- Author: Jose A Hidalgo, MD; Chief Editor: Michael Stuart Bronze, MD more...
Candidiasis (see the image below) is a fungal infection caused by yeasts from the genus Candida. Candida albicans is the predominant cause of the disease.
Essential update: FDA approves marketing of first rapid blood test for 5 Candida species
In September 2014, the FDA gave marketing approval for the T2Candida Panel and T2Dx Instrument (T2Candida), the first direct blood test for detecting five Candida species that cause bloodstream infections (C albicans and/or C tropicalis, C parapsilosis, C glabrata and/or C krusei).[1, 2] T2Candida can use single blood sample to identify these five yeasts within 3-5 hours, whereas traditional testing methods can take up to 6 days to detect, and even longer to identify, Candida species. Therefore, this test potentially allows earlier administration of appropriate antifungal therapy and may reduce disease severity and/or the mortality risk from sepsis.[1, 2] However, blood cultures should be used to confirm T2Candida results owing to the potential for false-positive results.
Approval was based on a study of 1500 patients, in which T2Candida correctly categorized almost 100% of negative specimens as negative for the presence of Candida, and another study of 300 blood samples with specific concentrations of yeast, in which the test correctly identified the organism in 84%-96% of positive samples.[1, 2]
Signs and symptoms
Chronic mucocutaneous candidiasis
Findings reveal disfiguring lesions of the face, scalp, hands, and nails. Chronic mucocutaneous candidiasis is occasionally associated with oral thrush and vitiligo.
Individuals with oropharyngeal candidiasis (OPC) usually have a history of HIV infection, wear dentures, have diabetes mellitus, or have been exposed to broad-spectrum antibiotics or inhaled steroids. Although patients are frequently asymptomatic, when symptoms do occur, they can include the following:
Sore and painful mouth
Burning mouth or tongue
Thick, whitish patches on the oral mucosa
Physical examination reveals a diffuse erythema and white patches that appear on the surfaces of the buccal mucosa, throat, tongue, and gums.
The following are the 5 types of OPC:
Membranous candidiasis - One of the most common types; characterized by creamy-white, curdlike patches on the mucosal surfaces
Chronic atrophic candidiasis (denture stomatitis) - Also thought to be one of the most common forms of the disease; presenting signs and symptoms include chronic erythema and edema of the portion of the palate that comes into contact with dentures
Erythematous candidiasis - Associated with an erythematous patch on the hard and soft palates
Angular cheilitis - Inflammatory reaction characterized by soreness, erythema, and fissuring at the corners of the mouth
Mixed - A combination of any of the above types is possible
Patients with esophageal candidiasis may be asymptomatic or may have 1 or more of the following symptoms:
Normal oral mucosa (>50% of patients)
Nausea and vomiting
Physical examination almost always reveals oral candidiasis.
Nonesophageal gastrointestinal candidiasis
The following symptoms may be present:
Nausea and vomiting
Fever and chills
Abdominal mass (in some cases)
Genitourinary tract candidiasis
The types of genitourinary tract candidiasis are as follows:
Vulvovaginal candidiasis (VVC) - Erythematous vagina and labia; a thick, curdlike discharge; and a normal cervix upon speculum examination 
Candida balanitis - Penile pruritus and whitish patches on the penis
Candida cystitis - Many patients are asymptomatic, but bladder invasion may result in frequency, urgency, dysuria, hematuria, and suprapubic pain
Asymptomatic candiduria - Most catheterized patients with persistent candiduria are asymptomatic
Ascending pyelonephritis - Flank pain, abdominal cramps, nausea, vomiting, fever, chills and hematuria
Fungal balls - Intermittent urinary tract obstruction with subsequent anuria and ensuing renal insufficiency
See Clinical Presentation for more detail.
