Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Biology of Candida infections

Wiley A Schell, MS
Section Editor
Carol A Kauffman, MD
Deputy Editor
Anna R Thorner, MD


Candidiasis refers to the range of infections caused by species of the fungal genus Candida; these infections can be acute or chronic, localized or systemic. Disseminated candidiasis is life threatening. The great majority of candidiasis is caused by Candida albicans. C. albicans is a common commensal organism in the oropharyngeal cavity, gastrointestinal tract, and vagina of humans but is capable of causing opportunistic infection following disruption of the normal flora, a breach of the mucocutaneous barrier, or a defect in host cellular immunity. C. albicans can be detected as normal flora in about 50 percent of individuals [1].

The basic mycology and pathogenesis of candidiasis will be reviewed here. An overview of Candida infections and the epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment of candidemia and invasive candidiasis are presented separately; other forms of candidiasis are also discussed elsewhere. (See "Overview of Candida infections" and "Epidemiology and pathogenesis of candidemia in adults" and "Clinical manifestations and diagnosis of candidemia and invasive candidiasis in adults" and "Treatment of candidemia and invasive candidiasis in adults".)


The genus Candida encompasses more than 350 species. They can be found among humans and other mammals, birds, insects, arthropods, fish, animal waste, plants, mushrooms, naturally occurring high-sugar substrates (eg, honey, nectar, grapes) and fermentation products, dairy products, soil, freshwater, seawater, and on airborne particles [2-4].

Infection in humans was first described as oral thrush by Hippocrates in the fifth century BC. In 1853, Charles Robin microscopically observed budding cells and filaments in epithelial scrapings, and he named the fungus Oidium albicans. Subsequently, more than 160 synonyms, including Monilia albicans, were used before Candida albicans became the accepted name for this species.

As many as 30 Candida species have caused infection in humans [5]. The most common of these are C. albicans, C. glabrata, C. krusei, C. parapsilosis, and C. tropicalis. C. parapsilosis has been recognized as a heterogeneous species, and it was proposed that it be split into three morphologically and physiologically indistinguishable species: C. parapsilosis, C. metapsilosis, and C. orthopsilosis [6]. Phylogenetic analyses show that C. glabrata is more closely related to Saccharomyces cerevisiae than to the Candida albicans group [7-9], and future taxonomic revision is possible.

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Oct 30, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Naglik JR, Challacombe SJ, Hube B. Candida albicans secreted aspartyl proteinases in virulence and pathogenesis. Microbiol Mol Biol Rev 2003; 67:400.
  2. Barnett JA, Payne RW, Yarrow D. Yeasts: Characteristics and Identification, 2nd ed, Cambridge University Press, Cambridge 1990.
  3. Meyer AS, Payne RW, Yarrow D. Candida Berkhout. In: The Yeasts: A Taxonomic Study, 4th ed, Kurtzman CP, Fell JW (Eds), Elsevier, New York Vol 1998, p.454.
  4. Nunn MA, Schäefer SM, Petrou MA, Brown JR. Environmental source of Candida dubliniensis. Emerg Infect Dis 2007; 13:747.
  5. Brandt ME, Lockhart SR. Recent Taxonomic Developments with Candida and Other Opportunistic Yeasts. Curr Fungal Infect Rep 2012; 6:170.
  6. Tavanti A, Davidson AD, Gow NA, et al. Candida orthopsilosis and Candida metapsilosis spp. nov. to replace Candida parapsilosis groups II and III. J Clin Microbiol 2005; 43:284.
  7. Wong S, Fares MA, Zimmermann W, et al. Evidence from comparative genomics for a complete sexual cycle in the 'asexual' pathogenic yeast Candida glabrata. Genome Biol 2003; 4:R10.
  8. Diezmann S, Cox CJ, Schönian G, et al. Phylogeny and evolution of medical species of Candida and related taxa: a multigenic analysis. J Clin Microbiol 2004; 42:5624.
  9. Turner SA, Butler G. The Candida pathogenic species complex. Cold Spring Harb Perspect Med 2014; 4:a019778.
  10. Sullivan DJ, Westerneng TJ, Haynes KA, et al. Candida dubliniensis sp. nov.: phenotypic and molecular characterization of a novel species associated with oral candidosis in HIV-infected individuals. Microbiology 1995; 141 ( Pt 7):1507.
