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At least 343 records · Page 19Linked to original sources
PubMed1972

Stable reagent for the detection of antibody to the specific fraction I antigen of Yersinia pestis.

A stable hemagglutinating antigen for detection of fraction I (FR-I) antibody of Yersinia pestis (Pasteurella pestis) is described. The antigen was prepared by sensitizing tanned, pyruvaldehyde-treated sheep erythrocytes (PAT SRBC) with FR-I antigen. Preliminary standardization by titration of each lot of FR-I was required to minimize the effect of molecular heterogeneity of specific FR-I antigen and to eliminate nonspecific reactions caused by the presence of a minor antigenic contaminant. In tests with sera from rabbits, dogs, and humans, FR-I PAT SRBC were as reactive as the previously employed standard antigen, FR-I-sensitized tanned erythrocytes. Fluid suspensions of FR-I PAT SRBC stored at 4 C for 3 months, or lyophilized preparations stored at ambient temperature for 6 months, showed no loss in antigenic activity.

Aldehydes↗
PubMed1973

Pathogenicity and immunogenic efficacy of a live attentuated plaque vaccine in vervet monkeys.

A live attenuated Yersinia pestis (Pasteurella pestis) vaccine strain designated EV51f, which had been passaged through guinea pigs previously treated with ferrous sulfate, was shown to be pathogenic for African green vervet monkeys (Cercopithecus aethips pygerythrus), but not for guinea pigs. The bacilli multiplied in the monkeys, as shown by positive blood cultures, caused an elevation of white cell counts and rectal temperatures, and resulted in death of 26% (13/50) of animals. Postmortem findings of these animals were typical of bubonic-septicemic plague. This vaccine did not cause deaths in 50 guinea pigs even in doses up to 100 million viable bacilli inoculated subcutaneously. It is suggested that the virulence of an attenuated Y. pestis strain which does not produce pigment on a defined medium containing hemin, but possesses all other known virulence determinants, is dependent on the availability of iron in vivo. The serological response of the monkeys as determined by the hemagglutinating and mouse protective antibodies was high one month after vaccination and also in guinea pigs, as shown by virulent challenge. This antibody level declined in monkeys over a period of nearly 6 months, and a decline in immunity was confirmed by virulent challenge which resulted in the death of 30% of vaccinated monkeys. The level of immunity in monkeys did not appear to be related to the dose of vaccine.

Animals↗
PubMed1956

Studies on resistance to bacterial infections in animals infected with Rickettsiae.

Data are presented, demonstrating that infection with Rickettsia typhi brings about a reduction of the death rates and a prolongation of the time of survival in animals subsequently challenged with Pasteurella pestis or Pasteurella tularensis. This interference with bacterial infection by previous rickettsial infection does not appear immediately after injection of the rickettsiae; it begins to appear around 16 hours after this injection and becomes more marked during the first 96 hours; later it decreases. The phenomenon is essentially a local tissue reaction with weaker systemic effects. The phenomenon of interference can be overcome by challenge with too large a number or too virulent a strain of bacteria. A strain of P. pestis subjected to 10 passages through mice infected with Rickettsia typhi failed to develop resistance to the interfering activity of the latter microbial species. This does not rule out, but might be evidence against, an assumption that the interfering action is due to antibiotic effects from the rickettsiae.

Animals↗
PubMed1962

Gluconate metabolism of Pasteurellapestis.

Mortlock, R. P. (U.S. Army Chemical Corps, Frederick, Md.). Gluconate metabolism of Pasteurella pestis. J. Bacteriol. 84:53-59. 1962.-During a study of gluconate metabolism by a virulent strain of Pasteurella pestis, evidence was obtained for the presence of gluconokinase, 6-phosphogluconate dehydrogenase, transketolase, and 2-keto-3-deoxy-6-phosphogluconate dehydrase in cell-free extracts. A study of the products of 6-phosphogluconate degradation by extracts indicated that 6-phosphogluconate was metabolized by both the 6-phosphogluconate dehydrogenase-transketolase pathway and the Entner-Doudoroff pathway. No evidence could be obtained for the presence of an active glucose-6-phosphate dehydrogenase.

Carbohydrate Metabolism↗
PubMed1977

Cyclic kinetics and mathematical expression of the primary immune response to soluble antigen. VII. The conveyer hypothesis and its mathematical expression.

The conveyer hypothesis is based on the fact that because of clone predetermination, antibody production takes place in an organism without the presence of antigen as a result of natural cell differentiation. Soluble antigen is an analogue of a specific mitogen which gives rise to reproduction mainly of cells carrying on their surface the immunoglobulin receptors to the given antigen. The mathematical model of the conveyer hypothesis takes into account the initial conditions, among them the background level of antibody-producing cells before injection of a soluble antigen, migration of precursor cells in the draining lymphoid organ, and the rate of precursor differentiation, including the rate of the change of the immunoglobulin receptor number on the cell surface. Changes of antigen concentration in blood determine the intensity of precursor proliferation. Comparison of real experiments (intraperitoneal injections of capsular antigen of Pasteurella pestis into inbred mice) with calculations done on the basis of the developed mathematical model shows a definite qualitative resemblance with the kinetics of antibody-producing cells and free antibodies as well as with the decrease of free antigen concentration in blood. In spite of some differences between model experiments and real experiments the conveyer hypothesis and its mathematical model appear suitable for describing the primary immune response of mice immunized with low doses of capsular antigen of Pasteurella pestis.

