The Distribution of Lizard Besnoitiosis in Panama, and Its Transfer to Mice

Schneider, Curt R.

doi:10.1111/j.1550-7408.1967.tb02060.x

Cited by 12 publications

(1 citation statement)

References 9 publications

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“…A cheap, effective animal model and the ability to passage the parasite in cell culture would aid the study of this poorly characterized parasite species. Different animal models have been used to isolate Besnoitia species, including outbred laboratory mice (Mus musculus), interferon-gamma gene knockout (c-IFN-KO) mice, rats, gerbils, guinea pigs, hamsters, and rabbits (Senaud et al 1974;Schneider 1976;Shkap et al 1987;Dubey et al 2002). Corticosteroids have proven useful in developing animal models to study coccidian parasitism (Dubey et al 1974;Boy et al 1990;Fenger et al 1997;Cutler et al 2001) because they suppress natural killer (NK) cell activity by acting directly on NK effector cells and they inhibit differentiation and antigen presentation by dendritic cells (Cox et al 1982;Pan et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone treatment induces susceptibility of outbred Webster mice to experimental infection with Besnoitia darlingi isolated from opossums (Didelphis virginiana)

2005

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The Sarcocystidae comprise a diverse, monophyletic apicomplexan parasite family, most of whose members form intracellular cysts in their intermediate hosts. The extent of pathology associated with such cyst formation can range widely. We currently lack experimental animal models for many of these infections. Here we explored dexamethasone treatment as a means to render outbred mice susceptible to Besnoitia darlingi infection and demonstrated that this approach allows viable parasites to be subsequently isolated from these mice and maintained in tissue culture. Besnoitia bradyzoites recovered from crushed cysts derived from naturally infected opossums (Didelphis virginiana) replicated and reproduced the development of besnoitiosis in mice treated with dexamethasone (0.5 mg/ml drinking water) daily for 12 days post infection (DPI). Isolates recovered from the peritoneal exudates of these mice were viable and were maintained in long-term tissue cultures. In contrast, control mice given saline without dexamethasone and challenged with similar bradyzoites remained clinically normal for up to 70 DPI. An additional group of mice challenged with the same inoculum of bradyzoites and given dexamethasone at the same concentration and treated with sulfadiazine (1 mg/ml drinking water) daily for 12 DPI also remained normal for up to 70 DPI. Severe disease developed more rapidly in dexamethasone-treated mice inoculated with culture-derived B. darlingi tachyzoites than in those inoculated with cyst-derived bradyzoites. B. darlingi tachyzoite-infected, untreated control mice developed signs of illness at 18 DPI. In contrast, mice treated with sulfadiazine showed no clinical signs up to 50 DPI. Although dexamethasone treatment was required to establish B. darlingi infection in outbred mice inoculated with opossum-derived B. darlingi bradyzoites, no such treatment was required for mice inoculated with culture-derived B. darlingi tachyzoites. Finally, sulfadiazine was highly effective in protecting mice from infection with the tachyzoite stage of B. darlingi.

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