Diagnostic tests for candidiasis include the following:
Mucocutaneous candidiasis - For a wet mount, scrapings or smears obtained from skin, nails, or oral or vaginal mucosa are examined under the microscope; a potassium hydroxide smear, Gram stain, or methylene blue is useful for direct demonstration of fungal cells
Cutaneous candidiasis - Using a wet mount, scrapings or smears obtained from skin or nails can be examined under the microscope; potassium hydroxide smears are also useful
Genitourinary candidiasis - A urinalysis should be performed; evidence of white blood cells (WBCs), red blood cells (RBCs), protein, and yeast cells is common; urine fungal cultures are useful
Gastrointestinal candidiasis - Endoscopy with or without biopsy
See Workup for more detail.
See the list below:
Cutaneous candidiasis - Most localized cutaneous candidiasis infections can be treated with any number of topical antifungal agents (eg, clotrimazole, econazole, ciclopirox, miconazole, ketoconazole, nystatin)
Chronic mucocutaneous candidiasis - This condition is generally treated with oral azoles
Oropharyngeal candidiasis - This can be treated with either topical antifungal agents or systemic oral azoles
Esophageal candidiasis - Treatment requires systemic therapy with fluconazole
VVC - Topical antifungal agents or oral fluconazole can be used 
Candida cystitis - In noncatheterized patients, Candida cystitis should be treated with fluconazole; in catheterized patients, the Foley catheter should be removed or replaced; if the candiduria persists after the catheter change, then patients can be treated with fluconazole
Candidiasis is caused by infection with species of the genus Candida, predominantly with Candida albicans.Candida species are ubiquitous fungi that represent the most common fungal pathogens that affect humans. The growing problem of mucosal and systemic candidiasis reflects the enormous increase in the number of patients at risk and the increased opportunity that exists for Candida species to invade tissues normally resistant to invasion. Candida species are true opportunistic pathogens that exploit recent technological advances to gain access to the circulation and deep tissues.
The increased prevalence of local and systemic disease caused by Candida species has resulted in numerous new clinical syndromes, the expression of which depends primarily on the immune status of the host. Candida species produce a wide spectrum of diseases, ranging from superficial mucocutaneous disease to invasive illnesses, such as hepatosplenic candidiasis, Candida peritonitis, and systemic candidiasis. The management of serious and life-threatening invasive candidiasis remains severely hampered by delays in diagnosis and the lack of reliable diagnostic methods that allow detection of both fungemia and tissue invasion by Candida species.
Advances in medical technology, chemotherapeutics, cancer therapy, and organ transplantation have greatly reduced the morbidity and mortality of life-threatening disease. Patients who are critically ill and in medical and surgical ICUs have been the prime targets for opportunistic nosocomial fungal infections, primarily due to Candida species. Studies suggest that the problem is not under control and, in fact, show it is worsening. On a daily basis, virtually all physicians are confronted with a positive Candida isolate obtained from one or more various anatomical sites. High-risk areas for Candida infection include neonatal, pediatric, and adult ICUs, both medical and surgical. Candida infections can involve any anatomical structure.
Candida species are yeastlike fungi that can form true hyphae and pseudohyphae. For the most part, Candida species are confined to human and animal reservoirs; however, they are frequently recovered from the hospital environment, including on foods, countertops, air-conditioning vents, floors, respirators, and medical personnel. They are also normal commensals of diseased skin and mucosal membranes of the gastrointestinal, genitourinary, and respiratory tracts.
