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The genus Candida encompasses more than 150 species, only a few of which cause disease in humans. With rare exceptions, the human pathogens are C. albicans, C. guilliermondii, C. krusei, C. parapsilosis, C. tropicalis, C. kefyr, C. lusitaniae, C. dubliniensis, and C. glabrata. Ubiquitous in nature, these organisms are found on inanimate objects, in foods, and on animals and are normal commensals of humans. They inhabit the gastrointestinal tract (including the mouth and oropharynx), the female genital tract, and the skin. Although cases of candidiasis have been described since antiquity in debilitated patients, the advent of Candida species as common human pathogens dates to the introduction of modern therapeutic approaches that suppress normal host defense mechanisms. Of these relatively recent advances, the most important is the use of antibacterial agents that alter the normal human microbial flora and allow nonbacterial species to become more prevalent in the commensal flora. With the introduction of antifungal agents, the causes of Candida infections shifted from an almost complete dominance of C. albicans to the common involvement of C. glabrata and the other species listed above. The non-albicans species now account for approximately half of all cases of candidemia and hematogenously disseminated candidiasis. Recognition of this change is clinically important, since the various species differ in susceptibility to the newer antifungal agents. In developed countries, where medical therapeutics are commonly used, Candida species are now among the most common nosocomial pathogens. In the United States, these species are the fourth most common isolates from the blood of hospitalized patients.
Candida is a small, thin-walled, ovoid yeast that measures 4–6 m in diameter and reproduces by budding. Organisms of this genus occur in three forms in tissue: blastospores, pseudohyphae, and hyphae. Candida grows readily on simple medium; lysis centrifugation enhances its recovery from blood. Species are identified by biochemical testing (currently with automated devices) or on special agar.
In the most serious form of Candida infection, the organisms disseminate hematogenously and form microabscesses and small macroabscesses in major organs. Although the exact mechanism is not known, Candida probably enters the bloodstream from mucosal surfaces after growing to large numbers as a consequence of bacterial suppression by antibacterial drugs; alternatively, in some instances, the organism may enter from the skin. A change from the blastospore stage to the pseudohyphal and hyphal stages is generally considered integral to the organism’s penetration into tissue. However, C. glabrata can cause extensive infection even though it does not transform into pseudohyphae or hyphae. Numerous reviews of cases of hematogenously disseminated candidiasis have identified the following predisposing factors or conditions: antibacterial agents, indwelling intravascular catheters, hyperalimentation fluids, indwelling urinary catheters, parenteral glucocorticoids, respirators, neutropenia, abdominal and thoracic surgery, cytotoxic chemotherapy, and immunosuppressive agents for organ transplantation. Patients with severe burns, low-birth-weight neonates, and persons using illicit IV drugs are also susceptible. HIV-infected patients with low CD4+ T cell counts and patients with diabetes are susceptible to mucocutaneous infection, which may eventually develop into the disseminated form when other predisposing factors are encountered. Women who receive antibacterial agents may develop vaginal candidiasis.
Innate immunity is the most important defense mechanism against hematogenously disseminated candidiasis, and the neutrophil is the most important component of this defense. Although many immunocompetent individuals have antibodies to Candida, the role of these antibodies in defense against the organism is not clear.
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