Vaginitis — Bacterial Vaginosis, Candidiasis and Trichomoniasis

• Bacterial vaginosis is not an infection but a dysbiosis: loss of hydrogen peroxide–producing lactobacilli with overgrowth of Gardnerella vaginalis and anaerobes. Thin grey-white discharge, a fishy odour, pH > 4.5, clue cells on saline microscopy and a positive whiff test with potassium hydroxide. Notably not inflammatory, so there are few white cells and little itch or erythema. Associated with preterm birth in pregnancy.
• Vulvovaginal candidiasis — usually Candida albicans. Thick white "cottage cheese" discharge with prominent itch and erythema, a normal pH (≤4.5), and pseudohyphae seen after potassium hydroxide. Risk rises with antibiotics, diabetes, pregnancy and immunosuppression.
• Trichomoniasis — Trichomonas vaginalis, a sexually transmitted flagellated protozoan. Frothy yellow-green discharge, pH > 4.5, motile trichomonads, and a "strawberry cervix" from punctate haemorrhages. Because it is sexually transmitted, partners require treatment.

Dysbiotic (non-inflammatory) — bacterial vaginosis

• Loss of lactobacilli: replacement of H₂O₂- and lactic acid–producing Lactobacillus crispatus/jensenii by a polymicrobial anaerobic community — Gardnerella vaginalis, Prevotella, Mobiluncus, Atopobium vaginae, Mycoplasma hominis.
• Modifiable: vaginal douching, new or multiple sex partners, female sex partners, smoking, intrauterine device use, and copious/receptive semen exposure (alkaline pH). Antibiotic courses that eliminate lactobacilli.
• Non-modifiable: Black race carries a higher prevalence of BV-associated microbiota; genetic determinants of the vaginal microbiome. BV is not classified as a sexually transmitted infection, though it is sexually associated — a favourite distractor.

Opportunistic fungal — vulvovaginal candidiasis

• Organism: Candida albicans in most cases; C. glabrata and C. krusei in recurrent or azole-refractory disease.
• Modifiable: broad-spectrum antibiotics (suppress lactobacilli), poorly controlled diabetes mellitus with glycosuria, SGLT2 inhibitors, systemic corticosteroids, high-oestrogen states including combined oral contraceptives, occlusive clothing.
• Non-modifiable: pregnancy (oestrogen-rich, glycogen-rich epithelium), HIV and other cell-mediated immunodeficiency, genetic predisposition in recurrent disease.

Sexually transmitted protozoal — trichomoniasis

• Organism: Trichomonas vaginalis, a flagellated protozoan transmitted almost exclusively by sexual contact; the stem names a new partner, inconsistent condom use, or another concurrent STI.
• Modifiable: unprotected intercourse, multiple partners, untreated partners (reinfection is the rule).
• Non-modifiable/associated: coexisting BV (the two frequently co-occur), incarceration, and HIV infection. The CDC recommends screening for T. vaginalis in women living with HIV at entry to care and at least annually, and testing anyone with vaginitis symptoms plus STI risk.

Bacterial vaginosis

• Loss of lactobacilli → pH rises above 4.5, permitting anaerobic overgrowth and Gardnerella biofilm adherent to the epithelial surface.
• Anaerobes decarboxylate amino acids to volatile amines (trimethylamine, putrescine, cadaverine). These are protonated and odourless at acid pH but volatilise when alkalinised — the mechanistic basis of the whiff test with potassium hydroxide and of the post-coital odour after alkaline semen.
• Biofilm-coated epithelial cells shed as clue cells. Because the anaerobes elicit little neutrophil recruitment, the process is a dysbiosis, not an inflammation — hence scant leukocytes, no dyspareunia, no erythema, and a thin homogeneous discharge that simply coats the walls.
• Sialidases and mucinases degrade cervical mucus, explaining the ascending-infection and preterm-birth associations.

Candidiasis

• Oestrogen, glycogen and antibiotic-induced loss of lactobacilli permit Candida to switch from commensal yeast to hyphal/pseudohyphal invasive form, which secretes candidalysin and aspartyl proteinases.
• Epithelial damage triggers a brisk neutrophilic and IgE-mediated hypersensitivity response — this is why the dominant symptom is pruritus and burning with erythema and fissures, while discharge is adherent and curd-like. Lactobacilli persist, so pH stays normal (≤4.5) and the whiff test is negative.

Trichomoniasis

• The flagellate is cytoadherent, phagocytoses lactobacilli and host cells, and releases cysteine proteinases — producing intense inflammation with purulent, frothy discharge (gas-producing co-anaerobes), an alkaline pH, and punctate cervical/vaginal haemorrhages seen as the strawberry cervix (colpitis macularis).
• Epithelial microulceration and recruitment of activated CD4 cells increase HIV acquisition and transmission efficiency.

