Esophageal candidiasis (EC), often referred to as esophageal thrush, is a fungal infection affecting the lining of the esophagus. This condition is categorized as an opportunistic infection, meaning the fungi responsible are normally present in the body but only cause disease when the host’s defenses are weakened. EC is a significant indicator of compromised immune function, though localized factors can also permit the organism to proliferate.
The Primary Fungal Pathogens
Esophageal candidiasis is almost always caused by a species from the Candida genus, a yeast that naturally colonizes the human gastrointestinal tract. Candida albicans remains the predominant pathogen, accounting for the vast majority of infectious esophagitis cases. This organism is considered a commensal, coexisting harmlessly with the host until the body’s protective mechanisms fail.
In recent years, there has been an increase in infections caused by non-albicans Candida species, such as C. glabrata and C. tropicalis. These secondary pathogens are of concern because they often exhibit reduced susceptibility to common antifungal treatments like fluconazole. The shift toward these drug-resistant species complicates treatment, particularly in patients who have a history of frequent or prolonged antifungal use.
Underlying Conditions Causing Systemic Immune Suppression
The most common risk factor for developing esophageal candidiasis is a systemic failure of T-cell mediated immunity, the body’s primary defense against fungal infections. Acquired immunodeficiency syndrome (AIDS) is the most significant systemic cause, with EC classified as an AIDS-defining illness. This infection is strongly correlated with a severely depleted count of CD4+ T-lymphocytes, typically occurring when the count drops below 200 cells per microliter of blood.
The use of powerful immunosuppressive drugs following solid organ or hematopoietic stem cell transplantation also creates an environment conducive to Candida overgrowth. These medications suppress the immune system to prevent organ rejection, removing the necessary fungal surveillance mechanism. Patients receiving treatment for various cancers are similarly vulnerable, particularly those undergoing chemotherapy or radiation therapy. Cytotoxic chemotherapy agents destroy rapidly dividing cells, including the immune cells needed to fight off opportunistic organisms.
Hematological malignancies, such as leukemia and lymphoma, further impair immune function directly, making EC a common complication. Beyond medical treatments, the immune system can be compromised by systemic factors, including severe malnutrition. A lack of adequate protein and micronutrients hinders the production and function of immune cells, leading to a diminished capacity for fungal defense. The natural decline in immune function associated with advanced age can also impair the body’s ability to mount an effective defense against Candida colonization.
Localized and Medication-Related Contributing Factors
Causes not related to systemic immune collapse often involve factors that locally impair esophageal defense or alter the natural microbial balance. The use of broad-spectrum antibiotics is a common cause, as these drugs eliminate commensal bacteria in the digestive tract. This removal of competing microorganisms allows the naturally present Candida yeast to proliferate without restraint, leading to an overgrowth that can extend into the esophagus.
Corticosteroids also contribute significantly to EC, especially in their inhaled form used for conditions like asthma or chronic obstructive pulmonary disease. While systemic steroids cause broad immune suppression, inhaled corticosteroids suppress the local immune response in the oropharynx and esophagus. The deposition of steroid particles on the mucosal lining diminishes local immune cell activity, making the tissue susceptible to colonization.
Chronic metabolic disease, specifically uncontrolled diabetes mellitus, creates a favorable environment for fungal growth. High blood glucose levels impair the function of phagocytic immune cells and provide a rich source of sugar for Candida to metabolize and multiply. This combination of impaired host defense and nutrient availability significantly elevates the risk of developing EC.
Conditions that physically damage the esophageal lining or impede its normal function also act as contributing factors. Severe gastroesophageal reflux disease (GERD) causes continuous chemical injury to the mucosal barrier, making the damaged tissue more vulnerable to fungal invasion. Prior radiation therapy administered to the chest or neck can induce local tissue injury, which provides a damaged surface for Candida adhesion. Furthermore, the use of proton pump inhibitors (PPIs) is considered a risk factor, as the reduction of stomach acid alters the gastrointestinal pH, promoting the survival and colonization of Candida species.