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PubMed1984

Does enteropathogenic Escherichia coli produce heat-labile enterotoxin, heat-stable enterotoxins a or b, or cholera toxin A subunits?

Although most enteropathogenic Escherichia coli strains do not produce recognized enterotoxins, we wished to examine whether they produce any factors like heat-stable enterotoxin b or cholera toxin active subunits that might be missed by conventional assay methods. E. coli strains E851 (O142) and E2348 (O127) that had caused diarrhea in volunteers were negative for heat-labile enterotoxin and heat-stable enterotoxin a in Chinese hamster ovary cell and suckling mouse assays, failed to cause secretion in ligated small bowel loops from 6- to 8-week-old pigs after 4 to 5 h (used to show heat-stable enterotoxin b), and did not activate adenylate cyclase in pigeon erythrocyte lysates (used to demonstrate cholera toxin A subunit). We conclude that crude, unconcentrated culture filtrates and sonicates do not mimic heat-labile or heat-stable enterotoxins or cholera toxin or its A subunit and that enteropathogenic strains of E. coli probably have yet another mechanism or group of mechanisms by which they cause diarrhea.

Animals↗

PubMed1987

[Immunochemical characteristics of the subunits of cholera enterotoxin and of thermolabile Escherichia coli enterotoxins of various origins].

Antigenic determinants of subunits A and B of cholera enterotoxin (CT), heat-labile enterotoxin from the human E. coli strain (hLT) and heat-labile enterotoxin from the porcine E. coli strain (pLT) were analysed by Ouchterlony double gel-diffusion test against antisera to B subunits of three toxins and antisera to three holotoxins. The results have shown the existence of the following antigenic determinants: in subunits B-1. antigenic determinants, common for B subunits of all three enterotoxins-B(chp); 2. group antigenic determinants, common for B subunits of two toxins in the pair-B(ch), B(hp); 3. antigenic determinants, unique for B subunits of each CT, hLT, pLT-(B(c), B(h), B(p); in subunits A.-1. antigenic determinants, common for A subunits of all three enterotoxins-A.(chp); 2. group antigenic determinants, common for A subunits of two enterotoxins (hLT and pLT/-A(hp); 3. antigenic determinants, unique for A subunit of CT-A(c). On the basis of these results antigenic formulas for subunits of CT, hLT, pLT were proposed.

Animals↗

PubMed1999

Infants colonized with enterotoxin-producing staphylococci at 3 months display a decreased frequency of interferon-gamma-producing CD45RO lymphocytes upon stimulation with staphylococcal enterotoxin A at birth but not at 6 months of age.

The aim of the study was to elucidate the relationship between the cytokine response to staphylococcal enterotoxin A (SEA) at birth and subsequent staphylococcal colonization in the first months of life. In a cohort of 45 newborns, cord blood lymphocytes were stimulated with SEA (10 ng/ml) in vitro, re-stimulated with PMA (phorbol myristate acetate) and ionomycin at day 3 and assessed for CD45RO expression and cytokine generation by flow cytometry. The infants were classified into three groups according to nasal staphylococcal colonization and enterotoxin generation at 3 months: There were 16 infants with either no colonization or non-enterotoxin-producing staphylococci, 16 infants with enterotoxins B, C, D and E, and 13 infants colonized with SEA-producing staphylococci. At birth, the group without subsequent colonization displayed a significantly higher frequency of CD45RO-positive interferon-gamma-producing cells (1.7%; range 0.0-9.3%) in comparison to the SEA-positive group (0.1%; range 0.0-0.4%) and also to the group positive for other enterotoxins (0.50%; range 0.0-2.5%). Comparable but less pronounced results were found for interleukin-5 but not for interleukins 2 and 4. At 6 months, no differences in cytokine generation were detected between the three groups. The results provide evidence that a non-specific immunologic immaturity at birth is a risk factor for early bacterial colonization. Furthermore, it is remarkable that this immaturity is similar to that seen in infants destined to be atopic with respect to disequilibrium of interferon-gamma to interleukin-4 generation. Thus the link between early staphylococcal colonization and subsequent atopy requires further investigation.

