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SYNOPSIS. Observations were made on the differentiation of fine structure during sporogonic development of Plasmodium berghei. The oocyst in the process of sporozoite formation is an encapsulated structure 30‐40 μ in diameter. It typically develops while in an extracellular position, attached to the basement membrane of the mosquito midgut and projecting into the mosquito hemocoel. Occasionally, however, ookinetes passing thru the midgut epithelial cells may become impacted within a cell so that the resulting oocyst develops intracellularly. Each oocyst has a large differentiating region, the sporoblastoid body. This body contains large dividing nuclei which are Feulgenpositive, and a cytoplasm which includes mitochondria, dense rodlike structures, cytoplasmic membranes, cisternae and vacuolar structures, Golgi material, and ribosomes which are both free and membrane‐associated. Sporozoite budding takes place along the surface of the sporoblastoid body. Bits of a new membrane condense under the plasma membrane which bounds the sporoblastoid body. These 2‐membraned sites then bulge out, continue to elongate, and eventually become sporozoites. The various nuclear and cytoplasmic components of the sporoblastoid body are passed into the sporozoites during their elongation. In addition, the sporozoite develops a system of elogate, subpellicular microtubules, possibly contractile in function. The pellicle of the sporozoite is broken by an opening, the cytostome (micropyle). The anterior end is truncate.

The genetic basis of virulence in a line (YM) of Plasmodium yoelii yoelii was investigated in a cross with a mild line (A/C). The blood forms of the virulent line developed extensively in mature erythrocytes of mice, causing death of the host within 7 days; infections with the mild line were normally restricted to reticulocytes, infected animals recovering after three weeks. Lines YM and A/C differed additionally in enzyme and drug-sensitivity markers. Studies on infections established from each line alone from sporozoite mixtures of the two lines and from the cross between the lines showed that the appearance of virulence had been caused by a genetic change in the parasite, and not by other factors such as a concurrent infection with another organism. An analysis of the characters of 56 clones derived from the cross showed that the virulence character had undergone recombination with the other markers, and appeared to be inherited in Mendelian fashion. Three clones exhibited atypical virulence, although it was not clear whether this had been produced by genetic recombination.

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