Yeast infection wikipedia

Yeast infection wikipedia DEFAULT

Fungal infection

Fungal infection of animals, including humans

"Mycoses" redirects here. For the journal, see Mycoses (journal).

Medical condition

Other namesMycoses,[1] fungal disease,[2] fungal infection[3]
ICD-10CM codes: Mycoses B35-B49 [4]
Pulmonary aspergillosis.jpg
Micrograph showing a mycosis (aspergillosis). The Aspergillus (which is spaghetti-like) is seen in the center and surrounded by inflammatory cells and necrotic debris. H&E stain.
SpecialtyInfectious Diseases[5]
TypesSystemic, superficial, subcutaneous[3]
CausesPathogenic fungus: dermatophytes, yeasts, molds[6][7]
Risk factorsImmunodeficiency, cancer treatment, organ transplant,[6]COVID-19,[8]tuberculosis
Diagnostic methodBased on symptoms, culture, microscopic examination[6]
Deaths1.7 million (2020)[10]

Fungal infection, also known as mycosis, is disease caused by fungi.[5][11] Different types are traditionally divided according to the part of the body affected; superficial, subcutaneous, and systemic.[3][6] Superficial fungal infections include common tinea of the skin, such as tinea of the body, groin, hands, feet and beard, and yeast infections such as pityriasis versicolor.[7] Subcutaneous types include eumycetoma and chromoblastomycosis, which generally affect tissues in and beneath the skin.[1][7] Systemic fungal infections are more serious and include cryptococcosis, histoplasmosis, pneumocystis pneumonia, aspergillosis and mucormycosis.[3] Signs and symptoms range widely.[3] There is usually a rash with superficial infection.[2] Fungal infection within the skin or under the skin may present with a lump and skin changes.[3]Pneumonia-like symptoms or meningitis may occur with a deeper or systemic infection.[2]

Fungi are everywhere, but only some cause disease.[11] Fungal infection occurs after spores are either breathed in, come into contact with skin or enter the body through the skin such as via a cut, wound or injection.[3] It is more likely to occur in people with a weak immune system.[12] This includes people with illnesses such as HIV/AIDS, and people taking medicines such as steroids or cancer treatments.[12]Fungi that cause infections in people include yeasts, molds and fungi that are able to exist as both a mold and yeast.[3] The yeast Candida albicans can live in people without producing symptoms, and is able to cause both superficial mild candidiasis in healthy people, such as oral thrush or vaginal yeast infection, and severe systemic candidiasis in those who cannot fight infection themselves.[3]

Diagnosis is generally based on signs and symptoms, microscopy, culture, sometimes requiring a biopsy and the aid of medical imaging.[6] Some superficial fungal infections of the skin can appear similar to other skin conditions such as eczema and lichen planus.[7] Treatment is generally with antifungal medicines, usually in the form of a cream or by mouth or injection, depending on the specific infection and its extent.[13] Some require surgically cutting out infected tissue.[3]

Fungal infections have a world-wide distribution and are common, affecting more than one billion people every year.[9] An estimated 1.7 million deaths from fungal disease were reported in 2020.[10] Several, including sporotrichosis, chromoblastomycosis and mycetoma are neglected.[14]

A wide range of fungal infections occur in other animals, and some can be transmitted from animals to people.[15]

Signs and symptoms[edit]

Most common mild mycoses often present with a rash.[2] Infections within the skin or under the skin may present with a lump and skin changes.[3] Less common deeper fungal infections may present with pneumonia like symptoms or meningitis.[2]


Mycoses are traditionally divided into superficial, subcutaneous, or systemic, where infection is deep, more widespread and involving internal body organs.[3][9] They can affect the nails, vagina, skin and mouth.[16] Some types such as blastomycosis, cryptococcus, coccidioidomycosis and histoplasmosis, affect people who live or visit certain parts of the world.[16] Others such as aspergillosis, pneumocystis pneumonia, candidiasis, mucormycosis and talaromycosis, tend to affect people who are unable to fight infection themselves.[16] Mycoses might not always conform strictly to the three divisions of superficial, subcutaneous and systemic.[3] Some superficial fungal infections can cause systemic infections in people who are immunocompromised.[3] Some subcutaneous fungal infections can invade into deeper structures, resulting in systemic disease.[3]Candida albicans can live in people without producing symptoms, and is able to cause both mild candidiasis in healthy people and severe invasive candidiasis in those who cannot fight infection themselves.[3][7]

ICD-11 codes[edit]

ICD-11 codes include:[5]

  • 1F2D Non-dermatophyte superficial dermatomycoses

Superficial mycoses[edit]

Superficial mycoses include candidiasis in healthy people, common tinea of the skin, such as tinea of the body, groin, hands, feet and beard, and malassezia infections such as pityriasis versicolor.[3][7]


Subcutaneous fungal infections include sporotrichosis, chromoblastomycosis, and eumycetoma.[3]


Systemic fungal infections include histoplasmosis, cryptococcosis, coccidioidomycosis, blastomycosis, mucormycosis, aspergillosis, pneumocystis pneumonia and systemic candidiasis.[3]

Systemic mycoses due to primary pathogens originate normally in the lungs and may spread to other organ systems. Organisms that cause systemic mycoses are inherently virulent.[further explanation needed].[citation needed] Systemic mycoses due to opportunistic pathogens are infections of people with immune deficiencies who would otherwise not be infected. Examples of immunocompromised conditions include AIDS, alteration of normal flora by antibiotics, immunosuppressive therapy, and metastatic cancer. Examples of opportunistic mycoses include Candidiasis, Cryptococcosis and Aspergillosis.[citation needed]


Mycoses are caused by certain fungi; yeasts, molds and some fungi that can exist as both a mold and yeast.[3][6] They are everywhere and infection occurs after spores are either breathed in, come into contact with skin or enter the body through the skin such as via a cut, wound or injection.[3]Candida albicans is the most common cause of fungal infection in people, particularly as oral or vaginal thrush, often following taking antibiotics.[3]

Risk factors[edit]

Fungal infections are more likely in people with weak immune systems.[12] This includes people with illnesses such as HIV/AIDS, and people taking medicines such as steroids or cancer treatments.[12] People with diabetes also tend to develop fungal infections.[17] Very young and very old people, also, are groups at risk.[18][dead link]

Individuals being treated with antibiotics are at higher risk of fungal infections.[19]

Children whose immune systems are not functioning properly (such as children with cancer) are at risk of invasive fungal infections.[20]


During the COVID-19 pandemic some fungal infections have been associated with COVID-19.[8][21][22] Fungal infections can mimic COVID-19, occur at the same time as COVID-19 and more serious fungal infections can complicate COVID-19.[8] A fungal infection may occur after antibiotics for a bacterial infection which has occurred following COVID-19.[23] The most common serious fungal infections in people with COVID-19 include aspergillosis and invasive candidiasis.[24] COVID-19–associated mucormycosis is generally less common, but in 2021 was noted to be significantly more prevalent in India.[8][25]


Fungal infections occur after spores are either breathed in, come into contact with skin or enter the body through a wound.[3]


Diagnosis is generally by signs and symptoms, microscopy, biopsy, culture and sometimes with the aid of medical imaging.[6]

Differential diagnosis[edit]

Some tinea and candidiasis infections of the skin can appear similar to eczema and lichen planus.[7] Pityriasis versicolor can look like seborrheic dermatitis, pityriasis rosea, pityriasis alba and vitiligo.[7]

Some fungal infections such as coccidioidomycosis, histoplasmosis, and blastomycosis can present with fever, cough, and shortness of breath, thereby resembling COVID-19.[26]


Keeping the skin clean and dry, as well as maintaining good hygiene, will help larger topical mycoses. Because some fungal infections are contagious, it is important to wash after touching other people or animals. Sports clothing should also be washed after use.[clarification needed][citation needed]


Treatment depends on the type of fungal infection, and usually requires topical or systemicantifungal medicines.[13]Pneumocystosis does not respond to anti-fungals is treated with co-trimoxazole.[27] Sometimes, infected tissue needs to be surgically cut away.[3]


Worldwide, every year fungal infections affect more than one billion people.[9] An estimated 1.6 million deaths from fungal disease were reported in 2017.[28] The figure has been rising, with an estimated 1.7 million deaths from fungal disease reported in 2020.[10] Fungal infections also constitute a significant cause of illness and mortality in children.[29]

According to the Global Action Fund for Fungal Infections, every year there are over 10 million cases of fungal asthma, around 3 million cases of long-term aspergillosis of lungs, 1 million cases of blindness due to fungal keratitis, more than 200,000 cases of meningitis due to cryptococcus, 700,000 cases of invasive candidiasis, 500,000 cases of pneumocystosis of lungs, 250,000 cases of invasive aspergillosis, and 100,000 cases of histoplasmosis.[30]


In 500BC, an apparent account of ulcers in the mouth by Hippocrates may have been thrush.[31] The Hungarian microscopist based in Paris David Gruby first reported that human disease could be caused by fungi in the early 1840s.[31]

SARS 2003[edit]

During the 2003 SARS outbreak, fungal infections were reported in 14.8–33% of people affected by SARS, and it was the cause of death in 25–73.7% of people with SARS.[32]

Other animals[edit]

A wide range of fungal infections occur in other animals, and some can be transmitted from animals to people, such as Microsporum canis from cats.[15]

See also[edit]


  1. ^ abJohnstone, Ronald B. (2017). "25. Mycoses and Algal infections". Weedon's Skin Pathology Essentials (2nd ed.). Elsevier. pp. 438–465. ISBN .
  2. ^ abcde"Fungal Diseases Homepage | CDC". 29 March 2021. Retrieved 17 June 2021.
  3. ^ abcdefghijklmnopqrstuvwxyBarlow, Gavin; Irving, Irving; moss, Peter J. (2020). "20. Infectious diseases". In Feather, Adam; Randall, David; Waterhouse, Mona (eds.). Kumar and Clark's Clinical Medicine (10th ed.). Elsevier. pp. 559–563. ISBN .
  4. ^ICD-10CM. mycoses B35-B49.
  5. ^ abc"ICD-11 - ICD-11 for Mortality and Morbidity Statistics". Retrieved 25 May 2021.
  6. ^ abcdefgWillinger, Birgit (2019). "1. What is the target? Clinical mycology and diagnostics". In Elisabeth Presterl (ed.). Clinically Relevant Mycoses: A Practical Approach. Springer. pp. 3–19. ISBN .
  7. ^ abcdefghKutzner, Heinz; Kempf, Werner; Feit, Josef; Sangueza, Omar (2021). "2. Fungal infections". Atlas of Clinical Dermatopathology: Infectious and Parasitic Dermatoses. Hoboken: Wiley Blackwell. p. 77-108. ISBN .
  8. ^ abcd"Fungal Diseases and COVID-19 | CDC". 7 June 2021. Retrieved 7 August 2021.
  9. ^ abcdNakazato, Gerson; Alesandra, Audrey; Lonni, Stringhen Garcia; Panagio, Luciano Aparecido; de Camargo, Larissa Ciappina; Goncalves, Marcelly Chue; Reis, Guilherne Fonseca; Miranda-Sapla, Milena Menegazzo; Tomiotto-Pellissier, Fernanda; Kobayashi, Renata Katsuko Takayama (2020). "4. Applications of nanometals in cutaneous infections". In Rai, Mahendra (ed.). Nanotechnology in Skin, Soft Tissue, and Bone Infections. Switzerland: Springer. ISBN .
  10. ^ abcKainz, Katharina; Bauer, Maria A.; Madeo, Frank; Carmona-Gutierrez, Didac (2020). "Fungal infections in humans: the silent crisis". Microbial Cell. 7 (6): 143–145. doi:10.15698/mic2020.06.718. ISSN 2311-2638. PMC 7278517. PMID 32548176.
  11. ^ abRichardson, Malcolm D.; Warnock, David W. (2012). "1. Introduction". Fungal Infection: Diagnosis and Management (4th ed.). John Wiley & Sons. pp. 1–7. ISBN .
  12. ^ abcd"Fungal Infections | Fungal | CDC". 29 January 2019. Retrieved 16 June 2021.
  13. ^ abGraininger, Wolfgang; Diab-Elschahawi, Magda; Presterl, Elisabeth (2019). "3. Antifungal agents". In Elisabeth Presterl (ed.). Clinically Relevant Mycoses: A Practical Approach. Springer. pp. 31–44. ISBN .
  14. ^Queiroz-Telles, Flavio; Fahal, Ahmed Hassan; Falci, Diego R.; Caceres, Diego H.; Chiller, Tom; Pasqualotto, Alessandro C. (1 November 2017). "Neglected endemic mycoses". The Lancet Infectious Diseases. 17 (11): e367–e377. doi:10.1016/S1473-3099(17)30306-7. ISSN 1473-3099. PMID 28774696.
  15. ^ abSeyedmousavi, Seyedmojtaba; Bosco, Sandra de M G; de Hoog, Sybren; Ebel, Frank; Elad, Daniel; Gomes, Renata R; Jacobsen, Ilse D; Jensen, Henrik E; Martel, An; Mignon, Bernard; Pasmans, Frank; Piecková, Elena; Rodrigues, Anderson Messias; Singh, Karuna; Vicente, Vania A; Wibbelt, Gudrun; Wiederhold, Nathan P; Guillot, Jacques (April 2018). "Fungal infections in animals: a patchwork of different situations". Medical Mycology. 56 (Suppl 1): S165–S187. doi:10.1093/mmy/myx104. ISSN 1369-3786. PMC 6251577. PMID 29538732.
  16. ^ abc"Types of Fungal Diseases | Fungal Diseases | CDC". 27 June 2019. Retrieved 12 June 2021.
  17. ^"Thrush in Men". NHS. Retrieved 2013-07-13.
  18. ^"Fungal infections: Introduction". Retrieved May 26, 2010.
  19. ^Britt, L. D.; Peitzman, Andrew; Barie, Phillip; Jurkovich, Gregory (2012). Acute Care Surgery. p. 186. ISBN .
  20. ^Blyth, Christopher C; Hale, Katherine; Palasanthiran, Pamela; O'Brien, Tracey; Bennett, Michael H (2010-02-17). "Antifungal therapy in infants and children with proven, probable or suspected invasive fungal infections". Cochrane Database of Systematic Reviews (2): CD006343. doi:10.1002/14651858.cd006343.pub2. ISSN 1465-1858. PMID 20166083.
  21. ^Hoenigl, Martin; Talento, Alida Fe, eds. (2021). Fungal Infections Complicating COVID-19. MDPI. ISBN .
  22. ^Gangneux, J.-P.; Bougnoux, M.-E.; Dannaoui, E.; Cornet, M.; Zahar, J.R. (June 2020). "Invasive fungal diseases during COVID-19: We should be prepared". Journal De Mycologie Medicale. 30 (2): 100971. doi:10.1016/j.mycmed.2020.100971. ISSN 1156-5233. PMC 7136887. PMID 32307254.
  23. ^Saxena, Shailendra K. (2020). Coronavirus Disease 2019 (COVID-19): Epidemiology, Pathogenesis, Diagnosis, and Therapeutics. Singapore: Springer. p. 73. ISBN .
  24. ^"Fungal Diseases and COVID-19". 7 June 2021. Retrieved 7 August 2021.
  25. ^Qu, Jie-Ming; Cao, Bin; Chen, Rong-Chang (2021). COVID-19: The Essentials of Prevention and Treatment. Amsterdam, Netherlands: Elsevier. ISBN .
  26. ^"Fungal Diseases and COVID-19". 7 June 2021. Retrieved 19 June 2021.
  27. ^"CDC - DPDx - Pneumocystis". 22 January 2019. Archived from the original on 25 July 2021. Retrieved 25 July 2021.
  28. ^"Stop neglecting fungi". Nature Microbiology. 2 (8): 17120. 25 July 2017. doi:10.1038/nmicrobiol.2017.120. ISSN 2058-5276. PMID 28741610.
  29. ^Sehgal, Mukul; Ladd, Hugh J.; Totapally, Balagangadhar (2020-12-01). "Trends in Epidemiology and Microbiology of Severe Sepsis and Septic Shock in Children". Hospital Pediatrics. 10 (12): 1021–1030. doi:10.1542/hpeds.2020-0174. ISSN 2154-1663. PMID 33208389.
  30. ^Rodrigues, Marcio L.; Nosanchuk, Joshua D. (20 February 2020). "Fungal diseases as neglected pathogens: A wake-up call to public health officials". PLOS Neglected Tropical Diseases. 14 (2): e0007964. doi:10.1371/journal.pntd.0007964. ISSN 1935-2735. PMC 7032689. PMID 32078635.
  31. ^ abHomei, A.; Worboys, M. (11 November 2013). "1. Introduction". Fungal Disease in Britain and the United States 1850-2000: Mycoses and Modernity. Springer. p. 6. ISBN .
  32. ^Song, Ge; Liang, Guanzhao; Liu, Weida (31 July 2020). "Fungal Co-infections Associated with Global COVID-19 Pandemic: A Clinical and Diagnostic Perspective from China". Mycopathologia: 1–8. doi:10.1007/s11046-020-00462-9. ISSN 0301-486X. PMC 7394275. PMID 32737747.

