ROLE OF GENOTYPING FEATURES IN THE DEVELOPMENT OF RECURRENT VULVOVAGINAL CANDIDIASIS AND THERAPY TACTICS
https://doi.org/10.21518/2079-701X-2017-13-172-179
Abstract
Relevance: According to the literature, Vulvovaginal candidiasis (VVC) is diagnosed in 75% of women during life, and in 5-8% of women its recurrent course is developed (four or more episodes of exacerbation during 12 months). Recurrent vulvovaginal candidiasis (RVVC) is often observed in the presence of development risk factors, but often the recurrent course of the disease is developing among women without obvious risk factors. The literature shows that the development of a recurrent fungal infection is often caused by a violation of the local immune response, which is associated with the polymorphism of the immune system genes.
Objective of the study: To develop criteria for forecasting the recurrent current volvovaginal candidiasis to improve the effectiveness of therapy.
Study results: As a result of our study, it has been found that C. albicans remains the leading fungal species in the acute and recurrent VVC, but women with the recurrent course of VVC the prevalance of non-C. Albicans fungi is reliably higher than the patients with acute VVC (P = 0.037). Also, the sensitivity data obtained shows that most of the studied yeast fungi (97.5%) are sensitive to fluconazole. However, only in 10.5% of the non-C.Albicans strains resistance was detected. The determination of genetic predisposition to develop the recurrent current VVC, using the prediction model derived from our study, revealed that 77.8% of women with a genetic predisposition are developing a relapse of VVC. In view of these results and based on international recommendations (CDC, WHO, 2011) that it is appropriate to indicate the anti-recurring antifungal treatment to RVVC, it can be concluded that for patients with genetic predisposition to the development of recurrent VVC it is advisable to indicate the anti-recurrent antifungal therapy.
About the Authors
S. M. PogosyanRussian Federation
MD,
Moscow
E. A. Mezhevitinova
Russian Federation
PhD in medicine,
Moscow
A. E. Donnikov
Russian Federation
PhD in biology,
Moscow
V. V. Muravyova
Russian Federation
PhD in medicine,
Moscow
P. R. Abakarova
Russian Federation
Moscow
Y. S. Khlebkova
Russian Federation
Moscow
References
1. Sobel JD. Vulvovaginal candidosis. Lancet 369, 2007: 1961–1971.
2. Sobel JD. et al. Vulvovaginal candidiasis: Epidemiologic, diagnostic, and therapeutic considerations. Am. J. Obstet. Gynecol. 178, 203–211 (1998).
3. Foxman B, Muraglia R, Dietz J-P, Sobel JD. & Wagner J. Prevalence of recurrent vulvovaginal candidiasis in 5 European countries and the United States: results from an internet panel survey. J. Low. Genit. Tract Dis. 17, 340–5 (2013).
4. Sobel JD. et al. Vulvovaginal candidiasis: Epidemiologic, diagnostic, and therapeutic considerations. American Journal of Obstetrics and Gynecology 178, 203–211 (1998).
5. Beikert FC, Le MT, Koeninger A, Technau K. & Clad A. Recurrent vulvovaginal candidosis: Focus on the vulva. Mycoses 54, (2011).
6. Beigi RH, Meyn LA, Moore DM, Krohn MA & Hillier SL. Vaginal yeast colonization in nonpregnant women: a longitudinal study. Obstet. Gynecol. 104, 926–930 (2004).
7. Borges S, Silva J & Teixeira P. The role of lactobacilli and probiotics in maintaining vaginal health. Arch. Gynecol. Obstet. 289, 479–489 (2014).
8. Calderon L, Williams R, Martinez M, Clemons KV & Stevens DА. Genetic susceptibility to vaginal candidiasis. Med. Mycol. 41, 143–7 (2003).
9. Jaeger M, Plantinga TS, Joosten LA. B, Kullberg BJ & Netea MG. Genetic basis for recurrent vulvo-vaginal candidiasis. Curr. Infect. Dis. Rep. 15, 136–142 (2013).
10. Smeekens S.P., van de Veerdonk F.L., Kullberg B.J. & Netea M.G. Genetic susceptibility to Candida infections. EMBO Molecular Medicine 5, 805–813 (2013).
11. Rosentul D. et al. Polymorphism in innate immunity genes and susceptibility to recurrent vulvovaginal candidiasis. Journal de Mycologie Medicale 19, 191–196 (2009).
12. Puel A. et al. Inborn errors of human IL-17 immunity underlie chronic mucocutaneous candidiasis. Current Opinion in Allergy and Clinical Immunology 12, 616–622 (2012).
13. Babula O., Lazdane G., Kroica J., Ledger W.J. & Witkin S.S. Relation between recurrent vulvovaginal candidiasis, vaginal concentrations of mannose-binding lectin, and a mannose-binding lectin gene polymorphism in Latvian women. Clin. Infect. Dis. 37, 733–737 (2003).
14. Babula O. et al. Frequency of interleukin-4 (IL-4) -589 gene polymorphism and vaginal concentrations of IL-4, nitric oxide, and mannose-binding lectin in women with recurrent vulvovaginal candidiasis. Clin. Infect. Dis. 40, 1258–1262 (2005).
15. De Luca A. et al. IL-22 and IDO1 Affect Immunity and Tolerance to Murine and Human Vaginal Candidiasis. PLoS Pathog. 9, (2013).
16. Donders G.G.G, Babula O, Bellen G, Linhares IM & Witkin SS. Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis. BJOG An Int. J. Obstet. Gynaecol. 115, 1225– 1231 (2008).
