EXPERIMENTAL SUBCUTANEOUS CYSTICERCOSIS BY Taenia crassiceps IN BALB/c AND C57BL/6 MICE

Abstract

SUMMARYHuman cysticercosis is one of the most severe parasitic infections affecting tissues. Experimental models are needed to understand the host-parasite dynamics involved throughout the course of the infection. The subcutaneous experimental model is the closest to what is observed in human cysticercosis that does not affect the central nervous system. The aim of this study was to evaluate macroscopically and microscopically the experimental subcutaneous cysticercosis caused by Taenia crassiceps cysticerci in BALB/c and C57BL/6 mice. Animals were inoculated in the dorsal subcutaneous region and macroscopic and microscopic aspects of the inflammatory process in the host-parasite interface were evaluated until 90 days after the inoculation (DAI). All the infected animals presented vesicles containing cysticerci in the inoculation site, which was translucent at 7 DAI and then remained opaque throughout the experimental days. The microscopic analysis showed granulation tissue in BALB/c mice since the acute phase of infection evolving to chronicity without cure, presenting 80% of larval stage cysticerci at 90 DAI. While C57BL/6 mice presented 67% of final stage cysticerci at 90 DAI, the parasites were surrounded by neutrophils evolving to the infection control. It is possible to conclude that the genetic features of susceptibility (BALB/c) or resistance (C57BL/6) were confirmed in an experimental subcutaneous model of cysticercosis.

Histopathologic aspects of experimental cysticercosis and in situ cytokines profile in C57BL/6 mice

“…Other studies of NCC models 16 and in a subcutaneous model 22 showed that BALB/c mice are less efficient in the precocious destruction of the parasite, allowing its proliferation with greater inflammatory intensity in the acute phase of the infection, with a predominance of polymorphonuclear cells and macrophage infiltration. The C57BL/6 mice lineage is capable of inducing the parasite death with greater inflammatory intensity in the late phase of the infection with less tissue injury and a predominance of infiltration of mononuclear inflammatory cells.…”