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1.
G H Rabbani W B Greenough rd J Holmgren B Kirkwood 《BMJ (Clinical research ed.)》1982,284(6326):1361-1364
A randomised controlled trial was conducted to investigate the ability of chlorpromazine to reduce intestinal secretion in cholera. Chlorpromazine had reduced loss of intestinal fluid in animals with diarrhoea induced by cholera toxin, and in a preliminary study the drug had reduced purging in patients with cholera. Forty-six adults with cholera were included in the randomised trial. Of these, 34 were treated with chlorpromazine (1 mg/kg or 4 mg/kg either by mouth or intramuscularly) and 12 served as controls. After treatment with the drug there was a significantly greater reduction in the rate of fluid loss in the treated patients than in the controls during the first (p less than 0.005), second (p less than 0.05), and fourth (p less than 0.01) eight-hour periods, but not during the third eight-hour period; the dose of 4 mg/kg was only marginally more effective than 1 mg/kg. The effect of chlorpromazine was strikingly biphasic, with one peak during the first eight hours and another 24-32 hours after administration. Chlorpromazine also significantly reduced the duration of diarrhoea, frequency of vomiting, and amount of intravenous fluid required. The drug induced mild sedation and no hypotension in these well-hydrated patients. These findings confirm the effectiveness of chlorpromazine in reducing fluid loss in cholera. A sedative effect, however, especially in children, may limit its usefulness and requires further study. 相似文献
2.
Vonda G. Reeves-Darby John A. Turner Rajendra Prasad ashok K. Chopra Parvathi Chary Mary H. Clench Johnny W. Peterson John R. Mathias 《FEMS microbiology letters》1995,134(2-3):239-244
Abstract We analysed the small intestine myoelectric responses of anesthetized New Zealand albino rabbits to Escherichia coli lysates containing an enterotoxin cloned from Salmonella typhimurium . Migrating action potential complex, which consisted of rapid bursts of action potentials and secretion of fluid, was observed only in ileal loops injected with the enterotoxin-containing lysate. Migrating action potential complex produced by Stn usually propagated aborally, which was typical of cholera toxin, but orad or bidirectional propagation occurred from a single point of origin when activity was intense. Gell lysates from an E. coli clone containing vectors alone, as well as proximal control segments injected with phosphate-buffered saline, gave neither a change in motility nor fluid secretion. These results show that Stn caused dramatic changes in intestinal motility and substantial fluid production. 相似文献
3.
W. H. Frost 《CMAJ》1976,115(5):401-403
Cholera varies greatly in clinical severity; the mortality of untreated severe cholera may be as high as 60% The main clinical feature is dehydration; fluid lost in the stools may amount to 60/. Rehydration is the cornerstone of treatment. The amount of fluid required is approximately 10% of body weight in severe dehydration and 5 to 8% in moderate dehydration. Fluid therapy, which must be individualized, may be successful on its own, but chemo-therapy shortens the duration of illness. Tetracycline (in adults, 40 mg/kg for 2 days; in children, 50 mg/kg for 2 days) reduces the fluid loss and eliminates the causative organisms. Vaccination is of limited value. 相似文献
4.
The effects of indomethacin on intestine mucosal cAMP, intestinal fluid secretion, and mucosal and fluid PGE were studied in rabbits in vivo following challenge with cholera toxin. Indomethacin had no effect on cholera toxin-induced fluid secretion or cAMP accumulation. Inhibition of PGE synthesis was achieved by the administration of two but not one injection of indomethacin. These studies provide evidence against a role for PGE in mediating cholera toxin-induced secretion and point out the need to measure prostaglandin levels when using prostaglandin synthetase inhibitors in vivo. 相似文献
5.
Donald E. Wilson Suleiman El-Hindi Pearl Tao Larissa Poppe 《Prostaglandins & other lipid mediators》1975,10(6):581-587
The effects of indomethacin on intestine mucosal cAMP, intestinal fluid secretion, and mucosal and fluid PGE were studied in rabbits in vivo following challenge with cholera toxin. Indomethacin had no effect on cholera toxin-induced fluid secretion or cAMP accumulation. Inhibition of PGE synthesis was achieved by the administration of two but not one injection of indomethacin. These studies provide evidence against a role for PGE in mediating cholera toxin-induced secretion and point out the need to measure prostaglandin levels when using prostaglandin synthetase inhibitors in vivo. 相似文献
6.
