SCN5A encodes the alpha subunit of the cardiac sodium channel, NaV1.5, responsible for the sodium current INa which depolarises cardiac cells at the start of the action potential. Cardiac sodium channels normally inactivate rapidly, but the mutations involved in LQT3 slow their inactivation leading to a small sustained late sodium current. This continued inward current prolongs the action potential and thereby the QT interval.A large number of mutations have been characterized as leading to or predisposing to LQT3. Calcium has been suggested as a regulator of SCN5A protein, and the effects of calcium on SCN5A may begin to explain the mechanism by which some of these mutations cause LQT3. Furthermore, mutations in SCN5A can cause Brugada syndrome, cardiac conduction disease, and dilated cardiomyopathy. In rare situations, some individuals can have combinations of these diseases. Other subtypes
LQT5 is caused by variants in the KCNE1 gene. This gene is responsible for the potassium channel beta subunit MinK which, in conjunction with the alpha subunit encoded by KCNQ1, is responsible for the potassium current IKs, and variants associated with prolonged QT intervals decrease this current. The same variants in KCNE1 can cause the more severe Jervell and Lange-Nielsen syndrome when two copies are inherited (homozygous inheritance) and the milder LQT5 subtype of Romano–Ward syndrome when a single copy of the variant is inherited (heterozygous inheritance).The LQT6 subtype is caused by variants in the KCNE2 gene.
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.