overview of the current knowledge regarding the pathogenic mechanisms underlying VVC/RVVC, with particular emphasis on the key role played by host innate immunity, vaginal dysbiosis and Candida-related virulence factors. […] The adhesion of C. albicans to the vaginal mucosal surface is essential for its persistence in the host either as a commensal or pathogenic microorganism. This is a complex, dynamic, multifactorial process involving an intimate association between components of the fungal cell wall and epithelial surface proteins. VECs are continuously exposed to C. albicans, as this fungus is the main component of the healthy vaginal mycobiota. Interestingly, it has been demonstrated that VECs are able to discriminate between commensal and pathogenic forms of C. albicans. Moreover, the host innate immune response is dependent on both Candida morphotype and fungal load. Indeed, in healthy women, VECs are able to tolerate C. albicans yeast and low filamentous fungal burden. However, in the presence of a massive load of hyphae, VECs become susceptible to the fungus and trigger an intense inflammatory response.

• #39 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  This review provides an overview of the current knowledge regarding the pathogenic mechanisms underlying VVC/RVVC, with particular emphasis on the key role played by host innate immunity, vaginal dysbiosis and Candida-related virulence factors. […] The adhesion of C. albicans to the vaginal mucosal surface is essential for its persistence in the host either as a commensal or pathogenic microorganism. This is a complex, dynamic, multifactorial process involving an intimate association between components of the fungal cell wall and epithelial surface proteins. VECs are continuously exposed to C. albicans, as this fungus is the main component of the healthy vaginal mycobiota. Interestingly, it has been demonstrated that VECs are able to discriminate between commensal and pathogenic forms of C. albicans. Moreover, the host innate immune response is dependent on both Candida morphotype and fungal load. Indeed, in healthy women, VECs are able to tolerate C. albicans yeast and low filamentous fungal burden. However, in the presence of a massive load of hyphae, VECs become susceptible to the fungus and trigger an intense inflammatory response.

• #40 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #41 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #42 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #43 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #44 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #45 Vaginal Candidiasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459317/

  Candidal vulvovaginitis occurs when Candida species superficially penetrate the mucosal lining of the vagina and cause an inflammatory response. The dominant inflammatory cells are typically polymorphonuclear cells and macrophages. The inflammatory response results in copious thick discharge and vaginal irritation, excoriations, dysuria, itching, burning, dyspareunia, or swelling.[8] […] Candidal vulvovaginitis is caused by inflammatory changes in the vaginal and vulvar epithelium secondary to infection with Candida species, most commonly Candida albicans. However, Candida is part of the normal flora in many women, identified in 10% of asymptomatic women.[2] Therefore, candidal vulvovaginitis requires both the presence of Candida in the vagina and associated symptoms (eg, irritation, itching, dysuria, or inflammation).[3]

• #46 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  Candida albicans, along with other closely related Candida species, are the primary causative agents of vulvovaginal candidiasis (VVC) a multifactorial infectious disease of the lower female reproductive tract resulting in pathologic inflammation. […] While VVC is non-lethal, its high global incidence and profound negative impact on quality-of-life necessitates further understanding of the host and fungal factors that drive disease pathogenesis. […] Common disease symptoms include vaginal itching, burning, pain and redness. […] However, symptomatic infection can result from exuberant mucosal inflammation that is caused primarily by fungal overgrowth in the vagina and subsequent epithelial invasion and production of virulence effectors. […] The capacity to transition between these morphologies is the primary virulence attribute of C. albicans, as strains unable to undergo this switch are severely attenuated in pathogenicity or colonization.

• #47 Alan G. – Residual pain from yeast infection | TMS Forum (The Mindbody Syndrome)

  https://www.tmswiki.org/forum/threads/residual-pain-from-yeast-infection.8439/

  Yeast infections are a know cause of persisting vulvar pain. […] The infection itself is a painful stimulus that irritates the vulvar tissue. The pelvic floor muscles contract in response to the pain from the infection and may remain tight after the infection has cleared. Additionally, the vulvar connective tissue and nerves will be also be negatively affected by the infection. […] These impairments and symptoms can be treated with medical management to prevent further infections and to help manage the pain and pelvic floor physical therapy to address the musculoskeletal consequences of the infection.

• #48 Alan G. – Residual pain from yeast infection | TMS Forum (The Mindbody Syndrome)

  https://www.tmswiki.org/forum/threads/residual-pain-from-yeast-infection.8439/

  Yeast infections are a know cause of persisting vulvar pain. […] The infection itself is a painful stimulus that irritates the vulvar tissue. The pelvic floor muscles contract in response to the pain from the infection and may remain tight after the infection has cleared. Additionally, the vulvar connective tissue and nerves will be also be negatively affected by the infection. […] These impairments and symptoms can be treated with medical management to prevent further infections and to help manage the pain and pelvic floor physical therapy to address the musculoskeletal consequences of the infection.

• #49 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  Candida albicans, along with other closely related Candida species, are the primary causative agents of vulvovaginal candidiasis (VVC) a multifactorial infectious disease of the lower female reproductive tract resulting in pathologic inflammation. […] While VVC is non-lethal, its high global incidence and profound negative impact on quality-of-life necessitates further understanding of the host and fungal factors that drive disease pathogenesis. […] Common disease symptoms include vaginal itching, burning, pain and redness. […] However, symptomatic infection can result from exuberant mucosal inflammation that is caused primarily by fungal overgrowth in the vagina and subsequent epithelial invasion and production of virulence effectors. […] The capacity to transition between these morphologies is the primary virulence attribute of C. albicans, as strains unable to undergo this switch are severely attenuated in pathogenicity or colonization.

