Cutaneous Candidiasis

Updated: Jan 17, 2020
Author: Richard Harold "Hal" Flowers, IV, MD; Chief Editor: Dirk M Elston, MD 



Cutaneous candidiasis and other forms of candidiasis are infections caused by the yeast Candida albicans or other Candida species. Yeasts are unicellular fungi that typically reproduce by budding, which entails progeny pinching off of the mother cell. C albicans, the principal infectious agent in human infection, is an oval yeast 2-6 µm in diameter.

Superficial infections of skin and mucous membranes are the most common types of cutaneous candidiasis. These include intertrigo, diaper dermatitis, erosio interdigitalis blastomycetica, perianal dermatitis, and candidal balanitis. Candidal infections of the skin have become more prevalent in recent years, principally because of the increased numbers of immunocompromised patients. Less common types of candidiasis include esophagitis, septicemia, endocarditis, peritonitis, and urinary tract infections.

Although C albicans is the most common cause of human infection, the genus Candida includes more than 150 species. Candida tropicalis, Candida parapsilosis, Candida guilliermondi, Candida krusei, Candida kefyr, Candida zeylanoides, and Candida glabrata (formerly Torulopsis glabrata) are less common causes of human disease. Candida auris is an emerging pathogen often showing antifungal resistance.

Humans carry yeast, including Candida species, throughout the gastrointestinal tract (mouth through anus) as part of the normal commensal flora. The vagina is commonly colonized by yeast, most often by C albicans and C glabrata. The commensal oral isolation of candidal species ranges from 30-60% in healthy adults.[1] Candida species are not part of the normal flora of the skin but may colonize fingers or body folds transiently.

Also see the articles Mucosal Candidiasis and Candidiasis.


Candida is a versatile fungus that can exist commensally in many locations of the human body. Several different adaptive mechanisms help Candida survive in such diverse anatomical areas. The ability of C albicans to adjust to the different pH environments found in regions such as the bloodstream, at a neutral pH, versus the vagina, which has a more acidic pH, is explained by the differential expression of pH-regulated genes. In acidic environments, C albicans expresses PHR2, while in environments of pH 5.5 or higher, PHR1 is expressed to a greater extent.[2]

Another critical virulence factor is the ability of Candida to adhere to the host tissue. The protein Hwp1 is vital for C albicans to form attachments to host tissue, as is CaMnt1p, a mannosyl transferase.[3, 4] The ability of yeast forms to adhere to the underlying epithelium is an important step in the production of hyphae and tissue penetration.

In a broader view, a 2013 review of pathologic mechanisms of C albicans cited (1) the secretion of hydrolases, (2) molecules that mediate adhesion with concomitant invasion into host cells, (3) the yeast-to-hypha transition, (4) biofilm formation, (5) contact sensing and thigmotropism, (6) phenotypic switching, and (7) a variety of fitness attributes.[5] Candida species also produce proteases, which contribute to pathogenicity.

In a more narrow lens, additional research has elucidated the effect of Candida on keratinocytes. Within the epidermis, C albicans phospholipomannan triggers an inflammatory response through Toll-like receptor (TLR)–2.[6] Additionally, C albicans aborts the expression of interferon-gamma–inducible protein-10 in human keratinocytes.[7] Once C albicans invades the keratinocytes, the host cells express host defense proteins and secrete chemokines and cytokines.[4, 8] Melanocytes also play a role in the innate immune system; these cells detect C albicans through TLR4 and begin producing antimicrobial products and melanin, which can sequester and, in some cases, kill, the fungi. Langerhans cells detect C albicans via Dectin-1 and initiate a Th17 response via interleukin (IL)–6.[8] Furthermore, CD103+ dermal Langerhans cells, upon interaction with TLR-2, enhance Th1 production in secondary lymphoid organs.[8]

