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At least 37 records · Page 2Linked to original sources
PubMed1979

Synergistic protection against experimental cholera by immunization with cholera toxoid and vaccine.

Rabbits were immunized with two parenteral injections of Wellcome toxoid PX389A, Wyeth toxoid 20101, or Merck bivalent vaccine. Other groups of rabbits were immunized with combinations of the Merck vaccine and each of the two toxoids. Antitoxin responses were monitored in each group of rabbits before livecell challenge of each animal by the ligated intestinal loop assay. Inaba and Ogawa strains of Vibrio cholerae were used for challenge experiments. Basically, the data indicate that the toxoids were equivalent in antigenic potency and antitoxin responses were unaffected by combination of the toxoids with the whole-cell vaccine. The 50 microgram doses of each toxoid as well as the 4 X 10(9) cells of the bivalent vaccine provided the same magnitude of protection against live-cell challenge with either Inaba or Ogawa vibrios. Immunization with either toxoid in combination with the bivalent vaccine resulted in a synergistic protective response against live-cell challenge of intestinal loops with V. cholerae. Synergistic protection was observed when toxoid and vaccine were administered together by the oral and parenteral routes. Maximum protection was obtained when rabbits were immunized with the combined toxoid-whole-cell vaccine administered by both oral and parenteral routes.

Animals↗
PubMed1979

[The antigenic relationships between Candida albicans, Salmonella cholerae suis, and Salmonella cholerae suis var. Kunzendorf O antigens].

In this study a common antigenic factor (s) between C. albicans CBS-562 and S. cholerae suis 211 (0:6(2),7) was shown with agglutination and absorption tests. This common antigenic factor (s) is different than previously shown Salmonella 0:7 antigen. This new factor (s) is not present in S. cholerae suis var. kunzendorf 1350 (0:6(1), 7) and S. cholerae suis var. kunzendorf 5210 (0:6(2),7) serotypes.

Antigens, Bacterial↗
PubMed1976

Cell-mediated immunity to Vibrio cholerae with ribonucleic acid-protein fractions of V. cholerae L-form lysates.

Different L-form lysate vaccines of Vibrio cholerae serotypes Ogawa and Inaba and their combination along with ethyl alcohol-precipitated ribonucleic acid (E-RNA) and phenol-extracted RNA (P-RNA) fractions of V. cholerae Ogawa lysates were tested for production of cell-mediated immunity. Both E-RNA and P-RNA fractions induced an increase in leukocyte migration inhibition, macrophage migration inhibition, and macrophage aggregation. They also induced delayed hypersensitivity in rabbits. More consistent results were obtained with the P-RNA fraction.

Animals↗
PubMed1976

Vibrio cholerae adherence and colonization in experimental cholera: electron microscopic studies.

Colonization of the intestinal epithelium by Vibrio cholerae was examined in two model systems, in ligated ileal loops of adult rabbits and in the patent gut of infant rabbits, using both scanning and transmission electron microscopy. Time studies in the adult model showed a lag period of up to 1 h before the attachment of significant numbers of the vibrios. The bacteria appeared initially in small patches on the sides of the villi, predominantly along the transverse furrows. The number of adherent bacteria steadily increased, reaching a maximum between 4 and 7 h, when a dense mat of bacteria several layers thick covered much of the villi. After this time there was a rapid decline in the number of V. cholerae bound. By 12 to 16 h only a few bacteria could be seen on the surface of the villi, which had a rough, patchy appearance at these later times. Globular protrusions, with vibrios attached, may play a role in the clearance of bacteria. Colonization and clearance in the patent intestine of the infant rabbit occurred much as in the adult model. However, the bacteria adhered more uniformly and there was no lag in attachment. In both models the majority of bacteria were aligned horizontally with the epithelial surface, but some were attached in an end-on manner, with their flagella extending into the lumen. The bacteria adhered via their surface coats directly to the tips of the microvilli, except for a few vibrios that were partly embedded into the brush border. Some changes in the microvilli occurred as a consequence of the bacterial attachment.

Animals↗
PubMed1977

Study of intestinal immunity against V. cholerae: role of antibody to V. cholerae haemagglutinin in intestinal immunity.