Age Factors↗

PubMed2001

Production of a mouse antiserum to Bacteroides fragilis enterotoxin using a recombinant enterotoxin precursor.

The precursor of the Bacteroides fragilis metalloprotease enterotoxin was cloned and expressed in Escherichia coli, which was not able to process the precursor into the biologically active enterotoxin. Mouse antiserum elicited to the recombinant precursor reacted with the purified enterotoxin and with a crude enterotoxin preparation from an enterotoxigenic strain. The antiserum neutralized the cytotoxic activity of the enterotoxin in HT-29 cells.

Animals↗

PubMed1982

Further evaluation of the Biken test (modified Elek test) for detection of enterotoxigenic Escherichia coli producing heat-labile enterotoxin and application of the test to sampling of heat-stable enterotoxin.

A total of 2,229 strains of Escherichia coli isolated from subjects with traveller's diarrhea were tested for heat-labile enterotoxin production by the Biken test (Honda et al., J. Clin. Microbiol. 13:1--5, 1981). Results of the Biken test showed a 99.0% coincidence with those obtained by Chinese hamster ovary cell assay. The use of antiserum against E. coli heat-labile enterotoxin gave sharper and clearer results than did the use of antiserum against cholera enterotoxin. Samples for heat-stable enterotoxin assay were obtained from the agar plates used for the Biken test, and the heat-stable enterotoxin activities of these samples were compared with those of samples obtained from standard liquid cultures. Results for samples of 2,229 strains from the Biken agar plates and from liquid cultures were almost identical.

Bacteriological Techniques↗

PubMed1978

Detection of Clostridium perfringens enterotoxin in human fecal samples and anti-enterotoxin in sera.

By using counterimmunoelectrophoresis (CIEP), Clostridium perfringens enterotoxin was successfully demonstrated in fecal samples collected within 1 day of attack from sick individuals involved in a bacteriologically and epidemiologically proven outbreak of C. perfringens food poisoning. In contrast, enterotoxin was not demonstrable in fecal samples of apparently healthy individuals both at high- and low-risk exposure to the organism and enterotoxin or in fecal samples collected 4 to 5 days after a food poisoning outbreak. A 100% prevalence of C. perfringens anti-enterotoxin in sera of human volunteers at high- as well as low-risk exposure to the organism and enterotoxin was recorded with CIEP.

Allied Health Personnel↗

PubMed2001

Prevalence of the enteroaggregative Escherichia coli heat-stable enterotoxin 1 gene and its relationship with fimbrial and enterotoxin genes in E. coli isolated from diarrheic piglets.

A total of 720 Escherichia coli strains isolated from diarrheic piglets on 756 swine farms were screened for the presence of the enteroaggregative E. coli heat-stable enterotoxin 1 (EAST1) gene by polymerase chain reaction (PCR). Escherichia coli strains that carried EAST1 genes were also tested by PCR for the presence of 4 fimbriae (F4, F5, F6, F41), 2 heat-stable enterotoxins (STa and STb), and 1 heat-labile enterotoxin (LT) gene. One hundred sixty-four (22.7%) of the 720 E. coli isolates carried genes for EAST1. Of these 164 isolates, 62 (37.8%) carried EAST1 genes only, 11 (6.7%) carried genes for at least 1 of the fimbrial adhesins, 51 (31.1%) carried genes for at least 1 of the enterotoxins, and 40 (23.8%) carried genes for at least 1 of the fimbrial adhesins and enterotoxins. Forty-six percent of strains that carried EAST1 genes carried STa genes, and 16% of strains that carried EAST1 genes carried F4. The isolation rate of enterotoxigenic E. coli strains carrying genes for EAST1 gene was 63%. The 6 major genotypes observed in this study (in decreasing order) were EAST1+, EAST1+STa+, EAST1+STa+STb+, EAST1+STa+F5+, EAST1+STa+F4+, and EAST1+STb+F4+. EAST1 is widely prevalent among diarrheagenic strains of E. coli and may represent an important virulence determinant in the pathogenesis of enteric colibacillosis of preweaned pigs.

