British Association for Sexual Health and HIV national guideline for the management of vulvovaginal candidiasis (2019)

Offers clinical recommendations on the diagnostic tests, treatment regimens, and health promotion principles for the effective management of acute and recurrent vulvovaginal candidiasis.

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1Key Changes, Scope, and Definitions

ScopeApplies to individuals aged 16 years and older presenting to healthcare professionals offering Level 3 sexually transmitted infection (STI) care in the UK.
TerminologyThe terms 'uncomplicated' and 'complicated' VVC have been retired in favor of 'acute' and 'recurrent' VVC.
Acute VVCDefined as the first or a single isolated presentation of vulvovaginal candidiasis.
- Patients typically present with signs and symptoms of acute vulvovaginitis.
- Diagnosis is supported by the detection of Candida species via microscopy and/or culture.
Recurrent VVCDefined as at least four symptomatic episodes within a 12-month period.
- At least two of these episodes must be confirmed by microscopy or culture when symptomatic.
- At least one of the confirmed episodes must be verified by culture showing moderate or heavy growth.
- Pattern 1: Good or complete response to therapy, but with asymptomatic intervals between episodes.
- Pattern 2: Poor or partial response to therapy, with persistent symptoms between active treatment courses.
Chronic VVCProposed as a distinct condition from recurrent VVC, characterized by chronic, continuous symptoms.
- Symptoms may improve during menses and typically remit with active antifungal therapy.

2Aetiology, Epidemiology, and Pathogenesis

PathogensCandida species are eukaryotic, unicellular microorganisms capable of forming pseudohyphae and biofilms.
- Candida albicans is the causative organism in 80–89% of VVC cases.
- Non-albicans Candida (NAC) species cause the remainder of cases, including Candida glabrata, Candida tropicalis, Candida krusei, Candida parapsilosis, and Saccharomyces cerevisiae.
- Candida yeasts are normal flora of the skin (moist areas), respiratory tract, GI tract, and female genital tract; infection is caused by overgrowth rather than simple presence.
EpidemiologyVVC is highly prevalent among women of reproductive age.
- An estimated 75% of women will experience at least one lifetime episode of VVC.
- 40–45% of women will experience two or more lifetime episodes.
- Approximately 6% (and up to 20% in some survey data) of reproductive-age women develop recurrent VVC.
- The cumulative probability of developing recurrent VVC after an initial infection is 10% by age 25, rising to 25% by age 50.
PathogenesisRecurrent VVC is primarily driven by host susceptibility factors rather than increased organism virulence or reintroduction.
- Symptoms of VVC correlate directly with fungal burden.
- Neutrophil infiltration (mediated by S100 alarmins operating independently of the Th17 pathway) is heavily involved in the production of clinical symptoms.
- Persistence of Candida species can occur (detectable by PCR) even when cultures are negative between symptomatic episodes.
GeneticsHost genetic polymorphisms significantly influence susceptibility to recurrent infections.
- Mannose-binding lectin (MBL) deficiency (specifically associated with the MBL codon 54 gene polymorphism) is a genetic risk factor.
- Possessing the MBL variant allele B heterozygous or homozygous genotype significantly increases VVC risk and treatment failure compared to healthy controls.
Systemic FactorsSeveral systemic, endocrine, and psychological states alter the vaginal microenvironment.
- Hormonal influence: Elevated endogenous or exogenous oestrogen (pregnancy, HRT, and potentially the combined oral contraceptive pill) increases susceptibility.
- Diabetes Mellitus: Poorly-controlled diabetes mellitus significantly predisposes to VVC.
- Immunosuppression: Systemic immunosuppression increases risk.
- Antibiotic use: Recent antibiotic use (up to 3 months prior to the episode) predisposes to VVC by disrupting protective vaginal flora.
- Psychological stress: Chronic stress (indicated by lower mean cortisol levels) and associated reductions in host antioxidant capacity show a weak association.
- Micronutrient deficiencies: Evidence linking iron deficiency anaemia, low zinc, low magnesium, or low calcium to recurrent VVC remains conflicting or weak.