Bacterial vaginosis — the "odour without inflammation" stem

• Thin, homogeneous grey-white discharge coating the vaginal walls, often noticed only as staining of underwear; from biofilm shedding rather than exudation.
• Fishy odour, worse after intercourse and after menses, because alkaline semen and blood volatilise amines.
• Absent pruritus, absent dysuria, non-tender vulva, no erythema — the negative findings are the diagnostic lever. Up to half of women are asymptomatic.
• Stem demographic: reproductive-aged woman who douches or has a new partner; or a preoperative/pregnant patient found incidentally.

Vulvovaginal candidiasis — the "itch" stem

• Intense vulvar pruritus and burning, external dysuria (urine crossing excoriated skin, not urethritis) and superficial dyspareunia — all from the hypersensitivity/neutrophilic response.
• Thick, white, adherent "cottage cheese" discharge, typically odourless.
• Examination: vulvar and vaginal erythema, oedema, satellite lesions and fissures; discharge clings to the walls.
• Stem demographic: recent course of antibiotics, poorly controlled type 2 diabetes or a patient on an SGLT2 inhibitor, pregnancy, or high-dose corticosteroids. Recurrent disease (≥3–4 episodes/year) should prompt HIV testing and a glucose check.

Trichomoniasis — the "STI" stem

• Frothy, malodorous yellow-green discharge with vulvar irritation, dysuria and postcoital bleeding.
• **Punctate cervical haemorrhages — the *strawberry cervix*** — is highly specific but seen in a minority on unaided speculum examination; diffuse vaginal erythema is more common.
• Frequently asymptomatic, particularly in men, who present as an untreated partner or with urethritis.
• Stem demographic: new or multiple partners, another concurrent STI, incarceration, or a woman living with HIV.

Initial office evaluation — the three-part bedside panel

• Vaginal pH on narrow-range paper from the lateral wall (avoid cervical mucus, semen and blood, which are alkaline): >4.5 in BV and trichomoniasis; ≤4.5 in candidiasis.
• Amine (whiff) test: 10% potassium hydroxide added to discharge releases a fishy odour — positive in BV and often in trichomoniasis.
• Microscopy: saline wet mount for clue cells (epithelial cells with stippled, obscured borders) and motile flagellated trichomonads; KOH preparation lyses host cells to reveal budding yeast and pseudohyphae. Abundant leukocytes point away from BV.

Criteria and scoring

• Amsel criteria diagnose BV clinically when 3 of 4 are present: thin homogeneous discharge, pH >4.5, positive whiff test, and clue cells on ≥20% of epithelial cells.
• Nugent score — Gram stain quantification of Lactobacillus, *Gardnerella*/*Bacteroides* and curved rods, scored 0–10, with the high range diagnostic of BV. This is the laboratory reference standard, used mainly in research.

Confirmatory testing

• Trichomoniasis: wet mount is specific but only modestly sensitive and loses sensitivity as the slide cools, so the CDC designates nucleic acid amplification testing as the most sensitive method and the test of choice; rapid antigen and culture are alternatives. Trichomonads reported on a Pap smear are not a reliable basis for diagnosis.
• Candidiasis: microscopy is confirmatory when positive, but is falsely negative in a substantial minority — fungal culture with speciation is indicated for recurrent, severe or azole-refractory disease to identify C. glabrata.
• Multiplex molecular vaginitis panels are available and sensitive, but should not replace pH and microscopy when those are diagnostic.

Bacterial vaginosis

• Nitroimidazoles — metronidazole 500 mg orally twice daily for 7 days is first line; intravaginal metronidazole gel or clindamycin cream are equivalent alternatives (clindamycin cream is oil-based and weakens latex condoms).
• Alternatives: oral tinidazole, oral clindamycin, or single-dose secnidazole granules.
• Partner treatment is not recommended — the classic distractor. Recurrence is common; suppressive intravaginal metronidazole may be used.
• Pregnancy: metronidazole is considered safe by the CDC and is used for symptomatic BV in any trimester.

Vulvovaginal candidiasis

• Uncomplicated: topical azole (clotrimazole, miconazole) for 1–7 days or oral fluconazole 150 mg as a single dose.
• Complicated (severe, recurrent, non-*albicans*, diabetic or immunocompromised): fluconazole 150 mg repeated every 72 hours for two to three doses, then weekly suppression for 6 months in recurrent disease. IDSA and CDC recommend intravaginal boric acid or nystatin for **azole-resistant *C. glabrata*; boric acid is fatal if swallowed** and contraindicated in pregnancy.
• Pregnancy: use topical azoles for 7 days; oral fluconazole is avoided, particularly in the first trimester, because high-dose exposure has been linked to congenital anomalies.