External links[edit]


Candida albicans

Species of fungus

Candida albicans is an opportunistic pathogenic yeast[4] that is a common member of the human gut flora. It can also survive outside the human body.[5][6] It is detected in the gastrointestinal tract and mouth in 40–60% of healthy adults.[7][8] It is usually a commensal organism, but it can become pathogenic in immunocompromised individuals under a variety of conditions.[8][9] It is one of the few species of the genus Candida that causes the human infection candidiasis, which results from an overgrowth of the fungus.[8][9] Candidiasis is, for example, often observed in HIV-infected patients.[10]C. albicans is the most common fungal species isolated from biofilms either formed on (permanent) implanted medical devices or on human tissue.[11][12]C. albicans, C. tropicalis, C. parapsilosis, and C. glabrata are together responsible for 50–90% of all cases of candidiasis in humans.[9][13][14] A mortality rate of 40% has been reported for patients with systemic candidiasis due to C. albicans.[15] By one estimate, invasive candidiasis contracted in a hospital causes 2,800 to 11,200 deaths yearly in the US.[16] Nevertheless, these numbers may not truly reflect the true extent of damage this organism causes, given new studies indicating that C. albicans can cross the blood brain barrier.[17][18]

C. albicans is commonly used as a model organism for fungal pathogens.[19] It is generally referred to as a dimorphic fungus since it grows both as yeast and filamentous cells. However, it has several different morphological phenotypes including opaque, GUT, and pseudohyphal forms.[20][21]C. albicans was for a long time considered an obligate diploid organism without a haploid stage. This is, however, not the case. Next to a haploid stage C. albicans can also exist in a tetraploid stage. The latter is formed when diploid C. albicans cells mate when they are in the opaque form.[22] The diploid genome size is approximately 29 Mb, and up to 70% of the protein coding genes have not yet been characterized.[23]C. albicans is easily cultured in the lab and can be studied both in vivo and in vitro. Depending on the media different studies can be done as the media influences the morphological state of C. albicans. A special type of medium is CHROMagar™ Candida, which can be used to identify different species of candida.[24][25]


Candida albicans can be seen as a tautology. Candida comes from the Latin word candidus, meaning white. Albicans itself is the present participle of the Latin word albicō, meaning becoming white. This leads to white becoming white, making it a tautology.

It is often shortly referred to as thrush, candidiasis, or candida. More than a hundred synonyms have been used to describe C. albicans.[2][26] Over 200 species have been described within the candida genus. The oldest reference to thrush, most likely caused by C. albicans, dates back to 400 BCE in Hippocrates' work Of the Epidemics describing oral candidiasis.[2][27]


Candida albicansvisualized using scanning electron microscopy. Note the abundant hyphal mass.

The genome of C. albicans is almost 16Mb for the haploid size (28Mb for the diploid stage) and consists of 8 sets of chromosome pairs called chr1A, chr2A, chr3A, chr4A, chr5A, chr6A, chr7A and chrRA. The second set (C. albicans is diploid) has similar names but with a B at the end. Chr1B, chr2B, ... and chrRB. The whole genome contains 6,198 open reading frames (ORFs). Seventy percent of these ORFs have not yet been characterized. The whole genome has been sequenced making it one of the first fungi to be completely sequenced (next to Saccharomyces cerevisiae and Schizosaccharomyces pombe).[10][23] All open reading frames (ORFs) are also available in Gateway-adapted vectors. Next to this ORFeome there is also the availability of a GRACE (gene replacement and conditional expression) library to study essential genes in the genome of C. albicans.[28][29] The most commonly used strains to study C. albicans are the WO-1 and SC5314 strains. The WO-1 strain is known to switch between white-opaque form with higher frequency while the SC5314 strain is the strain used for gene sequence reference.[30]

One of the most important features of the C. albicans genome is the high heterozygosity. At the base of this heterozygosity lies the occurrence of numeric and structural chromosomal rearrangements and changes as means of generating genetic diversity by chromosome length polymorphisms (contraction/expansion of repeats), reciprocal translocations, chromosome deletions, Nonsynonymous single-nucleotide polymorphisms and trisomy of individual chromosomes. These karyotypic alterations lead to changes in the phenotype, which is an adaptation strategy of this fungus. These mechanisms are further being explored with the availability of the complete analysis of the C. albicans genome.[31][32][33]

An unusual feature of the genus Candida is that in many of its species (including C. albicans and C. tropicalis, but not, for instance, C. glabrata) the CUG codon, which normally specifies leucine, specifies serine in these species. This is an unusual example of a departure from the standard genetic code, and most such departures are in start codons or, for eukaryotes, mitochondrial genetic codes.[34][35][36] This alteration may, in some environments, help these Candida species by inducing a permanent stress response, a more generalized form of the heat shock response.[37] However, this different codon usage makes it more difficult to study C. albicans protein-protein interactions in the model organism S. cerevisiae. To overcome this problem a C. albicans specific two-hybrid system was developed.[38]

The genome of C. albicans is highly dynamic, contributed by the different CUG translation, and this variability has been used advantageously for molecular epidemiological studies and population studies in this species. The genome sequence has allowed for identifying the presence of a parasexual cycle (no detected meiotic division) in C. albicans.[39] This study of the evolution of sexual reproduction in six Candida species found recent losses in components of the major meiotic crossover-formation pathway, but retention of a minor pathway.[39] The authors suggested that if Candida species undergo meiosis it is with reduced machinery, or different machinery, and indicated that unrecognized meiotic cycles may exist in many species. In another evolutionary study, introduction of partial CUG identity redefinition (from Candida species) into Saccharomyces cerevisiae clones caused a stress response that negatively affected sexual reproduction. This CUG identity redefinition, occurring in ancestors of Candida species, was thought to lock these species into a diploid or polyploid state with possible blockage of sexual reproduction.[40]


C. albicans exhibits a wide range of morphologicalphenotypes due to phenotypic switching and bud to hypha transition. The yeast-to-hyphae transition (filamentation) is a rapid process and induced by environmental factors. Phenotypic switching is spontaneous, happens at lower rates and in certain strains up to seven different phenotypes are known. The best studied switching mechanism is the white to opaque switching (an epigenetic process). Other systems have been described as well. Two systems (the high-frequency switching system and white to opaque switching) were discover by David R. Soll and colleagues.[41][42] Switching in C. albicans is often, but not always, influenced by environmental conditions such as the level of CO2, anaerobic conditions, medium used and temperature.[43] In its yeast form C. albicans ranges from 10 to 12 microns.[44] Spores can form on the pseudohyphae called chlamydospores which survive when put in unfavorable conditions such as dry or hot seasons.[45]

An opaque colony of C. albicansgrowing as yeast-like cells with filamentous C. albicanscells on top

Yeast-to-hypha switching[edit]

Although often referred to as dimorphic, C. albicans is, in fact, polyphenic (often also referred to as pleomorphic).[46] When cultured in standard yeast laboratory medium, C. albicans grows as ovoid "yeast" cells. However, mild environmental changes in temperature, CO2, nutrients and pH can result in a morphological shift to filamentous growth.[47][48] Filamentous cells share many similarities with yeast cells. Both cell types seem to play a specific, distinctive role in the survival and pathogenicity of C. albicans. Yeast cells seem to be better suited for the dissemination in the bloodstream while hyphal cells have been proposed as a virulence factor. Hyphal cells are invasive and speculated to be important for tissue penetration, colonization of organs and surviving plus escaping macrophages.[49][50][51] The transition from yeast to hyphal cells is termed to be one of the key factors in the virulence of C. albicans; however, it is not deemed necessary.[52] When C. albicans cells are grown in a medium that mimics the physiological environment of a human host, they grow as filamentous cells (both true hyphae and pseudohyphae). C. albicans can also form chlamydospores, the function of which remains unknown, but it is speculated they play a role in surviving harsh environments as they are most often formed under unfavorable conditions.[53]

The cAMP-PKA signaling cascade is crucial for the morphogenesis and an important transcriptional regulator for the switch from yeast like cells to filamentous cells is EFG1.[54][55]

Round, white-phase and elongated, opaque-phase Candida albicanscells: the scale bar is 5 µm
In this model of the genetic network regulating the white-opaque switch, the white and gold boxes represent genes enriched in the white and opaque states, respectively. The blue lines represent relationships based on genetic epistasis. Red lines represent Wor1 control of each gene, based on Wor1 enrichment in chromatin immunoprecipitation experiments. Activation (arrowhead) and repression (bar) are inferred based on white- and opaque-state expression of each gene.

High-frequency switching[edit]

Besides the well-studied yeast-to-hyphae transition other switching systems have been described.[56] One such system is the "high-frequency switching" system. During this switching different cellular morphologies (phenotypes) are generated spontaneously. This type of switching does not occur en masse, represents a variability system and it happens independently from environmental conditions.[57] The strain 3153A produces at least seven different colony morphologies.[58][59][60] In many strains the different phases convert spontaneously to the other(s) at a low frequency. The switching is reversible, and colony type can be inherited from one generation to another. Being able to switch through so many different (morphological) phenotypes makes C. albicans able to grow in different environments, both as a commensal and as a pathogen.[61]

In the 3153A strain, a gene called SIR2 (for silent information regulator), which seems to be important for phenotypic switching, has been found.[62][63]SIR2 was originally found in Saccharomyces cerevisiae (brewer's yeast), where it is involved in chromosomal silencing—a form of transcriptional regulation, in which regions of the genome are reversibly inactivated by changes in chromatin structure (chromatin is the complex of DNA and proteins that make chromosomes). In yeast, genes involved in the control of mating type are found in these silent regions, and SIR2 represses their expression by maintaining a silent-competent chromatin structure in this region.[64] The discovery of a C. albicans SIR2 implicated in phenotypic switching suggests it, too, has silent regions controlled by SIR2, in which the phenotype-specific genes may reside. How SIR2 itself is regulated in S. cerevisiae may yet provide more clues as to the switching mechanisms of C. albicans.

White-to-opaque switching[edit]

Next to the dimorphism and the first described high-frequency switching system C. albicans undergoes another high-frequency switching process called white to opaque switching, which is another phenotypic switching process in C. albicans. It was the second high-frequency switching system discovered in C. albicans.[41] The white to opaque switching is an epigenetic switching system.[65] Phenotypic switching is often used to refer to white-opaque switching, which consists of two phases: one that grows as round cells in smooth, white colonies (referred to as white form) and one that is rod-like and grows as flat, gray colonies (called opaque form). This switch from white cells to opaque cells is important for the virulence and the mating process of C. albicans as the opaque form is the mating competent form, being a million times more efficient in mating compared to the white type.[65][66][67] This switching between white and opaque form is regulated by the WOR1 regulator (White to Opaque Regulator 1) which is controlled by the mating type locus (MTL) repressor (a1-α2) that inhibits the expression of WOR1.[68] Besides the white and opaque phase there is also a third one: the gray phenotype. This phenotype shows the highest ability to cause cutaneous infections. The white, opaque and gray phenotypes form a tristable phenotypic switching system. Since it is often difficult to differentiate between white, opaque and gray cells phloxine B, a dye, can be added to the medium.[61]

A potential regulatory molecule in the white to opaque switching is Efg1p, a transcription factor found in the WO-1 strain that regulates dimorphism, and more recently has been suggested to help regulate phenotypic switching. Efg1p is expressed only in the white and not in the gray cell-type, and overexpression of Efg1p in the gray form causes a rapid conversion to the white form.[69][70]

White-GUT switch[edit]

A very special type of phenotypic switch is the white-GUT switch (Gastrointestinally-IndUced Transition). GUT cells are extremely adapted to survival in the digestive tract by metabolic adaptations to available nutrients in the digestive tract. The GUT cells live as commensal organisms and outcompete other phenotypes. The transition from white to GUT cells is driven by passage through the gut where environmental parameters trigger this transition by increasing the WOR1 expression.[71][72]

Role in disease[edit]

Main article: Candidiasis

Candida is found worldwide but most commonly compromises immunocompromised individuals diagnosed with serious diseases such as HIV and cancer. Candida are ranked as one of the most common groups of organisms that cause hospital-acquired infections. Especially high-risk individuals are patients that have recently undergone surgery, a transplant or are in the Intensive Care Units (ICU),[73]C. albicans infections is the top source of fungal infections in critically ill or otherwise immuncompromised patients.[74] These patients predominantly develop oropharyngeal or thrush candidiasis, which can lead to malnutrition and interfere with the absorption of medication.[75] Methods of transmission include mother to infant through childbirth, people-to-people acquired infections that most commonly occur in hospital settings where immunocompromised patients acquire the yeast from healthcare workers and has a 40% incident rate.[citation needed] People can become infected after having sex with a woman that has an existing vaginal yeast infection.[73] Parts of the body that are commonly infected include the skin, genitals, throat, mouth, and blood.[76] Distinguishing features of vaginal infection include discharge, and dry and red appearance of vaginal mucosa or skin. Candida continues to be the fourth most commonly isolated organism in bloodstream infections.[77] Healthy people usually do not suffer (severely) from superficial infections caused by a local alteration in cellular immunity as seen by asthma patients that use oral corticosteroids.[citation needed]