3Clinical Features and Differential Diagnosis

PresentationTypical presenting symptoms of VVC include vulval itch (pruritus) and a non-offensive vaginal discharge.
- Other symptoms: Vulval soreness or burning, superficial dyspareunia, superficial dysuria, and cyclical symptom patterns (often worsening premenstrually).
- Clinical signs: Erythema, fissuring, swelling/oedema, satellite lesions (pustules or erythematous papules), and excoriation marks.
- Vaginal discharge is typically non-offensive and curdy, but it may be thin or entirely absent.
Clinical CaveatsClinical features are not pathognomonic, and there can be a significant discrepancy between symptoms and signs, especially in chronic disease.
- Clinical signs and symptoms cannot be used to differentiate between C. albicans and non-albicans species.
- In recurrent VVC, clinicians should enquire about other recurrent fungal infections (e.g., oropharyngeal, skin, nails, dandruff) to screen for underlying immune defects.
ColonizationAsymptomatic colonization occurs in up to 20% of women of reproductive age (and 30-40% of pregnant women).
- These women do not require antifungal treatment.
- Candida colonization may co-exist incidentally in women whose vulval symptoms are actually caused by other conditions (e.g., eczema, lichen sclerosus).
DifferentialsMore than 50% of self-diagnosed women presenting with vulvovaginal symptoms have alternative conditions.
- Aerobic vaginitis: Consider if the primary complaint is a purulent, non-offensive vaginal discharge.
- Cytolytic vaginosis: Presents with curdy discharge and pruritus mimicking VVC, but microscopy and fungal cultures are negative.
- Provoked vestibulodynia / Vulvodynia: Chronic vulval pain/burning without active infection; provoked vestibulodynia may be triggered by prior VVC.

Symptomatic Comparison of VVC and Common Differential Diagnoses

Condition	Vulval Itch	Vulval Soreness	Discharge	Superficial Dyspareunia	Superficial Dysuria	Swelling	Response to Topical Steroids
Vulvovaginal Candidiasis	Yes	Yes (sometimes 'prickling')	Yes (odourless, curdy; can be thin/absent)	Possible	Possible	Possible	Improvement / No change / Worse
Lichen Sclerosus	Yes (severe)	Yes (severe)	No	Yes (especially if loss of architecture)	Possible	No	Improvement (requires high potency)
Vulvo-/Vestibulodynia	No	Burning is predominant	No	Yes (point penetration pain)	Not usually	No	No response
Contact Dermatitis / Eczema	Yes	Possible	Possible (exudate from inflamed skin, not true discharge)	Possible	Possible	Possible	Improvement
Chronic Lichen Simplex	Yes	Possible	No	Possible	Not usually	Possible (secondary to skin thickening)	Improvement

Sign Comparison of VVC and Common Differential Diagnoses

Sign	Vulvovaginal Candidiasis	Lichen Sclerosus	Vulvodynia	Contact Dermatitis	Chronic Lichen Simplex
Erythema	Yes	Yes (usually with other features)	Possible	Yes	Possible
Fissuring	Possible	Possible	No	Possible	Possible
Discharge	Yes (odourless, curdy, or thin/absent)	No (unless dual pathology)	No (unless dual pathology)	Possible (exudate from inflamed skin)	No (unless dual pathology)
Oedema	Possible	No	No	Possible	Possible
Other features	Satellite lesions	Pallor, atrophy, loss of architecture, haemorrhage, introital narrowing	Cotton tip provoked tenderness	Erythema, exudate	Lichenification (thickening of skin from scratching)
Excoriations	Possible	Possible	No	Often	Often

