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  • Title: Influence of dietary nivalenol exposure on gross pathology and selected immunological parameters in young pigs.
    Author: Hedman R, Thuvander A, Gadhasson I, Reverter M, Pettersson H.
    Journal: Nat Toxins; 1997; 5(6):238-46. PubMed ID: 9615312.
    Abstract:
    Young pigs were fed diets to which 0, 2.5, or 5 mg/kg of purified nivalenol (NIV) had been added. The exposure continued for 3 weeks without any signs of feed refusal, vomiting, or change in clinical appearance, and there were no changes in body or organ weights due to the exposure. However, the concluding macroscopic examination revealed gastrointestinal erosions and signs of nephropathy in most of the exposed pigs. There were no differences in total or differential blood leukocyte counts between control and exposed pigs in blood samples collected after 0, 1, or 3 weeks, nor in the number of thymocytes at the end of the trial. Spleen cell numbers showed a dose-dependent decrease after 3 weeks of exposure that was statistically different from controls in pigs exposed to 5 mg NIV/kg. Flow cytometric analysis of lymphocytes revealed decreased numbers of both the CD4+ and the CD8+ subpopulations in the spleen at this point in time, reflecting the lower numbers of splenocytes; but no proportional changes were seen. In blood, exposure to NIV caused a transient decrease in the proportion of CD4+ cells after 1 week of exposure. Analysis of IgG and IgA in plasma showed a time-dependent tendency of increasing plasma concentrations of IgA and decreasing concentrations of IgG in the 2.5 mg/kg group, but differences in Ig levels between experimental groups and controls were not observed at any time. No differences were seen in the mitogen-induced proliferation by lymphocytes from blood, spleen, or thymus. In conclusion, exposure of young pigs to NIV in the diet caused pathological alterations in the kidneys and gastrointestinal tract and reduced the number of splenocytes. The results also indicated that exposure to NIV caused a time-dependent increase in IgA production in the 2.5 mg/kg group.
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