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Biomedical subjects

A Bertin

Publications and source records attributed to A Bertin.

At least 19 recordsLinked to original sources
PubMed1998

Phenotypic expression of K88 adhesion alone or simultaneously with K99 and/or F41 adhesins in the bovine enterotoxigenic Escherichia coli strain B41.

F41-positive and F41-negative derivatives of bovine enterotoxigenic Escherichia coli strain B41 carrying K88 or K88 and K99 plasmids were investigated for stability and expression of genes for their fimbrial antigens. Either K88 plasmid alone or both K88 and K99 plasmids could be maintained in these strains though stability could depend on culture medium. K99 antigen could be detected in each strain bearing K99 plasmid. Clones that produced K88 antigen or clones that did not produce this antigen could be isolated from each strain, except from the strain that possessed K99 plasmid in the strain that did not possess the ability to produce F41 antigen. Strains possessing K88 plasmid in the strain able to produce F41 antigen produced clones expressing either both K88 and F41 antigens, (also F41 appeared strongly expressed in some clones) or clones that produced only F41 antigen or no antigen at all. Clones that produced only K88 antigen or others that did not produce this antigen could be produced from a strain bearing only K88 plasmid and that did not possess the ability to produce F41 antigen. None of these strains bearing K88 plasmid alone or additionally K99 plasmid produced mannose-resistant hemagglutination of horse or sheep erythrocytes at 20 degrees C as found for K99 and F41 ETEC natural strains, respectively. These results suggested that the structures of pili when several genetic determinants were present simultaneously may not be identical to those of original strains. In this study, clones expressing either one, two or three adhesin bearing antigens could be obtained from the strain B41.

Adhesins, Escherichia coli↗
PubMed1995

[Midazolam versus placebo before spinal anesthesia].

The goal of this randomized, double blind and multicentric study was to compare the effects of midazolam (M) and placebo (P) administered by titration before puncture for spinal anaesthesia on the comfort of 211 patients scheduled for elective surgery after oral premedication with hydroxyzine. The administered dose of midazolam was 3.4 +/- 1.3 mg (mean +/- SD). Anxiety was nil in 92% of the patients of the M group and in 64% of the patients of the P group (p < 0.001) and memorization of the pain of the puncture was reported in 34% of the patients of the M group and in 66% of the patients of the P group (p < 0.001). However cooperation of the patient and easiness of the puncture were similar in both groups. In conclusion titrated sedation with midazolam before puncture for spinal anaesthesia increases the comfort of the patient.

Adjuvants, Anesthesia↗
PubMed1992

Plasmid content and localisation of the STaI (STaP) gene in enterotoxigenic Escherichia coli with a non-radioactive polynucleotide gene probe.

Enterotoxigenic Escherichia coli (ETEC) strain P2200 of porcine origin possessed eight possibly plasmid-determined characters (K88+ Raf+ Hly+ Col+ Smr Tcr Su(r) STa+) and six plasmid DNA bands of 4.2-93 kb. Analysis of the spontaneous loss of characters and the results of matings with other E. coli strains revealed that the K88, Raf, Hly, Smr, Tcr and Su(r) characters could be transferred, and that the presence of the K88 and Raf characters was associated with an 83-kb plasmid. The presence and location of the STaI gene was investigated in several ETEC strains of bovine or porcine origin. Hybridisation with a non-radioactive polynucleotide probe associated the STaI gene with a plasmid in each strain; these plasmids were of 32-142 kb. In contrast, plasmids from a P2200 STa- variant and plasmids from two STa- variants of the bovine ETEC strain B41* (strain B41 obtained from a different source) did not hybridise with the probe. One of the B41*STa- variants had lost the STa plasmid, whereas the second variant retained a plasmid of the same size which did not hybridise. In contrast, a third B41*STa- variant retained a plasmid of the same size that still hybridised with the STaI probe. Plasmid DNA restriction fragment analysis, followed by hybridisation with the STaI probe, showed that the STaI gene was associated with 8.3-, 6.8- and 3.5-kb plasmid fragments in strain B41, and with 4.9-, 6.8- and 3.5-kb plasmid fragments in strain B41*, following digestion with EcoRI, BamHI, or EcoRI + BamHI, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Comparison of susceptibility of inbred and outbred infant mice to Escherichia coli heat-stable enterotoxin STa.

Comparison of the susceptibility of outbred OF1 and inbred BALB/c, C57BL/6, DBA/2, and CBA mice to heat-stable toxin (STa) of enterotoxigenic Escherichia coli was made at different levels of induced secretion. STa was able to elicit fluid accumulation into the intestine of each strain of mice; however, quantitatively different results were obtained. Results were as usual expressed by gut weight/remaining body weight ratios. Fluid accumulation weight and fluid accumulation weight/remaining body weight ratios were also estimated. Values obtained for BALB/c and OF1 mice were never significantly different, but values for OF1 mice were significantly higher than those for DBA and C57BL/6 mice at the highest concentrations of toxin (toxin dilutions of 1/2, 1/4, and 1/5). At the highest toxin concentration, gut weight/remaining body weight ratio in C57BL/6 mice was significantly lower than that for every other strain, but the fluid accumulation value obtained for DBA mice did not differ from that for C57BL/6 mice. Fluid accumulation values for DBA mice were also significantly lower at toxin dilutions of 1/5 and 1/8 than those for every other strain, and this was also the case when estimating the fluid accumulation weight/remaining body weight ratio at a dilution of 1/8. Although the intestine of each strain of mice was able to respond to STa by fluid accumulation, differences in susceptibility of the STa receptor could exist and make DBA mice more resistant to enterotoxigenic E. coli diarrhea.

