Propagation of Giardia duodenalis cysts in immunosuppressed CF-1 mice

Abstract

This study developed and evaluated Giardia duodenalis cyst propagation using a dexamethasone immuno-suppressed CF-1 mouse model as an alternative to a previously described Mongolian gerbil model. The CF-1 mouse model shed significantly more cysts per animal during a 16 to18 h collection period compared to the gerbil (averages: 7.8 × 10 6 cysts/CF-1 mouse and 2.5 × 10 6 cysts/gerbil). In addition, the patency period for this model differed from both G. muris in mice and G. duodenalis in gerbils in that cysts were shed continuously for over 20 days. Results further showed that the β-giardin gene sequences from gerbil derived and mouse derived G. duodenalis were identical, after 34 serial passages through the CF-1 mouse model. Overall, since the CF-1 mouse model produced higher concentrations of cysts per animal, were genetically and phenotypically stable based on β-giardin gene sequences.

Male Swiss mice (Mus musculus) as a most suitable experimental model for the study of Giardia duodenalis BIV

“…The elimination of the first cysts of G. duodenalis in MS1 and MS2 groups occurred on the 6th dpi. This result is in agreement with Buret et al (1991), who also reported this pre-patency period; however, it differs from other studies that report elimination of cysts from the 3rd dpi (Pavanelli et al, 2018;Ware & Villegas, 2019). Some studies show that this period can vary from one to two weeks (Astiazarán-García et al, 2000;Soares et al, 2008).…”

“…Cysts of G. duodenalis BIV did not infect Balb/c and C57BL/6 mice, even with inoculum of 10 4 parasites. Infection with cysts in these two lineages was reported in malnourished C57BL/6 (Bartelt et al, 2013), in BALB/cAnUnib Specified Pathogen Free (SPF) (Nakada et al, 2018), and also in immunosuppressed CF1 heterogeneous mice (Ware & Villegas, 2019), indicating that nutritional status and other environmental factors during the maintenance of mice directly influence their capacity to resist to pathogens (Mizutani et al, 2017;Vaidya, 2017). The host's immune response is also a determining factor for infection.…”