Superficial and local infections[edit]

It commonly occurs as a superficial infection on mucous membranes in the mouth or vagina. Once in their lives around 75% of women will suffer from vulvovaginal candidiasis (VVC) and about 90% of these infections are caused by C. albicans.[citation needed] It may also affect a number of other regions. For example, higher prevalence of colonization of C. albicans was reported in young individuals with tongue piercing, in comparison to unpierced matched individuals.[78] To infect host tissue, the usual unicellular yeast-like form of C. albicans reacts to environmental cues and switches into an invasive, multicellular filamentous form, a phenomenon called dimorphism.[79] In addition, an overgrowth infection is considered a superinfection, the term usually applied when an infection becomes opportunistic and very resistant to antifungals. It then becomes suppressible by antibiotics[clarification needed][citation needed]. The infection is prolonged when the original sensitive strain is replaced by the antibiotic-resistant strain.[80]

Candidiasis is known to cause gastrointestinal (GI) symptoms particularly in immunocompromised patients or those receiving steroids (e.g. to treat asthma) or antibiotics. Recently, there is an emerging literature that an overgrowth of fungus in the small intestine of non-immunocompromised subjects may cause unexplained GI symptoms. Small intestinal fungal overgrowth (SIFO) is characterized by the presence of an excessive number of fungal organisms in the small intestine associated with gastrointestinal symptoms. The most common symptoms observed in these patients were belching, bloating, indigestion, nausea, diarrhea, and gas. The underlying mechanism(s) that predisposes to SIFO is unclear. Further studies are needed; both to confirm these observations and to examine the clinical relevance of fungal overgrowth.[8][9][81]

Systemic infections[edit]

Systemic fungal infections (fungemias) including those by C. albicans have emerged as important causes of morbidity and mortality in immunocompromised patients (e.g., AIDS, cancer chemotherapy, organ or bone marrow transplantation). C. albicans often forms biofilms inside the body. Such C. albicansbiofilms may form on the surface of implantable medical devices or organs. In these biofilms it is often found together with Staphylococcus aureus.[11][12][82][83] Such multispecies infections lead to higher mortalities.[84] In addition hospital-acquired infections by C. albicans have become a cause of major health concerns.[10][85] Especially once candida cells are introduced in the bloodstream a high mortality, up to 40–60% can occur.[10][86]

Although Candida albicans is the most common cause of candidemia, there has been a decrease in the incidence and an increased isolation of non-albicans species of Candida in recent years.[87] Preventive measures include maintaining a good oral hygiene, keeping a healthy lifestyle including good nutrition, the careful use of antibiotics, treatment of infected areas and keeping skin dry and clean, free from open wounds.[88][89]

Role of C. albicans in Crohn's disease[edit]

The link between C. albicans and Crohn's disease has been investigated in a large cohort. This study demonstrated that members of families with multiple cases of Crohn's disease were more likely to be colonized by C. albicans than members of control families.[90] Experimental studies show that chemically-induced colitis promotes C. albicans colonization. In turn, C. albicans colonization generates anti-Saccharomyces cerevisiae antibodies (ASCA), increases inflammation, histological scores and pro-inflammatory cytokine expression.[91][92]


There are relatively few drugs that can successfully treat Candidiasis.[93][94] Treatment commonly includes:[95]

Similarly to antibiotic resistance, resistance to many anti-fungals is becoming a problem. New anti-fungals have to be developed to cope with this problem since only a limited number of anti-fungals are available.[93][97] A general problem is that in contrast to bacteria, fungi are often overlooked as a potential health problem.[98]

Economic implications[edit]

Given the fact that candidiasis is the fourth- (to third-) most frequent hospital acquired infection worldwide it leads to immense financial implications. Approximately 60,000 cases of systemic candidiasis each year in the USA alone lead up to a cost to be between $2–4 billion.[99] The total costs for candidiasis are among the highest compared to other fungal infections due to the high prevalence.[100] The immense costs are partly explained by a longer stay in the intensive care unit or hospital in general. An extended stay for up to 21 more days compared to non-infected patients is not uncommon.[101]

Biofilm development[edit]

Biofilm formation steps[edit]

The biofilm of C. albicans is formed in four steps. First, there is the initial adherence step, where the yeast-form cells adhere to the substrate. The second step is called Intermediate step, where the cells propagate to form microcolonies, and germ tubes form to yield hyphae. In the maturation step, the biofilm biomass expands, the extracellular matrix accumulates and drug resistance increases. In the last step of biofilm formation, the yeast-form cells are released to colonize the surrounding environment (dispersion). Yeast cells released from a biofilm have novel properties, including increased virulence and drug tolerance.[102][103][104]


Zap1, also known as Csr1 and Sur1 (zinc-responsive activator protein), is a transcription factor which is required for the hypha formation in C. albicans biofilms. Zap1 controls the equilibrium of yeast and hyphal cells, the zinc transporters and zinc regulated genes in biofilms of C. albicans.[105]


Zinc (Zn2+) is important for cell function of C. albicans and Zap1 controls the Zinc levels in the cells through the zinc transporters Zrt1 and Zrt2. The regulation of zinc concentration in the cells is important for the cell viability and if the zinc levels get too high, it is toxic for the cells. The Zrt1 is transporting the zinc ions with high affinity and the Zrt2 is transporting the zinc ions with low affinity.[106]

Mechanisms and proteins important for pathogenesis[edit]


The ability to switch between yeast cells and hyphal cells is an important virulence factor. Many proteins play a role in this process. Filamentation in C. albicans is a very complex process.[107] The formation of hyphae can for example help Candida albicans to escape from macrophages in the human body.[108] Moreover, C. albicans undergo yeast-to-hyphal transition within the acidic macrophage phagosome. This initially causes phagosome membrane distension which eventually leads to phagosomal alkalinization by physical rupture, followed by escape.[109]


Main article: Hwp1

Hwp1 stands for Hyphal wall protein 1. Hwp1 is a mannoprotein located on the surface of the hyphae in the hyphal form of C. albicans. Hwp1 is a mammalian transglutaminase substrate. This host enzyme allows Candida albicans to attach stably to host epithelial cells.[110] Adhesion of C. albicans to host cells is an essential first step in the infection process for colonization and subsequent induction of mucosal infection.[citation needed]


The RNA-binding protein Slr1 plays a role in instigating hyphal formation and virulence in C. albicans.[111]


Candidalysin is a cytolytic 31-amino acid α-helical peptide toxin that is released by C. albicans during hyphal formation. It contributes to virulence during mucosal infections.[112]

Genetic and genomic tools[edit]

Due to its nature as a model organism, being an important human pathogen and the alternative codon usage (CUG translated into serine rather than leucine), several specific projects and tools have been created to study C. albicans.[10] The diploid nature and the absence of a sexual cycle, however, makes it a hard to study organism. In the last 20 years, however, many systems have been developed to study C. albicans in a more in depth genetic level.[19]

Selection markers[edit]

The most used selection markers in C. albicans are the CaNAT1 resistance marker (confers resistance against nourseothricin) and MPAr or IMH3r (confers resistance to mycophenolic acid).[113] Next to the above-mentioned selection makers a few auxotrophic strains were generated to work with auxotrophic makers. The URA3 marker (URA3 blaster method) is an often-used strategy in uridine auxotrophic strains; however, studies have shown that differences in URA3 position in the genome can be involved in the pathogeny of C. albicans.[114] Besides the URA3 selection one can also use the histidine, leucine and arginine autotrophy. The advantage of using those autotrophies lies in the fact that they exhibit wild-type or nearly wild-type virulence in a mouse model compared to the URA3 system.[115] One application of the leucine, arginine and histidine autotrophy is for example the candida two-hybrid system.[116]

Full sequence genome[edit]

The full genome of C. albicans has been sequenced and made publicly available in a Candida database. The heterozygous diploid strain used for this full genome sequence project is the laboratory strain SC5314. The sequencing was done using a whole-genome shotgun approach.[117]

ORFeome project[edit]

Every predicted ORF has been created in a gateway adapted vector (pDONR207) and made publicly available. The vectors (plasmids) can be propagated in E.coli and grown on LB+gentamicin medium. This way every ORF is readily available in an easy to use vector. Using the gateway system it is possible to transfer the ORF of interest to any other gateway adapted vector for further studies of the specific ORF.[29][118]

CIp10 integrative plasmid[edit]

Contrary to the yeast S. cerevisiae episomal plasmids do not stay stable in C. albicans. In order to work with plasmids in C. albicans an integrative approach (plasmid integration into the genome) thus has to be used. A second problem is that most plasmid transformations are rather inefficient in C. albicans; however, the CIp10 plasmid overcomes these problems and can be used with ease to transform C. albicans in a very efficient way. The plasmid integrates inside the RP10 locus as disruption of one RP10 allele does not seem to affect the viability and growth of C. albicans. Several adaptations of this plasmid have been made after the original became available.[119][120]

Candida two-hybrid (C2H) system[edit]

Due to the aberrant codon usage of C. albicans it is less feasible to use the common host organism (Saccharomyces cerevisiae) for two-hybrid studies. To overcome this problem a C. albicans two-hybrid (C2H) system was created. The strain SN152 that is auxotrophic for leucine, arginine and histidine was used to create this C2H system. It was adapted by integrating a HIS1 reporter gene preceded by five LexAOp sequences. In the C2H system the bait plasmid (pC2HB) contains the Staphylococcus aureus LexA BD, while the prey plasmid (pC2HP) harbors the viral AD VP16. Both plasmids are integrative plasmids since episomal plasmids do not stay stable in C. albicans. The reporter gene used in the system is the HIS1 gene. When proteins interact, the cells will be able to grow on medium lacking histidine due to the activation of the HIS1 reporter gene.[10][38] Several interactions have thus far been detected using this system in a low scale set up.[121][122] A first high-throughput screening has also been performed.[123][124] Interacting proteins can be found at the BioGRID.[125]

Bimolecular fluorescence complementation (BiFC)[edit]

Besides the C2H system, a BiFC system has been developed to study protein-protein interactions in C. albicans. With this systems protein interactions can be studied in their native sub cellular location contrary to a C2H system in which the proteins are forced into the nucleus. With BiFC one can study for example protein interactions that take place at the cell membrane or vacuolar membrane.[124][126][127]


Both DNA and protein microarrays were designed to study DNA expression profiles and antibody production in patients against C. albicans cell wall proteins.[120][128]

GRACE library[edit]

Using a tetracycline-regulatable promoter system a gene replacement and conditional expression (GRACE) library was created for 1,152 genes. By using the regulatable promoter and having deleted 1 of the alleles of the specific gene it was possible to discriminate between non-essential and essential genes. Of the tested 1,152 genes 567 showed to be essential. The knowledge on essential genes can be used to discover novel antifungals.[129]


CRISPR/Cas9 has been adapted to be used in C. albicans.[130] Several studies have been performed using this system.[131][132]

Application in engineering[edit]

C. albicans has been used in combination with carbon nanotubes (CNT) to produce stable electrically conductive bio-nano-composite tissue materials that have been used as temperature-sensing elements.[133]

Notable C. albicans researchers[edit]

See also[edit]


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  68. ^Morschhäuser J (2010). "Regulation of white-opaque switching in Candida albicans". Med Microbiol Immunol. 199 (3): 165–172. doi:10.1007/s00430-010-0147-0. PMID 20390300. S2CID 8770123.
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  71. ^Pande, Kalyan; Chen, Changbin; Noble, Suzanne M (2013). "Passage through the mammalian gut triggers a phenotypic switch that promotes Candida albicans commensalism". Nature Genetics. 45 (9): 1088–91. doi:10.1038/ng.2710. PMC 3758371. PMID 23892606.
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fungal infection due to any type of Candida

"Yeast infection" redirects here. For yeast infections affecting the vagina, see vaginal yeast infection.

For the invasive form of Candidiasis, see Candidemia.

Medical condition

Candidiasis is a fungal infection due to any type of Candida (a type of yeast).[4] When it affects the mouth, in some countries it is commonly called thrush.[3] Signs and symptoms include white patches on the tongue or other areas of the mouth and throat.[3] Other symptoms may include soreness and problems swallowing.[9] When it affects the vagina, it may be referred to as a yeast infection or thrush.[2][10] Signs and symptoms include genital itching, burning, and sometimes a white "cottage cheese-like" discharge from the vagina.[11] Yeast infections of the penis are less common and typically present with an itchy rash.[11] Very rarely, yeast infections may become invasive, spreading to other parts of the body.[12] This may result in fevers along with other symptoms depending on the parts involved.[12]

More than 20 types of Candida can cause infection with Candida albicans being the most common.[13] Infections of the mouth are most common among children less than one month old, the elderly, and those with weak immune systems.[5] Conditions that result in a weak immune system include HIV/AIDS, the medications used after organ transplantation, diabetes, and the use of corticosteroids.[5] Other risks include dentures, following antibiotic therapy, and breastfeeding.[5][14] Vaginal infections occur more commonly during pregnancy, in those with weak immune systems, and following antibiotic use.[15] Individuals at risk for invasive candidiasis include low birth weight babies, people recovering from surgery, people admitted to intensive care units, and those with an otherwise compromised immune system.[16]

Efforts to prevent infections of the mouth include the use of chlorhexidine mouthwash in those with poor immune function and washing out the mouth following the use of inhaled steroids.[6] Little evidence supports probiotics for either prevention or treatment, even among those with frequent vaginal infections.[17][18] For infections of the mouth, treatment with topicalclotrimazole or nystatin is usually effective.[6] Oral or intravenous fluconazole, itraconazole, or amphotericin B may be used if these do not work.[6] A number of topical antifungal medications may be used for vaginal infections, including clotrimazole.[19] In those with widespread disease, an echinocandin such as caspofungin or micafungin is used.[20] A number of weeks of intravenous amphotericin B may be used as an alternative.[20] In certain groups at very high risk, antifungal medications may be used preventatively.[16][20]

Infections of the mouth occur in about 6% of babies less than a month old.[7] About 20% of those receiving chemotherapy for cancer and 20% of those with AIDS also develop the disease.[7] About three-quarters of women have at least one yeast infection at some time during their lives.[8] Widespread disease is rare except in those who have risk factors.[21]

Signs and symptoms[edit]

Signs and symptoms of candidiasis vary depending on the area affected.[22] Most candidal infections result in minimal complications such as redness, itching, and discomfort, though complications may be severe or even fatal if left untreated in certain populations. In healthy (immunocompetent) persons, candidiasis is usually a localized infection of the skin, fingernails or toenails (onychomycosis), or mucosal membranes, including the oral cavity and pharynx (thrush), esophagus, and the genitalia (vagina, penis, etc.);[23][24][25] less commonly in healthy individuals, the gastrointestinal tract,[26][27][28]urinary tract,[26] and respiratory tract[26] are sites of candida infection.

