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PubMed1978

[Studies on staphylococcal enterotoxin B. II. Production and regulation (author's transl)].

Enterotoxigenic strain of Staphylococcus aureus (ATCC 14458) was grown under various conditions with constant shaking to determine the requirements for maximum toxin production. It was evident that 3% tryptic soy broth, 3% NZ-Amine NAK + 3% casein hydrolysate, 3% NZ-Amine NAK + 1% yeast extract, and 3% NZ-Amine NAK + 1% yeast extract + 0.2% glucose are most available toxin production media. But concentration of glucose could strictly triggered the enterotoxin producing efficiency. When glucose concentration was less than 0.5%, although with higher yield, the toxin production was delayed for certain period of time. However, if glucose concentration was up to more than 0.5%, the enterotoxin production was almost inhibited. Some metabolites of glucose to elucidate the inhibitory effect have also investigated. Our results indicated that glycerol and citric acid inhibited the toxin production directly, while the inhibitory effect of lactic acid and acetic acid were due to those acidic metabolites, decreased the pH value of media, and adversely suppressed the bacterial growth.

Culture Media↗
PubMed1988

[Identification of Salmonella enterotoxin by coagglutination reaction].

It has been shown that the intensity of enterotoxin production by various strains of Salmonella is different (it ranges from + to +). Thus, in addition to adhesive properties and skin permeability factors, the ability of various Salmonella strains to produce enterotoxin is one of the pathogenic factors of these microorganisms. Further biological characteristics of the infective agents will promote the detection of epidemiologically significant types of microorganisms during outbreaks of toxicoinfections.

Agglutination Tests↗
PubMed1978

Effects of intraluminal glucose on intestinal secretion induced by heat stable and heat labile Escherichia coli enterotoxin, cholera toxin and theophylline.

Glucose, l-alanine, l-aspartate, l-methionine and glycine enhanced net fluid and electrolyte absorption in acute isolated loops of the proximal jejunum of weanling swine. The effect of glucose on intestinal secretion induced by heat stable and heat labile Escherichia coli entero-toxin, cholera toxin and theophylline was examined in both the proximal and distal jejunum of weanling swine. In the proximal jejunum glucose enhanced the rate of net fluid and electrolyte absorption. This increase was accompanied by an increase in unidirectional dosium absorption. In loops exposed to either heat stable or heat labile enterotoxins, glucose significantly decreased the rate of net fluid and electrolyte secretion. The magnitude of glucose enhancement in loops exposed to heat stable and heat labile enterotoxins was similar to adjacent control loops. However, glucose enhancement did not occur in loops exposed previously to cholera toxin or concurrently to theophylline. Therefore, cholera toxin and theophylline may inhibit substrate dependent sodium absorption in the proximal jejunum. In the distal jejunum glucose enhancement did occur but the rate of enhancement was less than in the proximal jejunum. In this region glucose enhancement was not evident in loops exposed to either theophylline, heat stable, heat labile or cholera toxin.

Amino Acids↗
PubMed1978

Reversal of jejunal water secretion by glucose in rats exposed to coliform enterotoxins.

Glucose absorption and glucose-facilitated water transport were assessed in rats exposed to semipurified preparations of the heat-labile (LT) and heat-stable (ST) enterotoxins of Escherichia coli, Klebsiella pneumoniae, and Enterobacter cloacae by in vivo jejunal perfusion of these toxins alone and with varying amounts of glucose. Progressive increases in the glucose concentration of from 12 to 56 mM resulted in incremental rises in water absorption from perfusates containing each of these toxins, with similar delta water values to those for the electrolyte perfusion solution without toxins. Water secretion was reversed to absorption by the addition of 12 mM glucose when secretion was mild, but 24 mM was required to achieve this in the presence of severe secretion; absolute values for water transport did not return to normal in any instance. Glucose absorption from solutions containing 24 and 56 mM glucose was severely reduced by all of the ST toxins and marginally reduced by some of the LT toxins; the effect of LT was not attributable to the toxin itself, however, but to another unidentified factor present in LT, but not ST, preparations from both toxigenic and nontoxigenic strains. These observations indicate that glucose-facilitated water transport remains intact in intestinal tissue exposed to various coliform enterotoxins and that this occurs despite the presence of impaired glucose absorption in some instances. They provide a rational basis for treatment with oral glucose-electrolyte solutions of persons whose diarrhea is caused by toxigenic coliform bacteria.

Animals↗
PubMed1986

[Immunofluorescence method of detecting cholera enterotoxin].

The quantitative immunofluorescent assay for the determination of cholera enterotoxin is proposed. The assay is based on the selective sorption of cholera enterotoxin by gangliosides incorporated into polyacrylamide granules. The preliminary treatment of gangliosides with neuraminidase enhances the sensitivity of this assay. The assay permits the detection of cholerigen in an amount of 20 ng.