Cell-bound haemagglutinin as an adhesive factor of Vibrio cholerae has been partially purified from E1 Tor vibrios using 0.05 M cyclohexylaminopropane sulfonic acid buffer pH 9.5 and gel filtration column chromatography. Rabbits were immunized with the precipitin complexes of the haemagglutinin and its antibody. The antiserum is tested for the protective ability against the oral challenge with Vibrio cholerae strain of which the haemagglutinin has been prepared. The results indicate definite protection of the haemagglutinin antiserum.

Agglutinins↗
PubMed1979

Endocytosis of cholera toxin in GERL-like structures of murine neuroblastoma cells pretreated with GM1 ganglioside. Cholera toxin internalization into Neuroblastoma GERL.

Cholera toxin (CT), covalently attached to horseradish peroxidase (HRP), is a specific cytochemical marker for GM1 ganglioside (GM1) and retains the ability of the native toxin to raise levels of cyclic AMP in avian erythrocytes. Using a cytochemical stain for HRP, we found that 9% of control cultured murine neuroblastoma cells bound cholera toxin-horseradish peroxidase conjugates (CT-HRP) on their surfaces after incubations for 1 h at 4 degrees C. Exogenous GM1, the natural receptor of CT, becomes associated in the culture medium with the plasma membranes of these cells so that 96% of cells are stained. Cells preincubated with GM1 at 4 degrees C were exposed to CT-HRP for 1 h at 4 degrees C. After washing, cells were incubated at 37 degrees C for 30 min-24 h. Endocytosis of CT-HRP occurred within 30 min and CT-HRP remained, throughout the 24-h period, in tubules, vesicles, and cisternae often found near the Golgi apparatus; this aggregate of peroxidase-positive elements probably corresponds to Golgi apparatus-endoplasmic reticulum-lysosomes (GERL) of neurons. In metaphase cells, CT-HRP was observed in aggregates of vesicles and tubules clustered near the centriole. Conjugates of HRP with subunit B, the GM1 binding component of CT, were internalized by cells pretreated with GM1 as was CT-HRP. The 9% of neuroblastoma cells binding CT-HRP in the absence of exogenous GM1 internalized the ligand in a manner indistinguishable from that of the treated cells. These findings indicate that, in neuroblastoma cells, a system of vesicles, tubules, and cisternae, analogous to GERL of neurons, is the primary recipient of adsorptive endocytosis of CT bound to endogenous or exogenously introduced GM1.

Animals↗
PubMed1979

Purification and characterization of a hemolysin produced by Vibrio cholerae biotype El Tor: another toxic substance produced by cholera vibrios.

A thermolabile direct hemolysin from an El Tor cholera vibrio strain has been isolated and partially characterized as a simple protein of ca. 20,000 molecular weight. In addition to its hemolytic activity, the hemolysin is cytotoxic, cardiotoxic, and rapidly lethal. In these respects it resembles the thermostable direct hemolysin/cytotoxin/cardiotoxin/lethal toxin of Vibrio parahaemolyticus and certain other bacterial hemolysins, although there are other significant differences. Because identical diseases are produced by both hemolytic and nonhemolytic cholera vibrios, the El Tor hemolysin may be presumed to be pathogenetically irrelevant. These observations raise the question of "When is a toxic substance also a toxin?"

Adrenal Glands↗
PubMed1979

Evaluation of two intravenous rehydration solutions in cholera and non-cholera diarrhoea.

A clinical trial was carried out with 126 male patients over 2 years of age suffering from diarrhoea requiring intravenous rehydration, 80 of the patients suffering from cholera and 46 from non-cholera diarrhoea. A new "diarrhoea treatment solution" (DTS) containing sodium at a concentration of 118 mmol/litre and glucose at 44 mmol/litre was compared with the usual Dacca intravenous solution (DS) which has a sodium concentration of 133 mmol/litre and contains no glucose. The other constituents and their concentrations were the same in both solutions. All the patients responded well clinically and made an uneventful recovery. Oral water intake measured during the first 24 h was higher in the group receiving the DS. This group also excreted a significantly higher quantity of sodium in the urine. A significant fall in the level of blood glucose from the admission values occurred in both the groups; the fall was relatively less in the DTS group, this solution containing 44 mmol of glucose per litre. Further work is required to find the optimum concentration of glucose in the solution for infants and young children.

