Abstract

An integral part of fundamental research regarding the causative agents of coccidioidomycosis are experiments related to modeling the infectious process on a biological model. It has been shown that introducing an animal into a state of immunosuppression makes it possible to increase its susceptibility to pathogens and reproduce the generalization of the process in a shorter time. To model immunosuppression in experimental animals, the use of a synthetic glucocorticosteroid, dexamethasone, has become widespread. The purpose of our work was to study the effectiveness of the use of dexamethasone in modeling immunosuppression in animals with experimental coccidioidomycosis. Materials and methods. The infectious process was modeled by a single intraperitoneal injection of a fungal suspension into BALB/c mice and outbred mice with artificial immunosuppression caused by dexamethasone. Pathoanatomical dissection of dead and sacrificed mice was performed on the same day. Species identification of the isolated cultures was carried out using light, fluorescence and electron microscopy. Results. Infection of mice with strains of coccidioidomycosis pathogens was accompanied by the development of clinical symptoms, and in some cases, the death of animals. Characteristic pathological-anatomical changes were observed in the fallen individuals. Quadruple intraperitoneal administration of dexamethasone led to significant differences in the life expectancy of animals when compared with groups of mice without immunosuppression (p<0.05). Conclusions. This study demonstrated the effectiveness of dexamethasone in modeling acute coccidioidomycosis. It has been shown that intraperitoneal administration of dexamethasone at a concentration of 0.04 mg/mouse for 4 days before infection leads to increased susceptibility of the animal and, as a consequence, the development of an acute form of the disease.

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