• #50

  https://consensus.app/questions/vaginal-yeast-infection/

  Vaginal yeast infections, primarily caused by Candida species, are among the most common female genital tract infections. […] The pathophysiology involves the ability of Candida species to switch between yeast and hyphal forms, a key virulence factor that facilitates tissue invasion and immune response evasion. […] Additionally, the secretion of aspartyl proteinase by Candida albicans and Candida parapsilosis is linked to their pathogenicity, distinguishing them from non-proteolytic species. […] Recent research has focused on understanding the complex interactions between Candida species and host immune responses, which are crucial for developing effective treatments. […] Candida virulence factors and host immune response play crucial roles in the pathogenesis of vulvovaginal candidiasis, with host cell interactions and innate immune mechanisms also playing a role.

• #51 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. […] It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. […] These exciting new studies highlight the immunopathological response as a crucial element of vaginitis pathogenesis. […] C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen.

• #52

  https://consensus.app/questions/vaginal-yeast-infection/

  The yeast-to-hypha transition and associated morphogenetic response are crucial for the immunopathogenesis of Candida vaginitis, with implications for transitioning from benign colonization to symptomatic infection. […] Recurrent candidal vaginitis may result from an acquired Candida antigen-specific immunological deficiency, with no definitive cure but effective therapeutic maintenance regimens using azoles to control symptomatic infection.

• #53

  https://consensus.app/questions/vaginal-yeast-infection/

  The yeast-to-hypha transition and associated morphogenetic response are crucial for the immunopathogenesis of Candida vaginitis, with implications for transitioning from benign colonization to symptomatic infection. […] Recurrent candidal vaginitis may result from an acquired Candida antigen-specific immunological deficiency, with no definitive cure but effective therapeutic maintenance regimens using azoles to control symptomatic infection.

• #54 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  This review provides an overview of the current knowledge regarding the pathogenic mechanisms underlying VVC/RVVC, with particular emphasis on the key role played by host innate immunity, vaginal dysbiosis and Candida-related virulence factors. […] The adhesion of C. albicans to the vaginal mucosal surface is essential for its persistence in the host either as a commensal or pathogenic microorganism. This is a complex, dynamic, multifactorial process involving an intimate association between components of the fungal cell wall and epithelial surface proteins. VECs are continuously exposed to C. albicans, as this fungus is the main component of the healthy vaginal mycobiota. Interestingly, it has been demonstrated that VECs are able to discriminate between commensal and pathogenic forms of C. albicans. Moreover, the host innate immune response is dependent on both Candida morphotype and fungal load. Indeed, in healthy women, VECs are able to tolerate C. albicans yeast and low filamentous fungal burden. However, in the presence of a massive load of hyphae, VECs become susceptible to the fungus and trigger an intense inflammatory response.

• #55 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  The initial interaction between the fungus and the vaginal epithelium is mediated by passive forces, i.e., van der Waals forces and hydrophobic interactions. Subsequently, the adhesion is strengthened and stabilized by the binding of the fungal adhesins with specific surface epithelial cell receptors and host extracellular matrix components. […] Once Candida has adhered to the vaginal mucosa, the dimorphic transition from the yeast to the hyphal form results in the expression of additional adhesins associated with the hyphal morphotypes, namely, Als3p, Hwp1p (hyphal wall protein 1) and Ssa1p. These proteins reinforce the adhesion of the fungus to epithelial cells by interacting with E-cadherin, a key component of intercellular junctions, and with a heterodimeric receptor complex composed of epidermal growth factor receptor (EGFR) and Her2 (EGFR/Her2).

• #56 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #57 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #58

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The pathogenicity in VVC seems to be an interplay between vaginal microbiome dysbiosis followed by the vaginal epithelium invasion by Candida, colonization, and immune escape. […] The virulence feature of Candida include polymorphism, surface expression of adhesins, hydrolytic enzymes for invasion, immune evasion, biofilm formation which altogether support its colonization and sustenance. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane. […] The presence of secreted aspartyl proteinases (SAP) in vaginal secretions of women with symptomatic vaginitis caused by pathogenic Candida spp. suggest key role of these enzymes in virulence. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane.

• #59

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The pathogenicity in VVC seems to be an interplay between vaginal microbiome dysbiosis followed by the vaginal epithelium invasion by Candida, colonization, and immune escape. […] The virulence feature of Candida include polymorphism, surface expression of adhesins, hydrolytic enzymes for invasion, immune evasion, biofilm formation which altogether support its colonization and sustenance. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane. […] The presence of secreted aspartyl proteinases (SAP) in vaginal secretions of women with symptomatic vaginitis caused by pathogenic Candida spp. suggest key role of these enzymes in virulence. […] The pathogenicity of Candida spp. in VVC depends on its adherence properties, which are related to both abiotic surfaces and mucous membrane.

• #60 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #61 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #62 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #63 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #64 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #65 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. […] It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. […] These exciting new studies highlight the immunopathological response as a crucial element of vaginitis pathogenesis. […] C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen.

