Candida glabrata: a case report and the importance of azole resistance

A patient diagnosed with type I diabetes mellitus undergoes a transplant procedure, receiving a new kidney and a new pancreas. A week after the procedure, the patient develops acute pancreatitis for which the pancreas was removed and the patient was given prophylactic therapy with antibiotics and fluconazole. Soon after, he develops a systemic fungal infection with rupture of a branch of the external iliac artery from which Candida glabrata is isolated. A new treatment with caspofungin is started, but without success, as the patient develops peritonitis. He is switched to higher doses of fluconazole and the evolution improves. The important fact about this case is that it draws attention to C. glabrata infections and its intrinsic resistance to fluconazole. The latter is mediated by mutations in a transcription factor that controls the expression of genes coding for ATP bindig cassette (ABC) transporters. These transporters act like efflux pumps, removing the azoles molecules from the yeast. The mutations not only confer the azoles resistance, but increase the virulence of the pathogen, making it harder for the immune system to fight against. Fungal infections are a poorly recognized burden of the medical world and must not be neglected when dealing with patients with immunodeficiencies.