Observing the effects of deficiency in key regulatory molecules has helped elucidate host defense against Candida. For example, IL-17 is essential to combat C albicans infections.[9, 10, 11] Thus, phenotypes that knock out IL-17 are more susceptible to C albicans and drugs such as secukinumab, an IL-17 blocker used for psoriasis, can increase the incidence of candidal infections. Relatedly, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED)—secondary to mutations in the autoimmune regulator (AIRE) gene—predispose to mucocutaneous Candida infection. In patients with this disease, autoantibodies to IL-17A can be linked to mucocutaneous candidiasis severity.[12]

STAT1 gain-of-function mutations, as well as STAT3 loss-of-function mutations (which cause the autosomal dominant hyper-IgE syndrome), are both associated with mucocutaneous candidiasis.[13, 14] Mucocutaneous Candida infections can be the presenting sign of IL-12 receptor β1 deficiency.[15]  Additionally, Candida is a catalase-positive fungi; therefore, patients with chronic granulomatous disease (CGD), which is due to a mutation in the NADPH oxidase complex involved in respiratory burst, are at increased risk for Candida infection.[16] In those with CGD, Candida is the most common cause of meningitis, fungemia, and lymphadenitis.[17]


Host factors that predispose patients to infections include local factors, endocrine diseases, nutritional deficiencies, and systemic immunodeficiency. Local factors such as tissue damage resulting from trauma, xerostomia, radiation-induced mucositis, ulcerations, skin maceration, or occlusion enhance adhesion and predispose patients to increased infection rates. Cutaneous candidiasis has been reported to be more common in women than in men.[18, 19]

Nutritional deficiencies may alter host defense mechanisms or epithelial barrier integrity, allowing increased adherence or penetration. Iron deficiency anemia and deficiencies including vitamins B-1, B-2, B-6, C, and folic acid are associated with heightened infection rates.[20, 21]

Endocrine diseases such as diabetes mellitus, Cushing syndrome, hypoparathyroidism, hypothyroidism, and polyendocrinopathy are also associated with increased susceptibility to infection. The mechanism by which diabetes mellitus is believed to raise infection rates is through increased tissue glucose, altered yeast adhesion, and decreased phagocytosis.[22] Chronic mucocutaneous candidiasis refers to recurrent and chronic Candida infections of the epidermis, nails, and mucosal membranes. It is associated with a variety of autoimmune conditions and endocrine disorders.[23]

T-lymphocyte–mediated immunity plays an important immunologic role against infection through phagocytosis and killing by polymorphonuclear cells and macrophages. Individuals with deficient T-lymphocyte function, such as patients with AIDS, appear to be particularly vulnerable to mucosal or cutaneous candidiasis. Patients with primary immune deficiencies, such as lymphocytic abnormalities, phagocytic dysfunction, IgA deficiency, viral-induced immune paralysis, and severe congenital immunodeficiencies, often are affected by oropharyngeal candidiasis and other fungal mycoses.[24]


Candida species are a common cause of intertrigo in both elderly and diabetic patients. Candida species currently are the fourth leading cause of bloodstream infections in the United States, with occurrence at a disproportionately high rate in persons aged 65 years and older.[25]


Neonatal cutaneous and systemic candidiasis have become increasingly prevalent in neonatal intensive care nurseries. Postnatal acquisition has been attributed to increased survival rates of low-birth-weight babies in association with an increased number of invasive procedures and widespread use of broad-spectrum antibiotics. In neonates, parenteral nutrition, time in the intensive care unit, and mechanical ventilation are major risk factors for infection.[26] Neonatal candidiasis presents 3-7 days after birth with oral thrush and diaper dermatitis. This has been attributed to mucosal contact with the organism during labor and delivery. Neonatal candidiasis is distinct from congenital candidiasis, a more common infection, which occurs after birth as opposed to in utero and often preferentially involves the oral area.[27]

The number of candidal infections has risen dramatically in recent years, mirroring the increasing number of patients who are immunocompromised.[28] Increased age appears to be associated with increased morbidity and mortality.[29] Older adults are more likely to be exposed to situations that increase the risk of invasive candidiasis, including treatment with broad-spectrum antibiotics, hyperalimentation, and increased contact with invasive monitoring devices in an intensive care unit.[30]

Candidal infections are exacerbated by certain medications (eg, antibiotics), poor self-care, and decreased salivary flow (oral candidiasis), all of which often are associated with aging. In addition, treatment with cytotoxic agents (eg, methotrexate, cyclophosphamide) for dermatologic and rheumatic conditions or aggressive chemotherapy for malignancy in elderly patients puts them at higher risk.