In immunocompromised individuals, Candida infections in the esophagus occur more frequently than in healthy individuals and have a higher potential of becoming systemic, causing a much more serious condition, a fungemia called candidemia.[23][29][30] Symptoms of esophageal candidiasis include difficulty swallowing, painful swallowing, abdominal pain, nausea, and vomiting.[23][31]


Infection in the mouth is characterized by white discolorations in the tongue, around the mouth, and throat. Irritation may also occur, causing discomfort when swallowing.[32]

Thrush is commonly seen in infants. It is not considered abnormal in infants unless it lasts longer than a few weeks.[33]


Infection of the vagina or vulva may cause severe itching, burning, soreness, irritation, and a whitish or whitish-gray cottage cheese-like discharge. Symptoms of infection of the male genitalia (balanitis thrush) include red skin around the head of the penis, swelling, irritation, itchiness and soreness of the head of the penis, thick, lumpy discharge under the foreskin, unpleasant odour, difficulty retracting the foreskin (phimosis), and pain when passing urine or during sex.[34]


Signs and symptoms of candidiasis in the skin include itching, irritation, and chafing or broken skin.[35]

Invasive infection[edit]

Common symptoms of gastrointestinal candidiasis in healthy individuals are anal itching, belching, bloating, indigestion, nausea, diarrhea, gas, intestinal cramps, vomiting, and gastric ulcers.[26][27][28] Perianal candidiasis can cause anal itching; the lesion can be red, papular, or ulcerative in appearance, and it is not considered to be a sexually transmissible disease.[36] Abnormal proliferation of the candida in the gut may lead to dysbiosis.[37] While it is not yet clear, this alteration may be the source of symptoms generally described as the irritable bowel syndrome,[38][39] and other gastrointestinal diseases.[27][40]


Main article: Candida (fungus)

Candida yeasts are generally present in healthy humans, frequently part of the human body's normal oral and intestinal flora, and particularly on the skin; however, their growth is normally limited by the human immune system and by competition of other microorganisms, such as bacteria occupying the same locations in the human body.[41]Candida requires moisture for growth, notably on the skin.[42] For example, wearing wet swimwear for long periods of time is believed to be a risk factor.[43] Candida can also cause diaper rashes in babies.[35] In extreme cases, superficial infections of the skin or mucous membranes may enter the bloodstream and cause systemic Candida infections.

Factors that increase the risk of candidiasis include HIV/AIDS, mononucleosis, cancer treatments, steroids, stress, antibiotic usage, diabetes, and nutrient deficiency. Hormone replacement therapy and infertility treatments may also be predisposing factors.[44] Use of inhaled corticosteroids increases risk of candidiasis of the mouth.[45] Inhaled corticosteroids with other risk factors such as antibiotics, oral glucocorticoids, not rinsing mouth after use of inhaled corticosteroids or high dose of inhaled corticosteroids put people at even higher risk.[45] Treatment with antibiotics can lead to eliminating the yeast's natural competitors for resources in the oral and intestinal flora, thereby increasing the severity of the condition.[46] A weakened or undeveloped immune system or metabolic illnesses are significant predisposing factors of candidiasis.[47] Almost 15% of people with weakened immune systems develop a systemic illness caused by Candida species.[48] Diets high in simple carbohydrates have been found to affect rates of oral candidiases.[49]

C. albicans was isolated from the vaginas of 19% of apparently healthy women, i.e., those who experienced few or no symptoms of infection. External use of detergents or douches or internal disturbances (hormonal or physiological) can perturb the normal vaginal flora, consisting of lactic acid bacteria, such as lactobacilli, and result in an overgrowth of Candida cells, causing symptoms of infection, such as local inflammation.[50] Pregnancy and the use of oral contraceptives have been reported as risk factors.[51]Diabetes mellitus and the use of antibiotics are also linked to increased rates of yeast infections.[51]

In penile candidiasis, the causes include sexual intercourse with an infected individual, low immunity, antibiotics, and diabetes. Male genital yeast infections are less common, but a yeast infection on the penis caused from direct contact via sexual intercourse with an infected partner is not uncommon.[52]

Breast-feeding mothers may also develop candidiasis on and around the nipple as a result of moisture created by excessive milk-production.[14]

Vaginal candidiasis can cause congenital candidiasis in newborns.[53]


Micrograph of esophageal candidiasis showing hyphae, biopsyspecimen, PAS stain
Gram stainof Candida albicansfrom a vaginal swab. The small oval chlamydospores are 2-4 µmin diameter.

In oral candidiasis, simply inspecting the person's mouth for white patches and irritation may make the diagnosis. A sample of the infected area may also be taken to determine what organism is causing the infection.[54]

Symptoms of vaginal candidiasis are also present in the more common bacterial vaginosis;[55] aerobic vaginitis is distinct and should be excluded in the differential diagnosis.[56] In a 2002 study, only 33% of women who were self-treating for a yeast infection actually had such an infection, while most had either bacterial vaginosis or a mixed-type infection.[57]

Diagnosis of a yeast infection is done either via microscopic examination or culturing. For identification by light microscopy, a scraping or swab of the affected area is placed on a microscope slide. A single drop of 10% potassium hydroxide (KOH) solution is then added to the specimen. The KOH dissolves the skin cells, but leaves the Candida cells intact, permitting visualization of pseudohyphae and budding yeast cells typical of many Candida species.

For the culturing method, a sterile swab is rubbed on the infected skin surface. The swab is then streaked on a culture medium. The culture is incubated at 37 °C (98.6 °F) for several days, to allow development of yeast or bacterial colonies. The characteristics (such as morphology and colour) of the colonies may allow initial diagnosis of the organism causing disease symptoms.[58] Respiratory, gastrointestinal, and esophageal candidiasis require an endoscopy to diagnose.[28][59] For gastrointestinal candidiasis, it is necessary to obtain a 3–5 milliliter sample of fluid from the duodenum for fungal culture.[28] The diagnosis of gastrointestinal candidiasis is based upon the culture containing in excess of 1,000 colony-forming units per milliliter.[28]


Candidiasis may be divided into these types:


A diet that supports the immune system and is not high in simple carbohydrates contributes to a healthy balance of the oral and intestinal flora.[41][49] While yeast infections are associated with diabetes, the level of blood sugar control may not affect the risk.[64] Wearing cotton underwear may help to reduce the risk of developing skin and vaginal yeast infections, along with not wearing wet clothes for long periods of time.[15][43] For women who experience recurrent yeast infections, there is limited evidence that oral or intravaginal probiotics help to prevent future infections.[17][65] This includes either as pills or as yogurt.[17]

Oral hygiene can help prevent oral candidiasis when people have a weakened immune system.[5] For people undergoing cancer treatment, chlorhexidine mouthwash can prevent or reduce thrush.[5] People who use inhaled corticosteroids can reduce the risk of developing oral candidiasis by rinsing the mouth with water or mouthwash after using the inhaler.[5] People with dentures should also disinfect their dentures regularly to prevent oral candidiasis.[54]


Candidiasis is treated with antifungal medications; these include clotrimazole, nystatin, fluconazole, voriconazole, amphotericin B, and echinocandins.[20] Intravenous fluconazole or an intravenous echinocandin such as caspofungin are commonly used to treat immunocompromised or critically ill individuals.[20]

The 2016 revision of the clinical practice guideline for the management of candidiasis lists a large number of specific treatment regimens for Candida infections that involve different Candida species, forms of antifungal drug resistance, immune statuses, and infection localization and severity.[20] Gastrointestinal candidiasis in immunocompetent individuals is treated with 100–200 mg fluconazole per day for 2–3 weeks.[28]

Localized infection[edit]

Mouth and throat candidiasis are treated with antifungal medication. Oral candidiasis usually responds to topical treatments; otherwise, systemic antifungal medication may be needed for oral infections. Candidal skin infections in the skin folds (candidal intertrigo) typically respond well to topical antifungal treatments (e.g., nystatin or miconazole). For breastfeeding mothers topical miconazole is the most effective treatment for treating candidiasis on the breasts.[66]Gentian violet can be used for thrush in breastfeeding babies.[14] Systemic treatment with antifungals by mouth is reserved for severe cases or if treatment with topical therapy is unsuccessful. Candida esophagitis may be treated orally or intravenously; for severe or azole-resistant esophageal candidiasis, treatment with amphotericin B may be necessary.[6]

Vaginal yeast infections are typically treated with topical antifungal agents.[20] Penile yeast infections are also treated with antifungal agents, but while an internal treatment may be used (such as a pessary) for vaginal yeast infections, only external treatments – such as a cream – can be recommended for penile treatment.[67] A one-time dose of fluconazole by mouth is 90% effective in treating a vaginal yeast infection.[68] For severe nonrecurring cases, several doses of fluconazole is recommended.[20] Local treatment may include vaginal suppositories or medicated douches. Other types of yeast infections require different dosing. C. albicans can develop resistance to fluconazole, this being more of an issue in those with HIV/AIDS who are often treated with multiple courses of fluconazole for recurrent oral infections.[69]

For vaginal yeast infection in pregnancy, topical imidazole or triazole antifungals are considered the therapy of choice owing to available safety data.[70] Systemic absorption of these topical formulations is minimal, posing little risk of transplacental transfer.[70] In vaginal yeast infection in pregnancy, treatment with topical azole antifungals is recommended for 7 days instead of a shorter duration.[70]

For vaginal yeast infections, many complementary treatments are proposed, however a number have side effects.[71] No benefit from probiotics has been found for active infections.[18]

Blood infection[edit]

Treatment typically consists of oral or intravenous antifungal medications.[72] In candidal infections of the blood, intravenous fluconazole or an echinocandin such as caspofungin may be used.[20]Amphotericin B is another option.[20]


Among individuals being treated in intensive care units, the mortality rate is about 30–50% when systemic candidiasis develops.[73]


Oral candidiasis is the most common fungal infection of the mouth,[74] and it also represents the most common opportunistic oral infection in humans.[75] Infections of the mouth occur in about 6% of babies less than a month old.[7] About 20% of those receiving chemotherapy for cancer and 20% of those with AIDS also develop the disease.[7]

It is estimated that 20% of women may be asymptomatically colonized by vaginal yeast.[76] In the United States there are approximately 1.4 million doctor office visits every year for candidiasis.[77] About three-quarters of women have at least one yeast infection at some time during their lives.[8]

Esophageal candidiasis is the most common esophageal infection in persons with AIDS and accounts for about 50% of all esophageal infections, often coexisting with other esophageal diseases. About two-thirds of people with AIDS and esophageal candidiasis also have oral candidiasis.[31]

Candidal sepsis is rare.[78] Candida is the fourth most common cause of bloodstream infections among hospital patients in the United States.[79] The incidence of bloodstream candida in intensive care units varies widely between countries.[80]


Descriptions of what sounds like oral thrush go back to the time of Hippocratescirca 460–370 BCE.[22]

Vulvovaginal candidiasis was first described in 1849 by Wilkinson.[81] In 1875, Haussmann demonstrated the causative organism in both vulvovaginal and oral candidiasis is the same.[81]

With the advent of antibiotics following World War II, the rates of candidiasis increased. The rates then decreased in the 1950s following the development of nystatin.[82]

The colloquial term "thrush" refers to the resemblance of the white flecks present in some forms of candidiasis (e.g. pseudomembranous candidiasis) with the breast of the bird of the same name.[83] The term candidosis is largely used in British English, and candidiasis in American English.[81]Candida is also pronounced differently; in American English, the stress is on the "i", whereas in British English the stress is on the first syllable.

The genusCandida and speciesC. albicans were described by botanist Christine Marie Berkhout in her doctoral thesis at the University of Utrecht in 1923. Over the years, the classification of the genera and species has evolved. Obsolete names for this genus include Mycotorula and Torulopsis. The species has also been known in the past as Monilia albicans and Oidium albicans. The current classification is nomen conservandum, which means the name is authorized for use by the International Botanical Congress (IBC).[84]

The genus Candida includes about 150 different species; however, only a few are known to cause human infections. C. albicans is the most significant pathogenic species. Other species pathogenic in humans include C. auris, C. tropicalis, C. glabrata, C. krusei, C. parapsilosis, C. dubliniensis, and C. lusitaniae.

The name Candida was proposed by Berkhout. It is from the Latin word toga candida, referring to the white toga (robe) worn by candidates for the Senate of the ancient Roman republic.[81] The specific epithet albicans also comes from Latin, albicare meaning "to whiten".[81] These names refer to the generally white appearance of Candida species when cultured.

Alternative medicine[edit]

Main article: Chronic candidiasis

A 2005 publication noted that "a large pseudoscientific cult"[85] has developed around the topic of Candida, with claims stating that up to one in three people are affected by yeast-related illness, particularly a condition called "Candidiasis hypersensitivity".[86] Some practitioners of alternative medicine have promoted these purported conditions and sold dietary supplements as supposed cures; a number of them have been prosecuted.[86][87] In 1990, alternative health vendor Nature's Way signed an FTC consent agreement not to misrepresent in advertising any self-diagnostic test concerning yeast conditions or to make any unsubstantiated representation concerning any food or supplement's ability to control yeast conditions, with a fine of $30,000 payable to the National Institutes of Health for research in genuine candidiasis.[87]


High level Candida colonization is linked to several diseases of the gastrointestinal tract including Crohn's disease.[88][89]

There has been an increase in resistance to antifungals worldwide over the past 30–40 years.[90][91]


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How to CURE a yeast infection? (vaginal thrush) - Doctor Explains

Oral candidiasis

Fungal infection

Medical condition

Oral candidiasis, also known as oral thrush among other names,[1] is candidiasis that occurs in the mouth. That is, oral candidiasis is a mycosis (yeast/fungal infection) of Candida species on the mucous membranes of the mouth.

Candida albicans is the most commonly implicated organism in this condition. C. albicans is carried in the mouths of about 50% of the world's population as a normal component of the oral microbiota.[3] This candidal carriage state is not considered a disease, but when Candida species become pathogenic and invade host tissues, oral candidiasis can occur. This change usually constitutes an opportunistic infection by normally harmless micro-organisms because of local (i.e., mucosal) or systemic factors altering host immunity.


Traditional classification of oral candidiasis.[2]
  • Acute candidiasis:
    • pseudomembranous candidiasis (oral thrush)
    • atrophic candidiasis
  • Chronic candidiasis:
    • atrophic candidiasis
    • hyperplastic candidiasis
      • chronic oral candidiasis (Candida leukoplakia)
      • candidiasis endocrinopathy syndrome
      • chronic localized mucocutaneous candidiasis
      • chronic diffuse candidiasis.