• #66 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Subsequent to adhesion, Candida hyphae can penetrate epithelial cells through two distinct mechanisms: endocytosis and active penetration. […] The former is induced by the interaction of the C. albicans proteins Ssa1p and Als3p with cadherins and EGFR/Her2, while the latter occurs when the growing hyphal tip pushes the epithelial cell membrane and leads to cell damage through the release of various virulence factors, including the cytolytic peptide toxin candidalysin, secretory aspartyl proteinases (SAPs), lipases and phospholipases. Recognition of the filamentous forms of Candida by VECs leads to sustained activation of all three mitogen-activated protein kinase (MAPK) pathways (p38, JNK and ERK1/2), which in turn, leads to c-fos activation via p38 and release of antimicrobial peptides, such as alarmins and pro-inflammatory cytokines (GM-CSF, G-CSF, IL-6, IL-1α, IL-1β, IL-36γ and CCL20) that are essential for the recruitment of innate immune cells, mainly neutrophils and macrophages.

• #67 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #68 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #69 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #70 Vulvovaginal Candidiasis: A Current Understanding and Burning Questions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7151053/

  C. albicans is capable of eliciting vaginal inflammation, but how? […] C. albicans (as well as the NAC species) exert their damage primarily through two major mechanisms: direct invasion by hyphal filaments or secretion of virulence effectors. […] Candidalysin is a fungal peptide toxin critical for mucosal infection. […] Disruption of the ECE1 locus or the region specifically encoding for candidalysin results in severe attenuation of pathogenicity in multiple infection models, including murine invasive and oral candidiasis, zebrafish swim bladder infection, and a variety of cell culture systems. […] The NLRP3 inflammasome plays an important role during disease pathogenesis, as IL-1R pathway genes were increased during VVC. […] The role of the NLRP3 inflammasome as a partial driver of innate inflammatory events during VVC was plausible. […] C. albicans possesses multiple, redundant pathogenicity mechanisms for triggering inflammatory processes within the host.

• #71 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #72

  https://www.aaaai.org/allergist-resources/ask-the-expert/answers/old-ask-the-experts/candidiasis-normal-immune

  In general, in spite of a few earlier reports, Candida lymphocyte stimulation assays do not show good correlation with susceptibility to mucocutaneous candidiasis. […] It is essential that any results of proliferation assays (as with any laboratory tests) must be interpreted in the light of clinical findings to be of any use. […] Vaginal thrush (which she has) is very frequently seen in otherwise healthy women and (amazingly!) relatively infrequently in patients with CMC. […] It is believed that vaginal immunity is dependent on local and environmental factors (such as micobicidal peptides, pH etc) far more than on TB cell immunity and is therefore not seen as a sign of systemic immune deficiency. […] There is not much to justify further immunological assessments but she needs to have her current clinical problems (CFS, recurrent sinusitis, oral ulcers, skin rash, rhinoconjunctivitis asthma) controlled.

• #73

  https://www.aaaai.org/allergist-resources/ask-the-expert/answers/old-ask-the-experts/candidiasis-normal-immune

  In general, in spite of a few earlier reports, Candida lymphocyte stimulation assays do not show good correlation with susceptibility to mucocutaneous candidiasis. […] It is essential that any results of proliferation assays (as with any laboratory tests) must be interpreted in the light of clinical findings to be of any use. […] Vaginal thrush (which she has) is very frequently seen in otherwise healthy women and (amazingly!) relatively infrequently in patients with CMC. […] It is believed that vaginal immunity is dependent on local and environmental factors (such as micobicidal peptides, pH etc) far more than on TB cell immunity and is therefore not seen as a sign of systemic immune deficiency. […] There is not much to justify further immunological assessments but she needs to have her current clinical problems (CFS, recurrent sinusitis, oral ulcers, skin rash, rhinoconjunctivitis asthma) controlled.

• #74 Treatment of Recurrent Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0601/p3306.html

  Antibiotics are often implicated as a cause of recurrent vulvovaginal candidiasis. Frequent antibiotic use decreases protective vaginal flora and allows colonization by Candida species. […] Diabetes mellitus is often considered a predisposing factor for recurrent vulvovaginal candidiasis. Hyperglycemia enhances the ability of C. albicans to bind to vaginal epithelial cells. […] Contraceptive methods may also promote recurrences of vulvovaginal candidiasis. Use of spermicidal jellies and creams increases susceptibility to infection by altering the vaginal flora and increasing the adhesion of Candida organisms. […] Women who are prone to recurrent vulvovaginal candidiasis may have deficient cell-mediated immunity. […] Mechanical factors may also be important. Perspiration associated with tightly fitted clothes or poorly ventilated underwear increases local temperature and moisture.

• #75

  https://www.aaaai.org/allergist-resources/ask-the-expert/answers/old-ask-the-experts/candidiasis-normal-immune

  The widespread occurrence of mucosal infections caused by Candida, in particular recurrent vulvovaginal candidiasis among fertile-age women, together with the paucity of safe candidacidal antimycotics, have prompted a great number of investigations into the immunotherapy of candidal vaginitis. […] Although impairment of the T-cell response is associated with persistent or recurrent candidiasis, data on immunologic responses in patients with RVC are controversial. […] Mononuclear cells from patients with RVC stimulated with C albicans antigen have low or absent IFN- production.