Animals↗
PubMed1971

Mutations Influencing the Assimilation of Nitrogen by Yersinia pestis.

Cells of 20 isolates of Yersinia (Pasteurella) pestis exhibited an unusual nutritional requirement which could be fulfilled by glycine or l-threonine. Meiotrophic mutants which required neither of these amino acids (Gly/Thr(+)) were isolated from cultures of all 20 strains at a frequency of 10(-7). Wild-type and Gly/Thr(+) cells of 14 strains failed to utilize l-amino acids or urea (0.01 m) as primary sources of nitrogen and grew slowly in the presence of low concentrations of NH(4) (+) (<== 5 mm). Cells of six strains (termed N(+)) utilized certain l-amino acids and urea (0.01 m) as primary sources of nitrogen and grew rapidly in the presence of <== 5 mm NH(4) (+). N(+) but not N(-) organisms cultivated with NH(4) (+) (0.01 m) as a primary source of nitrogen excreted a complete spectrum of naturally occurring amino acids; under this condition of growth the aspartase and particulate nicotinamide adenine dinucleotide phosphate transhydrogenase activities of N(+) and N(-) cells were repressed. N(+) meiotrophs arose at a frequency of 10(-6) in cultures of all 14 N(-) isolates, and urease-positive meiotrophs could be selected at a frequency of 10(-7) from N(+) but not N(-) cells of all 20 strains on a medium containing urea (0.01 m) as a primary source of nitrogen. These findings illustrate a reversible loss of genetic potential which has occurred during the evolution of Y. pestis as an obligate parasite and suggest that this organism is unable to efficiently remove dispensable deoxyribonucleic acid from its chromosome.

Journal Article↗
PubMed1965

DETECTION OF AN ENZOOTIC PLAGUE FOCUS BY SEROLOGICAL METHODS.

Complement-fixation and haemagglutination tests, utilizing a highly purified, specific Fraction 1 antigen of Pasteurella pestis, have been employed to detect specific plague antibody in the sera of rodents resident in a sylvatic plague focus. The data show that while the isolation of P. pestis is seasonal and rather rare, antibodies can be detected for long periods of time and with great frequency in rodents surviving infection. The authors recommend that serological methods be incorporated into epidemiological surveys and control programmes involving rodent plague.

Animals↗
PubMed1963

ACTION OF PLAGUE MURINE TOXIN ON MITOCHONDRIA FROM RESISTANT AND SUSCEPTIBLE ANIMALS.

Kadis, Solomon (Albert Einstein Medical Center, Philadelphia, Pa.), Samuel J. Ajl, and James H. Rust, Jr. Action of plague murine toxin on mitochondria from resistant and susceptible animals. J. Bacteriol. 86:757-765. 1963.-Purified murine Pasteurella pestis toxin inhibited the respiration of liver mitochondria isolated from both the rat and the rabbit. Toxin had little or no effect on the respiration of rabbit sarcosomes, but when they were disrupted with either sodium deoxycholate or sonic vibration their respiration was inhibited. The respiration of heart mitochondria from rats immunized with toxoid-adjuvant mixtures was inhibited only slightly by the toxin, whereas the respiration of liver mitochondria from immunized rats was inhibited to the same degree as that from nonimmunized animals. Toxin caused the heart mitochondria of the rat to swell, but had little or no effect on the heart mitochondria of the rabbit. Also, brain mitochondria were not swollen by the toxin.

Animals↗
PubMed1961

Pesticins. I. Pesticinbacterium interrelationships, and environmental factors influencing activity.

Brubaker, Robert R. (U. S. Army Biological Laboratories, Fort Detrick, Frederick, Md.) and Michael J. Surgalla. Pesticins. I. Pesticin-bacterium interrelationships, and environmental factors influencing activity. J. Bacteriol. 82: 940-949. 1961-A second bacteriocin-like substance produced by all tested strains of Pasteurella pestis and P. pseudotuberculosis is described. This activity, termed pesticin II, is active against the two avirulent P. pestis strains, A12 and Java. These strains do not produce pesticin I, which inhibits the growth of type I strains of P. pseudotuberculosis. Pesticin I was also found to be active against certain strains of Escherichia coli, strain A12, but not strain Java, and some P. pestis isolates which also produce pesticin I. A number of E. coli strains produce a substance which also inhibits the growth of strains A12 and Java; the activity of this substance is dependent upon the presence of high concentrations of Ca(++). The activity of both pesticins is inhibited under anaerobic conditions or in the presence of antiserum. The activity of pesticin I, but not pesticin II, is suppressed by Fe(+++), hemin, certain hemin-containing proteins, Mg(++), and inorganic phosphate. Suppression of pesticin I activity by Fe(+++) can be reversed by the addition of either Ca(++) or Sr(++) or by metal chelating agents. All tested strains of P. pestis and P. pseudotuberculosis produce a metabolite which suppresses the activity of pesticin I. The activity of this substance, termed pesticin I inhibitor, is enhanced by Fe(+++), and to a lesser extent by Mg(++) or by inorganic phosphate; its activity is suppressed by Mn(++) and by protamine sulfate.

Bacteriocins↗