Cutaneous Candidiasis

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


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