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Candida spp.
Berkhout, 1923 nom. cons.

Say Me

(described by Bennett in 1844)

Taxonomic classification

Kingdom: Fungi
Phylum: Ascomycota
Subphylum: Ascomycotina
Class: Ascomycetes
Order: Saccharomycetales
Family: Saccharomycetaceae
Genus: Candida

Description and Natural Habitats

Candida is a yeast and the most common cause of opportunistic mycoses worldwide. It is also a frequent colonizer of human skin and mucous membranes. Candida is a member of normal flora of skin, mouth, vagina, and stool. As well as being a pathogen and a colonizer, it is found in the environment, particularly on leaves, flowers, water, and soil. While most of the Candida spp. are mitosporic, some have known teleomorphic state and produce sexual spores. See the page on individual species for more detailed information on teleomorphic genera.


The genus Candida includes around 154 species. Among these, six are most frequently isolated in human infections. While Candida albicans is the most abundant and significant species, Candida tropicalis, Candida glabrata, Candida parapsilosis, Candida krusei, and Candida lusitaniae are also isolated as causative agents of Candida infections. Importantly, there has been a recent increase in infections due to non-albicans Candida spp., such as Candida glabrata and Candida krusei [4, 29, 117]. Patients receiving fluconazole prophylaxis are particularly at risk of developing infections due to fluconazole-resistant Candida krusei and Candida glabrata strains [186]. Nevertheless, the diversity of Candida spp. that are encountered in infections is expanding and the emergence of other species that were rarely in play in the past is now likely [158, 259, 288, 294].

Species Commonly Causing Invasive Candidiasis
Species Frequency
Candida albicans
Candida tropicalis
Candida glabrata
Candida parapsilosis
Candida krusei
Candida lusitaniae


See the summary of synonyms and teleomorph-anamorph relations for the Candida spp.

Pathogenicity and Clinical Significance

Infections caused by Candida spp. are in general referred to as candidiasis. The clinical spectrum of candidiasis is extremely diverse. Almost any organ or system in the body can be affected. Candidiasis may be superficial and local or deep-seated and disseminated. Disseminated infections arise from hematogenous spread from the primarily infected locus. Candida albicans is the most pathogenic and most commonly encountered species among all. Its ability to adhere to host tissues, produce secretory aspartyl proteases and phospholipase enzymes, and transform from yeast to hyphal phase are the major determinants of its pathogenicity. Several host factors predispose to candidiasis [242, 266, 270]:

Physiological Pregnancy, age (elderly and infancy)
Trauma Maceration, infection, burn wound
Hematological Neutropenia, cellular immunodeficiency (leukemia, lymphoma, AIDS, aplastic anemia)
Endocrinological Diabetes Mellitus, hypoparathyroidism, Addison's disease
Iatrogenic Chemotherapeutics, corticosteroids, oral contraceptives, antibiotics, catheters, surgery
Other Intravenous drug addiction, malnutrition, malabsorption, thymoma

Candidiasis is mostly an endogenous infection, arising from overgrowth of the fungus inhabiting in the normal flora. However, it may occasionally be acquired from exogenous sources (such as catheters or prosthetic devices) [167] or by person-to-person transmission (such as oral candidiasis in neonates of mothers with vaginal candidiasis or endophthalmitis following corneal transplantation from an infected donor) [210].

Macroscopic and Microscopic Features

The colonies of Candida spp. are cream colored to yellowish, grow rapidly and mature in 3 days. The texture of the colony may be pasty, smooth, glistening or dry, wrinkled and dull, depending on the species [1295].

The microscopic features of Candida spp. also show species-related variations. All species produce blastoconidia singly or in small clusters. Blastoconidia may be round or elongate. Most species produce pseudohyphae which may be long, branched or curved. True hyphae and chlamydospores are produced by strains of some Candida spp.

Although they are the members of the same genus, the various species do have some degree of unique behavior with respect to their colony texture, microscopic morphology on cornmeal tween 80 agar at 25°C (Dalmau method) and fermentation or assimilation profiles in biochemical tests [1295].

Choose a species for more detail:

Histopathologic Features

See our histopathology page.