4Diagnostic Investigations

Clinical examination of the external genitalia is recommended for all women presenting with symptoms suggestive of acute VVC to exclude alternative or co-existing pathologies.
- Women presenting with features of recurrent VVC must always undergo clinical examination.
- If clinical examination is not possible or required, a self-collected vaginal swab for microscopy/culture is a highly reliable alternative.
GPPEmpirical (syndromic) treatment for acute VVC based on reported symptoms may be given in non-specialist settings.
- If symptoms fail to resolve or recur, clinical examination and microbiological testing must be performed.
Grade 1BIn level 3 STI care settings, supporting the diagnosis of acute VVC with routine microscopy is good clinical practice.
- A high vaginal swab (HVS) of the discharge should be taken for Gram stain and/or phase contrast wet film microscopy.
- Blastospores + pseudohyphae + neutrophils indicate active infection by Candida species.
- Blastospores only + neutrophils may reflect infection caused by C. glabrata.
- Neutrophils indicate an active inflammatory response; the presence of Candida without neutrophils likely represents colonization rather than active infection.
CultureFungal culture utility varies significantly between acute and recurrent presentations.
- Acute VVC: Fungal culture is not cost-effective or reliable on its own because it cannot differentiate colonization from active infection.
- Recurrent VVC: Take an HVS of the discharge for direct plating onto solid fungal growth medium (Sabouraud plate) to enable quantification.
- Grade 1BAny fungal growth in recurrent VVC should ideally be identified to species level (or at least C. albicans vs. non-albicans) and tested for fluconazole sensitivity.
- Mixed infections (C. albicans and a non-albicans species) are not rare and should be actively sought by the laboratory.
- Grade 2CSelf-collected swabs done at home can be considered in recurrent VVC if initial clinic-collected samples are negative.
- Transport Medium Limitation: If direct plating is unavailable, transport medium is acceptable, but quantification is unreliable if kept in transport medium for >12 hours due to continued fungal growth.
Caution is required when interpreting standard in vitro susceptibility testing, as standard breakpoints may not apply in vivo.
- Standard susceptibility testing is performed at pH 7.0, but vaginal pH in VVC is typically acidic (pH 4.0–4.5).
- The activity of most azole antifungals (especially against non-albicans species) is significantly decreased in acidic environments.
- Isolates with elevated MICs are unlikely to respond to standard azole doses despite being designated as 'susceptible' (e.g., C. glabrata loses its marginal azole efficacy at pH 4.5).
- Clinical Rule: Reported resistance is highly likely to predict a poor clinical response, but apparent in vitro sensitivity does not guarantee clinical success.
DiagnosticsMolecular and point-of-care (POC) rapid antigen tests are highly sensitive but cannot differentiate colonization from infection.
STI ScreeningVVC is not an STI or a marker for STIs.
- The offer of STI screening should be based on individual risk assessment, noting that some clinical features of VVC overlap with STIs.

5General Management and Lifestyle Advice

GPPProvide all patients with information on proper vulval skin care.
- Avoid local irritants such as perfumed soaps, bubble baths, or wipes.
- Use an emollient as a soap substitute, moisturizer, and barrier cream (advise the patient that this is for external use only).
- Vulval emollients can provide symptomatic relief, as secondary vulval dermatitis (eczema) is commonly present.
HygieneCarefully review daily hygiene routines to identify unrecognized local irritants (e.g., washing hair in bath water, excessive cleaning).
- Avoid wearing poorly fitted clothing made from non-breathable fabrics.
- Avoid using intermenstrual or daily panty liners.
- Avoid vaginal douching.
Sexual HealthSexual intercourse does not need to be avoided from an infection perspective, as VVC is not an STI.
- Do not treat asymptomatic male sexual partners in cases of acute or recurrent VVC, as there is no evidence of clinical benefit.
- Women may choose to avoid sex until symptoms improve, particularly if vulval fissuring is present.
- If symptoms are linked to sexual activity, patients may consider using a gentle water-based lubricant.
- Discuss potential psychosexual and emotional impacts, such as reduced libido and arousal, which are common in chronic vulvovaginal conditions.