  11. Sullivan DJ, Moran GP, Coleman DC. Candida dubliniensis: ten years on. FEMS Microbiol Lett 2005; 253:9.
  12. Asmundsdóttir LR, Erlendsdóttir H, Agnarsson BA, Gottfredsson M. The importance of strain variation in virulence of Candida dubliniensis and Candida albicans: results of a blinded histopathological study of invasive candidiasis. Clin Microbiol Infect 2009; 15:576.
  13. Lockhart SR. Do hospital microbiology laboratories still need to distinguish Candida albicans from Candida dubliniensis? J Clin Microbiol 2011; 49:4415.
  14. Segal E, Elad D. Candida species and Blastoschizomyces capitus. In: Topley & Wilson's Microbiology and Microbial Infections, 9th ed, Ajello L, Hay RJ (Eds), Arnold, London 1998. Vol 4, p.423.
  15. Bennett RJ, Johnson AD. Completion of a parasexual cycle in Candida albicans by induced chromosome loss in tetraploid strains. EMBO J 2003; 22:2505.
  16. Bennett RJ, Uhl MA, Miller MG, Johnson AD. Identification and characterization of a Candida albicans mating pheromone. Mol Cell Biol 2003; 23:8189.
  17. Pujol C, Daniels KJ, Lockhart SR, et al. The closely related species Candida albicans and Candida dubliniensis can mate. Eukaryot Cell 2004; 3:1015.
  18. Kniemeyer O, Schmidt AD, Vödisch M, et al. Identification of virulence determinants of the human pathogenic fungi Aspergillus fumigatus and Candida albicans by proteomics. Int J Med Microbiol 2011; 301:368.
  19. Schell WA. New aspects of emerging fungal pathogens. A multifaceted challenge. Clin Lab Med 1995; 15:365.
  20. Liu K, Howell DN, Perfect JR, Schell WA. Morphologic criteria for the preliminary identification of Fusarium, Paecilomyces, and Acremonium species by histopathology. Am J Clin Pathol 1998; 109:45.
  21. Schell WA. Histopathology of fungal rhinosinusitis. Otolaryngol Clin North Am 2000; 33:251.
  22. Sudbery P, Gow N, Berman J. The distinct morphogenic states of Candida albicans. Trends Microbiol 2004; 12:317.
  23. Veses V, Casanova M, Murgui A, et al. ABG1, a novel and essential Candida albicans gene encoding a vacuolar protein involved in cytokinesis and hyphal branching. Eukaryot Cell 2005; 4:1088.
  24. Chen YL, Yu SJ, Huang HY, et al. Calcineurin controls hyphal growth, virulence, and drug tolerance of Candida tropicalis. Eukaryot Cell 2014; 13:844.
  25. Odds FC. Candida and candidosis: A Review and Bibliography, 2nd ed, Bailliere Tindall, London 1988.
  26. Crampin H, Finley K, Gerami-Nejad M, et al. Candida albicans hyphae have a Spitzenkörper that is distinct from the polarisome found in yeast and pseudohyphae. J Cell Sci 2005; 118:2935.
  27. Stevenson JS, Liu H. Regulation of white and opaque cell-type formation in Candida albicans by Rtt109 and Hst3. Mol Microbiol 2011; 81:1078.
  28. Hnisz D, Schwarzmüller T, Kuchler K. Transcriptional loops meet chromatin: a dual-layer network controls white-opaque switching in Candida albicans. Mol Microbiol 2009; 74:1.
  29. Calderone RA, Gow NA. Host recognition by Candida species. In: Candida and candidiasis, Calderone RA (Ed), ASM Press, Washington, DC 2002. p.67.
  30. Inglis DO, Johnson AD. Ash1 protein, an asymmetrically localized transcriptional regulator, controls filamentous growth and virulence of Candida albicans. Mol Cell Biol 2002; 22:8669.
  31. Cottier F, Mühlschlegel FA. Sensing the environment: response of Candida albicans to the X factor. FEMS Microbiol Lett 2009; 295:1.
  32. Shapiro RS, Uppuluri P, Zaas AK, et al. Hsp90 orchestrates temperature-dependent Candida albicans morphogenesis via Ras1-PKA signaling. Curr Biol 2009; 19:621.
  33. De Bernardis F, Mühlschlegel FA, Cassone A, Fonzi WA. The pH of the host niche controls gene expression in and virulence of Candida albicans. Infect Immun 1998; 66:3317.
  34. Fonzi WA. Downstream functions in Candida morphogenesis (abstract). ASM Conference on Candida and Candidiasis, American Society for Microbiology, Charleston, South Carolina 1999. p. 16.