Classification of oral candidiasis.[2]
  • Primary oral candidiasis (group I)
    • Pseudomembranous (acute or chronic)
    • Erythematous (acute or chronic)
    • Hyperplastic: plaque-like, nodular
    • Candida-associated lesions: Denture related stomatitis, angular stomatitis, median rhomboid glossitis, linear gingival erythema
  • Secondary oral candidiasis (group II)
    • Oral manifestations of systemic mucocutaneous candidiasis (due to diseases such as thymic aplasia and candidiasis endocrinopathy syndrome)

Oral candidiasis is a mycosis (fungal infection). Traditionally, oral candidiasis is classified using the Lehner system, originally described in the 1960s, into acute and chronic forms (see table). Some of the subtypes almost always occur as acute (e.g., acute pseudomembranous candidiasis), and others chronic. However, these typical presentations do not always hold true, which created problems with this system. A more recently proposed classification of oral candidiasis distinguishes primary oral candidiasis, where the condition is confined to the mouth and perioral tissues, and secondary oral candidiasis, where there is involvement of other parts of the body in addition to the mouth. The global human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) pandemic has been an important factor in the move away from the traditional classification since it has led to the formation of a new group of patients who present with atypical forms of oral candidiasis.[2]

By appearance[edit]

Three main clinical appearances of candidiasis are generally recognized: pseudomembranous, erythematous (atrophic) and hyperplastic.[4] Most often, affected individuals display one clear type or another, but sometimes there can be more than one clinical variant in the same person.[5]

Pseudomembranous candidiasis in the mouth and oropharynx.

Pseudomembranous candidiasis in a person with HIV


Acute pseudomembranous candidiasis is a classic form of oral candidiasis,[6] commonly referred to as thrush.[4] Overall, this is the most common type of oral candidiasis,[7] accounting for about 35% of oral candidiasis cases.[8]

It is characterized by a coating or individual patches of pseudomembranous white slough that can be easily wiped away to reveal erythematous (reddened), and sometimes minimally bleeding, mucosa beneath.[7] These areas of pseudomembrane are sometimes described as "curdled milk",[4] or "cottage cheese".[7] The white material is made up of debris, fibrin, and desquamated epithelium that has been invaded by yeast cells and hyphae that invade to the depth of the stratum spinosum.[4] As an erythematous surface is revealed beneath the pseudomembranes, some consider pseudomembranous candidiasis and erythematous candidiasis stages of the same entity.[4] Some sources state that if there is bleeding when the pseudomembrane is removed, then the mucosa has likely been affected by an underlying process such as lichen planus or chemotherapy.[5] Pseudomembraneous candidiasis can involve any part of the mouth, but usually it appears on the tongue, buccal mucosae or palate.[7]

It is classically an acute condition, appearing in infants, people taking antibiotics or immunosuppressant medications, or immunocompromising diseases.[6] However, sometimes it can be chronic and intermittent, even lasting for many years. Chronicity of this subtype generally occurs in immunocompromised states, (e.g., leukemia, HIV) or in persons who use corticosteroids topically or by aerosol.[4] Acute and chronic pseudomembranous candidiasis are indistinguishable in appearance.[6]


Erythematous (atrophic) candidiasis is when the condition appears as a red, raw-looking lesion.[8] Some sources consider denture-related stomatitis, angular stomatitis, median rhomboid glossitis, and antiobiotic-induced stomatitis as subtypes of erythematous candidiasis, since these lesions are commonly erythematous/atrophic. It may precede the formation of a pseudomembrane, be left when the membrane is removed, or arise without prior pseudomembranes.[6] Some sources state that erythematous candidiasis accounts for 60% of oral candidiasis cases.[8] Where it is associated with inhalation steroids (often used for treatment of asthma), erythematous candidiasis commonly appears on the palate or the dorsum of the tongue.[6] On the tongue, there is loss of the lingual papillae (depapillation), leaving a smooth area.[5]

Acute erythematous candidiasis usually occurs on the dorsum of the tongue in persons taking long term corticosteroids or antibiotics, but occasionally it can occur after only a few days of using a topical antibiotic.[9] This is usually termed "antibiotic sore mouth", "antibiotic sore tongue",[9] or "antibiotic-induced stomatitis" because it is commonly painful as well as red.

Chronic erythematous candidiasis is more usually associated with denture wearing (see denture-related stomatitis).


This variant is also sometimes termed "plaque-like candidiasis" or "nodular candidiasis".[6] The most common appearance of hyperplastic candidiasis is a persistent white plaque that does not rub off. The lesion may be rough or nodular in texture.[10] Hyperplastic candidiasis is uncommon, accounting for about 5% of oral candidiasis cases,[8] and is usually chronic and found in adults. The most common site of involvement is the commissural region of the buccal mucosa, usually on both sides of the mouth.[10]

Another term for hyperplastic candidiasis is "candidal leukoplakia". This term is a largely historical synonym for this subtype of candidiasis, rather than a true leukoplakia.[11] Indeed, it can be clinically indistinguishable from true leukoplakia, but tissue biopsy shows candidal hyphae invading the epithelium. Some sources use this term to describe leukoplakia lesions that become colonized secondarily by Candida species, thereby distinguishing it from hyperplastic candidiasis.[10] It is known that Candida resides more readily in mucosa that is altered, such as may occur with dysplasia and hyperkeratosis in an area of leukoplakia.

Associated lesions[edit]

Candida-associated lesions are primary oral candidiases (confined to the mouth), where the causes are thought to be multiple.[4] For example, bacteria as well as Candida species may be involved in these lesions.[6] Frequently, antifungal therapy alone does not permanently resolve these lesions, but rather the underlying predisposing factors must be addressed, in addition to treating the candidiasis.[4]

Angular cheilitis[edit]

Main article: Angular cheilitis

Angular cheilitis is inflammation at the corners (angles) of the mouth, very commonly involving Candida species, when sometimes the terms "Candida-associated angular cheilitis",[9] or less commonly "monilial perlèche" are used.[12]Candida organisms alone are responsible for about 20% of cases,[5] and a mixed infection of C. albicans and Staphylococcus aureus for about 60% of cases.[3] Signs and symptoms include soreness, erythema (redness), and fissuring of one, or more commonly both the angles of the mouth, with edema (swelling) seen intraorally on the commissures (inside the corners of the mouth). Angular cheilitis generally occurs in elderly people and is associated with denture related stomatitis.[13]

Denture-related stomatitis[edit]

Main article: Denture-related stomatitis

This term refers to a mild inflammation and erythema of the mucosa beneath a denture, usually an upper denture in elderly edentulous individuals (with no natural teeth remaining). Some report that up to 65% of denture wearers have this condition to some degree.[14] About 90% of cases are associated with Candida species,[13] where sometimes the terms "Candida-associated denture stomatitis",[14] or "Candida-associated denture-induced stomatitis" (CADIS),[15] are used. Some sources state that this is by far the most common form of oral candidiasis.[15] Although this condition is also known as "denture sore mouth",[5] there is rarely any pain.[15]Candida is associated with about 90% of cases of denture related stomatitis.[2]

Median rhomboid glossitis[edit]

Main article: Median rhomboid glossitis

This is an elliptical or rhomboid lesion in the center of the dorsal tongue, just anterior (in front) of the circumvallate papillae. The area is depapillated, reddened (or red and white) and rarely painful. There is frequently Candida species in the lesion, sometimes mixed with bacteria.[13]

Linear gingival erythema[edit]

Main article: Linear gingival erythema

This is a localized or generalized, linear band of erythematous gingivitis (inflammation of the gums). It was first observed in HIV infected individuals and termed "HIV-gingivitis", but the condition is not confined to this group.[4]Candida species are involved, and in some cases the lesion responds to antifungal therapy, but it is thought that other factors exist, such as oral hygiene and human herpesviruses. This condition can develop into necrotizing ulcerative periodontitis.[16]


Chronic multifocal oral candidiasis[edit]

This is an uncommon form of chronic (more than one month in duration) candidal infection involving multiple areas in the mouth, without signs of candidiasis on other mucosal or cutaneous sites. The lesions are variably red and/or white. Unusually for candidal infections, there is an absence of predisposing factors such as immunosuppression, and it occurs in apparently healthy individuals, normally elderly males. Smoking is a known risk factor.[13]

Chronic mucocutaneous candidiasis[edit]

Main article: Chronic mucocutaneous candidiasis

This refers to a group of rare syndromes characterized by chronic candidal lesions on the skin, in the mouth and on other mucous membranes (i.e., a secondary oral candidiasis). These include Localized chronic mucocutaneous candidiasis, diffuse mucocutaneous candidiasis (Candida granuloma), candidiasis–endocrinopathy syndrome and candidiasis thymoma syndrome. About 90% of people with chronic mucocutaneous candidiasis have candidiasis in the mouth.[6]

Signs and symptoms[edit]

Signs and symptoms are dependent upon the type of oral candidiasis. Often, apart from the appearance of the lesions, there are usually no other signs or symptoms. Most types of oral candidiasis are painless, but a burning sensation may occur in some cases.[8] Candidiasis can, therefore, sometimes be misdiagnosed as burning mouth syndrome. A burning sensation is more likely with erythematous (atrophic) candidiasis, whilst hyperplastic candidiasis is normally entirely asymptomatic.[5] Acute atrophic candidiasis may feel like the mouth has been scalded with a hot liquid.[5] Another potential symptom is a metallic, acidic, salty or bitter taste in the mouth.[5][8] The pseudomembranous type rarely causes any symptoms apart from possibly some discomfort or bad taste due to the presence of the membranes.[5][6] Sometimes the patient describes the raised pseudomembranes as "blisters."[5] Occasionally there can be dysphagia (difficulty swallowing), which indicates that the candidiasis involves the oropharynx or the esophagus,[7] as well as the mouth. The trachea and the larynx may also be involved where there is oral candidiasis, and this may cause hoarseness of the voice.[15]



The causative organism is usually Candida albicans,[5] or less commonly other Candida species such as (in decreasing order of frequency) Candida tropicalis,[17]Candida glabrata,[17]Candida parapsilosis,[17]Candida krusei,[17] or other species (Candida stellatoidea,[17]Candida pseudotropicalis,[17]Candida famata,[17]Candida rugosa,[17]Candida geotrichium,[13]Candida dubliniensis,[13] and Candida guilliermondii).[17]C. albicans accounts for about 50% of oral candidiasis cases,[18] and together C. albicans, C. tropicalis and C. glabrata account for over 80% of cases.[6] Candidiasis caused by non-C. albicans Candida (NCAC) species is associated more with immunodeficiency.[13] For example, in HIV/AIDS, C. dubliniensis and C. geotrichium can become pathogenic.[13]

About 35-50% of humans possess C. albicans as part of their normal oral microbiota.[5] With more sensitive detection techniques, this figure is reported to rise to 90%.[6] This candidal carrier state is not considered a disease, since there are no lesions or symptoms of any kind. Oral carriage of Candida is pre-requisite for the development of oral candidiasis. For Candida species to colonize and survive as a normal component of the oral microbiota, the organisms must be capable of adhering to the epithelial surface of the mucous membrane lining the mouth.[19] This adhesion involves adhesins (e.g., hyphal wall protein 1), and extracellular polymeric materials (e.g., mannoprotein).[13] Therefore, strains of Candida with more adhesion capability have more pathogenic potential than other strains.[6] The prevalence of Candida carriage varies with geographic location,[6] and many other factors. Higher carriage is reported during the summer months,[6] in females,[6] in hospitalized individuals,[6] in persons with blood group O and in non-secretors of blood group antigens in saliva.[6] Increased rates of Candida carriage are also found in people who eat a diet high in carbohydrates, people who wear dentures, people with xerostomia (dry mouth), in people taking broad spectrum antibiotics, smokers, and in immunocompromised individuals (e.g., due to HIV/AIDS, diabetes, cancer, Down syndrome or malnutrition).[13] Age also influences oral carriage, with the lowest levels occurring in newborns, increasing dramatically in infants, and then decreasing again in adults. Investigations have quantified oral carriage of Candida albicans at 300-500 colony forming units in healthy persons.[20] More Candida is detected in the early morning and the late afternoon. The greatest quantity of Candida species are harbored on the posterior dorsal tongue,[13] followed by the palatal and the buccal mucosae.[20] Mucosa covered by an oral appliance such as a denture harbors significantly more candida species than uncovered mucosa.[20]

When Candida species cause lesions - the result of invasion of the host tissues - this is termed candidiasis.[2][19] Some consider oral candidiasis a change in the normal oral environment rather than an exposure or true "infection" as such.[7] The exact process by which Candida species switch from acting as normal oral commensals (saprophytic) state in the carrier to acting as a pathogenic organism (parasitic state) is not completely understood.[6]

Several Candida species are polymorphogenic,[18] that is, capable of growing in different forms depending on the environmental conditions. C. albicans can appear as a yeast form (blastospores), which is thought to be relatively harmless; and a hyphal form associated with invasion of host tissues.[5] Apart from true hyphae, Candida can also form pseudohyphae — elongated filamentous cells, lined end to end.[4] As a general rule, candidiasis presenting with white lesions is mainly caused by Candida species in the hyphal form and red lesions by yeast forms.[13]C. albicans and C. dubliniensis are also capable of forming germ tubes (incipient hyphae) and chlamydospores under the right conditions. C. albicans is categorized serologically into A or B serotypes. The prevalence is roughly equal in healthy individuals, but type B is more prevalent in immunocompromised individuals.

Predisposing factors[edit]

The host defenses against opportunistic infection of candida species are

  • The oral epithelium, which acts both as a physical barrier preventing micro-organisms from entering the tissues, and is the site of cell mediated immune reactions.
  • Competition and inhibition interactions between candida species and other micro-organisms in the mouth, such as the many hundreds of different kinds of bacteria.
  • Saliva, which possesses both mechanical cleansing action and immunologic action, including salivary immunoglobulin A antibodies, which aggregate candida organisms and prevent them adhering to the epithelial surface; and enzymatic components such as lysozyme, lactoperoxidase and antileukoprotease.[13]

Disruption to any of these local and systemic host defense mechanisms constitutes a potential susceptibility to oral candidiasis, which rarely occurs without predisposing factors.[4] It is often described as being "a disease of the diseased",[2][4] occurring in the very young, the very old, or the very sick.[4][6][21]

Oral candidiasis in an infant. At very young ages, the immune system is yet to develop fully.


Immunodeficiency is a state of reduced function of the immune system, which can be caused by medical conditions or treatments.

Acute pseudomembranous candidiasis occurs in about 5% of newborn infants.[9] Candida species are acquired from the mother's vaginal canal during birth. At very young ages, the immune system is yet to develop fully and there is no individual immune response to candida species,[9] an infants antibodies to the fungus are normally supplied by the mother's breast milk.

Other forms of immunodeficiency which may cause oral candidiasis include HIV/AIDS,[22] active cancer and treatment, chemotherapy or radiotherapy.[3][23]

Corticosteroid medications may contribute to the appearance of oral candidiasis,[24] as they cause suppression of immune function either systemically or on a local/mucosal level, depending on the route of administration. Topically administered corticosteroids in the mouth may take the form of mouthwashes, dissolving lozenges or mucosal gels; sometimes being used to treat various forms of stomatitis. Systemic corticosteroids may also result in candidiasis.

