Candidiasis

Introduction

Candida is a genus of yeast that lives as a normal commensal of the skin, gastrointestinal tract and genital tract in most healthy people. Disease occurs when the local or systemic balance that keeps it in check is disrupted - by antibiotics removing competing bacterial flora, by a compromised immune system, or by a moist, occluded environment that favours overgrowth. Candida albicans remains the commonest cause of clinical candidiasis, but non-albicans species (C. glabrata, C. krusei, C. tropicalis, and the emerging C. auris) are increasingly important because they carry different, sometimes more concerning, resistance patterns.

Candidiasis spans an enormous range of severity, from a trivial and extremely common nuisance (oral or vaginal thrush) to a genuine bloodstream infection with mortality comparable to severe bacterial sepsis. This range is exactly why it is examined: the same organism, in a different host and a different site, demands an entirely different level of concern and a different management plan.

Risk factors

• Broad-spectrum antibiotics - suppress competing bacterial flora and allow Candida overgrowth
• Immunosuppression - HIV, chemotherapy, long-term corticosteroids, and other significant immunosuppressive treatment
• Diabetes mellitus
• Indwelling central venous catheters - a major risk factor for bloodstream candidaemia
• Neutropenia
• Total parenteral nutrition
• Pregnancy
• Occlusive moisture - skin folds, dentures, incontinence pads
• Inhaled corticosteroids without adequate mouth rinsing afterwards - a common and easily preventable cause of oral thrush

Clinical syndromes

Oropharyngeal candidiasis (oral thrush)

White plaques on the tongue and buccal mucosa that can be scraped off, sometimes revealing a raw or bleeding surface underneath - the feature that distinguishes it from leukoplakia, which does not wipe away. Angular cheilitis (cracking and inflammation at the corners of the mouth) often coexists.

Oesophageal candidiasis

Presents with dysphagia or odynophagia. It is an AIDS-defining illness in HIV and should prompt consideration of significant immunosuppression if there is no other obvious explanation. Diagnosis is often made on a strong clinical picture with a treatment trial, or confirmed at endoscopy if the diagnosis is uncertain or symptoms fail to respond.

Vulvovaginal candidiasis

Extremely common: pruritus with a thick, white, non-offensive ("cottage cheese") discharge and vulval erythema. Recurrent disease (generally defined as four or more episodes a year) should prompt a check for underlying diabetes or immunosuppression, though many cases occur in otherwise healthy women.

Cutaneous candidiasis

Typically presents as intertrigo - a moist, erythematous rash in skin folds (groin, under the breasts, abdominal folds), with satellite lesions - small papules or pustules scattered just beyond the main patch - a key distinguishing sign from other causes of intertrigo. Also causes nappy rash in infants and chronic paronychia around the nail folds.

Invasive candidiasis and candidaemia

Bloodstream infection with Candida, seen particularly in critically ill patients, those with central venous catheters, and the significantly neutropenic. It should be actively considered in unexplained sepsis in a patient with these risk factors, particularly where broad-spectrum antibacterial treatment has already failed to produce improvement.

Chronic mucocutaneous candidiasis

A rare condition, associated with specific T-cell immunodeficiencies (for example APECED syndrome), causing persistent, treatment-resistant candidiasis of the skin, mucosa and nails from early life.

Differential diagnosis

• Oral leukoplakia - a white patch that cannot be scraped off, and a premalignant condition rather than an infection
• Oral lichen planus - a lacy, reticular white pattern, distinct from the discrete plaques of thrush
• Bacterial vaginosis - a thin, grey, fishy-smelling discharge with a raised vaginal pH, versus the thick, non-offensive discharge and normal-to-low pH of candidiasis
• Trichomonas vaginalis - a frothy, yellow-green discharge, sometimes with a "strawberry cervix" on examination
• Other causes of intertrigo - bacterial (erythrasma, responding to Wood's lamp examination with coral-pink fluorescence), or inverse psoriasis, which lacks the satellite lesions of candidal intertrigo

Investigations

Superficial candidiasis is usually a clinical diagnosis. Investigation becomes important once invasive disease is a possibility, or where species identification will change management.

• Microscopy and culture of a swab - KOH preparation shows budding yeast and pseudohyphae; culture allows species identification
• Blood cultures - the standard test for candidaemia, though sensitivity is imperfect (often quoted around 50-70%), so a negative culture does not fully exclude invasive disease in a high-risk patient
• Beta-D-glucan assay - a fungal cell wall marker used as an adjunct in suspected invasive candidiasis, particularly where cultures are negative but suspicion remains high
• Echocardiography - for anyone with confirmed candidaemia, to look for endocarditis
• Dilated ophthalmological examination - for anyone with confirmed candidaemia, to look for endophthalmitis

Management

Superficial disease

• Oral thrush - topical nystatin suspension or miconazole gel for mild disease; oral fluconazole for more extensive disease or in the immunocompromised
• Oesophageal candidiasis - systemic (oral or IV) fluconazole, since topical treatment cannot adequately reach the oesophageal mucosa
• Vulvovaginal candidiasis - a single dose of oral fluconazole, or a topical azole pessary/cream (e.g. clotrimazole); recurrent disease is managed with a longer induction and maintenance regimen
• Cutaneous candidiasis - topical antifungal (clotrimazole or miconazole), and addressing contributing moisture or occlusion where possible

Invasive candidiasis and candidaemia

• An echinocandin (e.g. caspofungin) is generally first-line empirical therapy, particularly in unstable patients or those with recent azole exposure, reflecting broader activity against resistant species
• Step-down to fluconazole once the patient is stable and the isolate is confirmed susceptible
• Remove or replace any central venous catheter - source control is essential, since a line can act as a persistent nidus of infection that antifungals alone will not clear
• Treatment duration is typically at least 2 weeks from the first negative blood culture, extended for endocarditis, endophthalmitis or other deep-seated disease
• Ophthalmology review as above, since untreated endophthalmitis can threaten vision

Candida auris

An emerging species responsible for healthcare-associated outbreaks worldwide, notable for being frequently multidrug-resistant, sometimes to all three main antifungal classes. It persists on surfaces and skin, spreads readily between patients in healthcare settings, and can be difficult to identify with standard laboratory methods. Confirmed or suspected cases require strict contact precautions and prompt infection control team involvement, reflecting its status as a genuine and growing public health concern rather than simply another resistant organism.

Complications

• Endophthalmitis - can threaten vision if untreated, hence the routine ophthalmology review in candidaemia
• Endocarditis - particularly on prosthetic valves or in people who inject drugs
• Hepatosplenic candidiasis - classically seen in neutropenic patients as their neutrophil count recovers, presenting with fever and abdominal pain with characteristic imaging findings
• Sepsis and septic shock
• Death - candidaemia carries a significant mortality, commonly quoted around 30-40% even with appropriate treatment, reflecting how unwell the underlying patient population typically is

Red flags

Prognosis

Superficial candidiasis - oral, vaginal or cutaneous - responds well to appropriate topical or short-course oral treatment in the great majority of cases, though recurrence is common if the underlying risk factor is not addressed. Invasive candidiasis and candidaemia carry a substantial mortality, driven as much by the severity of the underlying illness (critical illness, profound immunosuppression) as by the infection itself, which is why prompt source control and species-directed antifungal therapy make a measurable difference to outcome.