6Pharmacological Treatment Regimens

Grade 1BEfficacy of Acute Treatments: All oral azoles and intravaginal imidazoles achieve clinical and mycological cure rates >80% in acute VVC.
- Oral and intravaginal routes are equally effective and tolerable; selection is guided by cost and convenience.
- Fluconazole 150 mg single oral dose is 7 to 30 times cheaper than other listed regimens.
- A single dose of oral fluconazole may provide a more effective 7-day clinical cure than a prolonged 6-day course of intravaginal clotrimazole 200 mg.
Grade 1BSevere VVC Management: Defined as VVC presenting with extensive vulval erythema, oedema, excoriation, and fissure formation, regardless of recurrence history.
- Recommended regimen: Fluconazole 150 mg PO on Day 1 and Day 4 (or Clotrimazole 500 mg PV / Miconazole 1200 mg PV on Day 1 and Day 4 if oral is contraindicated).
- Repeating the dose after 3 days improves symptomatic response but does not influence the risk or rate of long-term recurrence.
- Low-potency corticosteroid creams can be used in conjunction with antifungals to accelerate symptomatic relief in severe vulval inflammation.
Grade 1ARecurrent VVC (RVVC) Management: Requires an induction regimen to achieve clinical remission, followed immediately by a maintenance regimen.
- Recommended induction: Fluconazole 150 mg PO every 72 hours for 3 doses (Days 1, 4, and 7).
- Recommended maintenance: Fluconazole 150 mg PO once weekly for 6 months.
- This regimen achieves clinical remission in 82–90% of patients. Recurrence rates post-therapy: 12% immediately after, 36% at 3 months, and 39% at 6 months.
- Avoid: Do not use low-dose protracted regimens (e.g., fluconazole 50 mg daily for 14–28 days) due to the risk of developing antifungal resistance.
- If a patient relapses between maintenance doses, consider increasing fluconazole to 150 mg PO twice weekly, or adding cetirizine 10 mg daily.
- If recurrences after the maintenance regimen are infrequent, treat each episode independently. If recurrent disease is re-established, repeat the full induction and maintenance regimens.
ContraindicationOral azoles (fluconazole, itraconazole) MUST be avoided in pregnancy, in those planning pregnancy, and during breastfeeding.
WarningIntravaginal and topical treatments can damage latex condoms and diaphragms, increasing the risk of unplanned pregnancy and STI transmission. Counsel patients appropriately.
Safety AlertOral ketoconazole is no longer recommended for the treatment of VVC due to the high risk of severe hepatotoxicity (suspended by the EMA).
GPPFluconazole Drug Interactions & QT Prolongation:
- Fluconazole is a moderate inhibitor of CYP2C9 and CYP3A4. Enzyme inhibition persists for 4–5 days post-discontinuation due to its long half-life.
- Fluconazole can prolong the QT interval. Perform an individual risk assessment if prescribing with other QT-prolonging drugs (risk factors: female sex, older age, cardiac disease, hypokalaemia).
- Co-administration of fluconazole with CYP3A4-metabolized QT-prolonging drugs (e.g., cisapride, astemizole, pimozide, quinidine, erythromycin) is strictly contraindicated.

