Cutaneous Candidiasis Clinical Presentation

  • Author: Noah S Scheinfeld, JD, MD, FAAD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Feb 05, 2016
 

History

Candidal vulvovaginitis

This common condition in women presents with itching, soreness, and a thick creamy white discharge (see the image below).

A moist, erosive, pruritic patch of the perianal s A moist, erosive, pruritic patch of the perianal skin and perineum (with satellite pustule formation) is demonstrated in this woman with extensive candidosis.

Although most candidal infections occur more frequently with advancing age, vulvovaginitis is unusual in older women. 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 (see the image below).

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.

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.[18]

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.

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

Congenital candidosis [19, 20]

This rarely reported candidal infection (70 cases during the 1990s) may be acquired by the infant in utero or during delivery. Presumably, congenital candidosis is an ascending intrauterine infection with cutaneous or systemic manifestations that typically present within 12 hours after birth. Although the congenital systemic form typically is fatal, congenital cutaneous infections usually have a more benign course. Prematurity and the presence of an intrauterine foreign body (intrauterine device) are associated with this condition. Untreated, infants are at higher risk for systemic infection, which is associated with a high mortality rate (70%). Some infants have respiratory distress and pneumonia secondary to in utero aspiration of infected amniotic fluid.

Oropharyngeal candidiasis [21]

This form is known more commonly as oral thrush and is considered by many to be 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 most commonly is 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 to uninfected mothers.

Oropharyngeal candidiasis 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 compared to a child aged several months who is not nearly as susceptible. Beyond the neonatal age, C albicans is considered a normal constituent of the oral and intestinal florae.

Candidosis of the nipple in the nursing mother is associated with infantile oropharyngeal candidiasis. Nipple candidosis almost always is bilateral, with the nipples appearing bright red and inflamed, with the look and feel of being sunburned or on fire. Unlike a painful-with-nursing cut or abrasion from local trauma by the infant (incorrect latch-on), nipple candidosis hurts between feedings. Merely having the clothing brush against the nipples is painful.

Candidal diaper dermatitis [21]

Infants with oropharyngeal candidiasis invariably harbor C albicans in the intestine and feces (85-90%). In most patients, candidal diaper dermatitis is the result of progressive colonization from oral and gastrointestinal candidiasis. Infected 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.

Diaper dermatitis candidiasis can result in an a generalized eruption known as an Id reaction, also known as autosensitization or an autoeczematization reaction.[22]

Oral candidiasis in adults

Use of broad-spectrum antibiotics and inhaled corticosteroids, diminished cell-mediated immunity, and xerostomia are all risk factors for candidiasis (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 be either primary resulting from the natural aging process or secondary resulting from the anticholinergic effect of certain drugs including psychoactive drugs such as phenothiazines and tricyclic antidepressants. A decrease in salivary production decreases both the amount of available mucosal secretory antibody (immunoglobulin A [IgA]) and the natural cleansing action provided by saliva.

In older adults, 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. Superficial mycoses may be the presenting sign in immunodepressed patients (especially AIDS).[23]

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 smokers or patients who are immunosuppressed.

Intertrigo

Most cases of cutaneous candidosis 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 candidosis

This is a particular form of cutaneous candidosis that occurs on the dorsal skin of chronically bedridden patients.[24]

Paronychia

Candida organisms occasionally cause 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. Immediate contact dermatitis to food allergens may play a role in the pathogenesis of the condition as well. Progression to total nail dystrophy has been associated specifically with C albicans and usually has been limited to women with 2 important predisposing conditions, ie, Cushing syndrome and Raynaud disease. Disease is more common in people who frequently submerge their hands in water and usually is not associated with the elderly population. One important exception to this generalization is the population of patients with diabetes.

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

Candidosis and HIV

Epidemiologic studies indicate that a very high percentage of patients infected with HIV contract some type of skin disorder during the course of the disease.[25, 26, 27] More specifically, most 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,[28] in 2007, reported on a case of disseminated candidiasis as an initial presentation of AIDS. Such cases often manifest with purpuric eruptions.

