European Journal of Cardiovascular Medicine

Vaginal discharge is a leading complaint among women of reproductive age, with infectious causes predominating: bacterial vaginosis (BV), vulvovaginal candidiasis (VVC), and Trichomonas vaginalis (TV) together account for most symptomatic vaginitis worldwide.^1,2 BV represents a dysbiosis marked by depletion of lactobacilli and overgrowth of anaerobes (e.g., Gardnerella spp.), diagnosed by Amsel criteria or Nugent score and associated with adverse reproductive outcomes and increased STI acquisition.^3,4 VVC, due to Candida spp., is frequently recurrent and increasingly involves non-albicans species (NAC) with reduced azole susceptibility.^5,6 TV remains the most prevalent non-viral STI globally and contributes to cervicitis, urethritis, and poor pregnancy outcomes; resistance to nitroimidazoles, although uncommon, is clinically relevant.^7,8

Accurate etiologic diagnosis is essential because symptomatology overlaps and empirical treatment without laboratory confirmation can drive antimicrobial resistance (AMR).⁹ Contemporary guidelines emphasize microscopy-based point-of-care tests (pH, whiff test, saline/KOH prep), Gram stain with Nugent scoring, wet-mount or Giemsa stain for TV, and Serological Tests like ELISA for Chlamydia trachomatis (CT)/Neisseria gonorrhoeae (NG), supplemented by culture for yeasts and aerobic vaginitis (AV) organisms.¹⁰ AV—characterized by inflammatory aerobic/facultative flora (e.g., E. coli, Enterococcus, Staphylococcus)—is increasingly recognized and often misclassified as BV, yet requires different therapy targeting aerobic bacteria and local inflammation.¹¹

AMR trends among urogenital isolates mirror broader patterns: declining susceptibility of Enterobacterales to fluoroquinolones and third-generation cephalosporins, relative preservation of nitrofurantoin and fosfomycin for lower-tract infections, and azole-reduced susceptibility among NAC.¹² For vaginitis, guideline-concordant regimens (metronidazole/clindamycin for BV; single-dose or 7-day nitroimidazoles for TV; topical azoles or oral fluconazole for VVC with maintenance for recurrent disease) remain first-line, but local data should calibrate empiric choices and stewardship practices. ¹³

Data from India and comparable LMIC settings show wide ranges in BV (15–46%), VVC (≈25–60%), and TV (≈6–10%) among symptomatic women, reflecting demographic, behavioral, and laboratory variability. ¹⁴ Given shifting AMR patterns and evolving guideline recommendations, we undertook a cross-sectional study to estimate the prevalence of etiologies among symptomatic women with vaginal discharge at a tertiary-care center and to describe antimicrobial susceptibility of aerobic bacterial and Candida isolates. Our objective was to generate practical, local evidence to refine diagnostic algorithms and empiric therapy and to support antimicrobial stewardship in gynecologic care. ¹⁵

This is a Cross-sectional study was conducted in the Department of Gynecology and Microbiology at tertiary-care teaching hospital over 12 months. Institutional ethics approval was obtained; written informed consent was taken.

Participants: Consecutive, non-pregnant women aged 18–49 years presenting with abnormal vaginal discharge +/- pruritus, malodor, dysuria, dyspareunia, or vulvovaginal discomfort.

Inclusion criteria: (i) 18–49 years; (ii) symptomatic vaginal discharge; (iii) no systemic antibiotics/antifungals or intravaginal therapy within 14 days; (iv) consented to pelvic exam and sampling.

Exclusion criteria: Pregnancy; active uterine bleeding; postpartum <6 weeks; known immunosuppression (e.g., chemotherapy, advanced HIV) unless stable and consenting; refusal of sampling.

