Taenia taeniaeformis (Cestoda) in the rat: ultrastructure of the host-parasite interface on days 1 to 7 postinfection.

Ultrastructural observation were made on the host-parasite interface from 1 to 7 days postinfection (DPI) with Taenia taeniaeformis in the rat. Over this period the organism developed from a multicellular oncospheral mass, equivalent in size to a host hepatocyte, into a fluid-filled, grossly visible vesicle, the walls of which showed the arrangement of syncytial tegument, cytoplasmic bridges and subtegumental cell bodies typical of older cestodes. Microvilli, often branched, extended from the free, tegumental surface of the parasite from 1 DPI onwards. Fragments of the microvilli were pinched off distally, and became segmented and distended. Some were seen in intercellular spaces as far as 40 micrometers from the free tegumental surface; others were ingested by nearby host phagocytic cells, and appeared to swell and rupture within phagosomes. Microvillar branching was less frequent after 4 DPI and the microvilli became progressively shorter. By 7 DPI the tegumental surface had become irregular and the microvillar bases were broad and knoblike. Electron-dense deposits were present on the outer membrane of microvilli, the tips of which had become truncated or globular. Although phagocytic host cells were seen in migratory tracks and in contact with some organisms as early as 1 DPI, they caused no detectable damage to the parasites. However, many host cells, including hepatocytes and endothelial cells, were injured or destroyed; their contents contributed to the debris surrounding the parasite at all stages. Inclusions, probably lipid, appeared within the tegument and subtegumental cell bodies from 3 DPI onwards, and similar droplets were seen in adjacent host cells. The great increase in surface area of postoncospheral forms over the first week of infection, augmented by the display of multiple, microvillar projections, may provide not only or the absorption of nutrients required for growth, but also for the enhanced release of factors that affect survival of host cells and stimulate immunological defense mechanisms.