The maintenance of L. simondi infections in nature from season to season among ducks is dependent upon the reservoir of parasties made available to the arthropod intermediate host by chronically infected birds. It has been known for some years that ducks which survive initial infestation during the summer relapse the following spring after an intervening winter period of parasitic dormancy. Naturally infected White Pekin and hybrid ducks were secured at the UMBS during the summers of 1948 and 1949. Laboratory studies conducted during the winter-spring periods of 1948-49 and 1949-50 with these ducks have shown this spring relapse to be consistently associated with the onset of reproductive activities among ducks infected the previous summer. Parasites were found only sporadically and in very low number during the winter months prior to this rise in parasitaemia. Preliminary observations indicated that within a matter of days after the ducks commenced egg-laying, the level of parasitaemia began to rise and that parasites were to be found thereafter in the peripheral circulation for periods ranging up to six months. As a result of photoperiodic manipulation it has been possible, within certain limits, to speed up or to delay the onset of sexual maturation and thereby to speed up or delay the occurrence of the parasitic relapse in ducks coming into their first breeding season. Birds exposed to 16 hours of artificial light per day during the winter went into egg-laying earlier and relapse earlier parasitologically than did controls under standard animal room conditions of light or ducks which had been exposed to only five and one half hours of artificial light per day. Studies designed to elucidate the relationship between the relapse of the haemosporidian infection and the physiological status of its avian host are still in progress and, in general, suggest that some hormonal mechanism probably underlies this phenomenon.