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Summary Table

Category	Details
Risk Factors	Recent antibiotic use, uncontrolled diabetes mellitus, pregnancy, oral contraceptive use, immunosuppression (HIV/AIDS, corticosteroids), obesity
Etiology	Candida albicans (85-90% of cases); non-albicans species (C. glabrata, C. tropicalis, C. krusei) account for the remainder
Patient Presentation	Intense vulvovaginal pruritus, vulvar burning/soreness, dysuria (external), dyspareunia
Classic Physical Exam	Vulvar erythema and edema, thick white "cottage cheese" discharge that is odorless, satellite lesions (erythematous papulopustules), excoriations from scratching
Key Diagnostic Results	Vaginal pH < 4.5 (normal acidic range), KOH wet mount showing pseudohyphae and budding yeast, negative whiff test
Management	Uncomplicated: oral fluconazole 150 mg single dose or short-course topical azole. Complicated/recurrent: extended fluconazole regimen. Pregnancy: topical azoles only (7-day course)
Keywords	"Cottage cheese discharge," "pruritus," "normal pH," "pseudohyphae on KOH," "recent antibiotic use," "no odor"

1. Pathophysiology

Candida species are normal commensals of the vaginal flora in approximately 20-30% of women. The organism exists in a balanced ecosystem alongside Lactobacillus species, which serve as the primary defense mechanism. Lactobacilli produce lactic acid and hydrogen peroxide, maintaining the vaginal pH in the acidic range (3.8 to 4.5) and inhibiting overgrowth of potentially pathogenic organisms including Candida.

Disease occurs when this equilibrium is disrupted. Antibiotic use is the most classic trigger tested on exams. Broad-spectrum antibiotics eliminate Lactobacillus populations, removing the competitive inhibition that keeps Candida in check. Without this restraint, the yeast transitions from its commensal yeast form to the pathogenic hyphal form, which penetrates the vaginal epithelium and triggers an inflammatory response. This is why pruritus, erythema, and edema dominate the clinical picture.

Estrogen plays a central role in susceptibility. Elevated estrogen levels (from pregnancy, combined oral contraceptives, or hormone replacement therapy) increase glycogen deposition in the vaginal epithelium. Glycogen is broken down into glucose, which serves as a carbon source for Candida proliferation. This explains why vulvovaginal candidiasis is rare before menarche and after menopause, and why it peaks during the reproductive years and pregnancy.

Diabetes mellitus promotes candidiasis through a related mechanism. Elevated blood glucose levels lead to increased glucose concentrations in vaginal secretions, directly fueling Candida growth. Poorly controlled diabetes also impairs neutrophil function, further weakening local immune defenses.

Cell-mediated immunity (T-helper type 1 response) is the dominant host defense against mucosal Candida infections. This is why patients with HIV/AIDS or those on immunosuppressive therapy are prone to recurrent and severe candidal infections. Notably, the vaginal pH remains normal (< 4.5) in candidiasis because the Lactobacillus population, while relatively suppressed, is not eliminated in the same way it is in bacterial vaginosis.

2. Classification and Clinical Manifestation

The distinction between uncomplicated and complicated disease is the single most important classification concept tested on exams, because it determines the treatment approach.

Feature	Uncomplicated	Complicated
Frequency	Sporadic or infrequent (< 4 episodes/year)	Recurrent (4 or more episodes/year)
Severity	Mild to moderate symptoms	Severe symptoms (extensive erythema, edema, excoriations, fissures)
Causative species	Likely C. albicans	Non-albicans species (C. glabrata, C. krusei)
Host factors	Immunocompetent, non-pregnant	Pregnant, uncontrolled diabetes, immunosuppressed (HIV, corticosteroid use)
Treatment approach	Single-dose or short-course therapy	Extended-duration or multi-dose therapy

Clinical Manifestation by Severity

Severity	Signs and Symptoms
Mild	Mild pruritus, scant discharge, minimal erythema
Moderate	Moderate pruritus and burning, visible "cottage cheese" discharge, vulvar erythema and edema
Severe	Intense pruritus with excoriations or fissure formation, extensive erythema, significant edema, possible satellite papulopustular lesions extending to the inguinal folds

A critical clinical point: the discharge in candidiasis is characteristically thick, white, curd-like, and odorless. The absence of odor is a strong discriminator from bacterial vaginosis (which has a "fishy" amine odor). Dysuria, when present, is external (burning when urine contacts the inflamed vulvar skin), not internal (which would point toward a urinary tract infection).