Breast pain

Andrews et al[29] studied 98 breastfeeding women, 20 who reported breastfeeding associated pain and 78 who were asymptomatic. Cultures were obtained from breast milk, areolae, and the infants' oropharynx. Six of the 20 symptomatic women returned breast milk cultures positive for yeast, compared with 6 of 78 controls (11 of 12 samples showed C albicans). The researchers suggested that Candida might play an etiologic role in breastfeeding-associated pain.

Ecthyma gangrenosum

In 2007, Agarwal et al[30] reported on a solitary ecthyma gangrenosum–like lesion that resulted from C albicans infection in a neonate.

Ulcers

Xi et al,[31] in 2007, reported a 51-year-old Cantonese woman who had a 1-year history of a large, deep-seated subcutaneous ulcer on her right shoulder for more than a year whose discharge showed C albicans and C parapsilosis. The researchers isolated C parapsilosis from the biopsy specimen.

Cutaneous candidiasis has manifested as an interdigital ulcer.[32]

Other

Cutaneous candidiasis was noted to occur under a ruby ring in a patient who was immunocompromised.[33]

Generalized cutaneous candidiasis can complicate Darier disease.[34]

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Physical

Candidal vulvovaginitis

Clinical examination reveals erythema of the vaginal mucosa and vulval 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 candidosis.

Congenital candidosis

In 2004, Diana et al[35] reported that cutaneous congenital candidiasis is a rare disease of term or premature infants. It typically manifests as an erythematous maculopapular eruption affecting the trunk and extremities; it resolves after extensive desquamation. Pustules and vesicles usually are superficial and resolve spontaneously or with topical treatment (see the image below). The presence of white microabscesses on the placenta and umbilical cord of an infant with such an eruption must suggest 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.

Oropharyngeal 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.

Candidal diaper dermatitis

The eruption of 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. The typical eruption begins with scaly papules that merge to form well-defined, weeping, 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 of candidal diaper dermatitis and represent the primary lesions. Candidiasis may be a presenting feature of diabetic ketoacidosis.[36]

Oral candidiasis in elderly persons

The most common clinical appearance of oropharyngeal candidiasis (pseudomembranous candidosis or oral thrush) in the adult population occurs as white plaques that are present on the buccal, palatal, or oropharyngeal mucosa overlying areas of mucosal erythema. Typically, the lesions are removed easily and may demonstrate areas with tiny ulcerations (see the image below). In addition, some patients may develop soreness and cracks at the lateral angles of the mouth (angular cheilitis). Denture stomatitis 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.

Intertrigo

Intertrigo typically presents with erythema, cracking, and maceration with soreness and pruritic symptoms. Lesions typically have an irregular margin with surrounding satellite papules and pustules. Web spaces of affected fingers or toes are macerated and have the appearance of soft white skin, which is a condition termed erosio interdigitalis blastomycetica (interdigital candidosis).

Paronychia

The nailfold becomes erythematous, swollen, and tender, with an occasional discharge. Loss of the cuticle occurs, along with nail dystrophy and onycholysis with discoloration around the lateral nailfold (see the image below). A greenish color with hyponychial fluid accumulation may occur that results entirely from Candida, and not Pseudomonas, infection. A potassium hydroxide (KOH) preparation is helpful and is likely to show yeast organisms.

Candida infection should be in the differential di Candida infection should be in the differential diagnosis when one or more nails become discolored, has subungual discoloration, nailplate separation from the nailbed, and lack evidence of a dermatophyte.
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Causes

Host factors that predispose patients to infections are numerous. Local factors such as tissue damage resulting from trauma, xerostomia, radiation-induced mucositis, ulcerations, skin maceration, or occlusion enhances adhesion and predisposes patients to increased infection rates.

Endocrine diseases such as diabetes mellitus, Cushing syndrome, hypoparathyroidism, hypothyroidism, and polyendocrinopathy are 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.

Nutritional deficiencies may alter host defense mechanisms or epithelial barrier integrity, allowing increased adherence or penetration. Iron deficiency anemia and deficiencies including vitamins B1, B2, B6, C, and folic acid are associated with heightened infection rates.

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 but not to systemic infection. 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.

