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In an attempt to elucidate the nature of the endotoxin-altering reaction, normal sera from animals of different phylogenetic levels were tested for capacity to inactivate endotoxin from Escherichia coli. Inactivation was assayed quantitatively by reduction in capacities of endotoxin to be precipitated by homologous antiserum and to kill mice, and by changes in its immunodiffusion pattern. Sera from species of Mammalia, Aves, Reptilia, Amphibia, Osteichthyes, and Chondrichthyes were shown to have similar capacities to inactivate endotoxin, whereas sera from cycIostomes and hemolymphs from crustaceans altered endotoxin only slightly or not at all. In general, the qualitative nature of the endotoxin-altering reaction by these sera was similar in that the reaction was inhibited by calcium (100 μmoles/ml) and, excepting carp and turtle sera, it was heat stable (56 C for 30 min). Inactivation was greater when endotoxin was incubated with serum at 37 C rather than at 3 C or 26 C. It is postulated that an endotoxin-altering mechanism similar to that of human serum originated phylogenetic ally between hagfish and shark. [ABSTRACT FROM PUBLISHER]

Two isolates of Candida tropicalis resistant to amphotericin B were obtained from a patient with pyelonephritis due to Candida. Isolate RI showed a twofold increase in resistance to amphotericin and to nystatin when compared with two sensitive strains of C. tropicalis and one of Candida albicans. Isolate R2 was extremely resistant to amphotericin B, etruscomycin, and nystatin. The sterols of RI, R2, and the sensitive strains of Candida were compared qualitatively by ultraviolet spectrophotometry, thin-layer chromatography, gas-liquid chromatography, and the Liebermann-Burchard reaction. Both polyene-resistant isolates had altered sterols. Rl contained an unidentified Δ5,7 sterol and little, if any, ergosterol; R2 was totally lacking in Δ5,7 sterols. Chromatographic analyses showed that R2 had three sterols that were distinguishable from lanosterol. It is concluded that the resistance of isolates R 1 and R2 to polyene antibiotics is a consequence of their altered sterol composition. [ABSTRACT FROM PUBLISHER]

The effect of tetracyclines on phagocytosis by human neutrophils was studied. Human leukocytes incubated with tetracycline hydrochloride or doxycycline in vitro showed a decreased capacity to phagocytize yeast and bacteria. Furthermore, leukocytes harvested from healthy volunteers after ingestion of tetracycline also demonstrated decreased phagocytic capacity for yeast. [ABSTRACT FROM PUBLISHER]

Secretion of fluid by rabbit ileum and the relation of the secretion to intestinal adenyl ate cyclase, phosphodiesterase, and cyclic adenosine 3′,5′-monophosphate (cyclic AMP) were compared in intestinal segments exposed to the enterotoxin of Shigella dysenteriae and/or the enterotoxin of Vibrio cholerae. Although there were some similarities in the gross appearance and kinetics of fluid secretion induced by the two toxins, the biochemical pathways appeared to differ. Shigella enterotoxin applied in vivo or to in vitro intestinal preparations did not produce the marked increase in adenylate cyclase or cyclic AMP noted after the application of V. cholerae enterotoxin. Moreover, despite known cytotoxic properties of shigella enterotoxin, prior treatment with this toxin did not prevent the intestine from responding to V. cholerae enterotoxin. [ABSTRACT FROM PUBLISHER]

Noninvasive, toxigenic Vibrio cholerae and the invasive enteropathogens Shigella flexneri and Salmonella typhimurium stimulate secretion of fluids in rabbit ileal loops. To assess similarities in secretory mechanisms and the possible involvement of prostaglandins in secretion, indomethacin (a rapid, intense inhibitor of prostaglandin synthesis) was used. Fluid secretion mediated by S. typhimurium was completely inhibited by treatment with indomethacin. Secretions stimulated by S. flexneri, V. cholerae, and cholera toxin were reduced by 40%–60%. Indomethacin affected neither the local invasiveness of S. typhimurium or S. flexneri nor the peripheral dissemination of S. typhimurium. Therefore, indomethacin dissociated the invasive process from the secretory event. These data are consistent with the participation of prostaglandins in these enteropathogen-stimulated secretory states. This conclusion must, however, be regarded as tentative in view of other possible mechanisms of indomethacin action. [ABSTRACT FROM PUBLISHER]