A J Bitonti 《Biochemical and biophysical research communications》1984,120(2):700-706
ADP-ribosylation by cholera toxin of the guanine nucleotide binding regulatory protein (Gs) of rat liver membrane adenylate cyclase was inhibited by 0.1-1 mM MDL 12330A or 0.1-1 mM chlorpromazine. Basal as well as cholera toxin activated adenylate cyclase activity in liver membranes was also inhibited by the two drugs. NAD glycohydrolase activity and self-ADP-ribosylation of cholera toxin were also inhibited by MDL 12330A and chlorpromazine. These effects of MDL 12330A and chlorpromazine may be related to their effects on cholera toxin-induced fluid secretion in vivo. 相似文献
7.
Blakely GW 《Molecular microbiology》2004,54(4):851-854
The seventh cholera pandemic emerged in the poorer nations of the world towards the end of the 20th century and continues to kill thousands of people per year. The causative agent of cholera, the Gram-negative bacterium Vibrio cholera, is only pathogenic when it contains a lysogenic bacteriophage, CTXphi, that encodes the toxin responsible for inducing massive fluid loss from the human host. Site-specific integration of CTXphi into chromosome I of V. cholera occurs at a site, dif, that is normally required for resolution of chromosome dimers generated by homologous recombination. An article in this issue of Molecular Microbiology reports the analysis of interactions between two host encoded recombinases, XerC and XerD, and the recombination sites involved in lysogeny. Surprisingly, recombination between the CTXphi attP site and the chromosomal dif site requires additional recombinase binding sites, downstream from the positions of strand exchange, which might play an architectural role. The positions of strand cleavage also differ significantly between the two sites, suggesting a novel recombination mechanism that implicates additional host factors in resolution of the Holliday junction intermediate. 相似文献
8.
Peterson JW King D Ezell EL Rogers M Gessell D Hoffpauer J Reuss L Chopra AK Gorenstein D 《Biochimica et biophysica acta》2001,1537(1):27-41
Mediators of cholera toxin (CT)-induced fluid secretion include 3',5'-adenosine monophosphate (cAMP), prostaglandin E(2) (PGE(2)), and 5-hydroxytryptamine (5-HT). Administration of L-histidine significantly reduced the net secretory response of the small intestine of mice challenged with CT and reduced the capacity of PGE(2) to stimulate Na+ transport in Ussing chambers. We demonstrated that L-histidine chemically modified the structure of PGE(2) but had no direct effect on cAMP or 5-HT. L-Histidine and imidazole reacted with PGE(2) in vitro in cell-free mixtures incubated at 37 degrees C and pH 7.0 under an atmosphere of N(2) with the formation of PGE(2)-imidazole and PGE(2)-histidine covalent adducts. Nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS) analysis of the purified adduct showed that imidazole catalyzed the dehydration of PGE(2). A Michael adduct then was formed between C11 of 11-deoxy-Delta(10) PGE(2) (PGA(2)) and the tau nitrogen in the imidazole ring of L-histidine. Importantly, the isolated PGE(2)-imidazole and PGE(2)-histidine adducts inhibited CT-induced fluid loss and cAMP accumulation in mouse intestinal loops. The protection provided by PGE(2)-imidazole, PGE(2)-histidine, and L-histidine against intestinal fluid loss could provide a basis for future therapy against cholera. 相似文献
9.
Biochemistry of Vibrio cholerae virulence: purification of cholera enterotoxin by preparative disc electrophoresis. 总被引:2,自引:0,他引:2
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Procedures for cholera enterotoxin purification previously developed in this labarotory were not applicable to large-scale purification, and these methods resulted in low yields of pure toxin. An efficient scheme has been developed whereby pure cholera enterotoxin can be obtained from 6 to 8 liters of culture supernatant fluid. This method consists of concentration by membrane ultrafiltration followed by gel filtration and cation-exchange chromatography. Pure cholera enterotoxin of high biological potency was obtained after a final step of preparative acrylamide gel electrophoresis. The degree of purity of the toxin-antigen as well as its biological activity were determined at various setps of purification. This alternate technique for purification is offered because of the widespread interest in cholera enterotoxin as a specific stimulator of adenyl cyclase. 相似文献
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11.
Satchell KJ 《Microbes and infection / Institut Pasteur》2003,5(13):1241-1247
Vibrio cholerae induces either non-inflammatory diarrhea or inflammatory gastroenteritis, depending on the presence of cholera toxin, a fluid secretion inducer and a modulator of host immunity. In the absence of cholera toxin, other toxins induce inflammation, resulting in gastroenteritis. Thus, multiple toxins likely affect the safety of live attenuated vaccines. 相似文献
12.