Inhaled corticosteroids (e.g., for treatment of asthma or chronic obstructive pulmonary disease), are not intended to be administered topically in the mouth, but inevitably there is contact with the oral and oropharyngeal mucousa as it is inhaled. In asthmatics treated with inhaled steroids, clinically detectable oral candidiasis may occur in about 5-10% of adults and 1% of children.[25] Where inhaled steroids are the cause, the candidal lesions are usually of the erythematous variety.[6] Candidiasis appears at the sites where the steroid has contacted the mucosa, typically the dorsum of the tongue (median rhomboid glossitis) and sometimes also on the palate.[26][27] Candidal lesions on both sites are sometimes termed "kissing lesions"[26][27] because they approximate when the tongue is in contact with the palate.

Denture wearing[edit]

Denture wearing and poor denture hygiene, particularly wearing the denture continually rather than removing it during sleep,[3] is another risk factor for both candidal carriage and oral candidiasis. Dentures provide a relative acidic, moist and anaerobic environment because the mucosa covered by the denture is sheltered from oxygen and saliva.[28] Loose, poorly fitting dentures may also cause minor trauma to the mucosa,[4] which is thought to increase the permeability of the mucosa and increase the ability of C. albicans to invade the tissues.[28][29] These conditions all favor the growth of C. albicans. Sometimes dentures become very worn, or they have been constructed to allow insufficient lower facial height (occlusal vertical dimension), leading to over-closure of the mouth (an appearance sometimes described as "collapse of the jaws"). This causes deepening of the skin folds at the corners of the mouth (nasolabial crease), in effect creating intertriginous areas where another form of candidiasis, angular cheilitis, can develop. Candida species are capable of adhering to the surface of dentures, most of which are made from polymethylacrylate. They exploit micro-fissures and cracks in the surface of dentures to aid their retention. Dentures may therefore become covered in a biofilm,[18] and act as reservoirs of infection,[7] continually re-infecting the mucosa. For this reason, disinfecting the denture is a vital part of treatment of oral candidiasis in persons who wear dentures, as well as correcting other factors like inadequate lower facial height and fit of the dentures.

Dry mouth[edit]

Both the quantity and quality of saliva are important oral defenses against candida.[6] Decreased salivary flow rate or a change in the composition of saliva,[8] collectively termed salivary hypofunction or hyposalivation is an important predisposing factor. Xerostomia is frequently listed as a cause of candidiasis,[3] but xerostomia can be subjective or objective, i.e., a symptom present with or without actual changes in the saliva consistency or flow rate.


Malnutrition,[3] whether by malabsorption,[17] or poor diet, especially hematinic deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis,[6] by causing diminished host defense and epithelial integrity. For example, iron deficiency anemia is thought to cause depressed cell-mediated immunity.[28] Some sources state that deficiencies of vitamin A or pyridoxine are also linked.[17]

There is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis.[9]In vitro and studies show that Candidal growth, adhesion and biofilm formation is enhanced by the presence of carbohydrates such as glucose, galactose and sucrose.[28]


Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for C. albicans, or that local epithelial alterations occur that facilitate colonization of candida species.[28]


Broad-spectrum antibiotics (e.g. tetracycline) eliminate the competing bacteria and disrupt the normally balanced ecology of oral microorganisms,[5][6] which can cause antibiotic-induced candidiasis.[3]

Other factors[edit]

Several other factors can contribute to infection, including endocrine disorders (e.g. diabetes when poorly controlled),[30] and/or the presence of certain other mucosal lesions, especially those that cause hyperkeratosis and/or dysplasia[4] (e.g. lichen planus). Such changes in the mucosa predispose it to secondary infection with candidiasis.[9][24] Other physical mucosal alterations are sometimes associated with candida overgrowth, such as fissured tongue (rarely),[7]tongue piercing, atopy,[6] and/or hospitalization.[4]


The diagnosis can typically be made from the clinical appearance alone,[7] but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.[6]

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears.[31] Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites.[3] Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated.[31] Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.[24]

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer.[32] Hyphae penetrate to the depth of the stratum spinosum,[4] and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.[32]

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.[32]

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.[32]


Oral candidiasis can be treated with topical anti-fungal drugs, such as nystatin, miconazole, Gentian violet or amphotericin B. Surgical excision of the lesions may be required in cases that do not respond to anti-fungal medications.[33]

Underlying immunosuppression may be medically manageable once it is identified, and this helps prevent recurrence of candidal infections.

Patients who are immunocompromised, either with HIV/AIDS or as a result of chemotherapy, may require systemic prevention or treatment with oral or intravenous administered anti-fungals. However there is strong evidence that drugs that are absorbed or partially absorbed from the GI tract can prevent candidiasis more effectively than drugs that are not absorbed in the same way.[34]

If candidiasis is secondary to corticosteroid or antibiotic use, then use may be stopped, although this is not always a feasible option. Candidiasis secondary to the use of inhaled steroids may be treated by rinsing out the mouth with water after taking the steroid.[15] Use of a spacer device to reduce the contact with the oral mucosa may greatly reduce the risk of oral candidiasis.[25]

In recurrent oral candidiasis, the use of azole antifungals risks selection and enrichment of drug-resistant strains of candida organisms.[30]Drug resistance is increasingly more common and presents a serious problem in persons who are immunocompromised.[13]

Prophylactic use of antifungals is sometimes employed in persons with HIV disease, during radiotherapy, during immunosuppressive or prolonged antibiotic therapy as the development of candidal infection in these groups may be more serious.[2]

The candidal load in the mouth can be reduced by improving oral hygiene measures, such as regular toothbrushing and use of anti-microbial mouthwashes.[18] Since smoking is associated with many of forms of oral candidiasis, cessation may be beneficial.[medical citation needed]

Denture hygiene[edit]

See also: Denture-related stomatitis § Treatment

Good denture hygiene involves regular cleaning of the dentures, and leaving them out of the mouth during sleep. This gives the mucosa a chance to recover, while wearing a denture during sleep is often likened to sleeping in one's shoes. In oral candidiasis, the dentures may act as a reservoir of Candida species,[7] continually reinfecting the mucosa once antifungal medication is stopped. Therefore, they must be disinfected as part of the treatment for oral candidiasis. There are commercial denture cleaner preparations for this purpose, but it is readily accomplished by soaking the denture overnight in a 1:10 solution of sodium hypochlorite (Milton, or household bleach).[7] Bleach may corrode metal components,[13] so if the denture contains metal, soaking it twice daily in chlorhexidine solution can be carried out instead. An alternative method of disinfection is to use a 10% solution of acetic acid (vinegar) as an overnight soak, or to microwave the dentures in 200mL water for 3 minutes at 650 watts.[13] Microwave sterilization is only suitable if no metal components are present in the denture. Antifungal medication can also be applied to the fitting surface of the denture before it is put back in the mouth. Other problems with the dentures, such as inadequate occlusal vertical dimension may also need to be corrected in the case of angular cheilitis.


The severity of oral candidiasis is subject to great variability from one person to another and in the same person from one occasion to the next.[8] The prognosis of such infection is usually excellent after the application of topical or systemic treatments. However, oral candidiasis can be recurrent.[8] Individuals continue to be at risk of the condition if underlying factors such as reduced salivary flow rate or immunosuppression are not rectifiable.[8]

Candidiasis can be a marker for underlying disease,[20] so the overall prognosis may also be dependent upon this. For example, a transient erythematous candidiasis that developed after antibiotic therapy usually resolves after antibiotics are stopped (but not always immediately),[15] and therefore carries an excellent prognosis—but candidiasis may occasionally be a sign of more sinister undiagnosed pathology, such as HIV/AIDS or leukemia.

It is possible for candidiasis to spread to/from the mouth, from sites such as the pharynx, esophagus, lungs, liver, anogenital region, skin or the nails.[13] The spread of oral candidiasis to other sites usually occurs in debilitated individuals.[15] It is also possible that candidiasis is spread by sexual contact.[13] Rarely, a superficial candidal infection such as oral candidiasis can cause invasive candidiasis, and even prove fatal. The observation that Candida species are normally harmless commensals on the one hand, but are also occasionally capable of causing fatal invasive candidiases has led to the description "Dr Jekyll and Mr Hyde".[35]

The role of thrush in the hospital and ventilated patients is not entirely clear, however, there is a theoretical risk of positive interaction of candida with topical bacteria.[36]


In humans, oral candidiasis is the most common form of candidiasis,[17] by far the most common fungal infection of the mouth,[5] and it also represents the most common opportunistic oral infection in humans[37] with lesions only occurring when the environment favors pathogenic behavior.

Oropharyngeal candidiasis is common during cancer care,[23] and it is a very common oral sign in individuals with HIV.[22] Oral candidiasis occurs in about two thirds of people with concomitant AIDS and esophageal candidiasis.[38]

The incidence of all forms of candidiasis have increased in recent decades. This is due to developments in medicine, with more invasive medical procedures and surgeries, more widespread use of broad spectrum antibiotics and immunosuppression therapies. The HIV/AIDs global pandemic has been the greatest factor in the increased incidence of oral candidiasis since the 1980s. The incidence of candidiasis caused by NCAC species is also increasing, again thought to be due to changes in medical practise (e.g., organ transplantation and use of indwelling catheters).[18]


Oral candidiasis has been recognized throughout recorded history.[18] The first description of this condition is thought to have occurred in the 4th century B.C. in "Epidemics" (a treatise that is part of the hippocratic corpus), where descriptions of what sounds like oral candidiasis are stated to occur with severe underlying disease.[20][39]

The colloquial term "thrush" refers to the resemblance of the white flecks present in some forms of candidiasis (e.g., pseudomembranous candidiasis), with the breast of the bird of the same name.[40]

Society and culture[edit]

Many pseudoscientific claims by proponents of alternative medicine surround the topic of candidiasis. Oral candidiasis is sometimes presented in this manner as a symptom of a widely prevalent systemic candidiasis, candida hypersensitivity syndrome, yeast allergy, or gastrointestinal candida overgrowth, which are medically unrecognized conditions. (See: Alternative medicine in Candidiasis)


  1. ^ abJames, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunders Elsevier. p. 308. ISBN . OCLC 62736861.
  2. ^ abcdefghScully, Crispian (2008). Oral and maxillofacial medicine: the basis of diagnosis and treatment (2nd ed.). Edinburgh: Churchill Livingstone. pp. 191–199. ISBN .
  3. ^ abcdefghKerawala C, Newlands C (editors) (2010). Oral and maxillofacial surgery. Oxford: Oxford University Press. pp. 446, 447. ISBN .CS1 maint: extra text: authors list (link)
  4. ^ abcdefghijklmnopqSamaranayake, LP (2009). Essential microbiology for dentistry (3rd ed.). Elseveier. pp. 178–180, 247, 293–297. ISBN .
  5. ^ abcdefghijklmnoBouquot, Brad W. Neville, Douglas D. Damm, Carl M. Allen, Jerry E. (2002). Oral & maxillofacial pathology (2. ed.). Philadelphia: W.B. Saunders. pp. 189–197. ISBN .
  6. ^ abcdefghijklmnopqrstuvwxyGreenberg MS, Glick M, Ship JA (2008). Burket's oral medicine (11th ed.). Hamilton, Ont.: BC Decker. pp. 79–84. ISBN .
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  12. ^Park, KK; Brodell, RT; Helms, SE (June 2011). "Angular cheilitis, part 1: local etiologies". Cutis; Cutaneous Medicine for the Practitioner. 87 (6): 289–95. PMID 21838086.
  13. ^ abcdefghijklmnopqrScully C (2013). Oral and maxillofacial medicine : the basis of diagnosis and treatment (3rd ed.). Edinburgh: Churchill Livingstone. pp. 254–267. ISBN .
  14. ^ abSalerno, C; Pascale, M; Contaldo, M; Esposito, V; Busciolano, M; Milillo, L; Guida, A; Petruzzi, M; Serpico, R (Mar 1, 2011). "Candida-associated denture stomatitis"(PDF). Medicina Oral, Patologia Oral y Cirugia Bucal. 16 (2): e139–43. doi:10.4317/medoral.16.e139. PMID 20711156.
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  16. ^(editors) Newman MG, Takei HH, Klokkevold PR, Carranza FA (2012). Carranza's clinical periodontology (11th ed.). St. Louis, Mo.: Elsevier/Saunders. p. 180. ISBN .CS1 maint: multiple names: authors list (link) CS1 maint: extra text: authors list (link)
  17. ^ abcdefghijklAnil Ghom; Shubhangi Mhaske (2010). Textbook of oral pathology. New Delhi: Jaypee Brothers Medical Publishers. pp. 498, 508–514. ISBN .
  18. ^ abcdefgWilliams, D; Lewis, M (Jan 28, 2011). "Pathogenesis and treatment of oral candidosis". Journal of Oral Microbiology. 3: 5771. doi:10.3402/jom.v3i0.5771. PMC 3087208. PMID 21547018.
  19. ^ abNaglik, Julian R.; Moyes, David L.; Wächtler, Betty; Hube, Bernhard (1 November 2011). "Candida albicans interactions with epithelial cells and mucosal immunity". Microbes and Infection. 13 (12–13): 963–976. doi:10.1016/j.micinf.2011.06.009. PMC 3185145. PMID 21801848.
  20. ^ abcdeLynch, DP (August 1994). "Oral candidiasis. History, classification, and clinical presentation". Oral Surgery, Oral Medicine, and Oral Pathology. 78 (2): 189–93. doi:10.1016/0030-4220(94)90146-5. PMID 7936588.
  21. ^Scully, C; el-Kabir, M; Samaranayake, LP (1994). "Candida and oral candidosis: a review". Critical Reviews in Oral Biology and Medicine. 5 (2): 125–57. doi:10.1177/10454411940050020101. PMID 7858080.
  22. ^ abLi, X; Lei, L; Tan, D; Jiang, L; Zeng, X; Dan, H; Liao, G; Chen, Q (May 2013). "Oropharyngeal Candida colonization in human immunodeficiency virus infected patients". APMIS. 121 (5): 375–402. doi:10.1111/apm.12006. PMID 23030258. S2CID 6427809.
  23. ^ abEpstein, JB; Thariat, J; Bensadoun, RJ; Barasch, A; Murphy, BA; Kolnick, L; Popplewell, L; Maghami, E (Nov–Dec 2012). "Oral complications of cancer and cancer therapy: from cancer treatment to survivorship". CA: A Cancer Journal for Clinicians. 62 (6): 400–22. doi:10.3322/caac.21157. PMID 22972543. S2CID 8521191.
  24. ^ abcOdell EW (Editor) (2010). Clinical problem solving in dentistry (3rd ed.). Edinburgh: Churchill Livingstone. pp. 161, 194, 216. ISBN .CS1 maint: extra text: authors list (link)
  25. ^ abInhaled steroids in asthma optimizing effects in the airways. [S.l.]: Marcel Dekker Incorporate. 2001. ISBN .
  26. ^ abJohn D. Da Silva; David A. Mitchell; Laura Mitchell (2007-11-23). Oxford American Handbook of Clinical Dentistry. Oxford University Press, USA, 2007. p. 433. ISBN .
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  29. ^Gendreau, L; Loewy, ZG (June 2011). "Epidemiology and etiology of denture stomatitis". Journal of Prosthodontics. 20 (4): 251–60. doi:10.1111/j.1532-849x.2011.00698.x. PMID 21463383.
  30. ^ abRautemaa, R; Ramage, G (November 2011). "Oral candidosis--clinical challenges of a biofilm disease". Critical Reviews in Microbiology. 37 (4): 328–36. doi:10.3109/1040841x.2011.585606. PMID 21777047. S2CID 38426846.
  31. ^ abKumaraswamy, KL; Vidhya, M; Rao, PK; Mukunda, A (Apr–Jun 2012). "Oral biopsy: oral pathologist's perspective". Journal of Cancer Research and Therapeutics. 8 (2): 192–8. doi:10.4103/0973-1482.98969. PMID 22842360.
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  33. ^Shah, N; Ray, J. G; Kundu, S; Sardana, D (2017). "Surgical management of chronic hyperplastic candidiasis refractory to systemic antifungal treatment". Journal of Laboratory Physicians. 9 (2): 136–139. doi:10.4103/0974-2727.199622. PMC 5320878. PMID 28367031.
  34. ^Clarkson, Jan E; Worthington, Helen V; Eden, Tim OB (2007-01-24). "Interventions for preventing oral candidiasis for patients with cancer receiving treatment". Cochrane Database of Systematic Reviews (1): CD003807. doi:10.1002/14651858.CD003807.pub3. ISSN 1465-1858. PMC 6746214. PMID 17253497.
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  36. ^Peleg, Anton Y., Deborah A. Hogan, and Eleftherios Mylonakis. "Medically important bacterial–fungal interactions." Nature Reviews Microbiology 8.5 (2010): 340-349.
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  39. ^Dolin, [edited by] Gerald L. Mandell, John E. Bennett, Raphael (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases (7th ed.). Philadelphia, PA: Churchill Livingstone/Elsevier. pp. Chapter 250. ISBN .CS1 maint: extra text: authors list (link)
  40. ^Scully, Crispian. "Mucosal Candidiasis (Medscape)". WebMD LLC. Retrieved 8 September 2013.

