Immunity to intra-erythrocytic protoza.

Intra-erythrocytic inclusion bodies were seen in Giemsa-stained smears of peripheral blood from mice infected with Babesia microti. These bodies, which were probably the pyknotic remnants of dead protozoa, increased as parasitaemia fell and the animal recovered. It is suggested that a soluble mediator liberated by cells of the host during infection penetrates the red blood-cell and leads to degeneration of the parasite.

Morphological features in a neutral lipid storage disease.

The morphological changes in a patient with a generalized storage disease characterized by the intracellular deposition of neutral lipid are described. There is widespread accumulation of lipid in the cytoplasm of many cells and in occasional nuclei. Diagnosis may be facilitated by the recognition of clear vacuoles in the cytoplasm of granulocytes in blood films.

Predominance of synovial fluid lymphocytes in early rheumatoid arthritis.

Evaluation of 158 synovial fluids, mainly from patients with rheumatoid arthritis (RA) and the crystal deposition fiseases (CDD), revealed differences in the differential white blood count and numbers of cytoplasmic inclusion bodies (CIB) present. Lymphocytes and CIB were increased in RA, suggesting a different pathologic mechanism from that of CDD. Lymphocyte-like cells contained CIB implying phagocytic capability.

Production, isolation, and partial characterization of three foot-and-mouth disease virus temperature-sensitive mutants.

Three high temperature-sensitive (ts) mutants of foot-and-mouth disease virus were characterized by their relative abilities to grow at 33 or 38.5 C, to kill infant mice, to infect guinea pigs, and to produce foot-and-mouth disease in steers. Mutants ts-24 and ts-42 did not grow at 38.

Planned splenectomy in treatment of idiopathic thrombocytopenic purpura.

The results of a policy of treatment in idiopathic thrombocytopenic purpura based on previous observations on the natural history of the disease and its response to corticosteroids are described. The results of splenectomy were better when the history was less than 100 days. Three patterns of response to splenectomy were observed: complete remission, symptomatic remission, and relapse.

Enhancement of primary antigen-specific resistance in infant mice with divinyl ether-maleic anhydride.

The early response of infant mice to foot-and-mouth disease viral antigens, measured by greater resistance and increased serum-neutralizing antibody, was enhanced by divinyl ether-maleic anhydride (DVE/MA). Preparations of known antigen concentration were used to study various parameters influencing this enhancement. Resistance and antibody levels were increased when DVE/MA was administered with aqueous or oil-emulsified antigens, whether given separately or mixed with the antigens, but was dependent on the dose and route of the DVE/MA and antigen.

Morphological observations on the cellular and subcellular destination of intravenously administered liposomes.

The cellular and subcellular fate of intravenously administered liposomes was traced by light and electron microscopy, using nitroblue tetrazolium (NBT) as a marker. Liposomes were found almost exclusively within phagocytic vacuoles of cells of the reticuloendothelial system. Fusion of lysosomes with phagocytic vacuoles and liposomal degradation were clearly visible.

Observations of cattle, goats and pigs after administration of synthetic interferon inducers and subsequent exposure to foot and mouth disease virus.

Polyriboinosinic-polyribocytidylic acid (poly [rI.rC]) was administered intravenously to 11 cattle and 13 goats in doses of 0.25 to 4.

Enhancement, by two carboxylic acid interferon inducers of resistance stimulated in mice by foot-and-mouth disease vaccine.

Simultaneous injection of divinyl ether-maleic amhydride (DVE/MA) or itaconic-acrylic acid and foot-and-mouth disease virus vaccine enhanced the survival of infant mice to subsequent injections of virus. This enhanced resistance was obtained even with doses of interferon inducers which, when administered alone, failed to protect the mice. There was some increase in serum-neutralizing antibody in mice 7 days after injection of DVE/MA and vaccine, as compared with mice given vaccine alone, but there was no clear connection between antibody level and amount of DVE/MA administered.