  35. Popolo L, Vai M. Defects in assembly of the extracellular matrix are responsible for altered morphogenesis of a Candida albicans phr1 mutant. J Bacteriol 1998; 180:163.
  36. Davis DA. How human pathogenic fungi sense and adapt to pH: the link to virulence. Curr Opin Microbiol 2009; 12:365.
  37. Lo HJ, Köhler JR, DiDomenico B, et al. Nonfilamentous C. albicans mutants are avirulent. Cell 1997; 90:939.
  38. Finkel JS, Mitchell AP. Genetic control of Candida albicans biofilm development. Nat Rev Microbiol 2011; 9:109.
  39. Albuquerque P, Casadevall A. Quorum sensing in fungi--a review. Med Mycol 2012; 50:337.
  40. Alfatah M, Bari VK, Nahar AS, et al. Critical role for CaFEN1 and CaFEN12 of Candida albicans in cell wall integrity and biofilm formation. Sci Rep 2017; 7:40281.
  41. Stoldt VR, Sonneborn A, Leuker CE, Ernst JF. Efg1p, an essential regulator of morphogenesis of the human pathogen Candida albicans, is a member of a conserved class of bHLH proteins regulating morphogenetic processes in fungi. EMBO J 1997; 16:1982.
  42. Wang A, Raniga PP, Lane S, et al. Hyphal chain formation in Candida albicans: Cdc28-Hgc1 phosphorylation of Efg1 represses cell separation genes. Mol Cell Biol 2009; 29:4406.
  43. Yaar L, Mevarech M, Koltin Y. A Candida albicans RAS-related gene (CaRSR1) is involved in budding, cell morphogenesis and hypha development. Microbiology 1997; 143 ( Pt 9):3033.
  44. Zheng X, Wang Y, Wang Y. Hgc1, a novel hypha-specific G1 cyclin-related protein regulates Candida albicans hyphal morphogenesis. EMBO J 2004; 23:1845.
  45. Chapa y Lazo B, Bates S, Sudbery P. The G1 cyclin Cln3 regulates morphogenesis in Candida albicans. Eukaryot Cell 2005; 4:90.
  46. Chen J, Zhou S, Wang Q, et al. Crk1, a novel Cdc2-related protein kinase, is required for hyphal development and virulence in Candida albicans. Mol Cell Biol 2000; 20:8696.
  47. Bastidas RJ, Heitman J, Cardenas ME. The protein kinase Tor1 regulates adhesin gene expression in Candida albicans. PLoS Pathog 2009; 5:e1000294.
  48. Enjalbert B, Whiteway M. Release from quorum-sensing molecules triggers hyphal formation during Candida albicans resumption of growth. Eukaryot Cell 2005; 4:1203.
  49. Hall RA, Cottier F, Mühlschlegel FA. Molecular networks in the fungal pathogen Candida albicans. Adv Appl Microbiol 2009; 67:191.
  50. Gow NA. Germ tube growth of Candida albicans. Curr Top Med Mycol 1997; 8:43.
  51. Davies JM, Stacey AJ, Gilligan CA. Candida albicans hyphal invasion: thigmotropism or chemotropism? FEMS Microbiol Lett 1999; 171:245.
  52. Sahand IH, Moragues MD, Eraso E, et al. Supplementation of CHROMagar Candida medium with Pal's medium for rapid identification of Candida dubliniensis. J Clin Microbiol 2005; 43:5768.
  53. Hamprecht A, Christ S, Oestreicher T, et al. Performance of two MALDI-TOF MS systems for the identification of yeasts isolated from bloodstream infections and cerebrospinal fluids using a time-saving direct transfer protocol. Med Microbiol Immunol 2014; 203:93.
  54. Spanu T, Posteraro B, Fiori B, et al. Direct maldi-tof mass spectrometry assay of blood culture broths for rapid identification of Candida species causing bloodstream infections: an observational study in two large microbiology laboratories. J Clin Microbiol 2012; 50:176.
  55. Vlek A, Kolecka A, Khayhan K, et al. Interlaboratory comparison of sample preparation methods, database expansions, and cutoff values for identification of yeasts by matrix-assisted laser desorption ionization-time of flight mass spectrometry using a yeast test panel. J Clin Microbiol 2014; 52:3023.
  56. Avni T, Leibovici L, Paul M. PCR diagnosis of invasive candidiasis: systematic review and meta-analysis. J Clin Microbiol 2011; 49:665.