• #76 Preventing Vaginal Yeast Infections

  https://www.everydayhealth.com/yeast-infection/guide/prevention/

  Vaginal yeast infections are most often caused by the yeast species Candida albicans and can include a number of symptoms, such as itching in the vaginal area and around the vulva (the opening of the vagina), burning sensations in the genitals, and a cottage-cheese-like discharge. […] One study found that a localized immune defect in the vagina might be behind many womens recurrent vulvovaginal candidiasis. […] Recurring yeast infections may also be the result of an intestinal or vaginal reservoir of Candida. About 20 percent of women (and 30 percent of pregnant women) are colonized by Candida this colonization doesnt cause symptoms until the balance of microbial communities is altered by antibiotic use, hormonal changes, and other factors. […] The idea is that, normally, certain bacteria live in the digestive tract, on the skin, and elsewhere on the body where they help with digestion and other bodily functions. Therefore, probiotics can help restore the bodys normal bacterial balance, preventing Candida yeast from growing out of control and causing an infection.

• #77

  https://consensus.app/questions/vaginal-yeast-infection/

  The yeast-to-hypha transition and associated morphogenetic response are crucial for the immunopathogenesis of Candida vaginitis, with implications for transitioning from benign colonization to symptomatic infection. […] Recurrent candidal vaginitis may result from an acquired Candida antigen-specific immunological deficiency, with no definitive cure but effective therapeutic maintenance regimens using azoles to control symptomatic infection.

• #78

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The infection of VVC is extremely distressful with itchy, burning, and wet sensation. […] The presence of Lactobacillus keeps the vagina healthy as well as checks the pathogenic trait of Candida, and hence monitoring this microbiome forms the basis of recommending probiotics-based therapy for VVC. […] The interaction between Lactobacillus and Candida in the vaginal region is facilitated via the secretion of metabolic products by Lactobacillus that either directly regulate the virulence traits of Candida or activate the immune response for extending protection. […] Any dysbiosis in this control system results in the development of Candida mediated disease state in the vaginal area. […] The vaginal region has varying amounts of short-chain aliphatic organic acids, lactic acid (LA), and acetic acid (AA), depending upon the dominant Lactobacillus species.

• #79 Best Probiotics For Vaginal Health: Top Probiotics To Treat

  https://www.globenewswire.com/news-release/2025/05/02/3073441/0/en/Best-Probiotics-For-Vaginal-Health-Top-Probiotics-To-Treat-Bacterial-Vaginosis-BV-pH-Balance-WOLFSON-BRANDS-UK-LIMITED.html

  YourBiology Gut+ includes 4 key probiotic strains, two of which are especially beneficial for vaginal flora: Lactobacillus acidophilus: Known for helping maintain an acidic vaginal pH and preventing overgrowth of harmful bacteria. […] Lactobacillus plantarum: Supports immune defense and can help in managing yeast overgrowth. These strains support the production of lactic acid and hydrogen peroxide substances that help prevent infections like bacterial vaginosis and candidiasis. […] Probiotics improve gut and vaginal health with live microorganisms. They can assist with anxiety, depression, and enhance immunity. They generally have few or minor side effects and can promote overall well-being. […] Probiotics are rapidly gaining recognition as a natural, effective, and preventative tool for promoting optimal vaginal health. With the increasing understanding of the importance of a balanced vaginal microbiome one that’s rich in beneficial Lactobacillus species more individuals are turning to probiotic supplements and probiotic-rich foods to help manage and prevent issues such as yeast infections, bacterial vaginosis, and urinary tract infections. […] Among the most effective strains for vaginal support are Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14, which have been extensively studied for their ability to colonize the vaginal tract and protect against infections.

• #80

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The infection of VVC is extremely distressful with itchy, burning, and wet sensation. […] The presence of Lactobacillus keeps the vagina healthy as well as checks the pathogenic trait of Candida, and hence monitoring this microbiome forms the basis of recommending probiotics-based therapy for VVC. […] The interaction between Lactobacillus and Candida in the vaginal region is facilitated via the secretion of metabolic products by Lactobacillus that either directly regulate the virulence traits of Candida or activate the immune response for extending protection. […] Any dysbiosis in this control system results in the development of Candida mediated disease state in the vaginal area. […] The vaginal region has varying amounts of short-chain aliphatic organic acids, lactic acid (LA), and acetic acid (AA), depending upon the dominant Lactobacillus species.

• #81

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  The supernatant of Lactobacillus rhamnosus containing LA does not inhibit the growth of Candida albicans and Candida glabrata. […] The supernatant of late stationary phase of Lactobacillus rhamnosus, Lactobacillus acidophilus, and Lactobacillus casei effectively exhibited a fungistatic effect against fungal growth. […] For successful colonization and infection, adherence of Candida to vaginal epithelial cell (VEC) is crucial. […] This surface contact is prevented by biosurfactant (BC1) produced by Lactobacillus species which resist adhesion of fungal cells to epithelium. […] Despite the preventive strategies, if Candida colonization persist, Lactobacillus also regulate morphological transformation in Candida to obstruct their attachment to epithelium. […] The key advantage of transforming ethnopharmacological knowledge into a VVC therapy is the effective mitigation of infection along with health benefits, as phytomolecules work via multiple pathways targeting several molecules with least toxicity.

• #82

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  In the era of globalization, the concept of world health needs to be practiced where a significant consideration should be given to women health. Of many issues, the most common and under-rated is vulvovaginal candidiasis (VVC); a superficial to invasive mucosal infection of lower reproductive tract in women, primarily caused by commensal yeast Candida. […] The present review aimed to highlight the problem and concerns of women related to VVC, covering all aspects of disease development, host response, conventional drug failure, and possibilities of formulating phytomolecule based VVC therapy. […] Any dysbiosis in vaginal microbiome disturbs the harmony between residing microbes and leads to commencement of VVC. Lactobacillus is key care-taker microbe that keeps check on over growth of Candida by various means. However, Candida have evolved numerous virulence traits to overcome the governance of Lactobacillus as well as host immune system.