Superficial candidal infections cause significant morbidity in older adults but are well treated with topical or oral therapy. Identification and cessation of triggers or aggravating factors is critical to prevent recurrence.

Systemic congenital candidiasis carries a grave prognosis and can lead to respiratory distress, meningitis, sepsis, or death.[31] Although the prognosis for congenital cutaneous candidiasis is generally good, untreated disease may carry a mortality rate of 8-40%.[27, 32]

Chronic mucocutaneous candidiasis (CMC) as an isolated cutaneous disease with a good prognosis. However, it is not curable and remains a chronic condition. It is often found in conjunction with endocrine and autoimmune disorders and, in some cases, may progress to an invasive infection; in both of these cases, there is high morbidity.[33] Furthermore, fatal conditions such as oral or esophageal squamous cell carcinoma and cerebral aneurysm, although rare, can be associated with CMC.[23, 34]

In patients with chronic granulomatous disease (CGD), those with Candida infection of the soft tissue or bone overall have a good prognosis.[35] However, if the infection becomes disseminated, significant morbidity may be observed.[35]

Patient Education

For patient education resources, Candidiasis (Yeast Infection), Yeast Infection Diaper Rash, and Yeast Infection Skin Rash.




Candidal vulvovaginitis

This common condition in women presents with itching, soreness, and a thick creamy white discharge (see the images below). Although most candidal infections occur more frequently with advancing age, vulvovaginitis is unusual in older women. It is most prevalent in women aged 25-34 years, and, based on survey data, globally nearly 75% of women experience vulvovaginitis at least once.[36] In the absence of estrogen stimulation, the vaginal mucosa becomes thin and atrophic, producing less glycogen. Candidal colonization of vaginal mucosa is estrogen dependent and subsequently decreases sharply after menopause.

Vaginal candidiasis. Erythema, edema, and cheesy w Vaginal candidiasis. Erythema, edema, and cheesy white discharge. Courtesy of Kenneth Greer, MD.
Vulvar candidiasis. Bright erythema with scaling, Vulvar candidiasis. Bright erythema with scaling, fissuring, and satellite papules. Courtesy of Kenneth Greer, MD.

In contrast, the likelihood of colonization increases during pregnancy (25-33%). The widespread use of hormone replacement for reduction of osteoporosis and heart disease may cause an increasing trend in candidal vulvovaginitis among older women. Cutaneous hypersensitivity to C albicans has been reported in persons with idiopathic vulvodynia.[37]

Candidal balanitis

Signs and symptoms of this candidal infection vary but may include tiny papules, pustules, vesicles, or persistent ulcerations on the glans penis (see the image below). Exacerbations following intercourse are common. Candidal balanitis may be associated with diabetes mellitus and an lack of circumcision in males.[38, 39]

Dry, red, superficially scaly, pruritic macules an Dry, red, superficially scaly, pruritic macules and patches on the penis represent candidal balanitis.

Congenital candidiasis

Congenital candidiasis[40, 41]  is rare, with 70 cases reported during the 1990s. It may be acquired by the infant in utero or during delivery. Presumably, congenital candidiasis is an ascending intrauterine infection with cutaneous or systemic manifestations generally within 12 hours after birth (see image below). Although the systemic form typically is fatal, congenital cutaneous infections usually have a more benign course unless untreated. Prematurity and the presence of an intrauterine foreign body (intrauterine device) are associated with this condition. Some infants have respiratory distress and pneumonia secondary to in utero aspiration of infected amniotic fluid.

