Critical illness
Long-term intensive care unit stay
Abdominal surgery (aggravated by anastomotic leakage or repeat laparotomies)
Immunosuppressive diseases
Acute necrotizing pancreatitis
Malignant hematologic disease
Solid-organ transplantation
Hematopoietic stem cell transplantation
Solid-organ tumors
Neonates (especially low birth weight and preterm infants)
Broad-spectrum antibiotic treatment
Central venous catheter
Internal prosthetic device
Total parenteral nutrition
Hemodialysis
Glucocorticoid use
Chemotherapy
Noninvasive Candida colonization (particularly if multifocal)

Transmission
Invasive candidiasis is a nosocomial infection with the majority of cases associated with hospital stays. Diagnosis
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.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. Diagnosis by culturing allows subsequent susceptibility testing of causative species. Sensitivity of blood culture is far from ideal, with a sensitivity reported to be between 21 and 71%. 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.Diagnosis of invasive candidiasis is supported by histopathologic evidence  (for example, yeast cells or hyphae) observed in specimens of affected tissues.Additionally, elevated serum β-glucan can demonstrate invasive candidiasis while a negative test suggests a low likelihood of systemic infection.The emergence of multidrug-resistant C. auris as a cause of invasive candidiasis has necessitated additional testing in some settings. C. auris-caused invasive candidiasis is associated with high mortality.
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. 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). 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. Prevention
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. For example, one group would be patients recovering from abdominal surgery that may have gastrointestinal perforations or anastomotic leakage. Antifungal prophylaxis can reduce the incidence of fungemia by approximately 50%, but has not been shown to improve survival. 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. Treatment
Antifungals are used for treatment with the specific type and dose depending on the patients 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.