Candida species also contain their own set of well-recognized but not well-characterized virulence factors that may contribute to their ability to cause infection. The main virulence factors include the following:
Surface molecules that permit adherence of the organism to other structures (eg, human cells, extracellular matrix, prosthetic devices)
Acid proteases and phospholipases that involve penetration and damage of cell envelopes
Ability to convert to a hyphal form (phenotypic switching)
As with most fungal infections, host defects also play a significant role in the development of candidal infections. Host defense mechanisms against Candida infection and their associated defects that allow infection are as follows:
Intact mucocutaneous barriers - Wounds, intravenous catheters, burns, ulcerations
Phagocytic cells - Granulocytopenia
Polymorphonuclear leukocytes - Chronic granulomatous disease
Monocytic cells - Myeloperoxidase deficiency
Complement - Hypocomplementemia
Immunoglobulins - Hypogammaglobulinemia
Cell-mediated immunity - Chronic mucocutaneous candidiasis, diabetes mellitus, cyclosporin A, corticosteroids, HIV infection
Mucocutaneous protective bacterial flora - Broad-spectrum antibiotics
Risk factors associated with invasive or systemic candidiasis include the following :
Bone marrow transplantation
Solid organ transplantation (liver, kidney)
Recent chemotherapy or radiation therapy
Recent bacterial infection
Gastrointestinal tract surgery
Central intravascular access devices
Acute and chronic renal failure
Mechanical ventilation for longer than 3 days
The first step in the development of a candidal infection is colonization of the mucocutaneous surfaces. All of the factors outlined above are associated with increased colonization rates. The routes of candidal invasion include (1) disruption of a colonized surface (skin or mucosa), allowing the organisms access to the bloodstream, and (2) persorption via the gastrointestinal wall, which may occur following massive colonization with large numbers of organisms that pass directly into the bloodstream.
Candida species are the most common cause of fungal infection in immunocompromised persons. Oropharyngeal colonization is found in 30%-55% of healthy young adults, and Candida species may be detected in 40%-65% of normal fecal flora.
Three of every 4 women experience at least one bout of vulvovaginal candidiasis (VVC) during their lifetime.
More than 90% of persons infected with HIV who are not receiving highly active antiretroviral therapy (HAART) eventually develop oropharyngeal candidiasis (OPC), and 10% eventually develop at least one episode of esophageal candidiasis.
In persons with systemic infections, Candida species are now the fourth most commonly isolated pathogens from blood cultures.
Clinical and autopsy studies have confirmed the marked increase in the incidence of disseminated candidiasis, reflecting a parallel increase in the frequency of candidemia. This increase is multifactorial in origin and reflects increased recognition of the fungus, a growing population of patients at risk (eg, patients undergoing complex surgical procedures, patients with indwelling vascular devices), and the improved survival rates among patients with underlying neoplasms or collagen-vascular disease and patients who are immunosuppressed.
Similar rates of mucocutaneous and systemic candidiasis/candidemia have been observed worldwide.[10, 11] In fact, throughout the world, Candida species have replaced Cryptococcus species as the most common fungal pathogens affecting immunocompromised hosts.
Mucocutaneous candidiasis: Most candidal infections are mucocutaneous and, as such, do not cause mortality. However, in patients with advanced immunodeficiency due to HIV infection, these mucosal infections can become refractory to antifungal therapy and may lead to severe oropharyngeal and esophageal candidiasis that initiates a vicious cycle of poor oral intake, malnutrition, wasting, and early death.
Candidemia and disseminated candidiasis: Mortality rates associated with these infections have not improved markedly over the past few years and remain in the range of 30%-40%. Systemic candidiasis causes more case fatalities than any other systemic mycosis. More than a decade ago, investigators reported the enormous economic impact of systemic candidiasis in hospitalized patients. Candidemia is associated with considerable prolongation in hospital stays (70 d vs 40 d in comparable patients without fungemia). Although mucocutaneous fungal infections, such as oral thrush and Candidaesophagitis, are extremely common in patients with AIDS, candidemia and disseminated candidiasis are uncommon.
Neither sex is predisposed to candidal colonization; however, VVC is the second most common cause of vaginitis in women.
Persons at the extremes of age (neonates and adults >65 y) are most susceptible to candidal colonization. Mucocutaneous candidiasis is also more prevalent in neonates and older adults. Very-low-birth-weight and extremely-low-birth-weight infants are at high risk for blood culture–proven late-onset candidiasis (defined as sepsis that develops after age 72 h).
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