Das Verhalten von Spro�pilzen am nicht verhornenden Plattenepithel

Schnell, J. D.; Voigt, W. H.

doi:10.1007/bf00668025

Cited by 9 publications

(3 citation statements)

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“…Auler et al [4] and Chassot et al [21] describe a biofilm phenomenon involving C. albicans on intrauterine pessaries. In systematic examinations of women with vulvovaginal candidosis in Berlin and China using a clear definition of biofilm, no Candida biofilms were found in numerous vaginal tissue samples; the well-known phenomenon that Candida pseudohyphae penetrate vaginal tissue 8-10 cell layers deep 126 and that numerous other bacteria in abnormal vaginal flora enable penetration was recently demonstrated in vulvovaginal candidosis using fluorescence in situ hybridisation. 139 The step between colonisation and vaginitis is not yet fully understood and highlights the importance of host factors.…”

Section: Virulence Factors Of C Albicansmentioning

confidence: 99%

Guideline: Vulvovaginal Candidosis (AWMF 015/072), S2k (excluding chronic mucocutaneous candidosis)

Mendling

2015

Mycoses

102

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The oestrogenised vagina is colonised by Candida species in at least 20% of women; in late pregnancy and in immunosuppressed patients, this increases to at least 30%. In most cases, Candida albicans is involved. Host factors, particularly local defence mechanisms, gene polymorphisms, allergies, serum glucose levels, antibiotics, psycho-social stress and oestrogens influence the risk of candidal vulvovaginitis. Non-albicans species, particularly Candida glabrata, and in rare cases also Saccharomyces cerevisiae, cause less than 10% of all cases of vulvovaginitis with some regional variation; these are generally associated with milder signs and symptoms than normally seen with a C. albicans-associated vaginitis. Typical symptoms include premenstrual itching, burning, redness and odourless discharge. Although itching and redness of the introitus and vagina are typical symptoms, only 35-40% of women reporting genital itching in fact suffer from vulvovaginal candidosis. Medical history, clinical examination and microscopic examination of vaginal content using 400× optical magnification, or preferably phase contrast microscopy, are essential for diagnosis. In clinically and microscopically unclear cases and in chronically recurring cases, a fungal culture for pathogen determination should be performed. In the event of non-C. albicans species, the minimum inhibitory concentration (MIC) should also be determined. Chronic mucocutaneous candidosis, a rarer disorder which can occur in both sexes, has other causes and requires different diagnostic and treatment measures. Treatment with all antimycotic agents on the market (polyenes such as nystatin; imidazoles such as clotrimazole; and many others including ciclopirox olamine) is easy to administer in acute cases and is successful in more than 80% of cases. All vaginal preparations of polyenes, imidazoles and ciclopirox olamine and oral triazoles (fluconazole, itraconazole) are equally effective (Table ); however, oral triazoles should not be administered during pregnancy according to the manufacturers. C. glabrata is not sufficiently sensitive to the usual dosages of antimycotic agents approved for gynaecological use. In other countries, vaginal suppositories of boric acid (600 mg, 1-2 times daily for 14 days) or flucytosine are recommended. Boric acid treatment is not allowed in Germany and flucytosine is not available. Eight hundred-milligram oral fluconazole per day for 2-3 weeks is therefore recommended in Germany. Due to the clinical persistence of C. glabrata despite treatment with high-dose fluconazole, oral posaconazole and, more recently, echinocandins such as micafungin are under discussion; echinocandins are very expensive, are not approved for this indication and are not supported by clinical evidence of their efficacy. In cases of vulvovaginal candidosis, resistance to C. albicans does not play a significant role in the use of polyenes or azoles. Candida krusei is resistant to the triazoles, fluconazole and itraconazole. For this reason, local imidazole, ciclopi...