Compare to

Candida spp. should be differentiated from other clinically encountered yeasts, such as Blastoschizomyces, Cryptococcus, Geotrichum, Malassezia, Rhodotorula, Saccharomyces, and Trichosporon. Morphology on cornmeal tween 80 agar, capsule production, urease activity, ability to grow in presence of cycloheximide, growth pattern in Sabouraud broth, and fermentation assimilation profiles help in differentiation of Candida from other yeasts. Well-developed pseudohyphae and one-celled blastoconidia characterize the common species of Candida. Candida differs from Cryptococcus by having well-developed pseudohyphae. The lack of arthroconidia is the major microscopic feature which differentiates Candida from Trichosporon and Geotrichum, the two genera that produce abundant arthroconidia [1295].

Laboratory Precautions

No special precautions other than general laboratory precautions are required.


Please see our extended discussion of the usual susceptibility patterns of Candida spp.

Candida spp.





4. Abi-Said, D., E. Anaissie, O. Uzun, I. Raad, H. Pinzcowski, and S. Vartivarian. 1997. The epidemiology of hematogenous candidiasis caused by different Candida species. Clin. Infect. Dis. 24:1122-1128.

29. Aisner, J., S. C. Schimpff, J. C. Sutherland, V. M. Young, and P. H. Wiernik. 1976. Torulopsis glabrata infections in patients with cancer: Increasing incidence and relationship to colonization. Am. J. Med. 61:23-28.

117. Arif, S., T. Barkham, E. G. Power, and S. A. Howell. 1996. Techniques for investigation of an apparent outbreak of infections with Candida glabrata. J Clin Microbiol. 34:2205-9.

158. Baily, G. G., C. B. Moore, S. M. Essayag, S. de Wit, J. P. Burnie, and D. W. Denning. 1997. Candida inconspicua, a fluconazole-resistant pathogen in patients infected with human immunodeficiency virus. Clin. Infect. Dis. 25:161-3.

167. Band, J. D., and D. G. Maki. 1979. Infections caused by arterial catheters used for hemodynamic monitoring. Am. J. Med. 67:735-741.

186. Barchiesi, F., V. Morbiducci, F. Ancarani, and G. Scalise. 1993. Emergence of oropharyngeal candidiasis caused by non-albicans species of Candida in HIV-infected patients (letter). Eur. J. Epidemiol. 9:455-456.

210. Behrens-Baumann, W., R. Ruechel, O. Zimmermann, and M. Vogel. 1991. Candida tropicalis endophthalmitis following penetrating keratoplasty. Br. J. Opthalmol. 75:565.

242. Bielsa, I., J. M. Miro, C. Herrero, E. Martin, X. Latorre, and J. M. Mascaro. 1987. Systemic candidiasis in heroin abusers. Cutaneous findings. Int. J. Dermatol. 26:314-9.

259. Blinkhorn, R. J., D. Adelstein, and P. J. Spagnuolo. 1989. Emergence of a new opportunistic pathogen, Candida lusitaniae. J. Clin. Microbiol. 27:236-240.

266. Bodey, G., B. Bueltmann, W. Duguid, D. Gibbs, H. Hanak, M. Hotchi, G. Mall, P. Martino, F. Meunier, S. Milliken, S. Naoe, M. Okudaira, D. Scevola, and J. van't Wout. 1992. Fungal infections in cancer patients: An international autopsy survey. Eur. J. Clin. Microbiol. Infect. Dis. 11:99-109.

270. Bodey, G. P. 1966. Fungal infections complicating acute leukemia. J. Chron. Dis. 19:667-687.

288. Bonomo, R. A., M. Strauss, R. Blinkhorn, and R. A. Salata. 1996. Torulopsis (Candida) glabrata: A new pathogen found in spinal epidural abscess. Clin. Infect. Dis. 22:588-589.

294. Borg-von Zepelin, M., H. Eiffer, M. Kann, and R. Rüchel. 1993. Changes in the spectrum of fungal isolates: results from clinical specimens gathered in 1987/88 compared with those in 1991/92 in the University Hospital Göttingen, Germany. Mycoses. 36:247-253.

1295. Larone, D. H. 1995. Medically Important Fungi - A Guide to Identification, 3rd ed. ASM Press, Washington, D.C.

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