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Candida Albicans— An Opportunistic Organism By Max Sherman The opportunistic fungal pathogen, Candida albicans, lives benignly in our bodies, on our skin and mucosa membranes, until it senses we are weak; then it quickly adapts and goes on the offensive. One of the diseases caused by this pathogen, vulvovaginal candidiasis, is commonplace and may affect up to 75% of women at least once in their lifetime. The fungus causes other diseases as well, including a sometimes fatal infection known as candidemia, in compromised patients. Unfortunately, reports of human infections with environmental (airborne) fungi are on the increase throughout the world. More importantly, fungal infections are becoming more resistant to current drugs.1 There have been recent reports that new dimorphic emmonsia species are infecting patients with advanced human immunodeficiency virus (HIV).2 Dimorphic organisms have the ability to switch between a yeast-like form and a filamentous form. In pathogenic fungi like C. albicans, this capacity has been correlated with virulence. This article describes the history of its discovery, characteristics, forms, opportunism, fungal infections and resistance. Discovery David Gruby, a Hungarian physician, generally is recognized as the discoverer of various fungi that produce diseases. He built an excellent microscope in the early 1840s and began a study of the pathology of body fluids. His attempt at microscopic differentiation of pus from other pathological substances, such as mucus or sputum, was a careful, original investigation in a new field of medicine. In 1841, Gruby found a fungus in favus, a contagious skin disease situated in hair follicles, and shortly thereafter discovered C. albicans (then called Oidium albicans), the cause of thrush in children.3 His work was recognized in The New England Journal of Medicine’s 200th anniversary issue.4 regulatoryfocus.org January 2014 1 In 1923, Christine Marie Berkhout named Candida albicans for the white robe, toga candida, worn by Roman senators and senatorial candidates.5 Albicans also comes from Latin albicare, meaning “to whiten.” The Organism and its Various Forms Candida albicans is a yeast that resides in the mouth, throat, intestines and genitourinary tract of most humans. It usually is considered a normal part of the bowel flora. Of the Candida species afflicting humans, C. albicans is by far the most common. It is a eukaryote and belongs to the class Ascomycetes and the family Saccharomycetaceae. C. albicans can live as a harmless commensal organism in many different body locations and is carried by almost half the population. The organism can change cellular morphology and grow as either ovoid, yeast form cells or as elongated filaments. This growth occurs in response to a change in the host environment when the yeast converts from a benign inhabitant into a disease-causing pathogen. The current view is that this ability to switch between the two forms underpins the success of C. albicans as a pathogen. Filaments are thought to be important for tissue invasion, whereas yeast cells are used for dissemination in the host.6 In addition to growth as yeast or filaments, C. albicans can switch to a multicellular form, growing as a biofilm. Biofilms are multicellular communities of yeast and filamentous cells surrounded by a coat of extracellular matrix. Biofilms of C. albicans form an attachment to surfaces and are an important issue in clinical settings.7 Biofilms readily form on implanted medical devices, such as catheters, pacemakers and prosthetic devices, giving the fungus access to the bloodstream for dissemination and causing life-threatening systemic infections. Maturation of biofilms is accompanied by development of drug resistance. What triggers drug resistance is not completely understood, but it likely is a result of physical properties of the biofilm and metabolic and gene expression changes.8 Fungal Infections Infections caused by C. albicans can be defined in two broad categories: superficial mucocutaneous and systematic invasive, which involves the spread of the organism to the bloodstream (candidemia) and to the major organs. Systemic invasive candidemia often is fatal. Superficial infections affect the various mucous membranes on body surfaces, such as in oral and vaginal thrush. (Thrush refers to the resemblance of the white flecks present in some forms of candidiasis with the breast of the bird with the same name.) The incidence of vulvovaginal candidiasis (vaginal thrush) has increased approximately