Vittal Mogasale Shantanu K. Kar Jong-Hoon Kim Vijayalaxmi V. Mogasale Anna S. Kerketta Bikash Patnaik Shyam Bandhu Rath Mahesh K. Puri Young Ae You Hemant K. Khuntia Brian Maskery Thomas F. Wierzba Binod Sah 《PLoS neglected tropical diseases》2015,9(9)
BackgroundService provider costs for vaccine delivery have been well documented; however, vaccine recipients’ costs have drawn less attention. This research explores the private household out-of-pocket and opportunity costs incurred to receive free oral cholera vaccine during a mass vaccination campaign in rural Odisha, India.MethodsFollowing a government-driven oral cholera mass vaccination campaign targeting population over one year of age, a questionnaire-based cross-sectional survey was conducted to estimate private household costs among vaccine recipients. The questionnaire captured travel costs as well as time and wage loss for self and accompanying persons. The productivity loss was estimated using three methods: self-reported, government defined minimum daily wages and gross domestic product per capita in Odisha.FindingsOn average, families were located 282.7 (SD = 254.5) meters from the nearest vaccination booths. Most family members either walked or bicycled to the vaccination sites and spent on average 26.5 minutes on travel and 15.7 minutes on waiting. Depending upon the methodology, the estimated productivity loss due to potential foregone income ranged from $0.15 to $0.29 per dose of cholera vaccine received. The private household cost of receiving oral cholera vaccine constituted 24.6% to 38.0% of overall vaccine delivery costs.InterpretationThe private household costs resulting from productivity loss for receiving a free oral cholera vaccine is a substantial proportion of overall vaccine delivery cost and may influence vaccine uptake. Policy makers and program managers need to recognize the importance of private costs and consider how to balance programmatic delivery costs with private household costs to receive vaccines. 相似文献
13.
Incubation of FRTL-5 rat thyroid cell membranes with [32P]NAD and pertussis toxin results in the specific ADP-ribosylation of a protein of about 40 kDa. This protein has the same molecular mass of the alpha i subunit of the adenylate cyclase regulatory protein Ni and is distinct from proteins ADP-ribosylated by cholera toxin in the same membranes. Prior treatment of FRTL-5 cells with pertussis toxin results in the ADP-ribosylation of Ni, as indicated by the loss of the toxin substrate in the ADP-ribosylation assay performed with membranes prepared from such cells. Preincubation of FRTL-5 cells with thyrotropin causes the same loss; cholera toxin has no such effect. Pertussis toxin, as do thyrotropin and cholera toxin, increases cAMP levels in FRTL-5 cells. Forskolin together with thyrotropin, cholera toxin or pertussis toxin causes a further increase in cAMP levels. Pertussis toxin and thyrotropin are not additive in their ability to increase adenylate cyclase activity, whereas both substances are additive with cholera toxin. A role of Ni in the thyrotropin regulation of the adenylate cyclase activity in thyroid cells is proposed. 相似文献
14.
Structure-function studies of cholera toxin and its A and B protomers. Modification of tryptophan residues 总被引:9,自引:0,他引:9
M J De Wolf M Fridkin M Epstein L D Kohn 《The Journal of biological chemistry》1981,256(11):5481-5488
The tryptophan residues on cholera toxin and its A and B protomers have been modified by reaction with 2-nitrophenylsulfenyl chloride and 2,4-dinitrophenylsulfenyl chloride. Modification of the tryptophan residues of cholera toxin results in complete loss of toxicity measured in a skin permeability assay. Modification of cholera toxin and its B protomer results in the complete loss of binding activity toward membrane receptors, the ganglioside galactosyl-N-acetylgalactosaminyl-[N-acetylneuraminyl]-galactosylceramide (GM1), and the oligosaccharide moiety of the ganglioside GM1. Modification of cholera toxin and its A protomer results in a complete loss of the ADP-ribosylation activity exhibited by their native counterparts. Modification of the A protomer results in no apparent change in its physical properties by sedimentation velocity in the ultracentrifuge or by gel filtration chromatography. Modification of the B protomer, either directly or when it remains a component part of the holo toxin structure, results in a change in its sedimentation value and its elution from gel filtration columns. The changes are compatible with a conversion of the B protomer from a pentameric moiety in aqueous solvents to its existence as a monomer unit, i.e. to the individual polypeptide chains comprising the native B pentamer. Thiolysis of the 2,4-dinitrophenylsulfenyl chloride derivative of the B protomer reaggregates the individual-polypeptide chains but does not return its ability to interact with GM1. 相似文献
15.