• #83 Vaginal yeast infection | Content for the lay public | Microbiota institute

  https://www.biocodexmicrobiotainstitute.com/en/vaginal-yeast-infection

  A vaginal yeast infection is an infection of the vulva and the vagina caused by a yeast-like fungus, in most cases Candida albicans. After bacterial vaginosis, it is the second most common infectious vaginal disease. It is important to consult a doctor to confirm diagnosis, since its symptoms are not very specific. The most common clinical symptoms are abnormal vaginal discharge (leukorrhea), genital itching, and a burning sensation accompanied by vaginal pain or irritation that can lead to dyspareunia or dysuria. […] A dysbiosis is when the vaginal ecosystem is unbalanced (due to antibiotic treatment, douching, stress, smoking, etc.): species of Lactobacillus no longer predominate and instead certain opportunistic species may proliferate. This is what happens with vaginal candidiasis: Candida yeasts normally present in the vagina and the gut proliferate abnormally and become pathogenic under specific conditions. It is estimated that 10%-30% of women contract yeast infections following antibiotic treatment.

• #84

  https://link.springer.com/article/10.1186/s12982-024-00274-y

  In the era of globalization, the concept of world health needs to be practiced where a significant consideration should be given to women health. Of many issues, the most common and under-rated is vulvovaginal candidiasis (VVC); a superficial to invasive mucosal infection of lower reproductive tract in women, primarily caused by commensal yeast Candida. […] The present review aimed to highlight the problem and concerns of women related to VVC, covering all aspects of disease development, host response, conventional drug failure, and possibilities of formulating phytomolecule based VVC therapy. […] Any dysbiosis in vaginal microbiome disturbs the harmony between residing microbes and leads to commencement of VVC. Lactobacillus is key care-taker microbe that keeps check on over growth of Candida by various means. However, Candida have evolved numerous virulence traits to overcome the governance of Lactobacillus as well as host immune system.

• #85 Vaginal yeast infection | Content for the lay public | Microbiota institute

  https://www.biocodexmicrobiotainstitute.com/en/vaginal-yeast-infection

  A vaginal yeast infection is an infection of the vulva and the vagina caused by a yeast-like fungus, in most cases Candida albicans. After bacterial vaginosis, it is the second most common infectious vaginal disease. It is important to consult a doctor to confirm diagnosis, since its symptoms are not very specific. The most common clinical symptoms are abnormal vaginal discharge (leukorrhea), genital itching, and a burning sensation accompanied by vaginal pain or irritation that can lead to dyspareunia or dysuria. […] A dysbiosis is when the vaginal ecosystem is unbalanced (due to antibiotic treatment, douching, stress, smoking, etc.): species of Lactobacillus no longer predominate and instead certain opportunistic species may proliferate. This is what happens with vaginal candidiasis: Candida yeasts normally present in the vagina and the gut proliferate abnormally and become pathogenic under specific conditions. It is estimated that 10%-30% of women contract yeast infections following antibiotic treatment.

• #86

  https://www.juno.bio/blogs/learn/is-it-really-a-yeast-infection?srsltid=AfmBOop53UbAn8sAsyhUzjEiLhyN6ijk8hXp4c4RVapFNoJWQ9yOYxo_

  This disruption can be triggered by antibiotics, diabetes, immunosuppressant medicine or changes in hormones. […] In a disrupted vaginal microbiome, protective vaginal bacteria known as Lactobacilli are depleted in number. […] Lactobacilli work to protect you from Candida growing out of control by producing lactic acid which creates an unfavourable environment for this fungus. […] So when this protective lactobacillus microbe population is disrupted, all hell can break loose.

• #87 Vaginal thrush | Hirslanden Switzerland

  https://www.hirslanden.com/en/international/disease-patterns/vaginal-thrush.html

  Vaginal thrush infections are common. Three out of every four women are affected by them at least once in their lives. They are usually yeast infections. Discharge, itching and burning in the vagina are typical symptoms. Antifungal medication, known as antimycotics, usually heals a vaginal fungal infection without difficulty in a few days. […] The mucous membrane of the vagina is usually well protected against fungal infections. Lactic acid bacteria guarantee an acidic environment in the vaginal mucous membrane. This controls the growth of fungi which are naturally present in the vagina in small amounts. If this natural protective mechanism is affected, this can lead to an infection with marked growth of the fungus. The following factors in particular can facilitate the development of a vaginal fungal infection: Antibiotic treatment, Mechanical irritation through tampons or vaginal diaphragms, Excessive intimate hygiene, Pregnancy, Lack of oestrogen, Disorders of the immune system, diabetes mellitus.

• #88 Best Probiotics For Vaginal Health: Top Probiotics To Treat

  https://www.globenewswire.com/news-release/2025/05/02/3073441/0/en/Best-Probiotics-For-Vaginal-Health-Top-Probiotics-To-Treat-Bacterial-Vaginosis-BV-pH-Balance-WOLFSON-BRANDS-UK-LIMITED.html

  The vaginal microbiome refers to the diverse population of microorganisms, predominantly bacteria, that inhabit the vaginal canal. A healthy vaginal microbiome is typically dominated by Lactobacillus species, which help protect against infections by producing lactic acid. This acid maintains the vaginal environment at an acidic pH (around 3.8 to 4.5), making it inhospitable to many harmful bacteria and yeast. […] When the balance shifts and harmful organisms like Gardnerella vaginalis or Candida albicans become dominant, it can result in conditions such as bacterial vaginosis or yeast infections. […] Maintaining a healthy vaginal microbiome is not only important for preventing discomfort and infection, but it also plays a role in fertility and pregnancy outcomes. An imbalanced microbiome has been linked to complications such as preterm birth and infertility.