Animals↗

PubMed1997

Oral tolerance to ovalbumin in mice: induction and long-term persistence unaffected by Staphylococcus aureus enterotoxin B and Clostridium perfringens type A enterotoxin.

Oral administration of dietary antigen (Ag) results in the systemic Ag-specific immunologic unresponsiveness termed oral tolerance. Its induction is of importance in the young where numerous symptoms are associated with IgE-mediated food-hypersensitivity reactions. Two related enterotoxins, cholera toxin and Escherichia coli heat-labile enterotoxin, have been shown to abrogate oral tolerance (i.e. IgG and IgE antibody (Ab) unresponsiveness) to an unrelated and simultaneously fed Ag. However, a critical role has been suggested for the gut flora in recovery of a hyporesponsive state. The purpose of the present study was to investigate whether the Staphylococcus aureus enterotoxin B (SEB) and Clostridium perfringens type A enterotoxin (CPE), involved in many diarrheas, could affect the induction and long-term persistence of oral tolerance to ovalbumin (OVA). Using conventional and germ-free mice fed once or twice with enterotoxin plus OVA, we investigated the possible role of the indigenous gut flora. In addition, we tested the influence of CPE synthesized in vivo in the digestive tract of gnotobiotic mice on the induction of OVA-specific oral tolerance. Mice were immunized intraperitoneally with OVA twice, and IgG and IgE Ab levels were measured by ELISA. Neither SEB nor CPE, orally given or synthesized in vivo (CPE), prevented the induction of oral tolerance to OVA. Moreover, the IgG Ab unresponsiveness persisted over 2 mo in the conventional mice fed with toxin plus OVA as also observed in the OVA controls. The results indicate that, independent of the gut flora's influence, SEB and CPE did not affect the induction nad long-term persistence of oral tolerance to co-ingested Ag.

Administration, Oral↗

PubMed1975

The application of QAE-Sephadex for the purification of two staphylococcal enterotoxins. II. Purification of enterotoxin A.

The last three steps described in the preceding communication Robern, H., Stavric, S. and Dickie, N. (1975) Biochim. Biophys. Acta 000,000-000) were utilized successfully for the purification of enterotoxin A. The enterotoxin appeared homogeneous by gel chromatography and in the analytical ultracentrifuge but showed two bands on polyacrylamide disc electrophoresis at pH 4.5. The emetic dose, ED50, by intravenous route in cynomolgus monkeys was 0.12 mug/kg of animal weight. After treatment with beta-mercaptoethanol, urea and sodium dodecylsulfate enterotoxin A formed one band corresponding to a molecular weight of about 27700 on sodium dodecylsulfate gel electrophoresis. Molecular-weight estimation by gel filtration gave a value of 26500. The amino acid composition data indicate that enterotoxin A consists of 241 amino acid residues.

Amino Acids↗

PubMed1996

Role of staphylococcal enterotoxins in pathogenesis of atopic dermatitis: growth and expression of T cell receptor V beta of peripheral blood mononuclear cells stimulated by enterotoxins A and B.