Clinical/laboratory procedures: Demographic and clinical data were recorded. External genital inspection and speculum exam were performed. Vaginal pH was measured (pH paper). Whiff test was performed with 10% KOH. Saline and KOH wet-mounts assessed clue cells, budding yeasts/pseudohyphae, leukocytes, and motile trichomonads. Gram-stained vaginal smears were scored using Nugent criteria (0–3: Normal flora, predominantly Lactobacillus. 4–6: Intermediate flora. 7–10: Bacterial Vaginosis) . A separate swab was inoculated for yeast culture and identification (chromogenic agar and biochemical/automated methods); AV work-up included aerobic culture from high vaginal swab with identification and semi-quantitative counts. Wet-mount positives for TV were confirmed by rapid antigen or Giemsa staining where available; Serum samples were collected for ELISA for Chlamydia. Cervical swabs collected for culture (in chocolate agar with CO₂ rich environment) and Gram staining of NG

Antimicrobial susceptibility: Aerobic bacterial isolates underwent disk diffusion/automated MIC testing as per CLSI M100 contemporary version, reporting nitrofurantoin, fosfomycin (if applicable), amoxicillin-clavulanate, cefixime/cefpodoxime (screen), ceftriaxone, ciprofloxacin, levofloxacin, cotrimoxazole, gentamicin, amikacin, and, for S. aureus/Enterococcus, penicillin G, clindamycin, tetracycline, linezolid/vancomycin (MIC). Yeasts underwent CLSI M27 broth microdilution for fluconazole, itraconazole, voriconazole, and amphotericin B; susceptibility was interpreted using species-specific breakpoints/epidemiologic cut-offs.

Outcomes and definitions: Primary outcomes—prevalence of BV (Nugent 7–10), VVC (positive microscopy and/or culture with symptoms), TV (wet-mount and/or Giemsa staining), AV (compatible microscopy plus significant aerobic growth with inflammation), CT (ELISA) , NG (compatible microscopy, culture). Mixed infection: ≥2 pathogens. Secondary outcomes—antimicrobial/antifungal susceptibility of aerobic isolates and Candida spp.

Sample size and analysis: Assuming combined infectious vaginitis prevalence of ~60% and 6–8% precision at 95% confidence, a minimum of 240 participants was required; we enrolled 300 to offset exclusions. Data were analyzed with descriptive statistics; proportions with 95% CIs. Group comparisons (e.g., BV vs non-BV) used χ² or t-tests as appropriate; p<0.05 considered significant

Table 1. Participant characteristics (N=300)

Typical reproductive-age cohort with substantial recurrence history.

Table 2. Etiologic distribution of symptomatic vaginal discharge

BV and VVC predominate; notable mixed infections and measurable AV/TV burden.

Table 3. Candida species distribution (n=89)

One-third NAC—relevant for azole selection and recurrent VVC management.

Table 4. Aerobic vaginitis (AV): leading isolates and susceptibilities

†For Enterococcus: penicillin 58%, high-level gentamicin 82%, vancomycin 100%, linezolid 100%.
NIT: nitrofurantoin; FOS: fosfomycin; AMC: amoxicillin-clavulanate; CRO: ceftriaxone; CIP: ciprofloxacin; SXT: cotrimoxazole; GEN: gentamicin; AMK: amikacin.
Fluoroquinolone activity is poor; nitrofurantoin/fosfomycin/amikacin retain activity in Enterobacterales; anti-MRSA options preserved.

Table 5. Antifungal susceptibility of Candida spp. (MIC interpretation)

Markedly reduced fluconazole susceptibility among NAC; amphotericin and voriconazole retain activity.

Table 6. Diagnostic yield of point-of-care tests

In this tertiary-care cohort, two-thirds of symptomatic vaginal discharge was due to BV and VVC, aligning with international and Indian reports that place BV and VVC as dominant etiologies among reproductive-age women. ¹⁶ Our BV prevalence (33%) falls within global ranges and mirrors recent summaries emphasizing BV’s high burden and relapse risk. ¹⁷ VVC (29.7%) similarly matches reports from South Asia and Africa, with ~40% due to NAC, a clinically important finding because NAC—especially C. glabrata—demonstrates reduced azole susceptibility and often necessitates topical non-azole or boric acid regimens for recurrent disease. ¹⁸

TV accounted for 7.7% of cases, consistent with multi-setting estimates and underscores guideline recommendations to incorporate molecular methods like Nucleic Acid Amplification Tests (NAAT) where feasible, given limited sensitivity of microscopy or wet-mount¹⁹; nevertheless, any positivity has implications for syndromic management and partner notification.²⁰