Animals↗
PubMed1990

Differences in susceptibility of inbred and outbred infant mice to enterotoxigenic Escherichia coli of bovine, porcine and human origin.

Infant mice from outbred Swiss OF1 and from inbred DBA/2, C57BL/6, BALB/cBy and CBA strains were screened for usefulness in the diarrhoea model with enterotoxigenic Escherichia coli (ETEC) strains of bovine, porcine and human origin. Mouse strains were either weakly susceptible or not susceptible to ETEC strains of porcine or human origin bearing antigen K88, 987P, CFA/I or CFA/II. In contrast, some mouse strains were highly susceptible to bovine and porcine ETEC strains bearing K99 or F41 or both antigens. Swiss OF1 and CBA infant mice were highly susceptible to one bovine ETEC strain bearing antigen K99, whereas DBA/2, BALB/cBy and C57BL/6 mice exhibited nearly complete resistance to the same ETEC strain. Except DBA/2, all mouse strains were highly susceptible to bovine and porcine ETEC strains bearing antigen F41 alone or in combination with antigen K99. Challenge ETEC strains colonised intestines of all infant mice, but they reached very high levels soon after inoculation in the diarrhoeic ones only.

Animals↗
PubMed1988

Morphological description of surface structures on strain B41 of bovine enterotoxigenic Escherichia coli bearing both K99 and F41 antigens.

In order to describe morphologically the structures on the cell surface of bovine enterotoxigenic Escherichia coli, variants of reference strain B41 (K99+F41+) either negative for K99 and positive for F41 antigens (variants B41A, B41*C), or phenotypically negative for both antigens (variants B41B1, B41B2, B41*CB), and a transconjugant harbouring the K99 plasmid and expressing the K99 adhesin [transconjugant B41 x H510a:H510(2)] were examined by transmission electron microscopy using negative staining. Several negative staining procedures were tested for strain B41 and variant B41A: direct harvesting of strains into ammonium molybdate (2%, w/v), with bacitracin (50 micrograms ml-1) as wetting agent, gave the best results. Three morphologically distinct structures on the cell surface could be identified in cultures grown on Minca medium. Firstly, thin, filamentous, flexible fibrillar structures, presenting a helical structure and a mean diameter of approximately 3 nm, were recognized as K99 fimbriae, since they were present on strain B41 and on transconjugant H510(2), but not on K99-negative variants nor on the recipient strain H510a. Secondly, coil-like structures with a diameter of about 17-20 nm were observed on strain B41 and on variants B41A and B41*C. These structures appeared to consist of two or more curled filaments (diameter 3 nm) joined to coil on themselves into dense spirals. They were very rare in variants B41B1 and B41B2 and were absent on variant B41*CB and on a transconjugant B41* x B41*CB, which had re-acquired the K99 plasmid and which again exhibited K99 fimbriae. Strains B41 and variant B41A gown at 37 degrees C for 24 h on sheep-blood agar exhibited coiled structures like those seen on Minca medium. In contrast, after growth at 18 degrees C for 48 h (which inhibits the synthesis of F41 antigen), coiled structures were no longer expressed on the cell surface of strain B41 and variants B41A and B41*C. Thus the presence of coiled structures correlated with the expression of F41 antigen in strains and variants, which suggests that F41 had a coiled morphology. Finally, straight fimbriae (diameter 6.5-7 nm) were observed on the cell surface of every strain and variant. Their expression on the cell surface was enhanced by several subcultures in th e static broth, and it was inhibited by subculture on agar, but not by culture at 18 degrees C after serial subcultures in static broth. These facts indicated that the straight fimbriae could be common fimbriae, and excluded their being F41 structures.

Animals↗
PubMed1985

F41 antigen as a virulence factor in the infant mouse model of Escherichia coli diarrhoea.