Vulvovaginal Candidiasis Treatment Options

Indication / Population	Preferred Regimen	Alternative Regimen
Acute VVC (Non-pregnant)	Fluconazole 150 mg PO stat If oral contraindicated: Clotrimazole 500 mg PV stat	• Clotrimazole vaginal cream (10%) 5 g stat • Clotrimazole pessary 200 mg PV nocte for 3 nights • Econazole pessary 150 mg PV stat OR 150 mg PV nocte for 3 nights • Fenticonazole capsule 600 mg PV stat OR 200 mg PV nocte for 3 nights • Itraconazole 200 mg BD for 1 day PO • Miconazole pessary 1200 mg PV stat OR 400 mg PV nocte for 3 nights • Miconazole vaginal cream (2%) 5 g PV nocte for 7 nights
Acute VVC (Pregnancy)	Clotrimazole pessary 500 mg PV nocte for up to 7 nights (1C)	• Clotrimazole vaginal cream (10%) 5 g nocte for up to 7 nights • Clotrimazole pessary 200 mg or 100 mg PV nocte for 7 nights • Econazole pessary 150 mg PV nocte for 7 nights • Miconazole pessary 1200 mg or 400 mg PV nocte for 7 nights • Miconazole vaginal cream (2%) 5 g PV nocte for 7 nights
Acute VVC (NAC sp. & Azole Resistance)	Nystatin pessaries 100,000 units PV nocte for 14 days	• Boric acid suppositories 600 mg PV nocte for 14 nights • Amphotericin B vaginal suppositories 50 mg PV nocte for 14 nights • Flucytosine 5 g cream OR 1 g pessary with amphotericin or nystatin PV nocte for 14 nights
Recurrent VVC (Non-pregnant)	Induction: Fluconazole 150 mg PO every 72 h for 3 doses Maintenance: Fluconazole 150 mg PO once weekly for 6 months	Induction: Topical imidazole therapy increased to 10–14 days based on symptoms Maintenance (6 months): • Clotrimazole pessary 500 mg PV once weekly • Itraconazole 50–100 mg daily PO
Recurrent VVC (Pregnancy)	Induction: Topical imidazole therapy increased to 10–14 days based on symptoms Maintenance: Clotrimazole pessary 500 mg PV weekly	N/A (Oral therapies contraindicated)
Recurrent VVC (NAC sp. & Azole Resistance)	Nystatin pessaries 100,000 units PV nocte for 14 nights/month for 6 months	Consider 14 nights per month for 6 months of the alternative regimens listed for acute NAC/azole resistance
Severe VVC	Fluconazole 150 mg PO on Day 1 and Day 4	• Clotrimazole pessary 500 mg PV on Day 1 and Day 4 • Miconazole nitrate capsule 1200 mg PV on Day 1 and Day 4
Breastfeeding	Topical imidazoles only (as per non-pregnant recommendations)	Avoid oral therapies

7Non-Albicans Candida and Azole Resistance

DiagnosticsSusceptibility profiles of common Candida species:
- C. albicans: Normally susceptible to all yeast-active antifungals; resistance is rare but can develop with prolonged or repeated azole courses.
- C. glabrata: The most common NAC species; most strains are reported as susceptible to azoles but have elevated Minimum Inhibitory Concentrations (MICs), leading to poor clinical response to standard doses.
- C. krusei: Intrinsically resistant to fluconazole.
- C. guilliermondii and C. parapsilosis: Normally susceptible to azoles; patients typically respond well to standard treatment.
PracticeDosing strategies for elevated MIC isolates:
- For isolates with elevated MIC but still designated susceptible, higher and more frequent dosing of fluconazole (200-300 mg OD every 48 hours for 1 week) may be effective.
- Repeated courses should be avoided to prevent further resistance development.
- For confirmed azole-resistant species, longer courses (suggested 2 weeks) of non-azole therapy are advised.
Grade 1BNystatin pessaries 100,000 units intravaginally nocte for 12–14 consecutive nights.
- For recurrent VVC due to azole-resistant Candida, use nystatin pessaries 100,000 units intravaginally nocte for 14 nights per month for 6 months.
Grade 1BBoric acid vaginal suppositories 600 mg daily for 14 days are a safe and effective alternative for resistant strains.
- If mucosal irritation occurs, the dose can be reduced to 300 mg daily (requires special compounding).
- Boric acid must be avoided in pregnancy or if there is a risk of pregnancy due to potential teratogenic risk.
Grade 2CAlternative non-azole regimens for resistant strains:
- Amphotericin B vaginal suppositories 50 mg once daily for 14 days.
- Flucytosine 5 g cream or 1 g pessary intravaginally combined with amphotericin or nystatin daily for 14 days (combination prevents resistance due to flucytosine's low genetic barrier).