External links[edit]


Infection wikipedia yeast

Invasive candidiasis

Serious and potentially fatal infection caused by Candida yeast

Medical condition

Invasive candidiasis is an infection (candidiasis) that can be caused by various species of Candida yeast. Unlike Candida infections of the mouth and throat (oral candidiasis) or vagina (Candidal vulvovaginitis), invasive candidiasis is a serious, progressive, and potentially fatal infection that can affect the blood (fungemia), heart, brain, eyes, bones, and other parts of the body.[1][2]

Signs and symptoms[edit]

Symptoms of invasive candidiasis can be confused with other medical conditions, however, the most common symptoms are fever and chills that do not improve with antibiotic treatment. Other symptoms develop as the infection spreads, depending on which parts of the body are involved.[3][2]


Invasive candidiasis can manifest as serious diseases including as fungemia, endocarditis, endophthalmitis, osteomyelitis, and central nervous system infections.[4]


Invasive candidiasis is caused by 15 of the more than 150 known species of Candida. These species, all confirmed by isolation from patients, are: C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, C. krusei, C. guilliermondii, C. lusitaniae, C. dubliniensis, C. pelliculosa, C. kefyr, C. lipolytica, C. famata, C. inconspicua, C. rugosa, and C. norvegensis.[4] Over the last 20–30 years, C. albicans has been responsible for 95% of infections, with, C. glabrata, C. parapsilosis, C. tropicalis, and C. krusei causing the majority of the remaining cases.[4] Recently, C. auris, a species first reported in 2009, has been found to cause invasive candidiasis. C. auris has attracted attention because it can be resistant to the antifungal medications used to treat candidiasis.[5]


Resistance to antifungal treatment can arise from species with intrinsic resistance that experience selection pressure or spontaneous induction of resistance in isolates from normally susceptible species. For Candida, the most common is the former, as seen by the emergence of resistant C. glabrata following the introduction of fluconazole and of C. parapsilosis where there was increased use of echinocandins. Insufficient dosing of azoles has also led to the emergence of resistance. Observed rates of echinocandin resistance for C. glabrata are between 2 and 12%. Acquired echinocandin resistance has also been reported for C. albicans, C. tropicalis, C. krusei, C. kefyr, C. lusitaniae, and C. dubliniensis.

Emergent species[edit]

Candida auris is an emerging multidrug-resistant yeast that can cause invasive candidiasis and is associated with high mortality.[6] It was first described in 2009.[6] Since then, C. auris infections, specifically fungemia, have been reported from South Korea, India, South Africa, Kuwait, Colombia, Venezuela, Pakistan, the United Kingdom and the United States.[6] The strains isolated in each region are genetically distinct, indicating that this species is emerging in different locations.[6] The reason for this pattern is unknown.[6]

Risk factors[edit]

Patients with the following conditions, treatments or situations are at increased risk for invasive candidiasis.[4][2][7]


Invasive candidiasis is a nosocomial infection with the majority of cases associated with hospital stays.[4]


Because many Candida species are part of the human microbiota, their presence in the mouth, the vagina, sputum, urine, stool, or skin is not definitive evidence for invasive candidiasis.[2]

Positive culture of Candida species from normally sterile sites, such as blood, cerebrospinal fluid, pericardium, pericardial fluid, or biopsied tissue, is definitive evidence of invasive candidiasis.[2] Diagnosis by culturing allows subsequent susceptibility testing of causative species.[8][7] Sensitivity of blood culture is far from ideal, with a sensitivity reported to be between 21 and 71%.[7] Additionally, whereas blood culture can establish a diagnosis during fungemia, the blood may test negative for deep-seated infections because candida may have been successfully cleared from the blood.[7]

Diagnosis of invasive candidiasis is supported by histopathologic evidence (for example, yeast cells or hyphae) observed in specimens of affected tissues.[2]

Additionally, elevated serum β-glucan can demonstrate invasive candidiasis while a negative test suggests a low likelihood of systemic infection.[9][2]

The emergence of multidrug-resistant C. auris as a cause of invasive candidiasis has necessitated additional testing in some settings.[6]C. auris-caused invasive candidiasis is associated with high mortality.[6] Many C. auris isolates have been found to be resistant to one or more of the three major antifungal classes (azoles, echinocandins, and polyenes) with some resistant to all three classes – severely limiting treatment options.[6] Biochemical-based tests currently used in many laboratories to identify fungi, including API 20C AUX and VITEK-2, cannot differentiate C. auris from related species (for example, C. auris can be identified as C. haemulonii).[6] Therefore, the Centers for Disease Control and Prevention recommends using a diagnostic method based on matrix-assisted laser desorption/ionization-time of flight mass spectrometry or a molecular method based on sequencing the D1-D2 region of the 28s rDNA to identify C. auris in settings where it may be present.[6]


Preventive antifungal treatment is supported by studies, but only for specific high-risk groups in intensive care units with conditions that put them at high risk for the disease.[7] For example, one group would be patients recovering from abdominal surgery that may have gastrointestinal perforations or anastomotic leakage.[7] Antifungal prophylaxis can reduce the incidence of fungemia by approximately 50%, but has not been shown to improve survival.[7] A major challenge limiting the number of patients receiving prophylaxis to only those that can potentially benefit, thereby avoiding the creation of selective pressure that can lead to the emergence of resistance.[7]


Antifungals are used for treatment with the specific type and dose depending on the patient's age, immune status, and specifics of the infection. For most adults, the initial treatment is an echinocandin class antifungal (caspofungin, micafungin, or anidulafungin) given intravenously. Fluconazole, amphotericin B, and other antifungals may also be used.[10] Treatment normally continues for two weeks after resolution of signs and symptoms and Candida yeasts can no longer can be cultured from blood samples. Some forms of invasive candidiasis, such as infections in the bones, joints, heart, or central nervous system, usually need to be treated for a longer period.[10] Retrospective observational studies suggest that prompt presumptive antifungal therapy (based on symptoms or biomarkers) is effective and can reduce mortality.[7]


Invasive candidiasis is estimated to affect more than 250,000 people and cause more than 50,000 deaths worldwide every year.[7] The CDC estimates that approximately 46,000 cases of healthcare-associated invasive candidiasis occur each year in the US.[11] The estimated mortality attributable to fungemia is 19-40%.[7][11] However, because the majority of people who develop invasive candidiasis are already sick, it can be difficult to determine if the cause of death is directly attributable to the fungal infection.[11] Fungemia is one of the most common bloodstream infections in the United States.[11] In general, observed incidence rates have been stable or trending higher but declining rates have been achieved with improvements in hygiene and disease management.[7]

Deep-seated infections in bones, muscles, joints, eyes, or central nervous system can arise from a bloodstream infection or direct inoculation of Candida may occur, for example, during intestinal surgery.[7]

The distribution of Candida species causing invasive candidiasis has changed over the past decades.[7]C. albicans had been the dominant pathogen but now accounts for just half of the isolates.[7] Increasing dominance of C. glabrata in northern Europe, the United States, and Canada has been observed while C. parapsilosis has become more prominent in southern Europe, Asia, and South America.[7] Regional species distribution guides treatment recommendations since the species exhibit different susceptibilities to azole and echinocandin classes of antifungals.[7]

The virulence of Candida species differs considerably, with C. parapsilosis and C. krusei being less virulent than C. albicans, C. tropicalis, and C. glabrata.[7] This variation is reflected in mortality rates.[7]


  1. ^"Invasive Candidiasis | Candidiasis | Types of Fungal Diseases | Fungal Diseases | CDC". Retrieved 2017-04-02.
  2. ^ abcdefg"Candidiasis (Invasive) – Infectious Diseases". MSD Manual Professional Edition. Retrieved 2017-04-06.
  3. ^"Symptoms | Invasive Candidiasis | Candidiasis | Types of Diseases | Fungal Diseases | CDC". Retrieved 2017-04-03.
  4. ^ abcdeYapar, Nur (2014-01-01). "Epidemiology and risk factors for invasive candidiasis". Therapeutics and Clinical Risk Management. 10: 95–105. doi:10.2147/TCRM.S40160. ISSN 1176-6336. PMC 3928396. PMID 24611015.
  5. ^"Fatal Fungus Linked to 4 New Deaths – What You Need to Know". 2016-11-07. Retrieved 2017-04-04.
  6. ^ abcdefghij"Clinical Alert to U.S. Healthcare Facilities – Fungal Diseases | CDC". June 2016. Retrieved 2017-04-06.
  7. ^ abcdefghijklmnopqrsKullberg, Bart Jan; Arendrup, Maiken C. (2015-10-08). "Invasive Candidiasis". The New England Journal of Medicine. 373 (15): 1445–1456. doi:10.1056/NEJMra1315399. hdl:2066/152392. ISSN 1533-4406. PMID 26444731.
  8. ^"Diagnosis and Testing | Invasive Candidiasis | Candidiasis | Types of Diseases | Fungal Diseases | CDC". Retrieved 2017-04-03.
  9. ^Vincenzi, V.; Fioroni, E.; Benvegnù, B.; De Angelis, M.; Bartolucci, L.; Gradoli, C.; Valori, C. (1985-05-12). "[Effects of calcium antagonists on pancreatic endocrine secretion]". Minerva Medica. 76 (19–20): 919–921. ISSN 0026-4806. PMID 3889722.
  10. ^ ab"Treatment | Invasive Candidiasis | Candidiasis | Types of Diseases | Fungal Diseases | CDC". Retrieved 2017-04-03.
  11. ^ abcd"Statistics | Invasive Candidiasis | Candidiasis | Types of Diseases | Fungal Diseases | CDC". Retrieved 2017-04-03.

Further reading[edit]

External links[edit]

Vaginal Yeast Infection: Symptoms, Causes and Tips to Avoid it

Candida (fungus)

Genus of ascomycete fungi

Candida is a genus of yeasts and is the most common cause of fungal infections worldwide.[1] Many species are harmless commensals or endosymbionts of hosts including humans; however, when mucosal barriers are disrupted or the immune system is compromised they can invade and cause disease, known as an opportunistic infection.[2] Candida is located on most of mucosal surfaces and mainly the gastrointestinal tract, along with the skin.[2]Candida albicans is the most commonly isolated species and can cause infections (candidiasis or thrush) in humans and other animals. In winemaking, some species of Candida can potentially spoil wines.[3]

Many species are found in gut flora, including C. albicans in mammalian hosts, whereas others live as endosymbionts in insect hosts.[4][5][6]Systemic infections of the bloodstream and major organs (candidemia or invasive candidiasis), particularly in patients with an impaired immune system (immunocompromised), affect over 90,000 people a year in the US.[7]

The genome of several Candida species has been sequenced.[7]

Antibiotics promote yeast (fungal) infections, including gastrointestinal (GI) Candida overgrowth and penetration of the GI mucosa.[8] While women are more susceptible to genital yeast infections, men can also be infected. Certain factors, such as prolonged antibiotic use, increase the risk for both men and women. People with diabetes or the immunocompromised, such as those infected with HIV, are more susceptible to yeast infections.[9][10]

Candida antarctica and Candida rugosa are a source of industrially important lipases, while Candida krusei is prominently used to ferment cacao during chocolate production. Candida rugosa is also used as an enzyme supplement to support fat digestion with its broad specificity for lipid hydrolysis.[11]


Agar plate culture of C. albicans

When grown in a laboratory, Candida appears as large, round, white or cream (albicans means "whitish" in Latin) colonies, which emit a yeasty odor on agar plates at room temperature.[12]C. albicans ferments glucose and maltose to acid and gas, sucrose to acid, and does not ferment lactose, which helps to distinguish it from other Candida species.[13]

Recent molecular phylogenetic studies show that the genus Candida, as currently defined, is extremely polyphyletic (encompassing distantly-related species that do not form a natural group).[14] Before the advent of inexpensive molecular methods, yeasts that were isolated from infected patients were often called Candida without clear evidence of relationship to other Candida species. For example, Candida glabrata, Candida guilliermondii, and Candida lusitaniae are clearly misclassified[14] and will be placed in other genera once phylogenetic reorganization is complete (for example, see Khunnamwong et al. 2015).[15]

Some species of Candida use a non-standard genetic code in the translation of their nuclear genes into the amino acid sequences of polypeptides.[16] The difference in the genetic code between species possessing this alternative code is that the codon CUG (normally encoding the amino acid leucine) is translated by the yeast as a different amino acid, serine. The alternative translation of the CUG codon in these species is due to a novel nucleic acid sequence in the serine-tRNA (ser-tRNACAG), which has a guanosine located at position 33, 5' to the anticodon. In all other tRNAs, this position is normally occupied by a pyrimidine (often uridine). This genetic code change is the only such known alteration in cytoplasmic mRNA, in both the prokaryotes, and the eukaryotes, involving the reassignment of a sense codon.[17] This novel genetic code may be a mechanism for more rapid adaptation to the organism's environment, as well as playing an important role in the evolution of the genus Candida by creating genetic barriers that encouraged speciation.[17]


