The ability of vitamin A deficient rats to resist infection with P. berghei was investigated. When 10 X 10(6) erythrocytes bearing the parasite/100 g body weight were given to the vitamin A protein energy undernourished rats, parasitemia developed in these animals at a faster pace than the controls. A high number (60% to 95%) of red blood cells (RBC) carrying the parasite were noticeable within 6 to 7 days after infection, at which time most animals in this group died. The pair-fed controls (protein-energy undernourished but supplemented with vitamin A) fared perceptibly better with an equivalent load of infection. Control ad libitum fed littermates were able to restrict the infection and neither high parasitemia nor death was noted in this group. Oral supplements of retinyl acetate to vitamin A deficient rats enabled the animals to recover from infection. A subclinical dose of 500 parasitized RBC given at an early stage of the vitamin A deficiency precipitated the deficiency symptoms at a faster rate and led to the development of higher order of parasitemia in these rats beginning from the 10th day after infection as compared to pair fed controls. The yield of glass adhering cells obtainable from peritoneal exudates was low in deficient rats. In vitro experiments further suggest a decrease in the capacity of the glass adhering peritoneal exudate cells in vitamin A deficient mice to clear the infection. This capacity was improved by addition of non glass adhering cells from sensitized control mice.