In order to investigate the role of staphylococcal enterotoxins in the pathogenesis of dermatitis in atopic patients, the growth and expression of T cell receptor V beta in peripheral blood mononuclear cells (PBMCs) from atopic dermatitis patients induced by stimulation with staphylococcal enterotoxin A (SEA) or staphylococcal enterotoxin B (SEB) were examined. Lymphocyte stimulation tests (LST) using SEA or SEB were performed in atopic dermatitis (AD) patients (n = 10) and normal controls (n = 5). PBMCs from AD patients displayed significantly stronger responses to SEA or SEB than those from the controls. To ascertain further whether SEA acts as a superantigen in atopic dermatitis, the expression of 22 genes in the variable region of the beta chain (V beta) of T cell receptors (TcR) was examined before and after stimulation with SEA by a reverse transcriptase-polymerase chain reaction (RT-PCR). Before stimulation, only weak expression of V beta was observed, and the expression of the various V beta segments was uniform in the normal controls (n = 3). In the AD patients (n = 3), the expression of V beta was enhanced, but was not uniform in 2 out of 3 patients and the pattern of expression was characteristic in each individual. This suggests that V beta expression varies in individual AD patients and displays restricted heterogeneity, reflecting the diversity of the etiology of the disease. After culture of the SEA-stimulated cells, no difference was observed in the expression of TcR V beta segments in the 3 normal controls as compared with that prior to stimulation, but particular V beta segments were intensely expressed in 3 AD patients, displaying distinct patterns (case I: V beta 9, V beta 10, V beta 18; case 2: V beta 6.1-3; case 3: V beta 6.1-3, V beta 18). Many of these V beta segments corresponded with those known to be induced by SEA. These results suggest oligoclonal proliferation of T cells in the peripheral blood of AD patients and high responsiveness in each clone, and since the expression of V beta segment after SEA stimulation was restricted, the actions of staphylococcal enterotoxins as superantigens were suggested.

Adolescent↗

PubMed1981

A new staphylococcal enterotoxin, enterotoxin F, associated with toxic-shock-syndrome Staphylococcus aureus isolates.

612 (93.8%) of 65 Staphylococcus aureus strains isolated from 65 patients with toxic-shock syndrome (TSS) produced an enterotoxin-like protein, tentatively identified as staphylococcal enterotoxin F (SEF). One of the other strains produced staphylococcal enterotoxin B and another exterotoxin C. In two blind studies all 34 TSS-associated S. aureau strains examined and 3 (11.5%) of 26 control S. aureau strains produced SEF. 2 of the latter strains were isolated from the vaginas of women who had no history of TSS. SEF was purified, and specific antibodies to it were prepared. Only 4 (4.6%) of 87 S. aureau strains from other sources were found to produce SEF. 5 (17.2%) of 29 TSS patients whose acute sera were available had anti-SEF antibody present in titres of greater than or equal to 1:100 as determined by radioimmunoassay, compared with 44 (78.6%) of 56 controls--demonstrating a greater serosusceptibility of TSS patients to SEF. It is suggested that staphylococcal enterotoxin, particularly SEF, may be a cause of the signs and symptoms of TSS.

Antibodies↗

PubMed1982

Enterotoxin production by strains of Staphylococcus aureus isolated from clinical and non-clinical specimens with special reference to enterotoxin F and toxic shock syndrome.

Enterotoxin production by strains of Staphylococcus aureus isolated from clinical specimens of human and animal origin and from healthy human carriers was investigated. All nine patients admitted to hospital with symptoms of toxic shock syndrome (TSS) yielded enterotoxin-producing strains of S. aureus. Eight of these produced staphylococcal enterotoxin F (SEF). A significantly smaller proportion of strains (42% of 50 strains tested) isolated from other clinical specimens of hospitalized patients produced SEF. Production of SEF by strains isolated from clinical specimens of animal origin (48 strains) was not observed. Twenty-nine per cent of 24 S. aureus strains isolated from noses of hospital staff produced SEF. This result was not significantly different from that obtained from strains isolated from clinical specimens other than TSS. A similar percentage of strains isolated from healthy human carriers outside hospital produced SEF (25% of 24 strains tested). The results indicated that enterotoxin production, especially that of SEF, is associated with S. aureus isolated from patients suspected of TSS. There was no indication of an association between S. aureus isolated from other staphylococcal infections and SEF production. All strains were phage typed and 79% of the strains belonging to the international phage-group I produced SEF. All strains lysed by phage 187 were found to produce SEF.

Bacteriophage Typing↗

PubMed2006

Staphylococcal enterotoxin-like toxins U2 and V, two new staphylococcal superantigens arising from recombination within the enterotoxin gene cluster.

