Host-Pathogen Molecular Factors Contribute to the Pathogenesis of spp. in Diabetes Mellitus.

PURPOSE OF REVIEW

Infectious diseases represent up to 12% of all deaths in people with diabetes mellitus (DM). The development and progression of DM generate a chronic inflammatory state with unique characteristics that have been exploited by some pathogens; one of them is spp., a fungus considered the causative agent of mucormycosis. This disease has a poor prognosis with high mortality rates, and the apparition of resistant isolates each year has become a worrying concern. DM is an actual and continuing health problem, and for that reason, it is of foremost importance to study the pathogenesis of mucormycosis to generate new prevention and treatment strategies.

RECENT FINDINGS

The worldwide incidence of mucormycosis has increased in recent years. The pathogenic mechanisms and factors identified in spp. are the cell wall, spore germination, proteins, and enzymes related to iron sequestration, CotH fungal protein, positive regulation of the GRP78 cell receptor, and immune evasion due to survival within phagocytes, among others. The physiopathology of DM offers favorable conditions for the successful replication of spp.

SUMMARY

The main reason for increase of incidence of mucormycosis caused by spp. has been associated with the rise of worldwide prevalence of DM. Knowing the fungal pathogenic mechanisms as well as the relationships between with the microenvironment found in the human body will undoubtedly help generate better antifungals to enhance treatment outcomes. Nowadays, some strategies to combat the fungus are based on the knowledge of its proteins, cellular interactions, and iron metabolism.