two-fold in the last decade9 There are more than 20 species of Candida yeasts that can cause infections in humans, and, although infections caused by these other species are increasing in prevalence, the majority of candidiasis is still caused by C. albicans.10 C. albicans acts a double agent. In most of us, it lives peacefully as a commensal microbe, but for people whose immune systems are compromised by HIV or other severe diseases, it frequently is deadly. Given the opportunity to breach the immune system defenses, the yeast can cross into the bloodstream and switch from peaceful coexistence to attack mode, producing long filaments that enter tissues and destroy them.11 C. albicans is the most common species of the Candida fungus and, as mentioned earlier, the leading cause of vaginal and oral yeast infections. It is the fourth most common hospital-acquired blood-borne pathogen in the US, and is present in the mouths of 30–50% of healthy adults.12 Because of the widespread nature of Candida, the potential for overgrowth and infection is common in the young, the elderly, immune-compromised individuals and people receiving corticosteroid or chemotherapy treatments. There is at least one other yeast to worry about. Researchers in Sweden have discovered that Candida glabrata is becoming more resistant to fungicidal medicine. It has become the second most-common yeast pathogen in humans. C. glabrata mutates surprisingly rapidly by reorganizing its chromosomes and making extra copies of large chromosome pieces. This process enables the yeast to tolerate higher doses of antifungal drugs. C. glabrata, like C. albicans, can be directly life-threatening to people with poor immune defense when it enters the bloodstream.13 regulatoryfocus.org January 2014 2 Final Thoughts During my research for this article I found a book written by a certified metabolic technician who categorizes C. albicans as the quiet epidemic.14 He claims our society is crawling with pollutants that enhance Candida and clobber us. As the book notes, our food is refined, additivized and chemicalized, and then so loaded with sugars and starch that we feed Candida very happily. The book goes on to recommend a regimen of antifungals, blood purifiers, intestinal cleansers, digestive aids, immune boosters, probiotics, detoxifiers and oxygen therapy. And I forgot to mention weekly colonic irrigations, which are part of a rigorous, eight-week treatment program. I am not expert enough to discourage anyone from trying the program, although it may be better than a once-recommended method of inhaling the breath of a duck. That treatment was used in an effort to cure children of thrush and other disorders of the mouth and throat. About the Author Max Sherman is head of Sherman Consulting Services in Warsaw, IN. He can be reached at [email protected]. References 1. Sudbery PE. “Growth of Candida albicans hyphae.” Nature Reviews/Microbiology. 2011; 9:737-48. 2. Papon N et al. “Emerging and emerged pathogenic Candida species: beyond the Candida albicans paradigm.” PLOS Pathogens. 2013; 9 (9):1-4. 3. Gruby D. Encyclopedia.com website. http://www.encyclopedia.com/doc/1G2-2830901758.html. Accessed 7 October 2013. 4. Fauci AS and Morens DM. “The perpetual challenge of infectious diseases.” New Engl J Med. 2012; 366(5):454-61. 5. Holland SM and Vinh DC. “Yeast infections—human genetics on the rise.” New Engl J Med. 2009; 361(18):1798-1801. 6. Op cit 2. 7. Uwamahoro N and Traven A. “Yeast, filaments and biofilms in pathogenesis of Candida albicans.” Australian Biochemist. 2010; 41(1):16-18. 8. Op cit 6. 9. Op cit 2. 10. Sudbery P et al. “The distinct morphogenic states of Candida albicans.” Trends in Microbiology. 2004; 12(7):317-24. 11. “Possible way to turn fungus from foe to friend.” Science Daily. http://sciencedaily.com/ releases/2013/09/130924122458.htm. Accessed 25 September 2013. 12. “New way the body fights fungal infections discovered.” Science Daily. http://www.sciencedaily.com/ releases/2009/06/090611120742.htm. Accessed 25 September 2013. 13. “Yeast infections worsening: rapidly mutating yeast causing more infections.” Science Daily. http://sciencedaily.com/ releases/2009/04/090401204205.htm. Accessed 25 September 2013. 14. Weinberger S. Candida albicans: the quiet epidemic. San Anselmo, CA: Healing Within Products; 2000. Cite as: Sherman, M. “Candida Albicans–An Opportunistic Organism.” Regulatory Focus. January 2014. Regulatory Affairs Professionals Society. © 2014 by the Regulatory Affairs Professionals Society. All rights reserved. regulatoryfocus.org January 2014 3