Enterotoxins↗
PubMed1978

Enterotoxin production by Shigella flexneri type 2A, strain no. M42-43.

Enterotoxin produced by Shigella flexneri type 2a, strain M42-43, is similar to "Shig-like" cytotoxic enterotoxin and shares common features with that of other S. flexneri strains. On the basis of molecular filtration and neutralization experiments it is suggested that the same molecule carries these biological characters.

Animals↗
PubMed1985

Effects of Escherichia coli heat-stable enterotoxin, atropine, clonidine, and morphine on chloride efflux from isolated enterocytes.

The effects of Escherichia coli heat-stable enterotoxin (ST) on chloride efflux rate were investigated in 3 fractions of enterocytes isolated in a villus-to-crypt gradient from porcine jejunum. There was no difference in chloride efflux rates between mature and immature cells from controls. Heat-stable enterotoxin significantly increased chloride efflux in all fractions. Morphine inhibited ST-augmented secretion in mature enterocytes. Atropine or clonidine had no effect. Calcium efflux rates and glucose or glutamic acid metabolism were not altered by ST. The results indicate that ST may stimulate chloride secretion in both villus and crypt cells and that opiates inhibit intestinal secretion by a direct action on villus epithelial cells.

Animals↗
PubMed1979

Shigella dysenteriae 1-like cytotoxic enterotoxins produced by Salmonella strains.

A Salmonella enteritidis strain produced a cytotoxin in addition to heat-labile (LT) and heat-stable (ST) enterotoxins. Two strains of serotypes Salmonella kapemba and Salmonella thompson were LT and ST negative, but exhibited a cytotoxic effect. After Sephadex G-100 fractionation of the crude S. enteritidis material, some high and low molecular fractions had both cytotonic and cytotoxic activities. Of the two other salmonellae, only some high molecular fractions contained the cytotoxic substance. Neutralization experiments revealed an antigenic relationship between the cytotoxins studied and Shigella dysenteriae 1 enterotoxin. On the basis of cross neutralization and other data, it seems that cytotoxic and LT-like characters are carried by the same molecule. In S. thompson and S. kapemba the LT fails to exert a biological effect, although it is antigenically related to the LT of Escherichia coli.

Animals↗
PubMed1979

Limitations of the infant mouse test for Escherichia coli heat stable enterotoxin.

A study was undertaken to evaluate the response of different test systems to preparations of heat-stable enterotoxin (ST) derived from Eschericihia coli strains recovered from diarrheal disease of humans, pigs and calves. Sterile broth culture supernatants of enterotoxigenic strains of E. coli were heated at 65 degrees C for 30 minutes and tested for the presence of heat-stable enterotoxin. Three test systems, namely, ligated intestine of weaned pigs, ligated intestine of rabbits and the infant mouse test were used in attempts to detect ST in the culture supernatants. Two patterns of reaction were observed in response to ST-containing preparations: either the preparation elicited a response in the three tests or the preparation elicited a reaction only in the ligated pig intestine. A response in all three tests were observed for 5/5 human ST-producing E. coli, 5/5 bovine enterotoxigenic E. coli, 5/5 "atypical" porcine enterotoxigenic E. coli, 3/3 St(+)LT(-) porcine E. coli of serogroup O138:K81 and 4/24 LT(+)ST(+) porcine E. coli. A response only in the ligated pig intestine was obtained with 5/5 ST(+)LT(-) porcine E. coli belonging to serogroups other than O138:K81 and to 20/24 ST(+)LT(+)E. coli from pigs. The results are consistent with the view that there are two kinds of ST, one of which (ST1) reacts in all three tests and the other (ST2) which reacts only in the ligated pig intestine. The findings underscore the limitations of the infant mouse test as a means of detecting ST in porcine isolates of E. coli, since the test fails to detect ST produced by a large number of these E. coli strains. There appeared to be a relationship between kind(s) of ST produced and the animal species from which the producing organism was recovered.

Animals↗
PubMed1985

Clinical and antibody responses to Clostridium perfringens type A enterotoxin in experimental sheep and calves.

Clostridium perfringens type A live cultures or sonicated sporulating cells, all containing enterotoxin, were repeatedly inoculated into sheep and calves by the intraduodenal route over periods of 30 to 35 days. Serum antibody to C. perfringens enterotoxin, tested by ELISA, developed in four of seven sheep and in two of four calves. The titers ranged from 400 to 1600. The live organism introduced into the duodenum did not become established in the bacterial flora of the intestinal tract.

Animals↗
PubMed1979

Quantitative determination of staphylococcal B-type enterotoxin with Laurell's electroimmune diffusion method.

The quantitative determination of B-type enterotoxin produced by Staphylococcus aureus is described. Pretreating the toxin with formaldehyde, the B-type enterotoxin could be demonstrated rapidly with appropriate sensitivity by Laurell's electroimmune diffusion method. Four to eight hours were required for the examination and 0.25 microgram/ml was the smallest demonstrable quantity of the toxin.