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Contributor Information and Disclosures
Author

Noah S Scheinfeld, JD, MD, 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, JD, MD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie<br/>Received income in an amount equal to or greater than $250 from: Optigenex<br/>Received salary from Optigenex for employment.

Coauthor(s)

Matthew C Lambiase, DO Dermatologist, Skin Cancer and Dermatology Institute, Reno, NV

Disclosure: Nothing to disclose.

Specialty Editor Board

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, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal 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, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Franklin Flowers, MD Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine

Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Surgery

Disclosure: Nothing to disclose.

Acknowledgements

Jessica M Allan, MD Private Practice

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.

Thomas K Vaughan, MD Assistant Chief, Dermatology Service, Madigan Army Medical Center

Disclosure: Nothing to disclose.

References
  1. Li M, Chen Q, Shen Y, Liu W. Candida albicans phospholipomannan triggers inflammatory responses of human keratinocytes through Toll-like receptor 2. Exp Dermatol. 2009 Jul. 18(7):603-10. [Medline].

  2. Shiraki Y, Ishibashi Y, Hiruma M, Nishikawa A, Ikeda S. Candida albicans abrogates the expression of interferon-gamma-inducible protein-10 in human keratinocytes. FEMS Immunol Med Microbiol. 2008 Oct. 54(1):122-8. [Medline].

  3. Mayer FL, Wilson D, Hube B. Candida albicans pathogenicity mechanisms. Virulence. 2013 Jan 9. 4(2):[Medline].

  4. Sonal C, Michael M, Daniele T, Paolo R. Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy. J Clin Aesthet Dermatol. 2012 Dec. 5(12):18-22. [Medline]. [Full Text].

  5. Proust-Lemoine E, Saugier-Veber P, Wémeau JL. Polyglandular autoimmune syndrome type I. Presse Med. 2012 Dec. 41(12 P 2):e651-62. [Medline].

  6. Ouederni M, Sanal O, Ikinciogullari A, et al. Clinical Features of Candidiasis in Patients With Inherited Interleukin 12 Receptor ß1 Deficiency. Clin Infect Dis. 2014 Jan. 58(2):204-13. [Medline]. [Full Text].

  7. Ouederni M, Sanal O, Ikinciogullari A, Tezcan I, Dogu F, Sologuren I, et al. Clinical features of Candidiasis in patients with inherited interleukin 12 receptor ß1 deficiency. Clin Infect Dis. 2014 Jan. 58(2):204-13. [Medline]. [Full Text].

  8. Sarkadi AK, Taskó S, Csorba G, Tóth B, Erdős M, Maródi L. Autoantibodies to IL-17A may be correlated with the severity of mucocutaneous candidiasis in APECED patients. J Clin Immunol. 2014 Feb. 34(2):181-93. [Medline].

  9. Nielsen J, Kofod-Olsen E, Spaun E, Larsen CS, Christiansen M, Mogensen TH. A STAT1-gain-of-function mutation causing Th17 deficiency with chronic mucocutaneous candidiasis, psoriasiform hyperkeratosis and dermatophytosis. BMJ Case Rep. 2015 Oct 22. 2015:[Medline].

  10. Conti HR, Whibley N, Coleman BM, Garg AV, Jaycox JR, Gaffen SL. Signaling through IL-17C/IL-17RE is dispensable for immunity to systemic, oral and cutaneous candidiasis. PLoS One. 2015 Apr 7. 10(4):e0122807. [Medline].

  11. Campois TG, Zucoloto AZ, de Almeida Araujo EJ, Svidizinski TI, Almeida RS, da Silva Quirino GF, et al. Immunological and histopathological characterization of cutaneous candidiasis. J Med Microbiol. 2015 Aug. 64(8):810-7. [Medline].

  12. Foureur N, Vanzo B, Meaume S, Senet P. Prospective aetiological study of diaper dermatitis in the elderly. Br J Dermatol. 2006 Nov. 155(5):941-6. [Medline].

  13. Kränke B, Trummer M, Brabek E, Komericki P, Turek TD, Aberer W. Etiologic and causative factors in perianal dermatitis: results of a prospective study in 126 patients. Wien Klin Wochenschr. 2006 Mar. 118(3-4):90-4. [Medline].