  57. Pfeiffer CD, Samsa GP, Schell WA, et al. Quantitation of Candida CFU in initial positive blood cultures. J Clin Microbiol 2011; 49:2879.
  58. Lussier M, Sdicu AM, Shahinian S, Bussey H. The Candida albicans KRE9 gene is required for cell wall beta-1, 6-glucan synthesis and is essential for growth on glucose. Proc Natl Acad Sci U S A 1998; 95:9825.
  59. Buurman ET, Westwater C, Hube B, et al. Molecular analysis of CaMnt1p, a mannosyl transferase important for adhesion and virulence of Candida albicans. Proc Natl Acad Sci U S A 1998; 95:7670.
  60. Bulawa CE, Miller DW, Henry LK, Becker JM. Attenuated virulence of chitin-deficient mutants of Candida albicans. Proc Natl Acad Sci U S A 1995; 92:10570.
  61. Chauhan N, Li D, Singh P, et al. The Wall of Candida spp. In: Candida and candidiasis, Calderone RA (Ed), ASM Press, Washington, DC 2002. p.159.
  62. Masuoka J. Surface glycans of Candida albicans and other pathogenic fungi: physiological roles, clinical uses, and experimental challenges. Clin Microbiol Rev 2004; 17:281.
  63. Timpel C, Strahl-Bolsinger S, Ziegelbauer K, Ernst JF. Multiple functions of Pmt1p-mediated protein O-mannosylation in the fungal pathogen Candida albicans. J Biol Chem 1998; 273:20837.
  64. Csank C, Schröppel K, Leberer E, et al. Roles of the Candida albicans mitogen-activated protein kinase homolog, Cek1p, in hyphal development and systemic candidiasis. Infect Immun 1998; 66:2713.
  65. Perfect JR, Schell WA. The new fungal opportunists are coming. Clin Infect Dis 1996; 22 Suppl 2:S112.
  66. Odds FC. Candida species and virulence. ASM News 1994; 60:313.
  67. Cutler JE. Putative virulence factors of Candida albicans. Annu Rev Microbiol 1991; 45:187.
  68. Calderone RA, Fonzi WA. Virulence factors of Candida albicans. Trends Microbiol 2001; 9:327.
  69. Blankenship JR, Wormley FL, Boyce MK, et al. Calcineurin is essential for Candida albicans survival in serum and virulence. Eukaryot Cell 2003; 2:422.
  70. Blankenship JR, Heitman J. Calcineurin is required for Candida albicans to survive calcium stress in serum. Infect Immun 2005; 73:5767.
  71. Chen YL, Brand A, Morrison EL, et al. Calcineurin controls drug tolerance, hyphal growth, and virulence in Candida dubliniensis. Eukaryot Cell 2011; 10:803.
  72. Robbins N, Uppuluri P, Nett J, et al. Hsp90 governs dispersion and drug resistance of fungal biofilms. PLoS Pathog 2011; 7:e1002257.
  73. McLellan CA, Whitesell L, King OD, et al. Inhibiting GPI anchor biosynthesis in fungi stresses the endoplasmic reticulum and enhances immunogenicity. ACS Chem Biol 2012; 7:1520.
  74. Staab JF, Bradway SD, Fidel PL, Sundstrom P. Adhesive and mammalian transglutaminase substrate properties of Candida albicans Hwp1. Science 1999; 283:1535.
  75. Gale CA, Bendel CM, McClellan M, et al. Linkage of adhesion, filamentous growth, and virulence in Candida albicans to a single gene, INT1. Science 1998; 279:1355.
  76. Thammahong A, Puttikamonkul S, Perfect JR, et al. Central Role of the Trehalose Biosynthesis Pathway in the Pathogenesis of Human Fungal Infections: Opportunities and Challenges for Therapeutic Development. Microbiol Mol Biol Rev 2017; 81.
  77. Hube B, Naglik J. Extracellular hydrolases. In: Candida and candidiasis, Calderone RA (Ed), ASM Press, Washington, DC 2002. p.107.
  78. Taylor BN, Staib P, Binder A, et al. Profile of Candida albicans-secreted aspartic proteinase elicited during vaginal infection. Infect Immun 2005; 73:1828.
  79. Schaller M, Korting HC, Borelli C, et al. Candida albicans-secreted aspartic proteinases modify the epithelial cytokine response in an in vitro model of vaginal candidiasis. Infect Immun 2005; 73:2758.
  80. Chen YC, Wu CC, Chung WL, Lee FJ. Differential secretion of Sap4-6 proteins in Candida albicans during hyphae formation. Microbiology 2002; 148:3743.
