In one line
Vaginal discharge is three common conditions wearing one symptom — bacterial vaginosis, vulvovaginal candidiasis and trichomoniasis — and the consultant task is to separate the dysbiosis from the yeast from the sexually transmitted protozoan, treat the right one, and recognise that South Africa's nurse-led syndromic vaginal-discharge algorithm trades aetiological precision for reach, undertreating candida and overtreating those without an STI while it catches the women who matter most.
Mechanism & pathophysiology
The healthy vagina is an oestrogen-dependent ecosystem. Oestrogen thickens the squamous epithelium and loads it with glycogen; lactobacilli (chiefly L. crispatus, L. iners, L. gasseri, L. jensenii) metabolise that glycogen to lactic acid, holding the pH at 3.8–4.5, and several strains generate hydrogen peroxide and bacteriocins that suppress competitors. Not all lactobacillary states are equally protective: a L. crispatus-dominant community is the most stable, whereas L. iners dominance is a more fragile state that transitions more readily into dysbiosis — which is part of why BV is harder to eradicate durably than to treat acutely. This low pH is the single most informative bedside number in the topic, because each of the three diagnoses sits in a predictable relationship to it, and the oestrogen-dependence explains the conditions' age distribution: BV and candida are diseases of the reproductive years, and a complaint of "discharge" in a hypo-oestrogenic prepubertal or postmenopausal woman should redirect attention to atrophic vaginitis, a foreign body, or malignancy rather than to this triad.
Bacterial vaginosis is a dysbiosis, not an infection by a single organism. Protective lactobacilli are displaced by a polymicrobial overgrowth — Gardnerella vaginalis, Prevotella, Atopobium vaginae, Mobiluncus, Mycoplasma hominis and other anaerobes — that raises the pH above 4.5. Gardnerella is the keystone: it adheres to the epithelium and lays down a dense polymicrobial biofilm into which the other anaerobes are recruited. That biofilm is the mechanistic explanation for the two clinical signatures of BV — the high recurrence rate (antibiotics suppress planktonic bacteria but the adherent biofilm persists and reseeds) and the volatile amines (putrescine, cadaverine, trimethylamine) released by anaerobic metabolism, which volatilise and produce the fishy odour when alkalinised. The long-standing teaching that BV is simply an imbalance, not transmitted, is now under direct challenge: the demonstration that treating male partners reduces recurrence reframes BV as, at least in part, sexually transmitted, with the organisms exchanged and re-exchanged between partners.
Vulvovaginal candidiasis is an inflammatory response to commensal yeast. Candida albicans (80–90%) colonises the vagina asymptomatically in a large minority of women; disease occurs when the yeast transforms from blastospore to the invasive hyphal form and provokes a brisk host inflammatory response — the symptoms are immunopathology, not tissue destruction. This is why VVC produces vulvar burning, pruritus and dyspareunia out of proportion to any odour, and why the discharge is thick and white ("cottage cheese") rather than malodorous. Crucially, candida thrives at the normal acidic pH, so a pH below 4.5 with florid symptoms points to yeast and away from BV or trichomonas. Oestrogen, pregnancy, poorly controlled diabetes, recent antibiotics and immunosuppression (including HIV) drive symptomatic disease. Non-albicans species, principally C. glabrata and C. krusei, matter disproportionately: they are intrinsically less susceptible to azoles, cause more chronic low-grade symptoms, and are over-represented in recurrent and refractory disease and in immunocompromised women.
Trichomoniasis is genuinely a sexually transmitted infection. Trichomonas vaginalis is a flagellated protozoan that infects the squamous epithelium of the vagina and lower urinary tract, raising pH above 4.5 and producing a frothy, sometimes greenish, malodorous discharge with vulvovaginal inflammation; the "strawberry cervix" (colpitis macularis) of punctate haemorrhages is specific but seen in a minority. Because it is an STI, its presence mandates partner notification, HIV testing and a search for co-infections in a way the other two do not.