  14. Nardin ME, Pelegri DG, Manias VG, Méndez Ede L. [Etiological agents of dermatomycoses isolated in a hospital of Santa Fe City, Argentina]. Rev Argent Microbiol. 2006 Jan-Mar. 38(1):25-7. [Medline].

  15. Nishimoto K. [An epidemiological survey of dermatomycoses in Japan, 2002]. Nippon Ishinkin Gakkai Zasshi. 2006. 47(2):103-11. [Medline].

  16. Peñate Y, Guillermo N, Melwani P, Martel R, Borrego L. Dermatologists in hospital wards: an 8-year study of dermatology consultations. Dermatology. 2009. 219(3):225-31. [Medline].

  17. El Ahmed HH, Cañadas-De la Fuente GA, Fernández-Castillo R, González-Jiménez E, Cantero-Hinojosa J, Lardón-Fernández M. [Generalized cutaneous candidiasis in newborn at term]. Biomedica. 2012 Jun. 32(2):170-3. [Medline].

  18. Ramirez De Knott HM, McCormick TS, Do SO, et al. Cutaneous hypersensitivity to Candida albicans in idiopathic vulvodynia. Contact Dermatitis. 2005 Oct. 53(4):214-8. [Medline].

  19. Gibney MD, Siegfried EC. Cutaneous congenital candidiasis: a case report. Pediatr Dermatol. 1995 Dec. 12(4):359-63. [Medline].

  20. Raval DS, Barton LL, Hansen RC, Kling PJ. Congenital cutaneous candidiasis: case report and review. Pediatr Dermatol. 1995 Dec. 12(4):355-8. [Medline].

  21. Hoppe JE. Treatment of oropharyngeal candidiasis and candidal diaper dermatitis in neonates and infants: review and reappraisal. Pediatr Infect Dis J. 1997 Sep. 16(9):885-94. [Medline].

  22. Chirac A, Brzezinski P, Chiriac AE, Foia L, Pinteala T. Autosensitisation (Autoeczematisation) reactions in a case of diaper dermatitis candidiasis. Niger Med J. 2014 May. 55(3):274-5. [Medline].

  23. Ramos-E-Silva M, Lima CM, Schechtman RC, Trope BM, Carneiro S. Superficial mycoses in immunodepressed patients (AIDS). Clin Dermatol. 2010 Mar 4. 28(2):217-25. [Medline]. [Full Text].

  24. Nico MM, Rivitti EA. Decubital candidosis': a study of 26 cases. J Eur Acad Dermatol Venereol. 2005 May. 19(3):296-300. [Medline].

  25. Aly R, Berger T. Common superficial fungal infections in patients with AIDS. Clin Infect Dis. 1996 May. 22 Suppl 2:S128-32. [Medline].

  26. Marquart KH. Electron microscopy reveals fungal cells within tumor tissue from two African patients with AIDS-associated Kaposi sarcoma. Ultrastruct Pathol. 2006 May-Jun. 30(3):187-92. [Medline].

  27. Wang SM, Yang YJ, Chen JS, Lin HC, Chi CY, Liu CC. Invasive fungal infections in pediatric patients with leukemia: emphasis on pulmonary and dermatological manifestations. Acta Paediatr Taiwan. 2005 May-Jun. 46(3):149-55. [Medline].

  28. Yanagisawa N, Suganuma A, Takeshita N, et al. [A case of disseminated candidiasis as an initial presentation of AIDS]. Kansenshogaku Zasshi. 2007 Jul. 81(4):459-62. [Medline].

  29. Andrews JI, Fleener DK, Messer SA, Hansen WF, Pfaller MA, Diekema DJ. The yeast connection: is Candida linked to breastfeeding associated pain?. Am J Obstet Gynecol. 2007 Oct. 197(4):424.e1-4. [Medline].

  30. Agarwal S, Sharma M, Mehndirata V. Solitary ecthyma gangrenosum (EG)-like lesion consequent to Candida albicans in a neonate. Indian J Pediatr. 2007 Jun. 74(6):582-4. [Medline].

