Bradyzoite‐Induced Murine Toxoplasmosis: Stage Conversion, Pathogenesis, and Tissue Cyst Formation in Mice Fed Bradvzoites of ‐ Different Strains of Toxoplasma gondii

Abstract

The development of Toxoplasma gondii was studied in mice fed bradyzoites. At one hour after oral inoculation (HAI), bradyzoites were found in cells of the surface epithelium and the lamina propria of the small intestine, primarily the ileum. Division into two tachyzoites was first observed at 18 HA1 in the intestine. At 24 HAI, organisms were also seen in mesenteric lymph nodes. Organisms were first detected in the brain at six days after oral inoculation with bradyzoites (DAI) but not consistently until 10 DAI. Immunohistochemical staining with bradyzoite specific (BAG-5 antigen) anti-serum showed that bradyzoites retained their BAG-5 reactivity even after the first division into two tachyzoites in the intestine at 18 HAL BAG-5 positive organisms were not seen 2-5 DAI. BAG-5 antigens reappeared in T. gondii at 6 DAI. Whole mice and individual tissues of mice fed bradyzoites were bioassayed in cats and mice for the presence of bradyzoites. Feces of cats fed murine tissues were examined for oocyst shedding for short prepatent periods. Bradyzoites were present in the intestines of mice up to 12 HA1 but not at 18 HAI, and tachyzoites and not bradyzoites disseminated to other tissues from the intestine. Bradyzoites were again detected 6 DAI. Using the mouse bioassay, T. gondii was first detected in peripheral blood at 24 HA1 and more consistently at 48 HAL Using a pepsin-digestion procedure and mouse bioassay, organisms were demonstrated in many tissues of mice 15 and 49 DAI.Supplementary key words. Cat feeding studies, immunohistochemical staining, oral infection, stage specific antibodies.NFECTIONS by Toxoplasma gondii are widely prevalent in hu-

Motile invaded neutrophils in the small intestine ofToxoplasma gondii-infected mice reveal a potential mechanism for parasite spread

“…Surprisingly little is known about how T. gondii behaves in the small intestine of orally infected hosts. There are isolated reports of dividing parasites in intestinal tissue 1 d after infection (dpi), and the parasite increases in number in the small intestine between 3 and 7 dpi (2,(4)(5)(6)9). However, we lack basic information concerning the distribution of parasites in the small intestine during the first week of infection and how this distribution…”

“…This model is useful to further our understanding of host-pathogen interactions in the intestine and of common mechanisms underpinning the development of inflammatory bowel disease (3). Nevertheless, we have limited understanding of how and in which cells infection is established in the intestine, the extent to which the parasite replicates and spreads within the intestine, and how these factors contribute to the development of pathology (2,(4)(5)(6)(7)(8)(9). The ability to label living parasites fluorescently and track them in the tissues of infected hosts provides an important tool for investigating these questions (10)(11)(12)(13)(14).…”

Congenital Toxoplasmosis: A Review of its Pathology, Immune Response and Current Treatment Options.

“…Crossing biological barriers, including the intestine, the blood barrier and the placenta, leading to dissemination within the host is a prerequisite for the establishment of T.gondii infections. Ingested parasites (oocysts or bradyzoite in tissue cysts) invade the intestine and differentiate into tachyzoites followed by spread of the organism haematogenously and via lymphatic tissue (Dubey, 1997). Tachyzoites are known to play important role in the pathogenesis of acute toxoplasmosis (Robert and Mcleod, 1999) and in reactivation of chronic infection in human (Reiter et al, 2000).…”

Toxoplasma gondii: 1908-2008, homage to Nicolle, Manceaux and Splendore

“…It has been possible using immuno-histology and stage specific antibodies to follow the distribution of the parasite during the development of the acute phase in orally infected mice and identify the changes associated with conversion from the acute to the chronic phase (Ferguson & Hutchison 1987b, Dubey 1997a, Dubey et al 1997. Recently, it has been possible to track parasites in live mice by using Fire-fly luciferase expressing parasites (Saeij et al 2005, Boyle et al 2007).…”