8Special Populations and Co-morbidities

PregnancyGeneral Considerations in Pregnancy:
- Asymptomatic Candida colonization is common (30–40%), and symptomatic VVC is more prevalent throughout pregnancy.
- There is no evidence linking asymptomatic Candida colonization or VVC to premature delivery or low birth weight.
- Oral azole therapies must be avoided during pregnancy.
- Topical imidazoles are safe and effective for symptomatic VVC in pregnancy.
- Longer courses of topical imidazoles are required in pregnancy (a 7-day course cures >90%, whereas a 4-day course cures just over 50%).
- Avoid using the applicator during insertion in late pregnancy to prevent mechanical trauma to the cervix.
SafetyFluconazole safety profile in pregnancy (reasons for avoidance):
- First-trimester use is associated with cleft lip with cleft palate and d-transposition of the great arteries (NBDPS study).
- Exposure between 7 and 22 weeks' gestation is associated with a statistically significant increased risk of spontaneous abortion.
- Potential anti-androgenic effect suggested by an association with shorter anogenital distance in male infants.
- Note: Accidental exposure to standard-dose fluconazole is not usually regarded as medical grounds for termination or additional fetal monitoring.
LactationFluconazole use during breastfeeding:
- Breast milk concentrations are expected to be very low and unlikely to be harmful.
- Breastfeeding can be maintained after a single 150 mg dose of fluconazole.
- Avoid breastfeeding after repeated or high doses of fluconazole; topical imidazoles remain the treatment of choice.
DiabetesDiabetes Mellitus Management:
- Symptomatic VVC is more prevalent and problematic in diabetic women with poor glycaemic control; improving glycaemic control should be encouraged.
- Non-albicans Candida species (specifically C. glabrata) are more prevalent in diabetic women.
- For confirmed C. albicans in acute VVC, prescribe oral fluconazole 150 mg as a single dose.
- For C. glabrata in symptomatic VVC, treat with boric acid 600 mg pessaries intravaginally at night for 14 consecutive nights (achieves a higher mycological cure rate at day 15 compared to a single dose of oral fluconazole 150 mg).
HIVHIV Infection Management:
- Treatment regimens for HIV-positive women should be identical to those for HIV-negative women, including suppressive therapy if required.
- VVC occurs more frequently and with greater persistence in HIV-infected women.
- Risk factors for symptomatic VVC in HIV: plasma HIV load >1000 copies/ml, CD4 count <200 cells/mm³, and absence of antiretroviral therapy (ART).
- Drug Safety: Clinicians must check www.hiv-druginteractions.org.uk for interactions between antifungals and antiretrovirals.
- VVC is not a risk factor for the acquisition of HIV.
HormonesHormones and Contraception:
- Hormone Replacement Therapy (HRT) is associated with an increased risk of VVC; symptomatic women with recurrent or persistent VVC should be informed of this link.
- Women with recurrent VVC using a combined oral contraceptive (COC), copper intrauterine device (Cu-IUD), or levonorgestrel intrauterine system (LNG-IUS) may trial alternative contraception.
- In vitro studies show Candida can adhere to vaginal rings and Cu-IUD surfaces, where it can produce a biofilm. In patients with refractory recurrent VVC (RVVC), removal of a biofilm-forming Cu-IUD may be required.
- Progestogen-only methods (desogestrel POP, implant, depot injection) theoretically reduce VVC by inducing anovulation and lowering oestrogen levels, but clinical evidence is limited and conflicting.

