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Cutaneous Candidiasis

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Cutaneous Candidiasis
Author: Noah S Scheinfeld, MD, JD, FAAD; Chief Editor: William D James, MD more...
Updated: Feb 13, 2013

Background
Cutaneous candidiasis and other forms of candidosis are infections caused by the yeast Candida albicans or other
Candida species. Yeasts are unicellular fungi that typically reproduce by budding, a process that entails a progeny
pinching off of the mother cell. C albicans, the principal infectious agent in human infection, is an oval yeast 2-6
m in diameter. C albicans (as well as most medically significant fungi) has the ability to exist in both hyphal and
yeast forms (termed dimorphism). If pinched cells do not separate, a chain of cells is produced and is termed
pseudohyphae.
Superficial infections of skin and mucous membranes are the most common types of candidal infections of the
skin. Common types of candidal skin infection include intertrigo, diaper dermatitis, erosio interdigitalis
blastomycetica, perianal dermatitis, and candidal balanitis. In certain subpopulations, candidal infection of the skin
has increased in prevalence in recent years, principally because of the increased numbers of patients who are
immunocompromised.
Esophagitis, septicemia, endocarditis, peritonitis, and urinary tract infections are less frequent types of
candidosis. 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 k rusei, Candida k efyr,
Candida zeylanoides, and Candida glabrata (formerly Torulopsis glabrata) are less common causes of human
disease.
Humans carry yeast fungi, including candidal species, throughout the gastrointestinal tract (mouth through anus)
as part of the normal commensal flora. The vagina also commonly is colonized by yeast (13% of women), most
commonly by C albicans and C glabrata. The commensal oral isolation of candidal species ranges from 30-60% in
healthy adults. Note that Candida species are not part of the normal flora of the skin; however, they may colonize
fingers or body folds transiently.
Also see the articles Candidiasis, Mucosal and Candidiasis.

Pathophysiology
Most candidal species are known to produce virulence factors including protease factors. Those strains lacking
virulence factors have been shown to be less pathogenic. The ability of yeast forms to adhere to the underlying
epithelium is an important step in the production of hyphae and tissue penetration. Removal of bacteria from the
skin, mouth, and gastrointestinal tract by exposing to tissue with its endogenous flora results in inhibition of
endogenous microflora, providing reduced environmental and nutritional competition that favors the growth of
candidal organisms.
Additional research has been performed on the cytokines and interleukins that candidal organisms affect in
keratinocytes. In keratinocytes, C albicans phospholipomannan triggers an inflammatory response through toll-like
receptor 2.[1] C albicans aborts the expression of interferon-gammainducible protein-10 in human keratinocytes.[2]
These factors probably explain how candidal infections occur in the skin, which has innate defenses against
candidal organisms.
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A 2013 review of pathologic mechanisms of C albicans cited (1) the secretion of hydrolases, (2) molecules that
mediate adhesion to 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.
[3]

Genetic conditions can make the skin susceptible to candidal infection. One such condition is autoimmune
polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED),[4] which manifests with at least 2 of 3
conditions: Addison disease, chronic mucocutaneous candidiasis, or hypoparathyroidism, called the Whitaker
triad or referred to as polyglandular autoimmune syndrome type 1 (PAS-1) or APECED.[5] . It is related to
autoimmune regulator (AIRE) genetic mutations.

Epidemiology
Frequency
United States
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.
International
A German study [6] investigated the different causes of diaper dermatitis in 46 men and women at a median age of
85 years. In 38 patients, a cause was established; specifically, 63% had candidiasis, 16% had irritant dermatitis,
11% had eczema, and 11% had psoriasis. Of these patients, 37 were treated and 73% were cured after 8 weeks
of treatment.
In Germany, Krnke et al[7] studied 126 patients with a presumptive diagnosis of anal eczema (age range, 7-82 y),
and most patients were male (57.1% male, 42.9% female). The clinical diagnosis was intertrigo/candidiasis in
42.9% of patients.
In Argentina, Nardin et al[8] analyzed 2073 samples of skin, hair, nails, and oral mucous membranes obtained from
1817 patients who attended the Microbiology Branch of the Central Laboratory at Dr. J.M. Cullen Hospital from
September 1999 to September 2003. The samples were examined and identified according to localization and the
type of lesion. Of the total samples, 55.67% were positive; 63% were recovered from females and 37% were
recovered from males. C albicans was the prevalent yeast species.
In Japan, Nishimoto[9] noted that cutaneous candidiasis was seen in 755 (1%) of 72,660 outpatients. Intertrigo
(347 cases) was the most common clinical manifestation of cutaneous candidiasis, erosio interdigitalis occurred in
103 cases, and diaper candidiasis was noted in 102 cases.
A Spanish study of 3,097 inpatient cases noted that cutaneous candidiasis accounted for 7.1% of consultations.
[10]

Mortality/Morbidity
Superficial candidal infections cause significant morbidity in older adults, which becomes a particular problem with
the use of certain types of medication, poor self-care, and decreased salivary flow. Age alone is not sufficient for
the development of candidal infection; however, increased morbidity is associated with both superficial and invasive
forms of disease. This is a result of an increased risk in patients of developing an underlying immunosuppressed
state, such as malignancy.

Age
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.
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.
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An interesting case from Spain was noted in 2012, in which a mother had subclinical vaginal candidal infection and
passed the infection to her full-term infant, who developed the disease 24 hours after being born.[11] Sepsis,
respiratory distress, and a positive culture in the blood for Staphylococcus aureus ensued. Biopsy proved Candida
was the provoking agent; the patient survived.
The number of candidal infections has risen dramatically in recent years, mirroring the increasing number of
patients who are immunocompromised. Specifically, increased age appears to be associated with increased
morbidity and mortality. 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. Superficial candidal infections, although typically believed to
be benign, cause significant morbidity in the elderly population.
Candidal infections are exacerbated by certain types of medication (eg, antibiotics), poor self-care, and decreased
salivary flow, 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.

Contributor Information and Disclosures

Author
Noah S Scheinfeld, MD, JD, FAAD Assistant Clinical Professor, Department of Dermatology, Weil Cornell
Medical College; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel
Medical Center, New York Eye and Ear Infirmary; Assistant Attending Dermatologist, New York Presbyterian
Hospital; Assistant Attending Dermatologist, Lenox Hill Hospital, North Shore-LIJ Health System; Private
Practice
Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of
Dermatology
Disclosure: Optigenex Consulting fee Independent contractor
Coauthor(s)
Matthew C Lambiase, DO Dermatologist, Skin Cancer and Dermatology Institute, Reno, NV
Disclosure: Nothing to disclose.
Daniel S Lehman, MD Fellow in Minimally Invasive Urology/Oncology, Department of Urology, Columbia
University Medical Center
Disclosure: Nothing to disclose.
Jessica M Allan, MD Consulting Staff, Private Practice
Disclosure: Nothing to disclose.
Specialty Editor Board
Franklin Flowers, MD Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology,
Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine
Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic
Surgery and Cutaneous Oncology
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University
Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology,
Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal
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Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology,
American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Catherine M Quirk, MD Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania
Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American
Academy of Dermatology
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director,
Department of Dermatology, University of Pennsylvania School of Medicine
William D James, MD is a member of the following medical societies: American Academy of Dermatology and
Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Additional Contributors
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author,
Thomas Vaughan, MD, to the development and writing of this article.

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