Antimicrobial susceptibility patterns among AV isolates reflected broader AMR trends: poor fluoroquinolone activity and moderate β-lactam performance against Enterobacterales, with preserved nitrofurantoin and fosfomycin utility—findings coherent with national AMR surveillance. ²¹ For Gram-positives, clindamycin and aminoglycosides remained active in most S. aureus isolates, and glycopeptide/oxazolidinone activity was universal in Enterococcus. These data argue against empiric fluoroquinolone therapy for presumed AV and favor targeted, short courses guided by culture. In yeasts, the sharp contrast in fluconazole susceptibility between C. albicans (86%) and NAC (28%) parallels recent Indian and global datasets and supports species-level identification in recurrent VVC. ²²

Practice implications are threefold. First, adhere to guideline-concordant therapy for BV (metronidazole/clindamycin; consider secnidazole/tinidazole alternatives), TV (nitroimidazoles with partner treatment), and VVC (topical azoles or single-dose oral fluconazole; multi-dose induction and maintenance regimens for recurrent disease). ²³ Second, incorporate low-cost microscopy (pH/whiff, saline/KOH) and Gram-stain routinely, adding ELISA or NAAT selectively (TV, CT/NG) and culture for AV/VVC to reduce diagnostic uncertainty and overtreatment. ²⁴ Third, embed antimicrobial stewardship: avoid empirical fluoroquinolones for AV, consider nitrofurantoin/fosfomycin for lower genital tract aerobic pathogens when susceptibility is likely, and escalate based on culture. ²⁵

Strengths include comprehensive bedside diagnostics and standardized susceptibility testing.

Limitations include single-center design, potential selection bias to OPD attendees, etc. Future work should include longitudinal follow-up for recurrence and randomized assessments of diagnostic algorithms in resource-limited settings.

BV and VVC are the leading causes of symptomatic vaginal discharge in reproductive-age women, with meaningful contributions from TV and AV and a non-trivial rate of mixed infections. Local AMR data caution against empirical fluoroquinolones for AV and highlight reduced azole susceptibility among NAC. A microscopy-first approach augmented by targeted NAAT/culture/Serological test supports accurate therapy, improved outcomes, and antimicrobial stewardship.