Contraceptive Methods and VVC Risk Associations

Contraceptive Method	Proposed Mechanism / Association	Evidence Quality & Clinical Findings
Copper IUD (Cu-IUD)	Candida can adhere to the device and produce a biofilm; identified as a possible risk factor for acute and recurrent VVC.	Mixed evidence of limited quality; some studies show higher rates of infection, others show no difference in symptomatic cases.
Levonorgestrel IUS (LNG-IUS)	Progestogen-releasing intrauterine device.	Mixed evidence of limited quality; conflicting data on whether it increases symptomatic VVC.
Combined Oral Contraceptive (COC)	Estrogen-induced changes in vaginal epithelium.	Inconsistent evidence; some studies show increased risk, others show no or negative association.
Vaginal Ring	In vitro studies show Candida adhesion to the ring surface.	Clinical studies do not demonstrate a higher incidence of VVC compared to COC users.
Progestogen-Only Methods (POP, Implant, Depot)	Theoretically protective by inducing anovulation and lowering systemic estrogen levels.	Limited and conflicting evidence. One study reported lower Candida carriage in POP/implant users compared to Cu-IUD/LNG-IUS users.

9Alternative and Supplementary Treatments

Grade 2CCetirizine 10 mg orally daily for six months may induce clinical remission in women who fail to achieve complete symptom resolution with suppressive fluconazole.
Grade 2CZafirlukast 20 mg orally twice daily for six months may be considered as maintenance prophylaxis for recurrent VVC, particularly in women with a history of atopy.
- Note: Zafirlukast was discontinued in the UK in 2018 for commercial reasons (no safety concerns). Montelukast is the closest available alternative, though it has not been studied specifically in VVC.
No EvidenceProbiotics (oral or vaginal Lactobacilli): Insufficient evidence to support use for treatment or prevention.
- Adjunctive use may improve clinical outcomes via inflammatory modulation rather than direct competition, but evidence is inconsistent.
No EvidenceTea tree and other essential oils: Antifungal in vitro, but may cause contact hypersensitivity; insufficient evidence for recurrent VVC.
No EvidenceDietary modifications: No evidence to support reducing dietary carbohydrates or yeast intake.
No EvidenceOral garlic: No evidence of benefit on Candida colonization.
- Side effects include heartburn, nausea, diarrhoea, flatulence, bloating, and offensive body odour.
UnderwearBreathable underwear with antimicrobial protection (Dermasilk) lacks sufficient evidence for routine recommendation.
- Small studies show some reduction in itching, burning, erythema, and recurrences compared to cotton briefs when used alongside standard suppressive fluconazole.
Yoghurt & HoneyVaginal applications of yoghurt and honey mixes are not supported by sufficient evidence, despite anecdotal reports of symptom improvement.

10Follow-up, Adverse Reactions, and Auditable Outcomes

Adverse EventsTreatment-related adverse events:
- Oral fluconazole (150 mg single dose): Most common side effects are headache, nausea, and abdominal pain.
- Hepatotoxicity: Low risk of idiosyncratic drug-induced hepatitis with oral azoles (fluconazole is less frequently associated with hepatotoxicity than itraconazole).
- Anaphylaxis: Rarely reported with fluconazole and itraconazole.
- Topical agents: Can cause local vulvovaginal irritation; consider this if symptoms worsen or persist.
Follow-UpFollow-up and test of cure (TOC) requirements:
- Acute VVC: Follow-up and TOC are unnecessary if symptoms resolve.
- Recurrent VVC: Advise patients to return if they have a poor or partial response. Repeat microscopy and culture are indicated to assess for microbiological cure or new resistance.
- Discordant response: Patients with microbiological cure but persistent clinical symptoms must be reassessed for alternative causes.
- Post-suppressive therapy: Advise patients on self-management of future acute episodes and when to return (e.g., recurrence frequency >4 episodes per year or acute symptoms failing to settle).
Grade 2CFurther Investigations in Recurrent VVC:
- Screen for diabetes mellitus using urinalysis, random blood glucose, or HbA1c if clinically indicated.
- Screen for iron-deficiency anaemia using a full blood count (FBC) or serum ferritin if clinical indicators are present.
- Consider screening for Mannose-Binding Lectin (MBL) deficiency in patients with suggestive clinical histories (e.g., recurrent upper respiratory tract infections, otitis media, or autoimmune conditions).