Main article: Candidiasis

Candida are almost universal in low numbers on healthy adult skin[13] and C.albicans is part of the normal flora of the mucous membranes of the respiratory, gastrointestinal and female genital tracts. The dryness of skin compared to other tissues prevents the growth of the fungus, but damaged skin or skin in intertriginous regions is more amenable to rapid growth.[18]

Overgrowth of several species, including C.albicans, can cause infections ranging from superficial, such as oropharyngeal candidiasis (thrush) or vulvovaginal candidiasis (vaginal candidiasis) and subpreputial candidiasis which may cause balanitis; to systemic, such as fungemia and invasive candidiasis. Oral candidiasis is common in elderly denture-wearers.[19] In otherwise healthy individuals, these superficial infections can be cured with topical or systemic antifungal medications[20] (commonly over-the-counter antifungal treatments like miconazole or clotrimazole). In debilitated or immunocompromised patients, or if introduced intravenously (into the bloodstream), candidiasis may become a systemic disease producing abscesses, thrombophlebitis, endocarditis, or infections of the eyes or other organs.[7][13] Typically, relatively severe neutropenia (low neutrophils) is a prerequisite for Candida to pass through the defenses of the skin and cause disease in deeper tissues; in such cases, mechanical disruption of the infected skin sites is typically a factor in the fungal invasion of the deeper tissues.[18] The most common way to treat invasive candida infections is with the use of amphotericin or fluconazole; other methods would include surgery.[21]


C. albicans has been used in combination with carbon nanotubes (CNT) to produce stable electrically-conductive bio-nano-composite tissue materials that have been used as temperature-sensing elements.[22]


Main article: List of Candida species

Among Candida species, C. albicans, which is a normal constituent of the human flora, a commensal of the skin and the gastrointestinal and genitourinary tracts, is responsible for the majority of Candida bloodstream infections (candidemia).[23] Yet, there is an increasing incidence of infections caused by C. glabrata and C. rugosa, which could be because they are frequently less susceptible to the currently used azole-group of antifungals.[24] Other medically important species include C. parapsilosis, C. tropicalis, C. dubliniensis.[7] and the more recent upcoming pathogen C. auris.[25]

Other Candida species, such as C. oleophila, have been used as biological control agents in fruit.[26]


  1. ^Manolakaki, D.; Velmahos, G.; Kourkoumpetis, T.; Chang, Y.; Alam, H. B.; De Moya, M. M.; Mylonakis, E. (2010). "Candida infection and colonization among trauma patients". Virulence. 1 (5): 367–75. doi:10.4161/viru.1.5.12796. PMID 21178472.
  2. ^ abKourkoumpetis TK, Velmahos GC, Ziakas PD, Tampakakis E, Manolakaki D, Coleman JJ, Mylonakis E (2011). "The effect of cumulative length of hospital stay on the antifungal resistance of Candida strains isolated from critically ill surgical patients". Mycopathologia. 171 (2): 85–91. doi:10.1007/s11046-010-9369-3. PMC 4093797. PMID 20927595.
  3. ^Fugelsang, K.; Edwards, C. (2010). Wine Microbiology (2nd ed.). Springer. pp. 3–28. ISBN .
  4. ^Spanakis EK, Kourkoumpetis TK, Livanis G, Peleg AY, Mylonakis E (2010). "Statin therapy and decreased incidence of positive Candida cultures among patients with type 2 diabetes mellitus undergoing gastrointestinal surgery". Mayo Clin. Proc. 85 (12): 1073–9. doi:10.4065/mcp.2010.0447. PMC 2996154. PMID 21123633.
  5. ^Nguyen NH, Suh SO, Blackwell M (2007). "Five novel Candida species in insect-associated yeast clades isolated from Neuroptera and other insects". Mycologia. 99 (6): 842–858. doi:10.3852/mycologia.99.6.842. PMID 18333508.
  6. ^Suh SO, Nguyen NH, Blackwell M (2008). "Yeasts isolated from plant-associated beetles and other insects: seven novel Candida species near Candida albicans". FEMS Yeast Res. 8 (1): 88–102. doi:10.1111/j.1567-1364.2007.00320.x. PMID 17986254.
  7. ^ abcdEnfert C, Hube B (editors) (2007). Candida: Comparative and Functional Genomics. Caister Academic Press. ISBN .CS1 maint: extra text: authors list (link)
  8. ^Kennedy MJ, Volz PA, Edwards CA, Yancey RJ (1987). "Mechanisms of association of Candida albicans with intestinal mucosa". J. Med. Microbiol. 24 (4): 333–41. doi:10.1099/00222615-24-4-333. PMID 3320372.
  9. ^Steckelberg, James M. (2012-09-18). "Male yeast infection: Can I get it from my girlfriend?". Mayo Clinic. Retrieved 2014-03-23.
  10. ^"Yeast Infections". MedlinePlus. Retrieved 2014-03-23.
  11. ^Menden, Ariane; Hall, Davane; Paris, Daniel; Mathura, Venkatarian; Crawford, Fiona; Mullan, Michael; Crynen, Stefan; Ait-Ghezala, Ghania (15 August 2019). "A fast, miniaturised in-vitro assay developed for quantification of lipase enzyme activity". Journal of Enzyme Inhibition and Medicinal Chemistry. 34 (1): 1474–1480. doi:10.1080/14756366.2019.1651312. PMC 6713963. PMID 31414611.
  12. ^"Candida species". Archived from the original on 2007-02-08. Retrieved 2007-02-09.
  13. ^ abcMeyers, Frederick H.; Jawetz, Ernest; Goldfien, Alan (1978). Review of Medical Pharmacology (6th ed.). Lange Medical Publications. ISBN .
  14. ^ abFitzpatrick, David A; Logue, Mary E; Stajich, Jason E; Butler, Geraldine (2006). "A fungal phylogeny based on 42 complete genomes derived from supertree and combined gene analysis". BMC Evolutionary Biology. 6: 99. doi:10.1186/1471-2148-6-99. PMC 1679813. PMID 17121679.
  15. ^Khunnamwong P, Lertwattanasakul N, Jindamorakot S, Limtong S, Lachance MA (2015). "Description of Diutina gen. nov., Diutina siamensis, f.a. sp. nov., and reassignment of Candida catenulata, Candida mesorugosa, Candida neorugosa, Candida pseudorugosa, Candida ranongensis, Candida rugosa and Candida scorzettiae to the genus Diutina". Int. J. Syst. Evol. Microbiol. 65 (12): 4701–9. doi:10.1099/ijsem.0.000634. PMID 26410375.
  16. ^"CGD Help: Non-standard Genetic Codes". Candida Genome Database. Retrieved 1 May 2015.
  17. ^ abSantos, Manuel A. S.; Ueda, Takuya; Watanabe, Kimitsuna; Tuite, Mick F. (31 October 2003). "The non-standard genetic code of Candida spp.: an evolving genetic code or a novel mechanism for adaptation?". Molecular Microbiology. 26 (3): 423–431. doi:10.1046/j.1365-2958.1997.5891961.x. PMID 9402014. S2CID 13575999.
  18. ^ abGoehring, Richard V. (2008). Mims' medical microbiology (4th ed.). Philadelphia, PA: Mosby Elsevier. p. 656. ISBN .
  19. ^Darwazeh A, Lamey P, Samaranayake L, MacFarlane T, Fisher B, Macrury S, MacCuish A (1990). "The relationship between colonisation, secretor status and in-vitro adhesion of Candida albicans to buccal epithelial cells from diabetics". J Med Microbiol. 33 (1): 43–9. doi:10.1099/00222615-33-1-43. PMID 2231671.
  20. ^"Yeast Infections (Candidiasis) in Men and Women". WebMD. 2012-11-12. Retrieved 2014-03-23.
  21. ^Gamaletsou, Maria N.; Rammaert, Blandine; Bueno, Marimelle A.; Sipsas, Nikolaos V.; Moriyama, Brad; Kontoyiannis, Dimitrios P.; Roilides, Emmanuel; Zeller, Valerie; Taj-Aldeen, Saad J. (January 2016). "Candida Arthritis: Analysis of 112 Pediatric and Adult Cases". Open Forum Infectious Diseases. 3 (1): ofv207. doi:10.1093/ofid/ofv207. ISSN 2328-8957. PMC 4742637. PMID 26858961.
  22. ^Di Giacomo, R (2013-03-07). "Candida albicans/MWCNTs: A Stable Conductive Bio-Nanocomposite and Its Temperature-Sensing Properties". IEEE Transactions on Nanotechnology. 12 (2): 111–114. Bibcode:2013ITNan..12..111D. doi:10.1109/TNANO.2013.2239308. ISSN 1536-125X. S2CID 26949825.
  23. ^Gow, Neil A. R.; Yadav, Bhawna (2017). "Microbe Profile: Candida albicans: a shape-changing, opportunistic pathogenic fungus of humans". Microbiology. 163 (8): 1145–1147. doi:10.1099/mic.0.000499. PMID 28809155.
  24. ^Pfaller, M. A.; Diekema, D. J.; Colombo, A. L.; Kibbler, C.; Ng, K. P.; Gibbs, D. L.; Newell, V. A. (2006). "Candida rugosa, an emerging fungal pathogen with resistance to azoles: geographic and temporal trends from the ARTEMIS DISK antifungal surveillance program". J. Clin. Microbiol. 44 (10): 3578–82. doi:10.1128/JCM.00863-06. PMC 1594768. PMID 17021085.
  25. ^Spivak, Emily S.; Hanson, Kimberly E. (2017). "Candida auris: an Emerging Fungal Pathogen". Journal of Clinical Microbiology. 56 (2). doi:10.1128/JCM.01588-17. PMC 5786713. PMID 29167291.
  26. ^"Efficacy of Candida oleophila strain 128 in preventing Penicillium Expansum infection in apricot fruit". Acta Hort. 485: 141–148. 1999.
  27. ^James, S. A.; Carvajal Barriga, E. J.; Bond, C. J.; Cross, K.; Núñez, N. C.; Portero, P. B.; Roberts, I. N. (2009). "Candida carvajalissp. Nov., an ascomycetous yeast species from the Ecuadorian Amazon jungle". FEMS Yeast Research. 9 (5): 784–788. doi:10.1111/j.1567-1364.2009.00518.x. PMID 19459983.
  28. ^Chang, C. F.; Lin, Y. C.; Chen, S. F.; Carvajal Barriga, E. J.; Barahona, P. P.; James, S. A.; Bond, C. J.; Roberts, I. N.; Lee, C. F. (2012). "Candida theae sp. nov., a new anamorphic beverage-associated member of the Lodderomyces clade". International Journal of Food Microbiology. 153 (1–2): 10–14. doi:10.1016/j.ijfoodmicro.2011.09.012. PMID 22088606.

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Candida hypersensitivity

Candida hypersensitivity is a pseudoscientific disease promoted by William G. Crook, M.D.[1] It is spuriously claimed that chronic yeast infections are responsible for many common disorders and non-specific symptoms including fatigue, weight gain, constipation, dizziness, muscle and joint pain, asthma, and others.[2]


Candida albicans is a fungus that colonizes a large majority of the population (meaning it is present in the body but not causing an infection or any problems). Under certain conditions, however, it can cause an infection. The most common manifestations are thrush (a superficial Candida infection in the mouth) and vaginitis, also commonly referred to as a yeast infection. Candida can also cause serious systemic infection, but this is almost always restricted to those with compromised immune systems, such as patients undergoing chemotherapy or with advanced AIDS.[2]


After reading publications by C. Orian Truss, M.D.,[3] Crook proposed the idea that a condition he termed systemic candidiasis, or Candida hypersensitivity, was responsible for a long list of common conditions and non-specific symptoms including fatigue, asthma, psoriasis, sexual dysfunction, and many others.[2] The list of symptoms is similar to that of multiple chemical sensitivity.[4] Many patients presenting with symptoms of environmental sensitivity claim to suffer from multiple "fashionable" syndromes.[5]


The American Academy of Allergy, Asthma, and Immunology strongly criticized the concept of "candidiasis hypersensitivity syndrome" and the diagnostic and treatment approaches its proponents use. AAAAI's position statement concludes: (1) the concept of candidiasis hypersensitivity is speculative and unproven; (2) its basic elements would apply to almost all sick patients at some time because its supposed symptoms are essentially universal; (3) overuse of oral antifungal agents could lead to the development of resistant germs that could menace others; (4) adverse effects of oral antifungal agents are rare, but some inevitably will occur; and (5) neither patients nor doctors can determine effectiveness (as opposed to coincidence) without controlled trials. Because allergic symptoms can be influenced by many factors, including emotions, experiments must be designed to separate the effects of the procedure being tested from the effects of other factors.[4][6]

By 2005, scientists were taking note of "a large pseudoscientific cult"[7] that had developed around the topic of yeast infections, with claims that up to one in three people were affected by yeast-related illnesses including Candida hypersensitivity.[4]

Legal action[edit]

Some practitioners of alternative medicine have promoted dietary supplements as supposed cures for this non-existent illness, rendering themselves liable to prosecution.[4][8] In 1990, alternative health vendor Nature's Way signed a FTC consent agreement not to misrepresent in advertising any self-diagnostic test concerning yeast conditions or to make any unsubstantiated representation concerning any food or supplement's ability to control yeast conditions, with a fine of US$30,000 payable to the National Institutes of Health for research in genuine candidiasis.[8]

See also[edit]


  1. ^Crook, William G. (1986). The Yeast Connection: A Medical Breakthrough. Vintage Books. ISBN .
  2. ^ abcNovella, Steven (25 September 2013). "Candida and Fake Illnesses". Science-Based Medicine. Retrieved 4 July 2018.
  3. ^Truss, CO (1983). The Missing Diagnosis. Birmingham, AL: The Missing Diagnosis, Inc.
  4. ^ abcdStephen Barrett, M.D. (October 8, 2005). "Dubious "Yeast Allergies"". Archived from the original on May 13, 2008.
  5. ^Stewart, Donna E. (1990). "The Changing Faces of Somatization". Psychosomatics. 31 (2): 153–158. doi:10.1016/S0033-3182(90)72188-3. ISSN 0033-3182.
  6. ^Anderson, J; Chai, H; Claman, H; Ellis, E; Fink, J; Kaplan, A; Lieberman, P; Pierson, W; Salvaggio, J; Sheffer, A (1986). "Candidiasis hypersensitivity syndromeApproved by the executive committee of the American academy of allergy and immunology". Journal of Allergy and Clinical Immunology. 78 (2): 271–273. doi:10.1016/S0091-6749(86)80073-2. ISSN 0091-6749. PMID 3734279.
  7. ^Odds, FC (1987). "Candida infections: an overview". Critical Reviews in Microbiology. 15 (1): 1–5. doi:10.3109/10408418709104444. PMID 3319417.
  8. ^ abJarvis WT. "Candidiasis Hypersensitivity". National Council Against Health Fraud. Retrieved 18 January 2014.

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