A E Libinzon G F Levanova G V Gal'tseva 《Zhurnal mikrobiologii, epidemiologii, i immunobiologii》1991,(2):20-23
For the first time V. fluvialis strains were detected on the territory of the USSR. The taxonomic position of these vibrios was determined by their nucleotide DNA composition (the content of guanine + cytosine was 49.3-51.0 mole%) and the characteristic features of their phenotype. The individual features of the strains consisted in their capacity for agglutination with cholera antisera, groups 01 and Inaba, in diagnostic dilutions in the presence of differences in genomes and phenotypes with cholera vibrios. Molecular hybridization DNA-DNA also gave no confirmation of their relationship to cholera vibrios (23-26% homology). The comparative study of V. fluvialis strains from the USSR and other countries by a broader set of their phenotypical signs confirmed their identity. 相似文献
16.
Fluid plain and adsorbed and freeze-dried cholera and tyhpoid vaccines of different composition were examined for thermostability by potency testing (by active mouse protection tests) after exposure to 37 degrees C for 1, 2, 3, 4, 8 and 12 weeks. Loss of potency was evaluated by comparison with samples stored at 4 degrees C. The fluid plain cholera vaccine remained fully potent for 1--3 weeks, the adsorbed vaccine for at least 4 weeks. The fluid typhoid vaccines showed greater thermosensitivity than the fluid plain cholera vaccine. The freeze-dried cholera and typhoid vaccines were both very stable, retaining fully potency after at least 12 weeks' exposure to 37 degrees C. It should be emphasized that the above results apply exclusively to vaccines prepared by the methods used by the authors and formulated to identical compositions. 相似文献
17.
Y Kamijo S I Ohkuma M Shimizu Y Shimizu 《National Institute of Animal Health quarterly》1977,17(4):133-140
Using antiserum against a particular strain of bovine viral diarrhea virus, the strains of hog cholera virus were divided into two groups, H and B, on the basis of the difference in the degree of neutralization. Group H consisted of strains reacting poorly in neutralization, and group B Consisted of strains reacting well with bovine viral diarrhea antiserum. Most of the strains of group H induced a typical clinical form of hog cholera in experimentally infected pigs. Inoculation of pigs with a strain of group B, however, resulted in a chronic type of illness. When immunized with bovine viral diarrhea virus, pigs succumbed to challenge with group H virus after showing clinical signs of hog cholera, but survived challenge with group B virus without manifesting any clinical sign. 相似文献
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19.
Effects of cholera toxin, Escherichia coli heat stable toxin and sodium deoxycholate on neurotensin release from the ileum in vivo 总被引:2,自引:0,他引:2
S Eklund L Karlstr?m A R?kaeus E Theodorsson M Jodal O Lundgren 《Regulatory peptides》1989,26(3):241-252
Neurotensin (NT) is a biologically active peptide found in specialized epithelial cells (N-cells) in the distal small intestine. In this study we tested the hypothesis that NT may be released by luminal secretagogues, i.e., cholera toxin, Escherichia coli heat-stable toxin and sodium deoxycholate. Cholera toxin elicited net fluid secretion in anesthetized cats. This secretion was accompanied by an increased release of NT-like immunoreactivity (NTLI) into the mesenteric vein when NTLI was measured with either a C-terminally or a N-terminally directed antibody. An increasing plasma NTLI concentration (N-terminally directed antibody) was recorded in the mesenteric vein and femoral artery in cholera experiments. These results indicate that cholera toxin releases NT from the small intestine. Since neurotensin causes intestinal fluid secretion at least in part via an activation of enteric nerves we propose that the N-cell functions as a 'receptor cell' which activates an intramural secretory reflex upon luminal stimulation by cholera toxin. This study does not support a similar role for NT in the secretion elicited by the heat stable toxin of Escherichia coli or by sodium deoxycholate since we were unable to demonstrate any intestinal release of NTLI after exposing the intestine to these secretory agents. 相似文献
20.
Lise Grout Isabel Martinez-Pino Iza Ciglenecki Sakoba Keita Alpha Amadou Diallo Balla Traore Daloka Delamou Oumar Toure Sarala Nicholas Barbara Rusch Nelly Staderini Micaela Serafini Rebecca F. Grais Francisco J. Luquero 《PLoS neglected tropical diseases》2015,9(12)