Studies of the chronic, winter parasitemia during the interval between the primary attack and the relapse in Leucocytozoon simondi infections in ducks have indicated that although parasites could be found only sporadically and in low number, there was no month (October through January) in which all slide examinations were consistently negative. Moreover, the discovery that immature parasites do occur during this period has served to strengthen earlier suggestions that some schizogony probably occurs during the winter months. The 3-year investigation of the spring relapse phenomenon in L. simondi infections has demonstrated that relapse is associated with the onset of reproductive activity in the avian host. This appears to represent the first complex in which it has been possible to establish a relationship between the relapse in a hemosporidian infection and a naturally occurring change in the physiology of the host. The results of these studies may be outlined as follows: (1) under ordinary laboratory conditions in Baltimore, parasitic relapses commenced in February and March; (2) the reappearance of parasites at this time was not the result of reinfection; (3) not all birds relapsed, and those which failed to do so are presumed to have overcome their infections ( self-cure); (4) in the female, relapse invariably occurred in conjunction with the onset of reproductive activity as manifested by the beginning of egg laying; (5) relapses occurred in males at about the same time as did those in females; (6) by subjecting females to increased hours of artificial light per day in the fall and winter it has been possible to precipitate egg laying several weeks to several months sooner than its time of occurrence in controls, with a concomitant shift in the time of onset of the parasitic relapse. There is no evidence that light per se induces relapse; it does, however, bring about the particular physiological condition in the host which permits of the acceleration of parasitic activity. Although no attempt has been made to induce premature relapse in drakes, the mere fact that they do relapse is considered sufficient evidence that egg laying in the female is probably not the fundamental cause of relapse, although it may represent a key to the underlying mechanism whereby the host is rendered vulnerable to renewed parasitic activity. In view of the complexity of the physiological changes which accompany sexual maturation in birds, renewed parasitic activity may (1) represent direct stimulation of the parasite by some hormonal or metabolic state, (2) involve alterations in the protective mechanisms of the host induced by this hormonal or metabolic condition, or (3) be a product of a dynamic complex of both (1) and (2). It is postulated that the anterior pituitary is probably involved in this process, since its functions are so basic to the physiological changes that accompany sexual maturation in the male as well as female. One of the characteristics of the observed relapses has been the very low level of parasitemia by which they are represented. It is estimated that the most intense degree of parasitemia in relapse may be but one-thousandth that of the primary attack. A second characteristic common to the relapses is that they were regularly initiated by relative and absolute increases in mature parasites, with immature parasites scarce, if present at all, during the first month of relapse. Several alternative explanations are presented, but this matter remains largely unresolved. In the final analysis, the association between relapse and the onset of reproductive activity of the host may be regarded as an adaptation of the parasite, and one with particular epizootiological significance. Thus, relapse serves to render a pool of parasites immediately available to the newly-emerging vector, while breeding activities on the part of the host shortly provide a population of young ducklings which are readily susceptible to infection.