Interactions between Vitamin A Deficiency and Plasmodium berghei Infection in the Rat

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Abstract
It has been claimed that vitamin A deficiency increases the severity of malarial infection in rats. We measured parasitemia, mortality, serum retinol, liver retinol, spleen weight, and degree of xerophthalmia in vitamin A—deficient rats (A-), pair-fed control rats (A+PF), and ad libitum—fed control rats (A+AL) infected with Plasmodium berghei, a rodent malarial parasite. In experiments 1 and 2 vitamin A deprivation began at weaning. Parasitemia and mortality among mildly deficient (expt. 1, mean serum retinol 19 µg/dl) or acutely deficient rats (expt. 2, mean serum retinol < 5 µg/dl) infected with P. berghei were not significantly different from those of infected A + AL or A + PF rats. Furthermore, when the mildly deficient rats were given a second, larger dose of P. berghel, all demonstrated complete immunity to the parasite. However, when vitamin A was withdrawn midway through pregnancy (expt. 3), the A- rats experienced significantly higher parasitemia and mortality during infection with P. berghei. Malaria caused a significant decrease in the serum retinol but not liver retinol of the A + PF and A + AL rats. Among the acutely deficient rats, xerophthalmia was significantly more prevalent and more severe among those infected with malaria than among those not infected with malaria. Malaria and vitamin A deficiency acted synergistically to increase spleen weight, and this interaction was highly significant. In these experiments, vitamin A deficiency decreased the rats' ability to recover from malaria, but only when the deficiency began early in life, was very severe, and the rats were young when infected. Malaria, even at low rates of parasitemia, decreased serum retinol in well-fed rats and exacerbated pre-existing vitamin A deficiency.