Discrete superficial pustules developed within hou Discrete superficial pustules developed within hours of birth on the hand of an otherwise healthy newborn. A potassium hydroxide preparation revealed spores and pseudomycelium, and culture demonstrated the presence of Candida albicans.

Candidal diaper dermatitis[42]

Infants with oropharyngeal candidiasis invariably harbor C albicans in the intestine and feces (85-90%). Colonized stools represent the most important focus for cutaneous infection. Moist macerated skin is particularly susceptible to invasion by C albicans. Additional factors that predispose infants to candidal diaper dermatitis include local irritation of the skin by friction; ammonia from bacterial breakdown of urea, intestinal enzymes, and stool; detergents; and disinfectants.

Oral candidiasis

Also known as oral thrush, this is considered as a minor problem of little significance that may clear spontaneously. However, without appropriate treatment, this can lead to a chronic condition that can result in discomfort and anorexia. Rarely, oropharyngeal infection leads to systemic candidiasis.

Oropharyngeal candidiasis in the neonate, commonly called oral thrush, is often acquired from the infected maternal mucosa during passage of the infant through the birth canal. Oropharyngeal candidiasis is 35 times more common in neonates of infected mothers compared with uninfected mothers and is the most common type of clinical presentation in infants and children. Immaturity of host defenses and incomplete establishment of the normal orointestinal flora are likely reasons why C albicans often acts as a pathogen in the neonate.

Use of broad-spectrum antibiotics and inhaled corticosteroids, diminished cell-mediated immunity, diabetes mellitus, dentures, and xerostomia are all risk factors for oral candidiasis in adults.

See the image below.

White plaques are present on the buccal mucosa and White plaques are present on the buccal mucosa and the undersurface of the tongue and represent thrush. When wiped off, the plaques leave red erosive areas.

Xerostomia may result from aging, medication, or conditions like Sjögren syndrome. A decrease in salivary production decreases both the amount of available mucosal secretory antibody (IgA) and the natural cleansing action provided by saliva.

The development of oral thrush in the absence of a known etiology should raise the clinician's index of suspicion for an underlying cause of immunosuppression, such as malignancy or AIDS.[43]

With denture stomatitis, the areas of erythema may be painful and may affect up to 65% of patients who wear dentures, especially those who wear full sets. Despite popular belief, denture stomatitis is not associated with smoking.[44]


Most cases of cutaneous candidiasis occur in skin folds where occlusion (by clothing or shoes) produces abnormally moist conditions. Sites such as the perineum, mouth, and anus, in which Candida organisms normally may be carried, are at further risk of infection. Candidal infection of the skin under the breasts or pannus occurs when those areas become macerated (see the image below).

Erythema, maceration, and satellite pustules in th Erythema, maceration, and satellite pustules in the axilla, accompanied by soreness and pruritus result in a form of intertrigo.

Decubital candidiasis

Decubital candidiasis is a particular form of cutaneous candidiasis that occurs on the skin of chronically bedridden patients.[45]


Candida occasionally causes infection in the periungual area and underneath the nailbed (see the image below). Candida species (not always C albicans) can be isolated from most patients with chronic paronychia. The yeast is believed to play an etiologic role in this condition, but bacteria also may act as co-pathogens. Disease is more common in people who frequently submerge their hands in water.

A nailfold with candidal infection becomes erythem A nailfold with candidal infection becomes erythematous, swollen, and tender with an occasional discharge.

Candidiasis and HIV

Many patients with HIV infection have some form of candidal infection during the illness. Recurrent episodes of oral candidiasis typically occur in patients in whom CD4 counts are less than 300/µL, an important marker of disease progression. Additionally, Yanagisawa et al,[46] in 2007, reported on a case of disseminated candidiasis as an initial presentation of AIDS. Such cases often manifest with purpuric eruptions.