3. Diagnostic Workup

Test	Role	Expected Finding
Vaginal pH	Initial bedside assessment	< 4.5 (normal). If pH is elevated, reconsider the diagnosis
KOH wet mount (10% KOH)	Best initial test	Pseudohyphae and/or budding yeast cells
Saline wet mount	Adjunct to rule out competing diagnoses	May show yeast; also used to evaluate for clue cells or trichomonads
Whiff test (KOH)	Exclusion of bacterial vaginosis	Negative (no fishy amine odor)
Vaginal culture	Most accurate/confirmatory test	Positive for Candida species; allows speciation

Vaginal pH is the first branch point in the diagnostic algorithm. A pH below 4.5 immediately narrows the differential to candidiasis. Both bacterial vaginosis and trichomoniasis produce an elevated pH (> 4.5), so a normal pH effectively rules those conditions out. This is a quick, inexpensive bedside test and is heavily tested.

The KOH preparation is the best initial diagnostic test. Adding 10% potassium hydroxide to a vaginal discharge sample lyses epithelial cells and bacteria, making fungal elements easier to visualize. The hallmark finding is pseudohyphae (elongated chains of yeast cells with constriction points) or budding yeast. However, the sensitivity of KOH prep is only around 50-70%, meaning a negative result does not exclude the diagnosis.

The whiff test is performed simultaneously by smelling the KOH-treated slide. A positive whiff test (release of volatile amines producing a "fishy" odor) indicates bacterial vaginosis, not candidiasis. In candidiasis, the whiff test is negative.

Vaginal culture (typically on Sabouraud agar or chromogenic media) is the most accurate test and is reserved for situations where clinical suspicion is high but the KOH prep is negative, or when non-albicans species are suspected (treatment-resistant or recurrent infections). Culture also allows speciation, which guides therapy. This is particularly relevant when dealing with C. glabrata, which is often resistant to fluconazole.

A practical exam pearl: you do not need a culture for a straightforward first episode of candidiasis with classic symptoms and a positive KOH prep. Culture becomes necessary in recurrent disease, treatment failure, or when the presentation is atypical.

4. Management and Treatment

Clinical Scenario	Regimen	Duration
Uncomplicated	Fluconazole 150 mg PO, single dose	One-time
Uncomplicated (topical alternative)	Clotrimazole 1% cream intravaginally or miconazole 200 mg suppository	3 to 7 days
Severe (complicated)	Fluconazole 150 mg PO on day 1 and day 4 (some guidelines add day 7)	Two to three doses
Recurrent (4+ episodes/year)	Induction: fluconazole 150 mg PO on days 1, 4, 7. Maintenance: fluconazole 150 mg PO weekly	Maintenance for 6 months
Pregnancy	Topical azole only (clotrimazole or miconazole intravaginally)	7-day course
*Non-albicans (C. glabrata)*	Intravaginal boric acid 600 mg capsule daily	14 days

Uncomplicated vulvovaginal candidiasis is treated with a single oral dose of fluconazole 150 mg. This is the first-line regimen due to its convenience, high efficacy (> 90% cure rate for C. albicans), and patient preference. Topical azoles (clotrimazole, miconazole, terconazole) are equally effective and serve as alternatives, particularly when oral therapy is not desired or is contraindicated. There is no proven benefit of treating the male sexual partner in uncomplicated cases.

For severe disease (marked by extensive vulvar erythema, edema, excoriation, or fissure formation), a single dose is insufficient. The recommended approach is fluconazole 150 mg on day 1 and day 4, with some guidelines adding a third dose on day 7. The rationale is that severe inflammation requires a longer duration of antifungal exposure to achieve clinical and mycological cure.

