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Immunohistochemical study of in vivo and in vitro IgA coating of candida species in vulvovaginal candidiasis.
  1. K Böhler,
  2. H Klade,
  3. C Poitschek,
  4. A Reinthaller
  1. Department of Dermatology, II University of Vienna, Medical School, Austria.


    OBJECTIVE--To evaluate whether quantitative or qualitative IgA deficiencies in cervicovaginal secretions can be identified in patients with recurrent vulvovaginal candidiasis. DESIGN--Prospective and controlled study. SETTING--Department of Dermatology, University of Vienna. SUBJECTS--30 patients with symptomatic and recurrent vulvovaginal candidiasis at the time of their presentation. 30 healthy women as a control group. INTERVENTION--Blood samples were drawn for measurement of serum IgA levels. Smears of the cervix and vagina were taken for direct microscopy and microbiological culture. Lavage of the vagina and ectocervix was performed with sterile saline solution for measurement of cervicovaginal IgA levels. MAIN OUTCOME MEASURES--IgA levels of serum and cervicovaginal secretion evaluated by Single Radial Immunodiffusion. IgA labelling was demonstrated on fungal elements in vaginal smears and subcultured blastospores after incubation with vaginal secretions by immunohistochemistry. RESULTS--We could not find any significant difference of IgA levels in serum and cervicovaginal secretions between the symptomatic group and healthy controls (p value for serum = 0.5796, p value for secretion = 0.2381). In vaginal smears yeasts revealed IgA coating on their surfaces, whereas three of the 61 subcultures were negative. Negative subcultures were assigned to three patients with recurrent candidiasis. No correlation was found between IgA levels of cervicovaginal secretions and staining intensity of subcultured blastospores after incubation with vaginal secretions (r = -0.0578). IgA levels of serum and vaginal secretion showed no correlation (r = -0.00012). CONCLUSION--Recurrent vulvovaginal candidiasis cannot be attributed to IgA deficiency. In some cases an IgA coating defect of yeasts might be involved. In addition inactivation of the IgA molecule by candida proteases might be of pathogenetic importance.

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