SYNOPSIS. An electron microscope study of Leishmania donovani revealed major differences between the intracellular leishmanial and the extracellular leptomonad stages. Parasites were also removed from infected hamster spleen, inoculated into cultures, and examined at intervals during incubation in order to follow changes during the transformation from one stage to the other. Prominent changes are evident primarily in the kinetoplast and the nucleoli after several hours of cultivation when the parasite is in an intermediate stage of transition. The kinetoplast, a composite organelk containing DNA and cristae mitochondriales, is a regular, sausage‐like structure in the leishmanial stage, but becomes irregular and enlarges extensively after a few hours in vitro, developing branches that are mitochondrial in nature and which, very likely, become new mitochondria. In the nucleus, significant nucleolar changes occur. The two homogeneous nucleoli characteristic of the leishmanial stage merge during transformation into one which is larger, less compact, and composed of small centrally located granules about 100 Å in diameter and larger particles over 200 Å in diameter at the periphery. These transformations of the kinetoplast and nucleolus are undoubtedly expressions of adaptive changes in the metabolic pattern of an intracellular parasite transferred to a markedly different extracellular environment of much lower temperature. It was also found that the leishmanial stage of the parasite has two unit membranes which extend over the flagellum and the flagellar pocket; the intermediate stage and the leptomonad have only a single membrane. Furthermore, some leishmanias in spleen cells were found to be covered by a capsule‐like structure formed by the deposition of fine granular material between the two unit membranes. Since two to four organisms were occasionally found within such capsules, it is possible that encapsulation is a preparatory step for reproduction.

Host IgG is a component of the surface coat of Trypanosoma lewisi; it is specifically acquired during infection in the rat, concomitant with a rise in titer of trypanostatic (ablastic) activity of host serum. Host IgG was eluted from trypomastigotes at 7 to 9 days postinfection with a high salt-low pH buffer. Surface coats and trypanosome ultrastructure were not notably altered by the elution procedure, as determined by electron microscopy. Rat IgG was removed and purified from the trypanosome eluates on an immunoadsorbent column made with the IgG fraction of anti-rat IgG serum coupled to Sepharose beads. Concentrated column eluates, by comparison with a standard, were shown to be rat IgG by immunoelectrophoresis and SDS polyacrylamide gel electrophoresis. As a control, IgG from normal rat serum was purified by the same technique. IgG-negative trypanosomes harvested from immunosuppressed rats bound IgG purified from surface coats of trypanosomes, but not IgG purified from normal rat serum, as demonstrated by subsequent labelling with FITC-conjugated, rabbit anti-rat IgG. The IgG purified from surface coats inhibited the reproduction of T. lewisi in an in vitro assay, but purified, normal IgG did not. These data show that antigen-specific host IgG, adsorbed to the surface of T. lewisi, is ablastic antibody.

No abstract

No abstract

No abstract