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Infect Agent Cancer. 2007 Nov 21;2:22. doi: 10.1186/1750-9378-2-22.

Cryptosporidium parvum, a potential cause of colic adenocarcinoma.

Author information

1
Ecologie du Parasitisme (EA3609 Université de Lille 2), IFR 142, Institut Pasteur de Lille, Lille, France.
2
Cátedra de Parasitología, Escuela de Medicina "José María Vargas", Universidad Central de Venezuela (UCV), Caracas, Venezuela.
3
Plateau d'Expérimentation Animale, Institut Pasteur de Lille, France.
4
Service d'Anatomie et de Cytologie Pathologiques, Groupe Hospitalier de l'Université Catholique de Lille, France.
5
Unité de Sécurité Microbiologique, Institut Pasteur de Lille, France.
6
Laboratoire Environnement et Santé, Université Catholique de Lille, France.
7
Parasitologie-Mycologie, Centre Hospitalier Régional et Universitaire de Lille, Université de Lille 2, France.
#
Contributed equally

Abstract

BACKGROUND:

Cryptosporidiosis represents a major public health problem. This infection has been reported worldwide as a frequent cause of diarrhoea. Particularly, it remains a clinically significant opportunistic infection among immunocompromised patients, causing potentially life-threatening diarrhoea in HIV-infected persons. However, the understanding about different aspects of this infection such as invasion, transmission and pathogenesis is problematic. Additionally, it has been difficult to find suitable animal models for propagation of this parasite. Efforts are needed to develop reproducible animal models allowing both the routine passage of different species and approaching unclear aspects of Cryptosporidium infection, especially in the pathophysiology field.

RESULTS:

We developed a model using adult severe combined immunodeficiency (SCID) mice inoculated with Cryptosporidium parvum or Cryptosporidium muris while treated or not with Dexamethasone (Dex) in order to investigate divergences in prepatent period, oocyst shedding or clinical and histopathological manifestations. C. muris-infected mice showed high levels of oocysts excretion, whatever the chemical immunosuppression status. Pre-patent periods were 11 days and 9.7 days in average in Dex treated and untreated mice, respectively. Parasite infection was restricted to the stomach, and had a clear preferential colonization for fundic area in both groups. Among C. parvum-infected mice, Dex-treated SCID mice became chronic shedders with a prepatent period of 6.2 days in average. C. parvum-inoculated mice treated with Dex developed glandular cystic polyps with areas of intraepithelial neoplasia, and also with the presence of intramucosal adenocarcinoma.

CONCLUSION:

For the first time C. parvum is associated with the formation of polyps and adenocarcinoma lesions in the gut of Dex-treated SCID mice. Additionally, we have developed a model to compare chronic muris and parvum cryptosporidiosis using SCID mice treated with corticoids. This reproducible model has facilitated the evaluation of clinical signs, oocyst shedding, location of the infection, pathogenicity, and histopathological changes in the gastrointestinal tract, indicating divergent effects of Dex according to Cryptosporidium species causing infection.

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