[Studies on a combined vaccine prepared from killed Vibrio comma and Pasteurella pestis].
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Certain metabolic requirements, upon initial interaction of sensitive cells with vibriocin, were a prerequisite for lethal activity. Transient "immunity" of these cells, manifested under suboptimal growth conditions, differed from the immunity of vibriocinogenic cells.
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Cary, Sylvia G. (Walter Reed Army Institute of Research, Washington, D.C.), and Eugene B Blair. New transport medium for shipment of clinical specimens. I. Fecal specimens. J. Bacteriol. 88:96-98. 1964.-A new transport medium for the collection and shipment of clinical specimens is described. Preliminary studies indicate that, with initial fecal specimens, Salmonella and Shigella can be recovered for as long as 49 days, Vibrio comma for 22 days, and Pasteurella pestis for at least 75 days.
It was shown that neuraminidase of Vibrio comma is inactivated by Ca..-binding anions like citrate, EDTA, oxalate, phosphate or tartrate. There is, however, no inhibition of the newly described enzymes of Erysipelothrix insidiosa and Streptococcus viridans. Pyruvate and, to a lesser extent, also citrate inactivate all the neuraminidases investigated independently of their activation by Ca..ions.
In 1883 Robert Koch isolated and characterized Vibrio comma as the etiological agent of cholera thereby creating a breakthrough in cholera research. Pathogenesis and pathophysiology of diarrheal diseases caused by V. cholerae and enterotoxigenic E. coli are cleared up by the production of enterotoxins and colonizing factors of microorganisms. Plasmids code for antibiotic resistance, distinct enterotoxins, colonization and other virulence factors. Sero-, bio-, phage-, colicino- and plasmid typing are important to epidemiological surveillance.
The mechanism of action of vibriocin, a bacteriocin produced by Vibrio comma, was investigated. Its lethal action (as defined by the loss in colony-forming ability) was reversed by tryptic digestion within 7 to 10 min after adsorption. The bacteriocin had a pronounced inhibitory effect on deoxyribonucleic acid (DNA) synthesis, whereas ribonucleic acid (RNA) and protein synthesis continued, although at a reduced rate. Chloramphenicol protected sensitive bacteria from the lethal action. Degradation of bacterial DNA prelabeled with (3)H-thymidine, as measured by changes in acid-precipitable radioactivity, occurred 10 min after treatment with vibriocin. The bacteriocin per se had no detectable deoxyribonuclease activity. Observation of vibriocin-treated cells by phase-contrast microscopy, measurement of ultraviolet light-absorbing capacity of extracellular fluid, and (42)K-efflux studies indicated a damaged bacterial membrane. This impairment of membrane function occurred in the presence of chloramphenicol and thus, unlike the lethal effect of vibriocin, was independent of protein synthesis.
There is a lack of agreement as to the significance of agglutination test results in cholera, and recent epidemics of "classic" Vibrio comma and El Tor infections have provided an opportunity to compare this test with two other serological procedures recently introduced in cholera work. These are determination of the circulating antitoxin expressed as the lethal toxin neutralizing power of a serum, and determination of the haemolysin neutralizing power through serial test-tube dilutions.Applying these tests to sera from cholera patients, convalescents, carriers and contacts and from immunized persons either exposed or not exposed to cholera, the authors found the agglutination test to be a less sensitive indicator of the immunological status than the other two procedures. They therefore recommend antitoxin and antihaemolysin titration for the study of cholera patients, convalescents and carriers. In the conditions of the experiments described, the results with exposed and non-exposed vaccinated individuals were less conclusive, but nevertheless suggest that antitoxin and antihaemolysin tests may be helpful in the follow-up of vaccination experiments.
Two types of inhibition of basic peptide-induced rat mast cell secretion are reported. Pretreatment of rat peritoneal mast cells with Vibrio comma neuraminidase, an enzyme which cleaves sialic acid from oligosaccharides, led to inhibition of 5-hydroxytryptamine release induced by the basic peptides polylysine, corticotropin 1-24 and a decapeptide sequence of human IgE. Inhibition was similarly observed when mast cells were challenged in the presence of the cationic cell membrane-active substance benzalkonium chloride. It is postulated that both of these experimental procedures inhibit basic peptide-induced secretion by depletion of cell surface negative charge. Sialic acid itself does not act as a specific receptor for basic peptides, since a molar excess of sialic acid in free solution failed to inhibit secretion by binding to basic peptides in the fluid phase.
A variety of bacteriophages specific for different hosts, including Bacillus cereus, Escherichia coli, Pseudomonas aeruginosa, Serratia marcescens, Shigella dysenteriae, Staphylococcus aureus, and Vibrio comma, were frozen at a controlled rate to liquid nitrogen temperatures, and then quick-thawed. Glycerol (10%) was used as a protective additive. Quantitative determinations showed from 10% to virtually 100% recovery in the various cases. Host specificity, plaque morphology, and, in one case, rate of inactivation of phage by homologous antiserum remained unchanged.
Contemporaneous with John Snow's famous study of the 1854 London cholera epidemic were 2 other investigations: a local study of the Broad Street outbreak and an investigation of the entire epidemic, undertaken by England's General Board of Health. More than a quarter-century prior to Koch's description of Vibrio comma, a Board of Health investigator saw microscopic "vibriones" in the rice-water stools of cholera patients that, in his later life, he concluded had been cholera bacilli. Although this finding was potential evidence for Snow's view that cholera was due to a contagious and probably live agent transmitted in the water supply, the Board of Health rejected Snow's conclusions. The Board of Health amassed a huge amount of information which it interpreted as supportive of its conclusion that the epidemic was attributable not so much to water as to air. Snow, by contrast, systematically tested his hypothesis that cholera was water-borne by exploring evidence that at first glance ran contrary to his expectations. Snow's success provides support for using a hypothetico-deductive approach in epidemiology, based on tightly focused hypotheses strongly grounded in pathophysiology.