Other rare presentations include ecthyma gangrenosum–like lesions in a neonate,[47] deep-seated subcutaneous ulcer,[48] interdigital ulcer,[49] and generalized cutaneous candidiasis complicating Darier disease.[50]

Physical Examination

Candidal vulvovaginitis

Clinical examination reveals erythema of the vaginal mucosa and vulvar skin, with curdy white flecks within the discharge. Erythema may spread to include the perineum and groin, with satellite pustules. Alternatively, the vaginal mucosa may appear red and glazed. A patient presenting with symptoms of vulvovaginitis with identification of yeasts in the vaginal discharge has a diagnosis of candidiasis.

Congenital candidiasis

Cutaneous congenital candidiasis typically manifests as an erythematous eruption of macules, papules and superficial pustules on the trunk and extremities, which resolves with extensive desquamation (see image below). The presence of white microabscesses on the placenta and umbilical cord of an infant with such an eruption suggests the diagnosis of cutaneous congenital candidiasis. It is always secondary to candidal chorioamnionitis, but it may pass unrecognized.

Fine superficial pustules on an erythematous patch Fine superficial pustules on an erythematous patchy base are suggestive of candidosis.

Candidal diaper dermatitis

Candidal diaper dermatitis usually starts in the perianal area, spreading to involve the perineum and, in severe cases, the upper thighs, lower abdomen, and lower back. Maceration of the anal mucosa and the perianal skin often is the first clinical manifestation. Scaly papules merge to form well-defined, weeping, and eroded lesions with a scalloped border. A collar of overhanging scales and an erythematous base may be demonstrated. Satellite flaccid vesicopustules around the primary intertriginous plaque also are characteristic and represent the primary lesions.

Rarer and severe forms of candidal diaper dermatitis include granuloma gluteale infantum and Jacquet erosive diaper dermatitis. Granuloma gluteale infantum can be a complication of diaper dermatitis and presents as erythematous-to-purplish nodules and plaques in the anogenital region of infants.[51] In addition to candidal diaper dermatitis, other risk factors that indicate a predisposition to granuloma gluteale infantum are restrictive synthetic pants and topical corticosteroid use. Jacquet erosive diaper dermatitis is an uncommon variant of diaper dermatitis often seen in occluded skin in lengthy contact with urine or feces.[52] It presents on the genital and perianal skin as superficial ulcerations or pustules.[52]

Oral candidiasis

In the infant, lesions become visible as pearly white patches on the mucosal surfaces. Buccal epithelium, gums, and the palate commonly are involved with extension to the tongue, pharynx, or esophagus in more severe cases. If the lesions are scraped away, an erythematous base is exposed. Lesions may progress to symptomatic erosion and ulceration.

The most common clinical appearance of oropharyngeal candidiasis (pseudomembranous candidiasis or oral thrush) in the adult population is white plaques on the buccal, palatal, or oropharyngeal mucosa overlying areas of mucosal erythema. Typically, the lesions are adherent, which, when removed, may demonstrate areas with tiny ulcerations. Sometimes, oral candidiasis manifests as diffuse erythema. A variant of oral candidiasis, median rheumatoid glossitis, presents as a discrete cherry-red patch on the posterior tongue. In addition, some patients may develop soreness and cracks at the lateral angles of the mouth called angular cheilitis (see image below). Denture stomatitis[17] presents as chronic mucosal erythema typically beneath the site of a denture.

Soreness and cracks at the lateral angles of the m Soreness and cracks at the lateral angles of the mouth (angular cheilitis) is a frequent expression of candidosis in elderly individuals.


Candidal intertrigo typically presents as an intensely pruritic, bright-pink, macerated rash with satellite papules and pustules. Erosio interdigitalis blastomycetica (interdigital candidiasis) manifests as hyperhidrosis and maceration and favors the skin between the third and fourth fingers.

Candidal paronychia

The proximal nailfold becomes chronically erythematous and swollen, with loss of the cuticle, nail dystrophy, and onycholysis (see the image below). This can usually be distinguished clinically from acute paronychia, which is caused by Staphylococcus aureus and presents with proximal abscess formation. This can be secondary to bacterial infection with Pseudomonas, which displays a green discoloration under the nail. A potassium hydroxide (KOH) preparation is helpful and is likely to show yeast organisms.

