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PubMed1965

GENETIC MAPPING OF VI AND SOMATIC ANTIGENIC DETERMINANTS IN SALMONELLA.

Johnson, E. M. (Walter Reed Army Institute of Research, Washington, D.C.), Barbara Krauskopf, and L. S. Baron. Genetic mapping of Vi and somatic antigenic determinants in Salmonella. J. Bacteriol. 90:302-308. 1965.-The Vi antigen and somatic antigen 9 were transferred to Salmonella typhimurium recipients by mating with S. typhosa Hfr TD-7, and the genetic determinants of these antigens were located. A gene responsible for Vi antigen expression, ViB was found to be associated with the inlpurA-pyrB linkage group, and the order ViB-inl-purA-pyrB was established. The determinant of somatic antigen 9 was found closely linked to the his gene, and cotransduction of these determinants was accomplished with phage PLT-22. Moreover, all conjugation and transduction hybrids which received the somatic antigen 9 determinant concurrently lost somatic antigen 4. Similarly, S. typhosa hybrids produced by transfer of his and the gene for somatic antigen 4 from S. typhimurium Hfr B2, or by cotransduction of these genes with PLT-22, also lost somatic antigen 9. These results indicated that the genetic determinants of the somatic antigen 9 and 4 are probably allelic. A second Vi antigen determinant, ViA, located near his, was discovered in matings of S. typhimurium Hfr B2 with a Vi-negative S. typhosa recipient. Vi-positive S. typhosa hybrids were obtained from this cross in which neither parent expressed the Vi antigen, indicating that this Vi determinant of S. typhosa is present also in S. typhimurium.

Agglutination↗
PubMed1967

Failure of bacterial endotoxin to produce the generalized Shwartzman reaction in the Syrian hamster.

The ability of bacterial endotoxin to produce the generalized Shwartzman reaction (GSR) in pregnant and nonpregnant hamsters was investigated. Endotoxins prepared from Escherichia coli O127:B8, Salmonella enteritidis, and S. typhosa 0-901 did not produce the GSR in nonpregnant hamsters. Injection of lead acetate did not make the hamsters susceptible to the GSR producing effects of endotoxin. Endotoxin administered to hamsters on either or both the 14th and 15th day of the 16-day gestation period caused fetal death, but did not provoke the GSR. The immunization of hamsters with boiled suspensions of gram-negative bacteria isolated from hamster feces did not protect against the GSR produced in pregnant hamsters by the injection of the antimitotic drug colchicine late in the gestation period. It appeared that colchicine was acting to produce the GSR by a mechanism other than the release of endogenous endotoxin through the damaged intestinal wall. Ascitic fluid, amniotic fluid, and serum obtained from pregnant hamsters developing the GSR after the administration of colchicine did not provoke the GSR in other pregnant hamsters.

Acetates↗
PubMed1960

A method for titrating endotoxic activity in the skin of rabbits.

The primary inflammatory response of rabbits to intradermal injection of bacterial products has been used as the basis of a sensitive assay for endotoxins. Injection of materials into the skin of the lateral surfaces, rather than the ventral surface of the abdomen, was essential. The method was evaluated by comparison with the mouse toxicity test. Statistical examination revealed an excellent correlation between the mean threshold dose for producing skin lesions in rabbits (SLD(50)) and the median lethal dose for mice (LD(50)). For potent endotoxins (LD(50) = 0.2-0.3 mg.) the skin test dose was about one-thousandth of the lethal dose for mice. Thereafter the LD(50) increased in the proportion of about 0.3 mg. per 1 microg. increase in SLD(50). The method of testing was devised for endotoxins prepared in various ways from Salmonella enteritidis and S. typhosa but was directly applicable to endotoxins from several other species of enteric Gram-negative bacteria.

Animals↗
PubMed1962

Production of tolerance to the toxicity of Candida albicans by nonfungal materials.

Hasenclever, H. F. (National Institute of Allergy and Infectious Diseases, Bethesda, Md.) and W. O. Mitchell. Production of tolerance to the toxicity of Candida albicans by nonfungal materials. J. Bacteriol. 84:1325-1329. 1962.-Tolerance in mice to the toxic manifestations of viable Candida albicans cells was elicited by injections of Salmonella enteritidis or S. typhosa lipopolysaccharides, or complete Freund's adjuvant. The greatest host stimulation occurred when the lipopolysaccharides were given 1 or 6 days before intravenous challenge. The highest level of tolerance produced by intraperitoneal preinfection with C. albicans was found when the yeast cells were injected 6 days before challenge. Older mice appeared to require larger amounts of endotoxin to demonstrate toxicity tolerance. Protection in mice that received both lipopolysaccharide injections and C. albicans intraperitoneal preinfection was slightly higher than in those mice given only the individual components.

Animals↗