Advancements in the Management of Chromoblastomycosis Among Immunocompromised Patients: an overview of a case

In the past decade, major advances have been made in understanding the host‐pathogen immune response in emerging fungal infections. The currently accepted theory is that an inefficient dysregulation by Treg/Th17 exists in immunocompromised hosts due to failure of pattern recognition receptors, i.e. the first line of defense against fungal infections. Recent studies indicate that C‐type lectin receptors(CLRs) play a prominent role in fungal immunity. We discuss a case of a 34 year‐old woman on immunosuppressive treatment after a renal transplant in 2010, who presented with a two year history of slowly progressing pruritic lesions on her left thigh, buttock lower back and right leg. She denied a history of local trauma, but had right hip prosthesis surgery due to avascular necrosis of the femoral head. Her current medications include omeprazole, tacrolimus, prednisone, azathioprine, propranolol and cephalexin; Treatment with antifungals medication was started. She has no known drug allergies and denies a history of similar skin lesions in the family. On examination: Hyperchromic, indurated, confluent nodules measuring 5 to 8 cm in diameter, adherent to subcutaneous tissue on her lower left buttock. Ulcer measuring 3 cm on her left thigh, regularly infiltrated, with hyperkeratotic borders and a purulent center. A similar but smaller lesion is observed on the right leg with infiltrated nodule surrounded by an erythematous halo on the lateral aspect of right leg, measuring 2 cm in diameter; The lesions are painless. Histological examination of the affected skin and mycological culture showing Fonsecaes pedrosoi confirmed the diagnosis of Chromoblastomycosis(CBM). Treatment was difficult and prolonged. Recently a mouse model has shown that F. pedrosoi , the major causative agent of CBM, is recognized primarily by CLR, specifically the β‐glucan receptor, Dectin‐1. This specific signaling pathway found in the spores from a subcutaneous infection promoted the differentiation of fungus‐specific CD4(+) T cells into Th17 cells. A secondary study testing topical applications of imiquimod for treatment of patients with CBM displayed a marked improvement of their lesions, both with and without concurrent oral antifungal therapy. This review focuses on the most recent finding regarding the immunopathogenesis of chromoblastomycosis and the different types of immune cells that play a role in antifungal host defense. Particular emphasis is given to recent clinical trials targeting topical immunomodulators as a possible adjuvant in the management of emerging fungal infections. Support or Funding Information