Reviewing the Etiologic Agents, Microbe-Host Relationship, Immune Response, Diagnosis, and Treatment in Chromoblastomycosis

Abstract

Chromoblastomycosis (CBM) is a neglected human disease, caused by different species of pigmented dematiaceous fungi that cause subcutaneous infections. This disease has been considered an occupational disease, occurring among people working in the field of agriculture, particularly in low-income countries. In 1914, the first case of CBM was described in Brazil, and although efforts have been made, few scientific and technological advances have been made in this area. In the field of fungi and host cell relationship, a very reduced number of antigens were characterized, but available data suggest that ectoantigens bind to the cell membrane of host cells and modulate the phagocytic, immunological, and microbicidal responses of immune cells. Furthermore, antigens cleave extracellular proteins in tissues, allowing fungi to spread. On the contrary, if phagocytic cells are able to present antigens in MHC molecules to T lymphocytes in the presence of costimulation and IL-12, a Th1 immune response will develop and a relative control of the disease will be observed. Despite knowledge of the resistance and susceptibility in CBM, up to now, no effective vaccines have been developed. In the field of chemotherapy, most patients are treated with conventional antifungal drugs, such as itraconazole and terbinafine, but these drugs exhibit limitations, considering that not all patients heal cutaneous lesions. Few advances in treatment have been made so far, but one of the most promising ones is based on the use of immunomodulators, such as imiquimod. Data about a standard treatment are missing in the medical literature; part of it is caused by the existence of a diversity of etiologic agents and clinical forms. The present review summarizes the advances made in the field of CBM related to the diversity of pathogenic species, fungi and host cell relationship, antigens, innate and acquired immunity, clinical forms of CBM, chemotherapy, and diagnosis.

Epidemiological, Clinical, and Histopathological Characteristics of Patients with Sporotrichoid Lymphocutaneous Infection in Southern Thailand: A 10-Year Retrospective Study

“…Although fungal pathogens are mainly found in soil, plants, and organic material, the disease was usually transmitted to humans by infected animals (e.g., cat or dog). 22 However, in previous studies, nearly half of the study population could not recall the source of their external cutaneous injuries. 13,23 The location of infection was found to be correlated with type of injury.…”

Mycetoma, chromoblastomycosis and other deep fungal infections: diagnostic and treatment approach

“…The antifungals of choice are azoles, itraconazole (200-400 mg per day) is the preferred one, but either terbinafine (250-500 mg per day) or 5flucytosne in combination with itraconazole are www.co-infectiousdiseases.com highly recommended. Potassium iodide may be used in refractory cases as well as posaconazole and voriconazole [13]. Duration of medical treatment is unknown, but usually prolonged therapy is needed.…”

A Lethal Case of Disseminated Cladosporium allicinum Infection in a Captive African Bullfrog

“…Nonetheless, these fungi usually cause allergic rhinitis and even life-threatening exacerbations in asthmatic patients [ 6 , 7 ], eventually leading to opportunistic phaeohyphomycosis (PHM) in humans and animals [ 2 , 8 , 9 ]. The term PHM is usually linked to infections caused by dematiaceous fungi of different genera (i.e., Phialophora, Cladosporium, Xylohypha, Curvularia, Exserohilum, Bipolaris, Lecythophora, Alternaria ), which are characterized by the presence of brown pigmented hyphae and yeasts in the histological section of tissues and by the low immunological competence of the host [ 10 , 11 ]. Among PHM, chromoblastomycosis (CBM) is one of the most prevalent invasive fungal infections caused by melanized or brown-pigmented fungi in the form of muriform cells, which causes pyogranulomatous inflammation and fibrosis in host tissues [ 12 ].…”