Child↗
PubMed1978

Interaction of cholera toxin and toxin derivatives with lymphocytes. III. Modulating effects in vivo by cholera toxin on the graft-versus-host reactivity of lymphoid cells: suggested inhibition of suppressor cells.

The influence of cholera toxin (CT), and thus probably of cyclic AMP, on the capacity of parental lymphoid cells to elicit a graft-versus-host reaction (GVHR) was studied. Toxin-treated DBA/1 mice were used as cell donors and untreated DBA/1xC57B1/6 F1 hybrid mice as recipients, and the GVHR reactivity of the transferred cells was estimated by their ability to induce spleen enlargement or stimulation of antibody formation ('allogenic effect') in the recipients. Spleen cells from donors intravenously injected with 1 microgram CT 1-3 days earlier, gave a significantly stronger GVHR than did spleen cells of untreated mice. Choleragenoid, a toxin analog devoid of the toxin's ability to activate plasma membrane adenylate cyclase even though it binds efficiently to cells, had no effect on the GVHR-inducing capacity of the spleen cells. The enhanced GVHR by spleen cells from toxin-treated DBA/1 animals was reduced to the normal level when the donor cells were transferred along with lymphoid cells from untreated animals of the same strain. Spleen was the most powerful source of the suppressive influence. No evidence for a redistribution of suppressor cells following administration of CT was found. Spleen cells from mice syngeneic with the recipients had no suppressive effect. The results suggest that parenterally administered CT, directly or indirectly, can inhibit a cell population in spleen which normally exerts an antigen-specific suppressive regulatory influence on the development of GVHR.

Cholera Toxin↗
PubMed1978

Prevention and reversal of cholera enterotoxin effects in rabbit jejunum by nicotinic acid.

The cholera enterotoxin produces intestinal secretion associated with an elevation of tissue levels of cyclic adenosine 3',5'-monophosphate levels of cyclic adenosine 3',5'-monosphosphate (cAMP). The objectives of this study were to determine whether intestinal secretion and cAMP elevation induced by cholera toxin could be prevented, or once initiated, reversed by nicotinic acid, an agent known to lower tissue levels of cAMP. In rabbits, four jejunal loops were constructed as alternating control (3-ml isotonic electrolyte solution) and cholera toxin (same solution containing 50 mug purified cholera toxin) loops. Net intestinal secretion was determined by measuring fluid accumulation, after which intestinal biopsies were taken for cAMP assay. The animals were pretreated either subcutaneously with 50 mg/kg nicotinic acid in saline 3 h and 1 h before the introduction of cholera toxin, or intraluminally with 200 mg/kg nicotinic acid in Ringer's lactate solution 15 min before the instillation of cholera toxin. Under these conditions, nicotinic acid blocked the cholera toxin-induced secretion and the rise in cAMP measured 3 h after the loops were exposed to cholera toxin. The effect of the nicotinic acid administered within the lumen on net intestinal secretion was studied. Maximal inhibition of net intestinal secretion was achieved with an intraluminally administered dose of nicotinic acid of 100 mg/kg. This dose was chosen for testing the ability of nicotinic acid to reverse the effects of cholera toxin. When nicotinic acid was instilled into a fifth loop constructed distally to the four experimental loops 3 h after exposure of these loops to cholera toxin, both intestinal secretion and elevation of cAMP were reversed. These results suggest that nicotinic acid can prevent and reverse the secretory effects of cholera toxin and may have a role in the therapy of cholera and other cAMP-associated diarrheal diseases.

Animals↗
PubMed1979

Endemicity of cholera in Surabaya, Indonesia.

As the seventh pandemic of cholera is caused by V. cholerae biotype El Tor, the former criteria for endemicity of cholera need to be reconsidered as regards their applicability in areas that are infected with cholera. As the mortality rate of cholera nowadays can be reduced to a very low level due to modern methods of treatment, it is suggested that the infection rates of cholera should be taken into consideration as criteria of cholera endemicity, i.e. 1. Five years persistence of cholera cases in a given area. 2. Five percent infection rate among family contacts of cholera cases. 3. Minimum infection rate of 1% in a vicinity where cholera cases occur. It was also found that in such an endemic area it is very difficult to eliminate V. cholerae infection from a locality, even when all family contacts are treated with the full dose of tetracycline.

Adolescent↗