Trichomoniasis

• Women: metronidazole 500 mg orally twice daily for 7 days — the multidose regimen outperformed single-dose 2 g in the CDC's current guidance. Men: metronidazole 2 g orally as a single dose. Tinidazole is an alternative.
• Treat all sexual partners and advise abstinence until therapy is complete and symptoms resolve; retest at 3 months because reinfection is frequent.
• Nitroimidazole allergy requires desensitisation — topical metronidazole is inadequate and should not be substituted.
• Counsel avoidance of alcohol during and shortly after nitroimidazole therapy (disulfiram-like reaction).

Bacterial vaginosis

• Preterm birth, preterm premature rupture of membranes, chorioamnionitis and postpartum endometritis — mucin- and IgA-degrading sialidases weaken the cervical mucus plug and fetal membranes, permitting ascending colonisation. Treatment of symptomatic BV in pregnancy is indicated, but screening asymptomatic low-risk pregnant patients has not been shown to prevent preterm birth (USPSTF).
• Post-procedural pelvic infection after hysterectomy, surgical abortion or IUD insertion, from anaerobic ascent.
• Increased susceptibility to HIV, gonorrhoea, chlamydia and herpes simplex virus, via loss of the protective acidic, H₂O₂-rich milieu.
• Pelvic inflammatory disease is an associated but less consistent risk — new cervical motion or adnexal tenderness with fever signals it and is a semi-urgent problem requiring empiric PID coverage.

Vulvovaginal candidiasis

• Excoriation with secondary bacterial cellulitis, and vulvar lichenification from chronic scratching.
• Recurrent or refractory disease is a sentinel finding: check for undiagnosed diabetes and HIV, and culture for C. glabrata.
• Invasive candidiasis does not arise from vaginitis in immunocompetent hosts — a common distractor.

Trichomoniasis

• Enhanced HIV acquisition and transmission from mucosal microulceration and CD4-cell recruitment — arguably the single most tested complication.
• Preterm birth, low birth weight and PPROM in pregnancy; PID, particularly in women living with HIV; infertility and possible association with cervical neoplasia.
• Reinfection from an untreated partner is the usual cause of "treatment failure"; true nitroimidazole resistance is uncommon and requires higher-dose tinidazole and specialised susceptibility testing.

Treatment-related

• Metronidazole/tinidazole: metallic taste, nausea, disulfiram-like reaction with alcohol, potentiation of warfarin, and — with prolonged or high-dose use — peripheral neuropathy and, rarely, encephalopathy or seizures (an emergency).
• Clindamycin: Clostridioides difficile colitis — new watery diarrhoea after therapy demands testing.
• Fluconazole: hepatotoxicity, QT prolongation and CYP-mediated interactions; teratogenicity at high doses.
• Boric acid: fatal on ingestion; vaginal-use-only counselling is mandatory.

• pH is the first discriminator: >4.5 → BV or trichomoniasis; ≤4.5 → candidiasis. If a stem gives a normal pH with a fishy odour, the numbers are inconsistent — re-read for contamination by blood or semen.
• ***Clue cells* + positive whiff test + thin grey discharge = bacterial vaginosis. Diagnosis needs 3 of 4 *Amsel criteria***; Nugent score on Gram stain is the laboratory reference standard.
• BV is inflammation-poor. Few leukocytes, no erythema, no itch. If the stem emphasises intense pruritus and vulvar erythema, it is candidiasis, not BV.
• Single best next step for suspected trichomoniasis is NAAT, not wet mount — wet mount is specific but insensitive and rapidly loses motile organisms as the slide cools. Strawberry cervix is the eponym.
• Treat partners in trichomoniasis; do not treat partners in bacterial vaginosis. This is the most reliably tested management distinction of the three.
• Women with trichomoniasis get metronidazole 500 mg twice daily for 7 days; men get a single 2 g dose — the CDC changed the female regimen away from single-dose therapy. Retest at 3 months.
• Recurrent candidiasis → check glucose and offer HIV testing; azole-refractory disease → culture for C. glabrata and treat with intravaginal boric acid (never oral — it is lethal ingested).
• In pregnancy, metronidazole is acceptable; oral fluconazole is not — use a 7-day topical azole for candidiasis. Do not confuse the two.
• Common distractors: postmenopausal patient with thin discharge, pH >4.5 and parabasal cells is atrophic vaginitis (treat with vaginal oestrogen), and cervical motion tenderness with fever means PID, not vaginitis.