One hundred twenty children infected with coxsackieviruses B-3 and B-4 in the fall of 1968 were later studied for evidence of diabetes mellitus. Specimens of fasting plasma were obtained from 94 of the children and were tested for glucose and insulin levels and, in many cases, for residual antibody to B-3 and B-4. There were no instances of hypoglycemia, hyperglycemia, or hypoinsulinism. Five children with slightly elevated insulin levels were given the oral glucose tolerance test, and all displayed normal tolerance. Twenty-two children had histories of diabetes in their families, and seven children had shown evidence of reinfection by B-3 and B-4 in the 1968 study; yet none of the 94 subjects with complete data and none of the 26 who had serum samples taken in 1969 and current histories had any record of diabetes symptoms or positive tests. Our data do not support the hypothesis that these viruses are related to the onset of juvenile diabetes. [ABSTRACT FROM PUBLISHER]

The method of preparation of typhoid vaccine influenced the adhesion of Vi antigen to the bacterial cell and the serologic and protective activity of the vaccine. The acetone-inactivated vaccine 6A and vaccine L, inactivated by heat and phenol, possessed approximately equal amounts of Vi antigen, extractable in 0.85% NaCl; the antigens had equal protective activity for mice. After extraction, bacteria in vaccine 6A retained a significant amount of Vi antigen, which was demonstrable by serologic and immunologic tests, whereas the bacteria in vaccine L retained practically no Vi antigen. Vaccine 6A decreased in potency only 2.5-fold, and vaccine L decreased ninefold. Heating at 56 C during preparation of vaccine L did not affect the non-Vi protective factor(s) or the protective activity of extracted Vi antigen. The superior potency of vaccine 6A was attributed to fixation of the Vi antigen to the bacteria by acetone. Treatment of bacterial cells with acetone slightly reduced endotoxicity for mice and mouse lymphoid cells, but the difference between vaccine 6A and vaccine L was not significant. The results reflect the variable differences in the reactions of man to vaccine K and vaccine L observed in the field trials. [ABSTRACT FROM PUBLISHER]

Tetracycline, in concentrations common during therapy, markedly depressed migration of human leukocytes in vitro. Sera from 12 of 13 volunteers who received oral tetracycline after infection with Mycoplasma pneumoniae inhibited leukotaxis of normal leukocytes. Random migration and chemotaxis of leukocytes from two additional subjects were depressed for up to 24 hr after a single 1-g dose of tetracycline. When tetracycline was tested over a wide range of concentrations, leukotaxis was depressed by lower concentrations (0.01–10 µg/ml) but was stimulated by higher concentrations (30–300 µg/ ml) of the antibiotic. Metabolic studies revealed that production of leukocyte lactate was elevated significantly in the presence of a high level of tetracycline. The mechanisms by which tetracycline affects leukotaxis are not known. [ABSTRACT FROM PUBLISHER]

Methods have been developed for the recognition of toxin production by individual colonies of Vibrio cholerae strain 569B Inaba and certain other (but not all) strains of V. cholerae. Following mutagenesis of strain 569B with nitrosoguanidine, mutants that produced less or no detectable enterotoxin were isolated. One mutant, which did not elaborate any toxin detectable in Oakley-Fulthorpe tests or in the rabbit skin test, was completely avirulent for infant rabbits, although it was prototrophic and colonized their intestines. A strain of V. cholerae biotype El Tor produced a toxin that lacked an antigenic determinant found in toxin elaborated by strain 569B Inaba. [ABSTRACT FROM PUBLISHER]