Practice EssentialsCandidiasis (see the image below) is a fungal infection caused by yeasts from the genus Candida. Candida albicans is the predominant cause of the disease. Show
 Signs and symptomsChronic mucocutaneous candidiasis Findings reveal disfiguring lesions of the face, scalp, hands, and nails. Chronic mucocutaneous candidiasis is occasionally associated with oral thrush and vitiligo. Oropharyngeal candidiasis 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:
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:
Esophageal candidiasis Patients with esophageal candidiasis may be asymptomatic or may have 1 or more of the following symptoms:
Physical examination almost always reveals oral candidiasis. Nonesophageal gastrointestinal candidiasis The following symptoms may be present:
Genitourinary tract candidiasis The types of genitourinary tract candidiasis are as follows:
See Clinical Presentation for more detail. DiagnosisDiagnostic tests for candidiasis include the following:
See Workup for more detail. ManagementSee the list below:
See Treatment and Medication for more detail. BackgroundCandidiasis 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. [3] Candida infections can involve any anatomical structure. PathophysiologyCandida 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. [4] The main virulence factors include the following:
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:
Risk factors associated with invasive or systemic candidiasis include the following [5] :
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. FrequencyUnited StatesCandida 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. [6] In persons with systemic infections, Candida species are now the fourth most commonly isolated pathogens from blood cultures. [7] 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. InternationalSimilar rates of mucocutaneous and systemic candidiasis/candidemia have been observed worldwide. [8, 9] In fact, throughout the world, Candida species have replaced Cryptococcus species as the most common fungal pathogens affecting immunocompromised hosts. Mortality/MorbidityMucocutaneous 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. SexNeither sex is predisposed to candidal colonization; however, VVC is the second most common cause of vaginitis in women. AgePersons 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). [10]
Author Jose A Hidalgo, MD Assistant Professor, Universidad Nacional Mayor de San Marcos; Attending Physician, Department of Internal Medicine, Division of Infectious Diseases, Guillermo Almenara Hospital, Peru Jose A Hidalgo, MD is a member of the following medical societies: HIV Medicine Association, Infectious Diseases Society of America Disclosure: Nothing to disclose. Coauthor(s) Jose A Vazquez, MD, FACP, FIDSA Chief, Division of Infectious Diseases, Professor, Department of Medicine, Medical College of Georgia at Augusta University Jose A Vazquez, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Society for Microbiology, HIV Medicine Association, Immunocompromised Host Society, Infectious Diseases Society of America, International AIDS Society, International Immunocompromised Host Society, International Society for Human and Animal Mycology, International Society for Infectious Diseases, Medical Mycological Society of the Americas, Michigan Infectious Disease Society, Mycological Society of America, National Foundation for Infectious Diseases Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cidara; Amplyx; F2G, Scynexis<br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan; Astellas. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape. Chief Editor Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation Disclosure: Nothing to disclose. Additional Contributors David Hall Shepp, MD Program Director, Fellowship in Infectious Diseases, Department of Medicine, North Shore University Hospital; Associate Professor, New York University School of Medicine David Hall Shepp, MD is a member of the following medical societies: Infectious Diseases Society of America Disclosure: Received salary from Gilead Sciences for management position. Can a yeast infection cause sediment in urine?The telltale symptom of a vaginal yeast infection (thick, white discharge) may come out in the urine, creating white particles. If you have a vaginal yeast infection, your doctor may have you take an antifungal cream, suppository, or ointment. You can also find over-the-counter versions of most of these.
Which of the following urine tests is usually positive when a patient has hepatitis?If bilirubin is found in your urine, it may be a sign that you have: A liver disease, such as hepatitis or cirrhosis.
What is fungal hyphae in urine?Fungal structures in the urine sediment can be used as a clinical sign of fungal UTI but should not be overinterpreted. The observation of yeasts and pseudohyphae can also be due to sample contamination, mainly when the sample is improperly collected.
What is the normal range of yeast cells in urine?It's normal to have one to five squamous epithelial cells per high power field (HPF) in your urine. Having a moderate number or many cells may indicate: a yeast or urinary tract infection (UTI) kidney or liver disease.
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Which of the following is usually found in the urine sediment of a patient with candidiasis?
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