  31. Xi L, Li X, Zhang J, Lu C, Xie T, Yin R. Good response in a patient with deep-seated subcutaneous ulcer due to Candida species. Mycopathologia. 2007 Aug. 164(2):77-80. [Medline].

  32. Luo DQ, Yang W, Wu LC, Liu JH, Chen WN. Interdigital ulcer: an unusual presentation of Candida infection. Mycoses. 2011 May 25. [Medline].

  33. Geddes ER, Polder K, Cutlan JE, Torres-Cabala CA, Hymes SR. Ulcerated plaque under a ruby ring in an immunosuppressed patient. Dermatol Online J. 2010 Aug 15. 16(8):4. [Medline].

  34. Weiler L, Poulalhon N, Debarbieux S, Thomas L. Darier's disease can be complicated by generalised cutaneous candidiasis: a case-report. Br J Dermatol. 2014 Aug 21. [Medline].

  35. Diana A, Epiney M, Ecoffey M, Pfister RE. "White dots on the placenta and red dots on the baby": congential cutaneous candidiasis--a rare disease of the neonate. Acta Paediatr. 2004 Jul. 93(7):996-9. [Medline].

  36. Williams MD, Sallee D, Robinson M. Diabetic ketoacidosis in toddler with a diaper rash. Am J Emerg Med. 2008 Sep. 26(7):834.e1-2. [Medline].

  37. Duong T, Ingen-Housz-Oro S, Gaulier A, Petit A, Dubertret L, Sigal-Grinberg M. [Extensive cutaneous candidiasis revealing cutaneous T-cell lymphoma: 2 cases]. Ann Dermatol Venereol. 2006 Jun-Jul. 133(6-7):566-70. [Medline].

  38. Lim CS, Lim SL. New contrast stain for the rapid diagnosis of dermatophytic and candidal dermatomycoses. Arch Dermatol. 2008 Sep. 144(9):1228-9. [Medline].

  39. Raz-Pasteur A, Ullmann Y, Berdicevsky I. The pathogenesis of Candida infections in a human skin model: scanning electron microscope observations. ISRN Dermatol. 2011. 2011:150642. [Medline]. [Full Text].

  40. Sundaram SV, Srinivas CR, Thirumurthy M. Candidal intertrigo: treatment with filter paper soaked in Castellani's paint. Indian J Dermatol Venereol Leprol. 2006 Sep-Oct. 72(5):386-7. [Medline].

  41. Pappas PG, Kauffman CA, Andes DR, Clancy CJ, Marr KA, Ostrosky-Zeichner L, et al. Executive Summary: Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2016 Feb 15. 62 (4):409-17. [Medline].

  42. Del Rosso JQ, Kircik LH. Optimizing topical antifungal therapy for superficial cutaneous fungal infections: focus on topical naftifine for cutaneous dermatophytosis. J Drugs Dermatol. 2013 Nov 1. 12(11):s165-71. [Medline].

  43. Macherla C, Sanchez DA, Ahmadi MS, et al. Nitric oxide releasing nanoparticles for treatment of Candida albicans burn infections. Front Microbiol. 2012. 3:193. [Medline]. [Full Text].

 
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A moist, erosive, pruritic patch of the perianal skin and perineum (with satellite pustule formation) is demonstrated in this woman with extensive candidosis.
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.
Dry, red, superficially scaly, pruritic macules and patches on the penis represent candidal balanitis.
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.
Erythema, maceration, and satellite pustules in the axilla, accompanied by soreness and pruritus result in a form of intertrigo.
A nailfold with candidal infection becomes erythematous, swollen, and tender with an occasional discharge
Soreness and cracks at the lateral angles of the mouth (angular cheilitis) is a frequent expression of candidosis in elderly individuals.
Fine superficial pustules on an erythematous patchy base are suggestive of candidosis.
Candida infection should be in the differential diagnosis when one or more nails become discolored, has subungual discoloration, nailplate separation from the nailbed, and lack evidence of a dermatophyte.
Candidiasis. Courtesy of Hon Pak, MD.
 
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