VVC in pregnancy

Understanding VVC during pregnancy assumes increasing importance, authors wrote, because recent research links the condition with suboptimal outcomes including low birth weight, preterm birth, spontaneous abortion, and stillbirth.^1-4 However, normal changes that occur in the genitourinary tract during pregnancy make VVC more common—and harder to treat—in pregnant women.

Due to geographic, ethnic, and socioeconomic factors, as well as variable testing techniques, rates of VVC and/or vaginal Candida colonization during pregnancy range from 90.3% in Kenya⁵ to 10% in the US.6 Although C. albicans is by far the most common culprit worldwide, research from Asia and Africa highlights notable increases in non-albicans species, most notably C. glabrata, during recent decades.^7,8

Physiologic factors clearly associated with VVC risk during pregnancy include reduced vaginal pH, elevated stress, and a weakened immune system. Increased levels of progesterone and estrogen also elevate VVC risk during pregnancy. Both hormones allow easier Candida implantation in the vagina, and they exert additional effects that support fungal overgrowth. High estrogen levels have been shown to suppress cell-mediated immunity,⁹ while progesterone shifts the balance of Th1 and Th2 responses toward the latter.¹⁰

“Predisposing host factors, such as HIV infection and other immunosuppressive diseases, play the leading role in the development of VVC,” review authors wrote. Additional clinical factors that appear to influence VVC risk during pregnancy range from past episodes of candidosis to behavioral variables such as use of oral contraceptives and frequent antibiotics.

Among socioeconomic factors, various studies suggest that education and employment status may influence VVC prevalence during pregnancy.^11,12 Differences in prevalence rates among illiterate and educated women may stem from improvement in personal hygiene and/or economic advancement resulting from education.¹²

In many respects, however, researchers found it difficult to draw firm conclusions. For example, authors said that due to contradictory evidence, the impact of intrauterine devices, tight and synthetic clothing, and dietary habits on VVC risk during pregnancy remains unclear.

Similarly, although most studies reviewed support increasing risk with length of gestation, research from Nepal, India, and Yemen reflects maximum risk in the first or second trimester.^8,12,13 Mechanistically, increased estrogen and corticoid levels may account for elevated VVC risk in the third trimester. Some research implicates additional issues such as repetitive vaginal and pelvic examinations and “failure to wash undies and pelvic areas due to fatigue or the tummy size of the pregnant mothers” during the third trimester.¹⁴

Because VVC is usually treated by observing clinical symptoms, authors concluded, “the data on the prevalence rate during pregnancy is not satisfying. Also, the role of associated factors with VVC is conflicting.” To more accurately assess real-world conditions, they recommend conducting additional research, especially in third-world countries.

REFERENCES:

1. Disha T, Haque F. Prevalence and risk factors of vulvovaginal candidosis during pregnancy: a review. Infect Dis Obstet Gynecol. 2022;2022:6195712. Published 2022 Jul 20. doi:10.1155/2022/6195712

2. Mølgaard-Nielsen D, Svanström H, Melbye M, Hviid A, Pasternak B. Association between use of oral fluconazole during pregnancy and risk of spontaneous abortion and stillbirth. JAMA. 2016;315(1):58-67. doi:10.1001/jama.2015.17844

3. Bliss JM, Basavegowda KP, Watson WJ, Sheikh AU, Ryan RM. Vertical and horizontal transmission of Candida albicans in very low birth weight infants using DNA fingerprinting techniques. Pediatr Infect Dis J. 2008;27(3):231-235. doi:10.1097/INF.0b013e31815bb69d

4. Roberts CL, Rickard K, Kotsiou G, Morris JM. Treatment of asymptomatic vaginal candidiasis in pregnancy to prevent preterm birth: an open-label pilot randomized controlled trial. BMC Pregnancy Childbirth. 2011;11:18. doi:10.1186/1471-2393-11-18

5. Nelson M, Wanjiru W, Margaret M. Prevalence of vaginal candidiasis and determination of the occurrence of Candida species in pregnant women attending the antenatal clinic of Thika District Hospital, Kenya. Open J Med Microbiol. 2013;3:264-272. doi: 10.4236/ojmm.2013.34040.

6. Cotch MF, Hillier SL, Gibbs RS, Eschenbach DA. Epidemiology and outcomes associated with moderate to heavy Candida colonization during pregnancy. Vaginal Infections and Prematurity Study Group. Am J Obstet Gynecol. 1998;178(2):374-380. doi:10.1016/s0002-9378(98)80028-8

7. Babic M, Hukic M. Candida albicans and non-albicans species as etiological agent of vaginitis in pregnant and non-pregnant women. Bosn J Basic Med Sci. 2010;10(1):89-97. doi:10.17305/bjbms.2010.2744

8. Yadav K, Prakash S. Prevalence of vulvovaginal candidiasis in pregnancy. Global J Med Sci. 2016;4:108-116.

9. Hagen C, Froland A. Depressed lymphocyte response to P.H.A. in women taking oral contraceptives. Lancet. 1972;1(7761):1185. doi:10.1016/s0140-6736(72)91415-8

10. Aguin TJ, Sobel JD. Vulvovaginal candidiasis in pregnancy. Curr Infect Dis Rep. 2015;17(6):462. doi:10.1007/s11908-015-0462-0

11. Toua V, Djaouda M, Gaké B, Menye DE, Christie E. Prevalence of vulvovaginal candidiasis amongst pregnant women in Maroua (Cameroon) and the sensitivity of Candida albicans to extracts of six locally used antifungal plants. Int Res J Microbiol. 2013;4: 89-97.

12. Al-Shamahy H, Al-Rukeimi A, Naser S. Prevalence and risk factors associated with vulvovaginal candidiasis during pregnancy in Sana’a, Yemen. Univers J Pharm Res. 2020;5:1-5. doi: 10.22270/ujpr.v5i3.407.

13. Kanagal DV, Vineeth VK, Kundapur R, Shetty H, Rajesh A. Prevalence of vaginal candidiasis in pregnancy among coastal South Indian women. Womens Health Issues. 2014;3:6. doi:10.4172/2325-9795.1000168

14. Okonkwo NJ, Umeanaeto PU. Prevalence of vaginal candidiasis among pregnant women in Nnewi Town of Anambra State, Nigeria. Afr Res Rev. 2011;4:539-548. doi:10.4314/afrrev.v4i4.69250