• #89 Treatment of Recurrent Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0601/p3306.html

  Vulvovaginal candidiasis is considered recurrent when at least four specific episodes occur in one year or at least three episodes unrelated to antibiotic therapy occur within one year. […] Known etiologies of recurrent vulvovaginal candidiasis include treatment-resistant Candida species other than Candida albicans, frequent antibiotic therapy, contraceptive use, compromise of the immune system, sexual activity and hyperglycemia. […] Although Candida albicans is the pathogen identified in most patients with vulvovaginal candidiasis, other possible pathogens include Candida tropicalis and Candida glabrata. […] In vitro studies have shown that imidazole antifungal agents such as miconazole and clotrimazole are not as effective against non C. albicans fungi. […] Although antifungal resistance can cause treatment failure, other factors may contribute to recurrent vulvovaginal candidiasis.

• #90 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Vulvovaginal candidiasis (VVC), which is primarily caused by Candida albicans, is an infection that affects up to 75% of all reproductive-age women worldwide. Recurrent VVC (RVVC) is defined as >3 episodes per year and affects nearly 8% of women globally. At mucosal sites of the vagina, a delicate and complex balance exists between Candida spp., host immunity and local microbial communities. In fact, both immune response and microbiota composition play a central role in counteracting overgrowth of the fungus and maintaining homeostasis in the host. If this balance is perturbed, the conditions may favor C. albicans overgrowth and the yeast-to-hyphal transition, predisposing the host to VVC. […] Understanding the host- and fungus-related factors that drive VVC pathogenesis is of paramount importance for the development of adequate therapeutic interventions to combat this common genital infection. This review focuses on the latest advances in the pathogenic mechanisms implicated in the onset of VVC and also discusses novel potential strategies, with a special focus on the use of probiotics and vaginal microbiota transplantation in the treatment and/or prevention of recurrent VVC.

• #91 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Candida albicans is the most common fungal pathogen associated with opportunistic infections in humans. As a member of the human mycobiota, C. albicans generally colonizes the mucosal surfaces of most healthy individuals. Under normal physiological conditions, mucosal sites are characterized by a delicate and complex balance between Candida, host immunity and local microbiota. In fact, both the immune response and microbiota composition play a central role in counteracting overgrowth of the fungus and maintaining host homeostasis. Dysfunction of the host immune defense mechanisms or alteration in microbial composition may promote fungal virulence and, thus, increase the risk of Candida infections. […] Among the known superficial mycotic infections, vulvovaginal candidiasis is the second most common cause of vaginitis worldwide. It has been estimated that VVC affects 75% of all women at least once in their lifetime, and it is predominant in women of reproductive age. When >3 episodes of VVC occur per year, the condition is diagnosed as RVVC, which affects nearly 8% of women globally.

• #92 What is a yeast infection?

  https://flo.health/menstrual-cycle/health/symptoms-and-diseases/what-is-a-yeast-infection

  It’s also commonly seen during pregnancy and among postmenopausal people on hormone replacement therapy whose estrogen levels are being artificially raised. Another risk factor is antibiotics. […] While antibiotics are great for clearing up bacterial infections caused by bad bacteria, they can also disrupt the natural balance of good bacteria that prevents candida fungus from overgrowing. […] You are more likely to get a yeast infection if your immune system has taken a dip (for instance, if you’re very stressed or run down) or if you have diabetes that isn’t well managed. […] As many as 8% of us have recurring or chronic vaginal yeast infections, defined as four or more flare-ups a year. […] A 2018 study, which appeared in The Lancet, estimated that 138 million people worldwide are affected by recurring yeast infections every year and case numbers are increasing.

• #93 Chronic Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2001/0215/p697.html

  Three primary theories have been proposed to explain why some women develop RVVC. The intestinal reservoir theory suggests that the recurrences are a result of persistence of the organism in the gastrointestinal tract and later reinfection of the vagina. This theory is based on uncontrolled data from the late 1970s in which a concordance of almost 100 percent was observed between rectal and vaginal cultures in women with RVVC. However, subsequent studies suggest that women with RVVC harbor yeast species in the gastrointestinal tract as often as control subjects. Furthermore, in women who experienced a recurrence after taking prolonged courses of systemic ketoconazole for RVVC and who experienced a recurrence following cessation of therapy, the recurrence often occurred in the presence of negative rectal cultures for yeast. The results from these two studies make it less likely that the intestinal reservoir theory satisfactorily explains the cause of RVVC.

• #94 Chronic Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2001/0215/p697.html

  The vaginal relapse theory maintains that, even after treatment, some women remain colonized with small numbers of yeast. Given the proper conditions, the yeast increase in number and cause a new clinical episode of vulvovaginal candidiasis. Support for this theory includes longitudinal studies that document persistence of the same strain of C. albicans causing repeated infections in the same women over several years of observation and after repeated treatment courses. According to this view, repeated episodes are not the result of reinfections, but rather caused by host factors. Although obvious exogenous factors such as diabetes, use of antibiotics and systemic corticosteroids, and infection with human immunodeficiency virus may play a role in RVVC, no obvious explanation exists for most recurrences. Much research is currently focused on possible abnormalities of the local vaginal immune response to yeast and their role in laying the groundwork for the patient’s next infection.