Chronic paronychia. Edema and erythema of the nail Chronic paronychia. Edema and erythema of the nailfolds with loss of the cuticle; note greenish discoloration of nails from likely pseudomonal coinfection. Courtesy of Kenneth Greer, MD.




Diagnostic Considerations

Differential diagnoses for candidal intertrigo are as follows[53, 54] :

  • Allergic contact dermatitis
  • Irritant contact dermatitis
  • Seborrheic dermatitis
  • Atopic dermatitis
  • Inverse psoriasis
  • Pemphigus vegetans
  • Hailey-Hailey disease

Differential diagnoses for oropharyngeal candidiasis are as follows[55, 56] :

  • Lichen planus
  • Herpes
  • Geographic tongue
  • Oral hairy leukoplakia
  • Aphthous ulcers
  • Erythema multiforme
  • Pernicious anemia
  • Leukoplakia
  • Chemotherapy-related mucositis
  • Squamous cell carcinoma
  • Zinc deficiency
  • Hairy tongue
  • White sponge nevus
  • Pemphigus


Laboratory Studies

KOH preparation is the easiest and most cost-effective method for diagnosing cutaneous candidiasis, but its use is not sufficient in the absence of other supporting clinical evidence.

Culture from an intact pustule, skin biopsy tissue, or desquamated skin can help to support the diagnosis.

Microscopic examination of skin scrapings prepared with calcofluor white stain is a simple way of detecting yeasts and pseudohyphae of C albicans. C albicans binds nonspecifically to polysaccharides found in fungal cell walls and produces a distinct bright color in a pattern characteristic for the organism when viewed under a fluorescence microscope.

Histologic Findings

A skin biopsy specimen stained with a periodic acid-Schiff stain reveals nonseptated hyphae. The presence of nonseptated hyphae allows cutaneous candidiasis to be distinguished from tinea. Classically, neutrophils are seen in the stratum corneum.[57] In the subsequent epidermis, focal spongiosis and mild acanthosis may be noted.[57]

Of all the types of Candida, the electron microscope shows that C albicans is the most confluent in its adherence to the skin.[58]



Approach Considerations

While topical antifungal drugs are used most frequently in the treatment of cutaneous C albicans infection, there is concern about rising resistance to these therapies. In particular, reports of Candida strains displaying resistance to azoles and echinocandins have increased in recent years and present a concerning development in the management of invasive candidiasis.[59] Furthermore, the rise of C auris, a pathogenic strain of Candida exhibiting antifungal resistance, is a concerning development and is often found in nosocomial settings. The increasing prevalence of this species is thought to be due to the use of prophylactic systemic antifungal agents such as fluconazole.[60] A 2020 report from the US Centers for Disease Control and Prevention described three chronically ill people in New York who were identified as having pan-resistant C auris infection.[61] The report stated that the pan-resistant C auris infection developed after the patients had received antifungal medications, including echinocandins, a class of drugs that targets the fungal cell wall. As a result, other treatment options are being considered, including antimicrobial peptides, blue/ultraviolet light, and probiotics.[62, 63, 64, 65]

Medical Care

Candidal vulvovaginitis

Topical antifungal agents, including nystatin, miconazole nitrate (Micatin, Monistat-Derm), or clotrimazole (Lotrimin, Mycelex) creams, are generally curative. One-time oral therapy with fluconazole (150 mg) or itraconazole (600 mg) is effective and may be a more attractive alternative to some patients.

Candidal balanitis

Topical therapy is sufficient in most patients. Asymptomatic sexual partners should be evaluated and treated if they are affected. If persistent lesions spread beyond the genitalia, diabetes should be considered.

