Mycotoxin T-2 and aflatoxin B1 as immunosuppressors in mice chronically infected with Toxoplasma gondii.

The aim of this study was to determine whether repeated ingestion of mycotoxin T-2 (T2) or aflatoxin B1 (AFL) at low doses could contribute to the activation of toxoplasmosis in experimentally infected mice. Mice were divided into two groups: Control (C) and Infected (I). The cyst-forming Beverley strain of Toxoplasma gondii was used to produce the infection one month before treatment with mycotoxins. Mycotoxins were given intragastrically for a 50-day period. The average weight gain was reduced in the groups treated with mycotoxins. Mice developed specific IgG to T. gondii. Histopathological studies showed severe encephalitis in all groups infected. The number of unruptured and ruptured cysts was established and the severity of the lesions was evaluated, the groups treated with mycotoxins being the most severely affected. Immunohistochemical studies of the brain showed free antigen in tissues surrounding ruptured cysts. It is suggested that low and repeated doses of mycotoxins, necessary to produce a subclinical intoxication, precipitate Toxoplasma cyst rupture and consequently the activation of chronic toxoplasmosis.
AuthorsM C Venturini, M A Quiroga, M A Risso, C D Lorenzo, Y Omata, L Venturini, H Godoy
JournalJournal of comparative pathology (J Comp Pathol) Vol. 115 Issue 3 Pg. 229-37 (Oct 1996) ISSN: 0021-9975 [Print] ENGLAND
PMID8923234 (Publication Type: Journal Article)
Chemical References
  • Antibodies, Protozoan
  • Antigens, Protozoan
  • Aflatoxin B1
  • T-2 Toxin
  • Aflatoxin B1 (pharmacology)
  • Animals
  • Antibodies, Protozoan (analysis)
  • Antigens, Protozoan (analysis)
  • Body Weight
  • Brain (pathology, ultrastructure)
  • Chronic Disease
  • Encephalitis (etiology, pathology)
  • Female
  • Immunohistochemistry
  • Immunosuppression
  • Liver (pathology)
  • Meningitis (etiology, pathology)
  • Mice
  • Microscopy, Electron
  • Organ Size
  • T-2 Toxin (pharmacology)
  • Toxoplasmosis, Animal (etiology, immunology)

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