Marginal vitamin A deficiency in pigs experimentally infected with Trichuris suis: a model for vitamin A inadequacy in children.

The development of an experimental model for marginal vitamin A deficiency in humans is of major interest, enabling the elucidation of possible interactions with helminth infections. We established a useful experimental model for human vitamin A deficiency in young pigs; deficiency was induced through a depletion method encompassing both sow and offspring. We report on a 2 x 2 study in which 18-week-old vitamin A deficient pigs and vitamin A sufficient littermates were infected with both of the intestinal nematodes Trichuris suis and Ascaris suum and followed for 14 weeks through 32 weeks of age. Forty-nine pigs were followed with respect to bodyweight, liver biopsies and blood samples for retinol concentration and faecal samples for parasite eggs and worms. Liver and serum concentrations of vitamin A were significantly diminished in the vitamin A deficient (VAD) group as compared to the vitamin A sufficient (VAS) group both before (P < 0.001) and after inoculation with T. suis and A. suum (P < 0.02). A significant correlation between retinol content in micro-biopsy needle samples and gross liver content was found (r = 0.457, n = 48, P = 0.001). The adult T. suis worms in the VAD group were marginally smaller (36.7 vs 40.2 mm; P = 0.08), more orally located (section 2.9 vs 3.9; P = 0.08) and had a higher proportion of males (0.58 vs 0.50; P = 0.08) whereas there were no effects of diet treatment on fecundity. The proportion of pigs with faecal T. suis egg excretion 12 weeks post inoculation (p.i.) was significantly lower in the VAD group compared with the VAS infected group (21 vs 78%; P = 0.036). In addition, faecal T. suis egg excretion was significantly lower in the VAD group at both week 11 (P = 0.040) and week 12 p.i. (P = 0.021). Vitamin A deficiency may have altered the functional integrity of the mucosal intestinal epithelium, disrupting the normally delicate attachment of T. suis and leading to the premature termination of infection. However, a possible antagonistic interaction, if verified, should not preclude interventions to improve vitamin A status, i.e., treatment should accompany anthelmintic treatment.