The properties responsible for the virulence in infant mice of the bovine enterotoxigenic Escherichia coli strain B41 were investigated. A B41K99- variant previously found to be nearly as virulent as the original strain B41 (B41K99+) possessed F41 antigen and haemagglutinating properties. Two variants that did not haemagglutinate sheep and human erythrocytes were isolated from strain B41K99-. These variants simultaneously lost their ability to agglutinate with F41 antiserum and their haemagglutinating properties. They still produced heat-stable enterotoxin. The first B41K99-F41- variant was much less virulent than strains B41K99+ and B41K99-, the second was not virulent at all. F41 properties were not acquired by other E. coli strains by plasmid transfers. Non-haemagglutinating variants could not be obtained from the original strain B41K99+. However, a B41K99+F41- strain was obtained by a four-step procedure: (i) spontaneous loss of the K99 plasmid, (ii) obtaining a nalidixic acid-resistant mutant, (iii) obtaining a non-haemagglutinating F41- variant, (iv) reacquisition of the K99 plasmid. This B41NalrK99+F41- strain, although producing heat-stable toxin, was not at all virulent, whereas reacquisition of the K99 plasmid by the strain B41NalrF41+ restored virulence. These results show that F41 antigen is an important virulence factor of strain B41 in the infant mouse model.

Animals↗
PubMed1983

Virulence factors of enterotoxigenic E. coli studied in the infant mouse model.

Enterotoxigenic E. coli (ETEC) strain B41 orally inoculated in infant mice at birth induces lethal diarrheoal disease. This model was used to study virulence factors of ETEC strains of bovine and porcine origins. Strains possessing different plasmid-coded virulence factors were obtained either after spontaneous loss of these factors from the original strain or by plasmid transfer to different E. coli. A clone B41A derived from the strain B41 did not produce K99 antigen, but still produced heat-stable (ST) toxin. This clone B41A was about as pathogenic as the strain B41 in that it caused death of nearly all animals less than 48 h after inoculation with 10(3) bacteria. Plasmids were transferred from the strain B41 to E. coli C600, to nalidixic acid resistant mutants of strains of serotypes O8, O9, O101 and to an E. coli strain isolated from a suckling mouse intestine. K99+ Ent+ transconjuguant clones were either not all or mildly pathogenic. Two strains of porcine origin K88+ Ent+ were mildly pathogenic for mice. Loss of factor K88 did not reduce virulence. In contrast, loss of both K88 and Ent characteristics suppressed virulence. Strain E. coli K12 that had acquired K88 virulence factor possibly with other plasmid-coded characteristics but not the ability to produce ST toxin was non-pathogenic. Hence factors K99 and K88 may not be essential for inducing mortality in the infant mouse model. Other factors may be involved in virulence of the strain B41A. These results were discussed from the viewpoint of pathogenicity for mice and for ETEC natural hosts.

Animals↗
PubMed1982

Effect of propranolol on the secretory activity of Escherichia coli heat-stable enterotoxin in the suckling mouse assay.

The effect of propranolol pretreatment on fluid accumulation induced in the suckling mouse by heat-stable toxin from Enterotoxigenic Escherichia coli strains of bovine and human origin was studies. The ratio of intestinal weight to body weight is reduced after subcutaneous and per os propranolol treatment when sub-maximal fluid accumulation is induced by diluted crude supernatants of cultures of ETEC reference strain B41. The effect is not dose-dependent above 6.25 m/kg. Propranolol can antagonize fluid accumulation induced by heat stable toxin from reference strain H 10407 at the same doses, although the results are only significant when a higher level of secretion is induced. The results show that, like other pharmacological agents whose action upon intestinal secretion by toxins is still unclear, propranolol can antagonize fluid accumulation induced in the infant mouse by heat-stable toxin.

Administration, Oral↗
PubMed1981

Chlorpromazine and propranolol extend survival of infant mice inoculated with enterotoxigenic Escherichia coli.

Effects of chlorpromazine and propranolol were tested in infant mice model of Enterotoxigenic Escherichia coli diarrhea. Reference strain B41 inoculated orally from 18 h to 48 h after birth causes death of almost all animals in less than 48 h. Both drugs, which are known to reverse submaximal induced secretion by heat-stable toxin in the suckling mouse assay, used as single treatment, were able to extend the survival of mice.

Administration, Oral↗
PubMed1979

Immobility induced by forced swimming in rats: effects of agents which modify central catecholamine and serotonin activity.

Rats were forced to swim in a restricted space will rapidly cease apparent attempts to escape and adopt a characteristic posture which we have termed "immobility". We show in previous experiments that immobility was reduced by a variety of antidepressant agents and thus suggested that the method could serve as a screening model for antidepressants. The present experiments showed that immobility was reduced by drugs which increase central dopaminergic and alpha-adrenergic activity but was less affected by drugs which act mainly on central serotonin. Conversely, immobility could be increased by drugs which diminish central catecholamine activity but not by drugs which inhibit central serotonin. It was concluded that immobility depended primarily on the activity of central catecholamines but that caution was required before ascribing immobility exclusively to activity within a single system.

Animals↗
PubMed1978

"Behavioural despair" in rats and mice: strain differences and the effects of imipramine.

Rats and mice when forced to swim in a restricted space will rapidly cease attempts to escape and become immobile. Previous experiments have shown that immobility was selectively reduced by antidepressant agents. The present experiments show that important differences exist between strains in both the amount of immobility observed and the effects of imipramine. Strain differences should therefore be taken into account in attempts to replicate results from one laboratory to another.

Animals↗