To test the hypothesis that the Staphylococcus aureus enterotoxin gene cluster (egc) can generate new enterotoxin genes by recombination, we analyzed the egc locus in a broad panel of 666 clinical isolates of S. aureus. egc was present in 63% of isolates, confirming its high prevalence. The archetypal organization of the egc locus, consisting of five enterotoxin genes plus two pseudogenes, was found in 409 of 421 egc-positive strains. The egc locus was incomplete in a few strains and occasionally harbored an insertion sequence and transposase genes. These strains may represent evolutionary intermediates of the egc locus. One strain with an atypical egc locus produced two new enterotoxins, designated SElV and SElU2, generated by (i) recombination between selm and sei, producing selv, and (ii) a limited deletion in the varphient1-varphient2 pseudogenes, producing selu2. Recombinant SElV and SElU2 had superantigen activity, as they specifically activated the T-cell families Vbeta 6, Vbeta 18, and Vbeta 21 (SElV) and Vbeta 13.2 and Vbeta 14 (SElU2). Immunoscope analysis showed a Gaussian CDR3 size distribution of T-cell receptor Vbeta chain junctional transcripts of expanded Vbeta subsets in toxin-stimulated cultures, reflecting a high level of polyclonality. These data show that egc is indeed capable of generating new superantigen genes through recombination.

Bacterial Toxins↗

PubMed1984

Cloning of enterotoxin gene from Aeromonas hydrophila provides conclusive evidence of production of a cytotonic enterotoxin.

Culture filtrates of two Aeromonas hydrophila strains which were isolated from patients with diarrhea and assumed to be causative agents of the infections were shown to contain enterotoxic, cytotoxic, and hemolytic activities. Modest heat treatment of the filtrates inactivated the cytotoxic and cytolytic activities, but not the enterotoxic activity. The construction of cosmid gene banks in Escherichia coli of DNA from both A. hydrophila strains demonstrated that the determinants of the three activities are located on three different segments of the A. hydrophila chromosome. Both heated culture filtrates of A. hydrophila and nonheated filtrates of an E. coli clone containing the A. hydrophila enterotoxin gene provoked fluid accumulation in the rabbit ileal loop and suckling mouse models and caused elongation of Chinese hamster ovary cells. Differences in the responses of the models to the A. hydrophila enterotoxin and to the heat-labile and heat-stabile toxins of E. coli indicated that the former is distinct from the latter two types of toxin. These results constitute conclusive evidence for the production by A. hydrophila of a cytotonic enterotoxin that is distinct from the A. hydrophila cytotoxin and hemolysin and known E. coli enterotoxins.

Aeromonas↗

PubMed1986

Plasmids coding for colonization factor antigens I and II, heat-labile enterotoxin, and heat-stable enterotoxin A2 in Escherichia coli.

Colonization factor antigens I and II (CFA/I and CFA/II) are important in the pathogenesis of diarrhea in humans caused by some enterotoxigenic Escherichia coli (ETEC). Plasmid DNA from 16 CFA/I+ and five CFA/II+ ETEC were examined by Southern blot analysis with enterotoxin gene probes and were compared with plasmid DNA from derivatives of the same ETEC that had lost the ability to produce these colonization factors. Among the 16 CFA/I+ ETEC strains, the loss of CFA/I was accompanied by the loss of a plasmid of between 34 and 68 megadaltons (MDa) coding for heat-stable enterotoxin A2 (ST-A2) in 12 strains, by the loss of a 60-MDa plasmid coding for heat-labile enterotoxin (LT) and ST-A2 in one strain, or by deletions of a segment of DNA encoding for ST-A2 in three strains. Among five CFA/II+ ETEC strains, the loss of CFA/II was associated with the loss of a plasmid of 75 MDa coding for LT and ST-A2 in three strains, with the loss of genes coding for LT and ST-A2 from a 68-MDa plasmid in one strain, or with no discernible loss of a plasmid or DNA sequences coding for enterotoxins in the remaining strain. The loss of CFA/I and CFA/II production was associated with the loss of DNA sequences encoding for ST-A2 in 20 of 21 ETEC examined.