Congenital candidiasis

Topical preparations usually are effective unless the infection is disseminated, in which case systemic medication is needed. Most patients can be treated with nystatin oral suspension. Usual treatment is 10-14 days or until 48-72 hours after resolution of symptoms. Dosage for preterm infants is 0.5 mL (50,000 U) to each side of mouth 4 times/day; dosage for infants is 1 mL (100,000 U) to each side of the mouth 4 times/day.

Candidal diaper dermatitis

Treatment for candidal diaper dermatitis includes practical measures that reduce the amount of time the diaper area is exposed to hot and humid conditions. Air drying, frequent diaper changes, and generous use of talc-free baby powders and zinc oxide paste are adequate preventive measures. For topical therapy of candidal diaper dermatitis, nystatin, amphotericin B, miconazole, and clotrimazole are effective and almost equivalent in efficacy. For more severe forms of diaper dermatitis, control of underlying causative factors, especially diarrhea, is necessary.

Oral candidiasis

Most patients can be treated with nystatin oral suspension. Usual treatment is 10-14 days or until 48-72 hours after resolution of symptoms. Dosage for preterm infants is 0.5 mL (50,000 U) to each side of mouth 4 times/day; dosage for infants is 1 mL (100,000 U) to each side of the mouth 4 times/day.

Treatment of adults with a topical agent such as nystatin (1:100,000 U/mL, 5 mL oral rinse and swallow four times daily) or clotrimazole troches (10 mg 5 times/day) usually is effective. In most patients, the duration of antifungal therapy should be at least twice as long as the termination of clinical signs and symptoms of candidiasis. Oral fluconazole, 100 mg once daily for 2 weeks, can be used for patients with more severe disease.

With denture stomatitis, improved oral hygiene with removal of dentures at night, vigorous brushing to remove plaque, and disinfecting (swish and spit) with chlorhexidine gluconate (Peridex) usually is adequate treatment. Topical therapy with clotrimazole troches or nystatin may be used for lesions that do not respond to the above measures. For more resistant cases, oral fluconazole, 100 mg/day for several weeks, in addition to the above measures, may prove effective.

Candidal intertrigo

Treatment is targeted at keeping the skin dry, with the addition of topical nystatin powder, clotrimazole, or miconazole twice daily, often in conjunction with a mild topical corticosteroid if needed for itching. Patients with extensive infection may require the addition of fluconazole (100 mg PO qd for 1-2 wk) or itraconazole (100 mg PO qd for 1-2 wk).


Treatment with topical agents may not be effective but can be attempted for chronic candidal paronychia.[66] Antifungal solutions are preferred over creams to allow drying. Exacerbating factors such as excessive exposure to moisture should be discontinued. Oral therapy itraconazole, fluconazole, or terbinafine may be used.

Candidiasis and HIV

Topical therapy with agents such as nystatin and clotrimazole are the mainstay of treatment. Treatment with topical therapies may be effective in the early stages of HIV infection. Oral treatment with a 2-week course of antifungal therapy (itraconazole, fluconazole, ketoconazole) is indicated in more refractory cases. In patients who are significantly immunocompromised, maintenance therapy on an intermittent (alternate days to twice weekly dosing of ketoconazole 200 mg or fluconazole 100 mg) or continuous basis may be required to provide symptomatic relief. In general, the goal is the cessation of therapy once clinical symptoms have subsided, since prolonged therapy may promote the development of drug-resistant organisms.


Related clinical guidelines have been released by the Infectious Diseases Society of America.[67] See Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America.


Owing to rising resistance in numerous antifungal drugs and the existence of undesirable adverse effects, as well as a general desire to avoid disease, it is preferable to prevent rather than treat Candida infections. The largest factor in preventing cutaneous Candida infection is removing moisture from the skin.[68] Accordingly, skin should be kept dry through means such as the use of breathable materials when indicated and possible. For example, in a clinical trial with infants (age 3-15 months), the use of a breathable diaper as opposed to a traditional diaper diminished C albicans colony count by nearly two thirds.[68]

Additionally, as demonstrated in infants, the use antibiotics increases the risk of Candida infection, a phenomenon that the authors attribute to the change in the gut microbiome, and judicious antibiotic use could lessen the likelihood of infection.[69]