Enterotoxins↗
PubMed1981

Antibody to staphylococcal enterotoxin A-induced human immune interferon (IFN gamma).

Antiserum to human gamma interferon (IFN gamma) was produced in rabbits immunized with partially purified (10(4.8) to 10(6.2) antiviral U/mg protein) staphylococcal enterotoxin A-induced IFN gamma. Staphylococcal enterotoxins, phytohemagglutinin M, concanavalin A, and pokeweed mitogen-induced antiviral activity in human leukocyte cultures was neutralized to undetectable levels by the antiserum. However, human leukocyte interferon (IFN alpha), human fibroblast interferon (IFN beta), and mouse interferons were not neutralized by the antiserum. After determining the antiserum was specific for IFN gamma and did not neutralize other known types of interferon, it was used with antibody to human IFN alpha to demonstrate the type(s) of interferon stimulated by some new inducers and antigens. Galactose oxidase- and calcium ionophore-induced interferons were neutralized to undetectable levels by the antiserum to IFN gamma. Interferon produced in leukocyte cultures from tuberculin-negative individuals stimulated with tuberculin-purified protein derivative or old tuberculin was IFN alpha, whereas interferon from tuberculin-positive individuals was a combination of alpha and gamma IFN. In addition, the antiserum neutralized the anticellular and natural killer cell enhancement activities of IFN gamma preparations. The specificity of this antiserum for IFN gamma indicates that it is an additional, powerful tool for identifying and classifying known and new interferons produced in vitro or in vivo and for investigating the role(s) of IFN gamma during the course of infectious, neoplastic, and autoimmune diseases.

Animals↗
PubMed1984

[Morphological and histochemical study of the action of a native Clostridium perfringens type A enterotoxin on a model of the ligated ileal loop in the rabbit].

Morphological studies carried out in the igated loop of the rabbit small intestine, used as a model, have revealed that the action of the enterotoxins of C. perfringens type A reference strain and C. perfringens type A strains isolated in the USSR on the intestinal mucosa is absolutely identical. This action is manifested by the destruction of epithelial cells on the tops of the villi, inflammatory infiltration and considerable exudation of fluid into the lumen of the intestinal loop. Early lesions of the brush border of enterocytes, accompanied by the loss of alkaline phosphatase activity and the disappearance of the glycocalix, have-been histochemically established. C. perfrinegens antienterotoxic serum has proved to be capable of completely neutralizing the histopathological activity of C. perfringens enterotoxin.

Alkaline Phosphatase↗
PubMedDate not supplied

[A cause, sub-estimated in France, of the deadly necrotic enteritis: the enterotoxin of welchia (author's transl)].

The symptoms and the lesions observed in the serious enteritis, often very severe, whose agent is W. perfringens A (and sometimes W. agni C) is an enterotoxin known only since the works of Hauschild (1971) and Duncan (1972). This enterotoxin is very different from the other toxinic factors of this anaerobic. This new toxin has been studied by foreign people and very little in France. It was isolated, purified and structured: it is a simple protein of PM +/- 34000, erythematous, inducing severe diarrhea, whose study was realized by the technic of ligatured ileal ansa of the rabbit. Its biosynthesis is related to the sporulation. In the experiment animal, it lyzes the intestinal villosities and denudes the membranes, what makes possible for the other toxins of A type to necrose the intestine. Its diagnostic evaluation is essential for a specific therapy.

Animals↗
PubMed1984

Primary structure of heat-labile enterotoxin produced by Escherichia coli pathogenic for humans.

Heat-labile enterotoxin of Escherichia coli pathogenic for humans (LTh) or for piglets (LTp) and Vibrio cholerae enterotoxin (CT) are structurally and functionally similar toxins. We have determined the complete nucleotide sequence of the toxA gene which encodes the subunit A of LTh (LTh A). The deduced amino acid sequence consists of 258 residues including a signal peptide of 18 residues. According to the previously completed LTh B sequence (103 residues), the predicted holotoxin (1A5B) of LTh comprises 755 residues and has Mr = 87,866. With respect to LTh A and LTh B, secondary structures, local hydrophilicity, and sites for antigenic determinants were predicted. Both codon usage and G + C content of the toxA gene and the LTh B gene (toxB) were markedly different from those observed with several E. coli chromosomal genes. Its relatively low G + C content was rather close to that of the V. cholerae chromosome. Although the toxA gene shares a common ancestor with the LTp A gene (eltA), the two genes are apparently distinguishable from each other in their sequences. Like LTh B reported previously, the predicted sequence of the catalytic fragment LTh A1 also showed more homology to that of CT A1 than did that of LTp A1. In contrast, unique sequences were found in LTh A2.

Amino Acid Sequence↗