Antigens, Bacterial↗

PubMed2004

Relative importance of heat-labile enterotoxin in the causation of severe diarrheal disease in the gnotobiotic piglet model by a strain of enterotoxigenic Escherichia coli that produces multiple enterotoxins.

Enterotoxigenic Escherichia coli (ETEC) strains that produce multiple enterotoxins are important causes of severe dehydrating diarrhea in human beings and animals, but the relative importance of these enterotoxins in the pathogenesis is poorly understood. Gnotobiotic piglets were used to study the importance of heat-labile enterotoxin (LT) in infection with an ETEC strain that produces multiple enterotoxins. LT(-) (DeltaeltAB) and complemented mutants of an F4(+) LT(+) STb(+) EAST1(+) ETEC strain were constructed, and the virulence of these strains was compared in gnotobiotic piglets expressing receptors for F4(+) fimbria. Sixty percent of the piglets inoculated with the LT(-) mutant developed severe dehydrating diarrhea and septicemia compared to 100% of those inoculated with the nalidixic acid-resistant (Nal(r)) parent and 100% of those inoculated with the complemented mutant strain. Compared to piglets inoculated with the Nal(r) parent, the mean rate of weight loss (percent per hour) of those inoculated with the LT(-) mutant was 67% lower (P < 0.05) and that of those inoculated with the complemented strain was 36% higher (P < 0.001). Similarly, piglets inoculated with the LT(-) mutant had significant reductions in the mean bacterial colony count (CFU per gram) in the ileum; bacterial colonization scores (square millimeters) in the jejunum and ileum; and clinical pathology parameters of dehydration, electrolyte imbalance, and metabolic acidosis (P < 0.05). These results indicate the significance of LT to the development of severe dehydrating diarrhea and postdiarrheal septicemia in ETEC infections of swine and demonstrate that EAST1, LT, and STb may be concurrently expressed by porcine ETEC strains.

Animals↗

PubMed1990

Stimulation of phosphorylation of rat brush-border membrane proteins by Escherichia coli heat-stable enterotoxin, cholera enterotoxin and cyclic nucleotides, and its inhibition by protein kinase inhibitors, isoquinolinesulfonamides.

Stimulation of phosphorylation of rat brush-border membrane proteins by the heat-stable enterotoxin of Escherichia coli (STh), cholera enterotoxin, cGMP and cAMP was demonstrated. Among at least 14 proteins examined, a protein with a molecular mass of 81,000 Da (81 kDa protein) was phosphorylated most in the presence of both STh and cholera enterotoxin, as well as in the presence of cGMP and cAMP. This phosphorylation was inhibited by N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide (H-8) or N-(2-aminoethyl)-5-isoquinoline-sulfonamide (H-9), which suggests that the phosphorylation occurs through cGMP- and cAMP-dependent protein kinases.

Animals↗

PubMed2003

Detection of the enteroaggregative Escherichia coli heat-stable enterotoxin 1 (EAST1) gene and its relationship with fimbrial and enterotoxin markers in E. coli isolates from pigs with diarrhoea.

The presence of the astA gene responsible for production of enteroaggregative Escherichia coli heat-stable enterotoxin 1 (EAST1) was examined in E. coli strains isolated from pigs with postweaning diarrhoea. Two hundred and seven isolates were tested using PCR for the astA marker and for heat-labile I (LTI), heat-stable I (STI), and heat-stable II (STII) enterotoxin genes. Moreover, the isolates were also analysed for their serotypes (O and K antigens) as well as for fimbrial adhesins using agglutination methods. It was shown that 96 (46.4%) of the isolates possessed the astA genetic determinant. The most common EAST1-positive E. coli serotype was O149:K91 and these strains were mostly LTI/STII-positive. A close correlation between the presence of F4 fimbriae and the EAST1 gene was also observed: 88 of 96 (91.7%) astA(+) isolates tested possessed the F4 antigen. Thus, EAST1 enterotoxin may represent an additional virulence determinant playing a role in the pathogenesis of porcine colibacillosis.

Agglutination Tests↗