Recurrent vulvovaginal candidiasis is defined as 4 or more symptomatic episodes in a 12-month period. This is a commonly tested threshold. Management involves two phases. The induction phase uses fluconazole 150 mg on days 1, 4, and 7 to achieve initial clearance. This is followed by a maintenance phase of fluconazole 150 mg once weekly for 6 months. After discontinuation, approximately 50% of patients will relapse, and some may need a longer or indefinite suppressive course. Culture and speciation should be performed to exclude non-albicans species before committing to a long-term azole regimen.

Pregnancy is a critical contraindication to oral fluconazole. Fluconazole, particularly at higher or repeated doses, is classified as teratogenic and has been associated with craniofacial and cardiac abnormalities. The only acceptable treatment in pregnancy is topical azoles (intravaginal clotrimazole or miconazole) for a full 7-day course. This is one of the most tested contraindications in this topic.

For infections caused by non-albicans species, particularly C. glabrata, standard fluconazole therapy often fails because these organisms carry intrinsic or acquired azole resistance. The recommended alternative is intravaginal boric acid 600 mg capsules daily for 14 days. If boric acid is unavailable or fails, intravaginal nystatin or flucytosine cream are second-line options. Importantly, boric acid is toxic if ingested orally and must only be used intravaginally.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Bacterial vaginosis (BV)	Both present with vaginal discharge	BV has a thin, grayish-white, homogeneous discharge with a fishy odor, pH > 4.5, positive whiff test, and clue cells on saline prep. Candidiasis has thick curd-like discharge, no odor, and normal pH.
Trichomoniasis	Both cause vulvovaginal irritation and dysuria	Trichomoniasis produces a frothy, yellow-green, malodorous discharge with pH > 4.5, "strawberry cervix" (punctate hemorrhages), and motile trichomonads on saline wet mount.
Contact dermatitis	Both cause vulvar pruritus and erythema	Contact dermatitis has a history of exposure to an irritant (new soap, detergent, spermicide). No abnormal discharge, negative KOH prep, normal vaginal flora.
Lichen sclerosus	Both cause vulvar pruritus	Lichen sclerosus shows "parchment paper" or "cigarette paper" skin with white plaques, labial fusion, and atrophic changes. Occurs more commonly in postmenopausal women. Biopsy is diagnostic.
Vulvar herpes (HSV)	Both cause vulvar pain/burning and dysuria	HSV presents with painful vesicles or shallow ulcers, systemic symptoms (fever, malaise) in primary outbreak, inguinal lymphadenopathy. Tzanck smear or PCR confirms.

The most commonly tested distractor is bacterial vaginosis. The exam writers rely on three branch points to distinguish them: discharge character (thick vs. thin), odor (absent vs. fishy), and pH (normal vs. elevated). Memorize these three parameters and you can reliably differentiate the two conditions.

6. Traps and High-Yield Pearls

The most common trap in exam questions on vulvovaginal candidiasis involves pH. Many students associate all forms of vaginitis with an elevated pH, but candidiasis is the notable exception. A vignette describing pruritus, vaginal discharge, and a pH of 4.0 should immediately point toward candidiasis. If the vignette gives a pH above 4.5, you need to pivot to bacterial vaginosis or trichomoniasis regardless of how "yeast-like" the discharge sounds.

The second major trap is fluconazole in pregnancy. A vignette will describe a pregnant woman with classic candidiasis and offer fluconazole as one of the answer choices. This is always wrong. The correct answer is a topical azole for 7 days. This tests whether you know the teratogenicity concern with oral azoles.

A third commonly tested angle involves treatment failure. When a patient returns with persistent symptoms after appropriate fluconazole therapy, the next step is to obtain a vaginal culture with speciation. The exam is testing whether you recognize that non-albicans species (particularly C. glabrata) are inherently resistant to fluconazole, and that boric acid is the appropriate alternative.

Finally, be careful with the KOH prep. A negative KOH prep does not rule out candidiasis. If clinical suspicion remains high (classic symptoms, normal pH, negative whiff test), the next step is culture, not reassurance. The core competency being tested across all these scenarios is pattern recognition of the classic presentation (pruritus, cottage cheese discharge, normal pH, pseudohyphae) combined with the ability to navigate contraindications and treatment-resistant cases.

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