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SMEDI and hog cholera viruses were shown to have marked effects upon the survival of the embryo (from conception to 30 days of gestation), the fetus (from 30 days of gestation until birth), and the neonatal pig (from birth until five days after birth). Embryonic infection was characterized by death and absorption of the embryo and in some instances the return to estrus after an irregular estrous cycle. Embryonic infection also may have been responsible for the development of some abnormal pigs. Fetal infection caused death with mummification of one or more fetuses and occasionally all fetuses in the uterus. Infection established in early gestation produced effects on the fetus which apparently persisted until after birth and varied from a persistent viremia (as in hog cholera infection) to an undefined lack of resistance in the newborn (as in SMEDI virus infection). Hog cholera vaccinal virus was the more virulent of the two virus types and reacted somewhat like rubella virus, in that infection apparently could be established in the fetus even in middle trimester of pregnancy, and possibly later. SMEDI viruses, in contrast, were less virulent and were most pathogenic when the dam was infected during the first 30 days of pregnancy. Immunity against either virus could be established in the nonpregnant gilt and was most effective in preventing intrauterine infections with that virus. However, with as many as 10 enteroviruses (five are known to cause intrauterine infection) it was believed that maintaining a closed breeding herd and introducing new stock into contact with the breeding herd at least 30 days before breeding time might be a safer means of control.