  81. Felk A, Kretschmar M, Albrecht A, et al. Candida albicans hyphal formation and the expression of the Efg1-regulated proteinases Sap4 to Sap6 are required for the invasion of parenchymal organs. Infect Immun 2002; 70:3689.
  82. Sundstrom P. Adhesins in Candida albicans. Curr Opin Microbiol 1999; 2:353.
  83. Sanglard D, Hube B, Monod M, et al. A triple deletion of the secreted aspartyl proteinase genes SAP4, SAP5, and SAP6 of Candida albicans causes attenuated virulence. Infect Immun 1997; 65:3539.
  84. Ghannoum MA. Potential role of phospholipases in virulence and fungal pathogenesis. Clin Microbiol Rev 2000; 13:122.
  85. Sundstrom P, Balish E, Allen CM. Essential role of the Candida albicans transglutaminase substrate, hyphal wall protein 1, in lethal oroesophageal candidiasis in immunodeficient mice. J Infect Dis 2002; 185:521.
  86. Stichternoth C, Ernst JF. Hypoxic adaptation by Efg1 regulates biofilm formation by Candida albicans. Appl Environ Microbiol 2009; 75:3663.
  87. Grahl N, Cramer RA Jr. Regulation of hypoxia adaptation: an overlooked virulence attribute of pathogenic fungi? Med Mycol 2010; 48:1.
  88. Holland SM, Vinh DC. Yeast infections--human genetics on the rise. N Engl J Med 2009; 361:1798.
  89. Mencacci A, Cenci E, Del Sero G, et al. IL-10 is required for development of protective Th1 responses in IL-12-deficient mice upon Candida albicans infection. J Immunol 1998; 161:6228.
  90. Lavigne LM, Schopf LR, Chung CL, et al. The role of recombinant murine IL-12 and IFN-gamma in the pathogenesis of a murine systemic Candida albicans infection. J Immunol 1998; 160:284.
  91. Vazquez-Torres A, Jones-Carson J, Wagner RD, et al. Early resistance of interleukin-10 knockout mice to acute systemic candidiasis. Infect Immun 1999; 67:670.
  92. Roilides E, Holmes A, Blake C, et al. Effects of granulocyte colony-stimulating factor and interferon-gamma on antifungal activity of human polymorphonuclear neutrophils against pseudohyphae of different medically important Candida species. J Leukoc Biol 1995; 57:651.
  93. Gaviria JM, van Burik JA, Dale DC, et al. Modulation of neutrophil-mediated activity against the pseudohyphal form of Candida albicans by granulocyte colony-stimulating factor (G-CSF) administered in vivo. J Infect Dis 1999; 179:1301.
  94. Ueta E, Tanida T, Doi S, Osaki T. Regulation of Candida albicans growth and adhesion by saliva. J Lab Clin Med 2000; 136:66.
  95. Martínez JP, Gil ML, López-Ribot JL, Chaffin WL. Serologic response to cell wall mannoproteins and proteins of Candida albicans. Clin Microbiol Rev 1998; 11:121.
  96. Casadevall A, Cassone A, Bistoni F, et al. Antibody and/or cell-mediated immunity, protective mechanisms in fungal disease: an ongoing dilemma or an unnecessary dispute? Med Mycol 1998; 36 Suppl 1:95.
  97. Han Y, Cutler JE. Assessment of a mouse model of neutropenia and the effect of an anti-candidiasis monoclonal antibody in these animals. J Infect Dis 1997; 175:1169.
  98. Cutler JE. Candida albicans antibodies and vaccine development (abstract). ASM Conference on Candida and Candidiasis, American Society for Microbiology, Charleston, South Carolina 1999, p. 20.
  99. Zhang MX, Kozel TR. Mannan-specific immunoglobulin G antibodies in normal human serum accelerate binding of C3 to Candida albicans via the alternative complement pathway. Infect Immun 1998; 66:4845.
  100. Spellberg BJ, Ibrahim AS, Avenissian V, et al. The anti-Candida albicans vaccine composed of the recombinant N terminus of Als1p reduces fungal burden and improves survival in both immunocompetent and immunocompromised mice. Infect Immun 2005; 73:6191.
  101. Gantner BN, Simmons RM, Canavera SJ, et al. Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. J Exp Med 2003; 197:1107.
  102. Kimberg M, Brown GD. Dectin-1 and its role in antifungal immunity. Med Mycol 2008; 46:631.