• #95 Vaginal yeast infection – Wikipedia

  https://en.wikipedia.org/wiki/Vaginal_yeast_infection

  Vaginal yeast infections are due to excessive growth of Candida. […] The causes of excessive Candida growth are not well understood, but some predisposing factors have been identified. […] There is some support for the theory that RVVC results from an especially intense inflammatory reaction to colonization. Candida antigens can be presented to antigen-presenting cells, which may trigger cytokine production and activate lymphocytes and neutrophils that then cause inflammation and edema. […] PRA1 gene (pH-regulated antigen) is strongly up-regulated during vaginal infections, which correlates with inflammation.

• #96 Vulvovaginal Candidiasis – STI Treatment Guidelines

  https://www.cdc.gov/std/treatment-guidelines/candidiasis.htm

  Vaginal culture or PCR should be obtained from women with complicated VVC to confirm clinical diagnosis and identify nonalbicans Candida. […] The pathogenesis of recurrent VVC is poorly understood, and the majority of women with recurrent VVC have no apparent predisposing or underlying conditions. […] C. glabrata and other nonalbicans Candida species are observed in 10%20% of women with recurrent VVC. […] Because C. albicans azole resistance is becoming more common, susceptibility tests, if available, should be obtained among symptomatic patients who remain culture positive despite maintenance therapy. […] Women with underlying immunodeficiency, those with poorly controlled diabetes or other immunocompromising conditions (e.g., HIV), and those receiving immunosuppression therapy (e.g., corticosteroid treatment) might not respond as well to short-term therapies.

• #97 Treatment of Recurrent Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0601/p3306.html

  Vulvovaginal candidiasis is considered recurrent when at least four specific episodes occur in one year or at least three episodes unrelated to antibiotic therapy occur within one year. […] Known etiologies of recurrent vulvovaginal candidiasis include treatment-resistant Candida species other than Candida albicans, frequent antibiotic therapy, contraceptive use, compromise of the immune system, sexual activity and hyperglycemia. […] Although Candida albicans is the pathogen identified in most patients with vulvovaginal candidiasis, other possible pathogens include Candida tropicalis and Candida glabrata. […] In vitro studies have shown that imidazole antifungal agents such as miconazole and clotrimazole are not as effective against non C. albicans fungi. […] Although antifungal resistance can cause treatment failure, other factors may contribute to recurrent vulvovaginal candidiasis.

• #98 Vulvovaginitis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2188931-overview

  The role of sexual transmission in recurrent infection remains unresolved. Most studies do not support treatment of sexual partners. […] Recurrences may be caused by other species of Candida that are not equally susceptible to the usual first-line treatments. In vitro studies have shown that imidazole antifungal agents, such as miconazole and clotrimazole, are not as effective against nonC albicans fungi. C tropicalis and C glabrata are 10 times less sensitive to miconazole than is C albicans. Appropriate fungal cultures may be taken to identify the species. Treatment entails longer courses of antimycotic therapy (10-14 days), regardless of the route of administration.

• #99 Treatment of Recurrent Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0601/p3306.html

  Vulvovaginal candidiasis is considered recurrent when at least four specific episodes occur in one year or at least three episodes unrelated to antibiotic therapy occur within one year. […] Known etiologies of recurrent vulvovaginal candidiasis include treatment-resistant Candida species other than Candida albicans, frequent antibiotic therapy, contraceptive use, compromise of the immune system, sexual activity and hyperglycemia. […] Although Candida albicans is the pathogen identified in most patients with vulvovaginal candidiasis, other possible pathogens include Candida tropicalis and Candida glabrata. […] In vitro studies have shown that imidazole antifungal agents such as miconazole and clotrimazole are not as effective against non C. albicans fungi. […] Although antifungal resistance can cause treatment failure, other factors may contribute to recurrent vulvovaginal candidiasis.

• #100 Vulvovaginitis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2188931-overview

  Vulvovaginal candidiasis can be an acute, chronic, recurrent, or persistent condition that can involve the vulva, vagina, and adjacent crural areas. The specific causative agent belongs to the genus Candida. These organisms are found in almost all humans and many animals. An estimated 10-50% of reproductive-aged American women are considered opportunistic carriers. […] The species C albicans is identified approximately 85-90% of the time. However, an increased frequency of other Candida species, such as C glabrata, C tropicalis, and C krusei, has been reported. The emergence of these other Candida species may possibly be due to widespread use of over-the-counter drugs, long-term use of suppressive azoles, and the use of frequent short courses of antifungal drugs. […] Any host factor that affects the vaginal environment or vaginal secretions can play a role in the initiation of Candida vulvovaginitis. Pregnancy is one of the most common predisposing factors. Studies have demonstrated that up to one third of pregnant women worldwide on any day can be affected. The high levels of reproductive hormones and an increase in the vaginal environments glycogen content create a favorable environment for Candida species, providing an abundant source of carbon for candidal growth, germination, and adherence.