17. Liu F, Liao Q. & Liu Z. Mannose-binding lectin and vulvovaginal candidiasis. Int. J. Gynaecol. Obstet. 92, 43–47 (2006).
18. Rosentul DC. et al. Gene polymorphisms in pattern recognition receptors and susceptibility to idiopathic recurrent vulvovaginal candidiasis. Front. Microbiol. 5, 483 (2014).
19. Nahum A, Dadi H, Bates A. & Roifman C. M. The biological significance of TLR3 variant, L412F, in conferring susceptibility to cutaneous candidiasis, CMV and autoimmunity. Autoimmunity Reviews 11, 341–347 (2012).
20. Plantinga T. S. et al. Toll-like receptor 1 polymorphisms increase susceptibility to candidemia. J. Infect. Dis. 205, 934–943 (2012).
21. Woehrle T. et al. Pathogen specific cytokine release reveals an effect of TLR2 Arg753Gln during Candida sepsis in humans. Cytokine 41, 322–329 (2008).
22. Ouederni M. et al. Clinical features of candidiasis in patients with inherited interleukin 12 Receptor ß1 Deficiency. Clin. Infect. Dis. 58, 204–213 (2014).
23. Ling Y. et al. Inherited IL-17RC deficiency in patients with chronic mucocutaneous candidiasis. J. Exp. Med. 212, 619–31 (2015).
24. Terças AL, Marques SG, Moffa EB, Alves MB, de Azevedo CM, Siqueira WL, M.C. No Title Antifungal Drug Susceptibility of Candida Species Isolated from HIV-Positive Patients Recruited at a Public Hospital in São Luís, Maranhão, Brazil. Front Microbiol. 2017 Mar 2;8298. doi 10.3389/fmicb.2017.00298. eCollection (2017). at .
25. PubMed, C. here to view optimized website for mobile devices J. is indexed with et al. No Title Identification and Antifungal susceptibility testing of Candida species: A Comparison of Vitek-2 system with conventional and molecular methods. 8, 139– 146 (2016).
26. Gharaghani M, Rezaei-Matehkolaei A, Zarei Mahmoudabadi A, K.B. No Title The Frequency, Antifungal Susceptibility and Enzymatic Profiles of Candida Species Isolated from Neutropenic Patients. Jundishapur J Microbiol (2016). at .
27. For U. ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists, Number 72, May 2006: Vaginitis. Obstet. Gynecol. 107, 1195–1206 (2006).
28. Mendling W. Guideline: Vulvovaginal candidosis (AWMF 015/072), S2k (excluding chronic mucocutaneous candidosis). Mycoses 58, 1–15 (2015).
29. Mahmoudi Rad M., Zafarghandi A.S., Amel Zabihi M., Tavallaee M. & Mirdamadi Y. Identification of candida species associated with vulvovaginal candidiasis by multiplex PCR. Infect. Dis. Obstet. Gynecol. 2012, (2012).
30. Holland J., Young M.L., Lee O. & C-A Chen, S. Vulvovaginal carriage of yeasts other than Candida albicans. Sex. Transm. Infect. 79, 249– 50 (2003).
31. Tortorano A.M. et al. Epidemiology of candidaemia in Europe: Results of 28-Month European Confederation of Medical Mycology (ECMM) hospital-based surveillance study. European Journal of Clinical Microbiology and Infectious Diseases 23, 317–322 (2004).
32. Chapman B, Slavin M, Marriott D, Halliday C, Kidd S, Arthur I, Bak N, Heath CH, Kennedy K, Morrissey CO, Sorrell TC, van Hal S, Keighley C, Goeman E, Underwood N, Hajkowicz K, Hofmeyr A, Leung M, Macesic N, Botes J, Blyth C. Australian and New Zealand Mycoses Interest Group. No Title Changing epidemiology of candidaemia in Australia. J Antimicrob Chemother. 2017 Apr 1;72(4)1103-1108. doi 10.1093/jac/dkw422. (2017). at .
33. Rosentul D. et al. Polymorphism in innate immunity genes and susceptibility to recurrent vulvovaginal candidiasis. J. Mycol. Med. 19, 191– 196 (2009).
34. Wojitani M.D. K.H, De Aguiar L.M, Baracat E.C. & Linhares I.M. Association between mannosebinding lectin and interleukin-1 receptor antagonist gene polymorphisms and recurrent vulvovaginal candidiasis. Arch. Gynecol. Obstet. 285, 149–153 (2012).
35. Giraldo P.C. et al. Mannose-binding lectin gene polymorphism, vulvovaginal candidiasis, and bacterial vaginosis. Obstet.Gynecol. 109, 1123– 1128 (2007).
36. Ferwerda B. et al. Human dectin-1 deficiency and mucocutaneous fungal infections. N Engl J Med 361, 1760–1767 (2009).
37. Plantinga T.S. et al. Early stop polymorphism in human DECTIN-1 is associated with increased candida colonization in hematopoietic stem cell transplant recipients. Clin. Infect. Dis. 49, 724–732 (2009).
38. Glocker E.-O. et al. A Homozygous CARD9 Mutation in a Family with Susceptibility to Fungal Infections. N. Engl. J. Med. 361, 1727– 1735 (2009).
Review
For citations:
Pogosyan SM, Mezhevitinova EA, Donnikov AE, Muravyova VV, Abakarova PR, Khlebkova YS. ROLE OF GENOTYPING FEATURES IN THE DEVELOPMENT OF RECURRENT VULVOVAGINAL CANDIDIASIS AND THERAPY TACTICS. Meditsinskiy sovet = Medical Council. 2017;(13):172-179. (In Russ.) https://doi.org/10.21518/2079-701X-2017-13-172-179