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SYNOPSIS Ultrastructure of the plasmodium wall and of sporogenesis were studied in Myxosoma funduli Kudo infecting the gills of Fundulus kansae (Garman). Plasmodia were located within the lamellar tissues adjacent to sinuses and capillaries. The plasmodium wall consisted of a single unit membrane which was continuous with numerous pinocytic canals extending into the parasite ectoplasm. The plasmodium membrane was covered by a surface coat of almost uniform thickness which prevented direct parasite‐host cell contact. Numerous generative cells and cell aggregates, representing early stages of spore development, were seen in immature plasmodia. Later stages of spore development, including mature spores, were observed in older plasmodia. Sporogenesis was initiated by envelopment of one generative cell, the sporont, by a 2nd, nondividing cell, the envelope cell. The sporont and its progeny proceeded through a series of divisions until there were 10 cells, all compartmentalized within the envelope cell. Subsequently, the 10 cells became structurally differentiated and arranged into two 5‐celled spore‐producing units, each consisting of 1 binucleate sporoplasm and 2 capsulogenic cells, all surrounded by 2 valvogenic cells. Observations of later developmental stages revealed the major events of capsulogenesis, valvogenesis, and sporoplasm maturation, which occurred concomitantly during spore construction.

Ultrastructural aspects of interlamellar Henneguya exilis infections in channel catfish are reported. The plasmodium wall of this form differs from that of other species in that it is composed of two outer unit membranes which give rise to a zone of numerous pinocytic canals. Single-membraned canals appeared to be a stable feature of the wall while double-membraned canals are interpreted as those actively carrying out pinocytosis. Evidence suggests that host cellular cytoplasm as well as interstitial material is taken in by plasmodia. Plasmodium wall integrity, aggregation of parasite ectoplasmic components, numbers of pinocytic canals, and number of mitochondria proximal to the wall vary among different plasmodium profiles and may be related to plasmodium maturity. The parasite causes extensive hyperplasia of basal cells, which in turn replaces most other cell types found in noninfected gill filaments. Cytoarchitectural differences between basal cells of noninfected filaments and basal cells adjacent to plasmodia include significantly shorter microfilament bundles in the latter.

The inter- and intralamellar types of Henneguya exilis Kudo (Myxosporida) infections from channel catfish are similar in spore structure and sporogenesis, but differ in the structure of their plasmodium wall and surface coat and in their relationship with the host cells. The 2 clinical types differ also in the sites of development and growth patterns of plasmodia within a gill filament. Interlamellar plasmodia are limited by 2 outer unit membranes which give rise to both single-and double-membraned pincytic canals. Intralamellar plasmodia are limited by a single outer unit membrane which gives rise to single-membraned pinocytic canals. Interlamellar plasmodia are covered by a fine granular coat of highly variable thicknesses; in some regions there is direct contact between the parasite and cells of the host. There is some evidence that host cell cytoplasm as well as interstitial material are taken in by interlamellar plasmodia. In contrast, intralamellar plasmodia are covered by a fine granular coat of almost uniform thickness, which prevents direct contact between the parasite and cells of the host; probably only interstitial material is taken by these plasmodia.

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