Medication Summary

The azoles are a group of synthetic antimycotic agents with a broad spectrum of activity. The primary drugs available include ketoconazole, miconazole, fluconazole, itraconazole, and econazole. The mechanism of action of azoles is blocking the synthesis of ergosterol, the primary sterol in the fungal cell membrane. The depletion of ergosterol alters the fluidity of the cell membrane and alters the action of the membrane-associated enzymes. This results in inhibition of replication and inhibition of the transformation of candidal yeast forms into hyphae, which is the invasive and pathogenic form of the parasite.

Nystatin and amphotericin are polyenes, which are active against some fungi but have little action on mammalian cells and no action on bacteria. They bind to cell membranes and interfere with permeability and transport functions. These antibiotics act as ionophores and cause leakage of cations.

Antifungal agents

Class Summary

Some antifungal agents exert their fungicidal effect by altering the permeability of fungal cell membranes. The mechanism of action also may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide toxic to the fungal cell.

Nystatin (Mycostatin)

Nystatin is a fungicidal and fungistatic antibiotic obtained from Streptomyces noursei. It is effective against various yeasts and yeastlike fungi. Nystatin changes the permeability of the fungal cell membrane after binding to cell membrane sterols, causing cellular contents to leak.


Class Summary

The azoles are a group of synthetic antimycotic agents with a broad spectrum of activity.

Clotrimazole (Gyne-Lotrimin-3 Combination Pack, Gyne-Lotrimin-3 Vaginal Cream, Gyne-Lotrimin-3 Vaginal Suppositories)

Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing death of fungal cells.

Fluconazole (Diflucan)

Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.

Itraconazole (Sporanox)

Itraconazole is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.


Questions & Answers


What is cutaneous candidiasis?

What is the pathophysiology of cutaneous candidiasis?

What causes cutaneous candidiasis?

What is the prevalence of cutaneous candidiasis?

Which patient groups are at highest risk for cutaneous candidiasis?

What is the prognosis of cutaneous candidiasis?

Where can patient education resources for cutaneous candidiasis be found?


Which clinical history findings are characteristic of candidal vulvovaginitis?

What are the signs and symptoms of candidal balanitis?

What are the risk factors for congenital candidiasis?

Which clinical history findings are characteristic of candidal diaper dermatitis?

What are the risk factors for oral candidiasis in adults?

What are common sites for intertrigo in patients with cutaneous candidiasis?

What is decubital candidosis?

Which history findings are characteristic of paronychia in patients with cutaneous candidiasis?

What is the prevalence of cutaneous candidiasis in patients with HIV?

What are other rare presentations of cutaneous candidiasis?

Which physical findings are characteristic of candidal vulvovaginitis?

Which physical findings are characteristic of congenital candidosis?

Which physical findings are characteristic of candidal diaper dermatitis?

Which physical findings are characteristic of oral candidiasis?

Which physical findings are characteristic of intertrigo?

Which physical findings are characteristic of paronychia?


Which conditions should be included in the differential diagnoses of cutaneous candidiasis?


What is the role of lab studies in the workup of cutaneous candidiasis?

Which histologic findings are characteristic of cutaneous candidiasis?


What are approach considerations in treating candidiasis?

What is included in the treatment of candidal vulvovaginitis?

What is included in the treatment of candidal balanitis?

What is included in the treatment of congenital candidiasis?

What is included in the treatment of candidal diaper dermatitis?

What are the treatment options for oral candidiasis?

What are the treatment options for candidal intertrigo?

What are the treatment options for paronychia?

What are the treatment options for candidiasis in HIV?

What guidelines have been published for the management of cutaneous candidiasis?

What measures can be taken to prevent candidal infections?


Which medications are used in the treatment of cutaneous candidiasis?

Which medications in the drug class Antifungal agents are used in the treatment of Cutaneous Candidiasis?

Which medications in the drug class Azoles are used in the treatment of Cutaneous Candidiasis?