• #101 Treatment of Recurrent Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0601/p3306.html

  Vulvovaginal candidiasis is considered recurrent when at least four specific episodes occur in one year or at least three episodes unrelated to antibiotic therapy occur within one year. […] Known etiologies of recurrent vulvovaginal candidiasis include treatment-resistant Candida species other than Candida albicans, frequent antibiotic therapy, contraceptive use, compromise of the immune system, sexual activity and hyperglycemia. […] Although Candida albicans is the pathogen identified in most patients with vulvovaginal candidiasis, other possible pathogens include Candida tropicalis and Candida glabrata. […] In vitro studies have shown that imidazole antifungal agents such as miconazole and clotrimazole are not as effective against non C. albicans fungi. […] Although antifungal resistance can cause treatment failure, other factors may contribute to recurrent vulvovaginal candidiasis.

• #102 Treatment of Recurrent Vulvovaginal Candidiasis | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0601/p3306.html

  Antibiotics are often implicated as a cause of recurrent vulvovaginal candidiasis. Frequent antibiotic use decreases protective vaginal flora and allows colonization by Candida species. […] Diabetes mellitus is often considered a predisposing factor for recurrent vulvovaginal candidiasis. Hyperglycemia enhances the ability of C. albicans to bind to vaginal epithelial cells. […] Contraceptive methods may also promote recurrences of vulvovaginal candidiasis. Use of spermicidal jellies and creams increases susceptibility to infection by altering the vaginal flora and increasing the adhesion of Candida organisms. […] Women who are prone to recurrent vulvovaginal candidiasis may have deficient cell-mediated immunity. […] Mechanical factors may also be important. Perspiration associated with tightly fitted clothes or poorly ventilated underwear increases local temperature and moisture.

• #103 Vulvovaginal Candidiasis – STI Treatment Guidelines

  https://www.cdc.gov/std/treatment-guidelines/candidiasis.htm

  Vaginal culture or PCR should be obtained from women with complicated VVC to confirm clinical diagnosis and identify nonalbicans Candida. […] The pathogenesis of recurrent VVC is poorly understood, and the majority of women with recurrent VVC have no apparent predisposing or underlying conditions. […] C. glabrata and other nonalbicans Candida species are observed in 10%20% of women with recurrent VVC. […] Because C. albicans azole resistance is becoming more common, susceptibility tests, if available, should be obtained among symptomatic patients who remain culture positive despite maintenance therapy. […] Women with underlying immunodeficiency, those with poorly controlled diabetes or other immunocompromising conditions (e.g., HIV), and those receiving immunosuppression therapy (e.g., corticosteroid treatment) might not respond as well to short-term therapies.

• #104 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #105 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  These initial signals, coupled with secondary amplification of immune effectors by recruited PMNs, contribute to symptomatic infection and characteristic immunopathology. […] Cumulatively, these studies confirm an important role for the morphogenetic response in vaginitis immunopathology. […] Vaginitis is a complex disease, requiring a perfect storm scenario to initiate infection. Estrogen production, microbiota disruption, pH modification, fungal virulence factor expression, and exuberant innate immune activity must synchronize to culminate in symptomatic infection. […] Current research has elucidated a major paradigm shift in the philosophy of Candida vaginitis pathogenesis, highlighting the role of the host innate immune response in disease immunopathology.

• #106 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Accumulating evidence has highlighted the critical role of the NLRP3 inflammasome in the molecular mechanism behind the immunopathogenesis of VVC. The activation of the inflammasome, both in the vaginal epithelium as well as in innate immune cells, is involved in host defense mechanisms against Candida infection, as the activated inflammasome mounts an effective immune response and, thus, limits fungal burden and inflammation. […] These findings provide evidence that NLRP3 inflammasome hyperactivation is a distinctive hallmark of VVC. […] In conclusion, it is clear that vaginal health is dependent on a complex and functional equilibrium between the host immune response, vaginal microbiota and C. albicans. Numerous factors that contribute to the variability of individuals and their microbiota, other than genetic and phenotypic variation among clinical isolates of C. albicans, further increase this immense complexity. Specifically, host-related factors, such as a dysregulated immune response triggered by C. albicans or an altered vaginal microbiota composition, may substantially contribute to individual variability, predisposing women to VVC.

• #107 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. […] It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. […] These exciting new studies highlight the immunopathological response as a crucial element of vaginitis pathogenesis. […] C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen.

• #108 Candida Vaginitis: When Opportunism Knocks, the Host Responds | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003965

  Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. […] It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. […] These exciting new studies highlight the immunopathological response as a crucial element of vaginitis pathogenesis. […] C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen.

• #109 The Interplay between Candida albicans, Vaginal Mucosa, Host Immunity and Resident Microbiota in Health and Disease: An Overview and Future Perspectives

  https://www.mdpi.com/2076-2607/11/5/1211

  Vulvovaginal candidiasis (VVC), which is primarily caused by Candida albicans, is an infection that affects up to 75% of all reproductive-age women worldwide. Recurrent VVC (RVVC) is defined as >3 episodes per year and affects nearly 8% of women globally. At mucosal sites of the vagina, a delicate and complex balance exists between Candida spp., host immunity and local microbial communities. In fact, both immune response and microbiota composition play a central role in counteracting overgrowth of the fungus and maintaining homeostasis in the host. If this balance is perturbed, the conditions may favor C. albicans overgrowth and the yeast-to-hyphal transition, predisposing the host to VVC. […] Understanding the host- and fungus-related factors that drive VVC pathogenesis is of paramount importance for the development of adequate therapeutic interventions to combat this common genital infection. This review focuses on the latest advances in the pathogenic mechanisms implicated in the onset of VVC and also discusses novel potential strategies, with a special focus on the use of probiotics and vaginal microbiota transplantation in the treatment and/or prevention of recurrent VVC.

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