The former paper (Huff and Marchbank, 1955) clearly indicated a general pattern among seven host-parasite combinations involving avian malarial parasites; this pattern being a rapid and continuing fall in the infectivity of gametocytes for mosquitoes during the course of infection in the bird. An analysis has been made in the present paper of the factors which might contribute to this change in infectivity of gametocytes. The aim has been the testing of two hypotheses to account for the decrease in this infectivity, namely (1) that it was due to a deficiency in the host which developed as the infection progressed, or (2) that an immune mechanism was responsible for the decrease. The following substances were administered to birds during the course of their infections: uninfected whole blood, coenzyme A, ferrous sulfate, sodium glutathione, calcium pantothenate, and sucrose. These substances did not enhance the infectivity of the gametocytes. In two experiments the hosts were bled daily during the course of their infections. No appreciable differences in oocysts numbers or infectivity values (oocyst-gametocyte ratios) were observed between the bled birds and the controls. Two experiments were performed testing whether mixed infections would yield evidence of a greater depleting effect. The results were not clearly conclusive but were suggestive that at least the principal cause of decrease in infectivity of the gametocytes was not a depleting effect. In one experiment in which blood infected with P. gallinaceum was transfused to a naturally immune host (duck) there was an appreciable increase in infectivity values of the mosquitoes. Two attempts to demonstrate effects on the gametocytes by the passive transfer of serum from hyperimmunized birds gave negative results. Two transfusion experiments were carried out in which infected blood was transmitted to birds with acquired immunity. No detectable change was observed in infectivity of gametocytes in one of these, while there were indications of a rapid fall in their infectivity in the second. Four experiments (three with P. gallinaceum in chickens and one with P. fallax in turkeys) testing the effect of immunization with killed parasites prior to the infecting inoculation uniformly indicated an early, more rapid fall in infectivity of gametocytes in the immunized than in the control animals. The results of all experiments can better be explained on the hypothesis that active immunity is the cause of decreasing infectivity of gametocytes than one in which this effect is assumed to result from a depletion effect of infection on the host. As in the former paper the lowering in mean numbers of merozoites produced by segmenters observed by other investigators during the crisis was not observed. However, significant differences were observed between the mean numbers of merozoites of infections in birds on adequate diets and those deficient in pantothenic acid.