Toxoplasma gondiicauses death and plastic alteration in the jejunal myenteric plexus

Abstract

It was concluded that infection with oocysts of ME-49 T. gondii strain caused quantitative and plastic alterations in the myenteric plexus of the jejunum in rats.

Toxoplasma gondii—A Gastrointestinal Pathogen Associated with Human Brain Diseases

“…Presumably this translocation of T. gondii into the blood stream is a consequence of localized intestinal inflammation and enteropathy generated by the parasite that collectively results in impaired integrity of the intestinal mucosa and gut-blood barrier. Indeed, the gut targeted inflammatory state elicited by T. gondii has been adapted for experimental animal models of inflammatory bowel diseases and of ileitis in particular, although evidence in support of cellular pathologies in the duodenum and jejunum is surfacing as well (Araujo et al, 2015; Trevizan et al, 2016). The intra- and para-cellular mechanisms for parasite invasion of gut epithelial or Peyer’s patch-associated cells are not known with certainty but are actively investigated topics (Briceno et al, 2016; Gregg et al, 2013).…”

Intestinal Dysmotility Syndromes following Systemic Infection by Flaviviruses

“…Bacterial (Porter et al, 2013), protozoan (Araujo et al, 2015; Soyturk et al, 2007) and enteric viral (Marshall et al, 2007; Porter et al, 2012; Zanini et al, 2012) agents that cause infectious gastroenteritis have been implicated in the development of GI dysmotility disorders (Klem et al, 2017). Multiple herpesviruses ( e.g ., herpes simplex virus 1 (HSV-1), varicella-zoster virus, and Epstein Barr virus) also can infect the ENS of humans or experimentally infected animals (Brun et al, 2010; Chen et al, 2011; Debinski et al, 1997; Khoury-Hanold et al, 2016).…”

Toxoplasma gondii promotes changes in VIPergic submucosal neurons, mucosal intraepithelial lymphocytes, and goblet cells during acute infection in the ileum of rats

“…Several studies have shown that infection with different strains of T. gondii causes changes in the neuronal subpopulations and epithelial cells of different segments of the gastrointestinal tract . However, little is known about the response of the submucosal plexus or the epithelial and inflammatory cells in the course of acute infection.…”