The reason any of this earns consultant attention beyond symptom relief is the downstream biology. A high vaginal pH and the loss of the lactobacillary barrier — the state shared by BV and trichomoniasis — amplifies HIV acquisition. The mucosal inflammation recruits activated CD4 target cells, the protective hydrogen-peroxide-producing flora is gone, the epithelial barrier is disrupted, and pooled epidemiological data put the increase in HIV-acquisition risk associated with BV at roughly 60%. There is biological reciprocity here: HIV-associated immunosuppression in turn predisposes to more frequent, more severe and more often non-albicans candidiasis, so the three vaginal conditions and HIV are not parallel problems but a connected system. In a country with South Africa's HIV incidence, a recurrent dysbiosis is not a nuisance diagnosis; it is a modifiable cofactor for the epidemic that dominates the rest of this domain — the HIV–gynaecology interface assumed from the Intermediate groundwork. BV and trichomoniasis are also linked to preterm birth and to post-procedural pelvic infection — untreated BV before instrumentation (termination, insertion of an intrauterine device, hysterectomy) raises the risk of post-operative endometritis and ascending infection, which is why they intersect with ascending pelvic infection and with the timing of elective gynaecological surgery.
Assessment
The history separates the three before any instrument is used. Odour (especially after intercourse, when alkaline semen volatilises the amines) with a thin grey discharge and minimal itch suggests BV; itch and burning with a thick white discharge and no odour suggests candida; a frothy, malodorous, irritating discharge, often with dysuria, raises trichomonas. None of these is reliable enough alone — symptom-based diagnosis is wrong often enough that office testing matters.
On speculum examination, look at the discharge (homogeneous grey film coating the walls in BV; white plaques adherent to an erythematous vagina in candida; frothy discharge with cervical petechiae in trichomonas) and at the cervix, because a mucopurulent cervix points past vaginitis to cervicitis and the STI cover that demands. The bedside tests, taken together, are diagnostic for most women:
- Vaginal pH (narrow-range paper against the lateral wall, away from cervical mucus and blood): >4.5 in BV and trichomonas, normal (<4.5) in candida. A normal pH effectively excludes BV.
- Whiff/amine test: a drop of 10% KOH on the discharge releases a fishy odour — positive in BV and frequently in trichomonas.
- Saline wet mount microscopy: clue cells (epithelial cells studded with adherent coccobacilli, borders obscured) for BV; motile, flagellated trichomonads the size of a leucocyte for trichomonas (sensitivity falls quickly as the slide cools and dries — examine it immediately).
- 10% KOH wet mount: lyses epithelial cells and reveals pseudohyphae and budding yeasts in candida.
These bedside findings are formalised in two scoring systems. Amsel criteria diagnose BV when three of four are present: thin homogeneous discharge, pH >4.5, positive whiff test, and ≥20% clue cells. The Nugent score is the Gram-stain laboratory reference standard, scoring the relative quantities of lactobacillary, Gardnerella/Bacteroides and curved gram-variable morphotypes from 0–10, with ≥7 diagnostic of BV (0–3 normal, 4–6 intermediate); the Hay–Ison system is a simpler Gram-stain alternative used in the same role. For trichomonas, wet-mount sensitivity is only 50–70% and falls further with delay, so where resources allow a nucleic acid amplification test (NAAT) is the most sensitive confirmation and is the modern standard in well-resourced settings; antigen point-of-care tests are an intermediate option, and the organism is sometimes reported incidentally on a routine cervical cytology slide, which counts as a real diagnosis but is too insensitive to use as a screen. Candidiasis deserves one caution at the microscope: up to half of symptomatic women have a negative KOH wet mount despite true infection, so a culture is warranted where symptoms are convincing, the wet mount is clear, or treatment has failed — both to confirm yeast and to speciate, since management diverges sharply for non-albicans disease.