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Section: Virulence Factors Of C Albicansmentioning

confidence: 99%

Guideline: Vulvovaginal Candidosis (AWMF 015/072), S2k (excluding chronic mucocutaneous candidosis)

Mendling

2015

Mycoses

102

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“…The ability of yeast cells to penetrate human cells in the absence of germ tubes has been documented previously (36,37). Although yeasts may initiate the metastatic process through the dissolution of the endothelial cell barrier, it is nevertheless likely that germ tube formation potentiates the invasive process (D. Rotrosen, J. E. Edwards, Jr., J. Moore, J. Adler, A. H. Cohen, and I.…”

Section: Discussionmentioning

confidence: 91%

Adherence and penetration of vascular endothelium by Candida yeasts

Klotz¹,

Drutz²,

Harrison³

et al. 1983

Infect Immun

133

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Metastatic infection after hematogenous dissemination of Candida species is presumably dependent on the fungus traversing the vascular endothelium. An in vitro model of the earliest events of metastatic Candida infection was developed with whole vascular strips. Freshly obtained porcine blood vessels were secured in a perforated Lucite template that allowed the application of yeasts directly to the endothelial surface. Multiple wells allowed experimental and control observations on the same vascular segments. Adherence to endothelium was greatest with Candida albicans and Candida tropicalis, less with Candida krulsei, and least with Candida parapsilosis, Candida pseudotropicalis, and Torullopsis glabrata. This hierarchy of adherence parallels that in other in vitro systems employing mucosal epithelial. cells or fibrin-platelet matrixes and reflects the known virulence of the respective species and their potential for hematogenous dissemination. C. albicans and C. tropicalis yeasts that adhered were capable of directly traversing the endothelial surface before the production of germ tubes. Heat or Formalin-killed yeasts and viridans group streptococci, although adherent, were incapable of vascular penetration, a process presumably attributable to enzymatic digestion of host tissue. Loss of integrity of penetrated endothelial tissue was verified by loss of dye exclusion, lactic dehydrogenase release, and ultramicroscopic changes. These two steps, adherence and penetration, provide direct insight into the earliest events in hematogenous Candida species dissemination and suggest that C. albicans and C. tropicalis yeasts are capable of initiating tissue invasion before germ tubes have had the opportunity to form and participate in the invasive process.

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“…Auler et al [4] and Chassot et al [21] describe a biofilm phenomenon involving C. albicans on intrauterine pessaries. In systematic examinations of women with vulvovaginal candidosis in Berlin and China using a clear definition of biofilm, non-Candida biofilms were found in numerous vaginal tissue samples; the well-known phenomenon that Candida pseudohyphae penetrate vaginal tissue 8 to 10 cell layers deep [126] and that numerous other bacteria in abnormal vaginal flora enable penetration was recently demonstrated in vulvovaginal candidosis using fluorescence in situ hybridization (FISH) [139]. Fig.…”

Section: Virulence Factors Of Candida Albicansmentioning

confidence: 99%

Vulvovaginal Candidosis (excluding chronic mucocutaneous candidosis). Guideline of the German Society of Gynecology and Obstetrics (AWMF Registry No. 015/072, S2k Level, December 2013)

Mendling

Friese

Mylonas

et al. 2015

Geburtshilfe Frauenheilkd

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The estrogenized vagina is colonized by Candida species in at least 20 % of women; in late pregnancy and in immunosuppressed patients this increases to at least 30%. In most cases Candida albicans is involved. Host factors, particularly local defense mechanisms, gene polymorphisms, allergies, serum glucose levels, antibiotics, psycho-social stress and estrogens influence the risk of candidal vulvovaginitis. Non-albicans species, particularly Candida glabrata, and in rare cases also Saccharomyces cerevisiae, cause less than 10 % of all cases of vulvovaginitis with some regional variation; these are generally associated with milder signs and symptoms than normally seen with a Candida albicans-associated vaginitis. Typical symptoms include premenstrual itching, burning, redness and odorless discharge. Although itching and redness of the introitus and vagina are typical symptoms, only 35-40 % of women reporting genital itching in fact suffer from vulvovaginal candidosis.

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Das Verhalten von Spro�pilzen am nicht verhornenden Plattenepithel

Cited by 9 publications

References 1 publication

Guideline: Vulvovaginal Candidosis (AWMF 015/072), S2k (excluding chronic mucocutaneous candidosis)

Guideline: Vulvovaginal Candidosis (AWMF 015/072), S2k (excluding chronic mucocutaneous candidosis)

Adherence and penetration of vascular endothelium by Candida yeasts

Vulvovaginal Candidosis (excluding chronic mucocutaneous candidosis). Guideline of the German Society of Gynecology and Obstetrics (AWMF Registry No. 015/072, S2k Level, December 2013)

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