1. van der Veer C, Bruisten SM, van Houdt R, Rentenaar RJ, van der Loeff MFS, de Vries HJC. Mycoplasma genitalium, Chlamydia trachomatis, and Neisseria gonorrhoeae infections among heterosexual men with urethritis in the Amsterdam area: a cross-sectional study. BMC Infect Dis. 2022;22(1):58.
2. Workowski KA, Bachmann LH, Chan PA, Johnston CM, Muzny CA, Park I, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep. 2021;70(4):1-187.
3. Unemo M, Lahra MM, Escher M, Eremin S, Cole MJ, Galarza P, et al. WHO global antimicrobial resistance surveillance for Neisseria gonorrhoeae 2017-18: a retrospective observational study. Lancet Microbe. 2021;2(11):e627-e36.
4. Chemaitelly H, Majed A, Abu-Hijleh F, Blondeel K, Matsaseng TC, Kiarie J, et al. Global epidemiology of Neisseria gonorrhoeae in infertile populations: systematic review, meta-analysis and metaregression. Sex Transm Infect. 2021;97(2):157-69.
5. Ferreira CS, de Souza RK, da Silva MR, de Araújo RS, da Silva LA, da Silva LBR. Prevalence of Candida albicans and non-albicans isolates from vaginal secretions: a systematic review and meta-analysis. Arch Gynecol Obstet. 2022;305(4):935-48.
6. Muzny CA, Kardas P. A narrative review of current challenges in the diagnosis and management of bacterial vaginosis. Sex Transm Dis. 2020;47(7):441-6.
7. Gaydos CA, Beqaj S, Schwebke JR, Lebed J, Smith B, Davis TE, et al. Clinical validation of a test for the diagnosis of vaginitis. Obstet Gynecol. 2017;130(1):181-9.
8. Peebles K, Velloza J, Balkus JE, McClelland RS, Barnabas RV. High global burden and costs of bacterial vaginosis: a systematic review and meta-analysis. Sex Transm Dis. 2019;46(5):304-11.
9. Semaan S, Doshi RH, Mitchell KM, Bärnighausen T, Kates J, Lantos PM, et al. Trends in Chlamydia trachomatis positivity among women attending sexually transmitted infection clinics in the United States, 2006-2019. Sex Transm Dis. 2022;49(4):e67-e71.
10. Bitew A, Abebaw Y, Bekele D, Mihret A. Prevalence of bacterial vaginosis and associated risk factors among women complaining of genital tract infection in Addis Ababa, Ethiopia. Int J Microbiol. 2020;2020:8893350.
11. Patel V, Pedersen HS, Nanda S, Awasthi S, Balakrishnan S. Aetiology and antimicrobial susceptibility patterns of urogenital pathogens in women with vaginal discharge in a tertiary care hospital in Gujarat, India. Indian J Med Microbiol. 2018;36(3):407-11.
12. Masha SC, Cools P, Descheemaeker P, Reynders M, Sanders EJ, Vaneechoutte M. Antimicrobial susceptibility of Neisseria gonorrhoeae isolates from women of reproductive age in Nairobi, Kenya. Microb Drug Resist. 2019;25(2):175-81.
13. Pfaller MA, Diekema DJ, Turnidge JD, Castanheira M, Jones RN. Twenty years of the SENTRY antifungal surveillance program: results for Candida species from 1997-2016. Open Forum Infect Dis. 2019;6(Suppl 1):S79-S94.
14. Mulu W, Yimer M, Zenebe Y, Abera B. Common causes of vaginal infections and antibiotic susceptibility of aerobic bacterial isolates in women of reproductive age attending at Felegehiwot referral Hospital, Ethiopia: a cross sectional study. BMC Womens Health. 2015;15:42.
15. Mohammed H, Blomquist P, Ogaz D, Duffell S, Furegato M, Checchi M, et al. 100 years of STIs in the UK: a review of national surveillance data. Sex Transm Infect. 2018;94(8):553-8.
16. Jensen JS, Cusini M, Gomberg M, Moi H. 2021 European guideline on the management of Mycoplasma genitalium infections. J Eur Acad Dermatol Venereol. 2022;36(5):641-50.
17. Murray GL, Bradshaw CS, Bissessor M, Danielewski J, Garland SM, Jensen JS, et al. Increasing macrolide and fluoroquinolone resistance in Mycoplasma genitalium. Emerg Infect Dis. 2017;23(5):809-12.
18. Aduloju OP, Akintayo AA, Aduloju T, Akin-Akintayo OO. Prevalence of Candida species among pregnant women with vulvovaginal pruritus in a Nigerian tertiary hospital. J Mycol Med. 2019;29(2):134-9.
19. Getaneh M, Tafesse K, Tsegaye A, Tadese M, Kassa M, Girma M. Prevalence of Trichomonas vaginalis infection among reproductive age women in Ethiopia: a systematic review and meta-analysis. BMC Infect Dis. 2023;23(1):202.
20. Rönn MM, Menzies NA, Gift TL, Chesson HW, Benedict C, Hsu K. Potential public health impact and cost-effectiveness of a gonococcal vaccine in the United States: a modelling study. Clin Infect Dis. 2023;76(3):e899-e907.
21. Taku O, Mtshali A, Mhlongo T, Mhlongo N, Mzimela N, Bhengu P, et al. Prevalence and antimicrobial resistance of Neisseria gonorrhoeae in South Africa: a systematic review and meta-analysis. Sex Transm Dis. 2022;49(7):488-97.
22. Bitew A, Woldeamanuel Y, Asrat D, Ayenew T, Gize A. Prevalence of Group B Streptococcus among pregnant women and neonates from a tertiary hospital in Addis Ababa, Ethiopia. Trop Med Int Health. 2020;25(6):722-30.
23. Price MJ, Ades AE, Angelis DD, Welton NJ, Macleod J, Soldan K, et al. Incidence of Chlamydia trachomatis infection in women in England: two methods of estimation. Epidemiol Infect. 2016;144(5):1072-85.
24. Mlynarczyk-Bonikowska B, Kowalewski C, Krolak-Ulinska A, Marusza W. Molecular mechanisms of drug resistance and epidemiology of multidrug-resistant variants of Neisseria gonorrhoeae. Int J Mol Sci. 2022;23(18):10499.
25. Abebe T, Tilahun G, Mekonnen E, Mulu A. Antimicrobial susceptibility pattern of bacterial isolates from women with vaginal discharge in Jimma Hospital, Southwest Ethiopia. Ethiop Med J. 2015;53(4):193-200.