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P Lintermans

Publications and source records attributed to P Lintermans.

At least 19 recordsLinked to original sources
PubMed1996

Characterization of F18 fimbrial genes fedE and fedF involved in adhesion and length of enterotoxemic Escherichia coli strain 107/86.

Infection of susceptible weaned pigs with oedema disease strains of E. coli is associated with bacterial adhesion to the small intestine. F18 fimbria (previously named F107) was the first colonisation factor described on oedema disease strains, and its genetic determinant was cloned. In the present study, genes fedE and fedF were positioned in the F18 gene cluster, downstream of the major structural subunit gene fedA. Two fedE and two fedF mutants were identified that had lost their capacity to adhere to isolated porcine villi. Moreover, these mutants produced significantly longer fimbriae. In vitro adhesion tests, electron microscopy study, transcomplementation tests, and nucleotide sequence analysis indicated that proteins FedE and FedF are F18 minor subunits essential for fimbrial adhesion and effecting fimbrial length.

Bacterial Adhesion↗
PubMed1995

Cloning and nucleotide sequence of the gene coding for the major 25-kilodalton outer membrane protein of Brucella abortus.

The cloning and sequencing of the Brucella abortus major 25-kDa outer membrane protein (OMP) is reported. The 25-kDa (group 3) OMP has been proposed, on the basis of amino acid composition, to be the counterpart of OmpA (D. R. Verstraete, M. T. Creasy, N. T. Caveney, C. L. Baldwin, M. W. Blab, and A. J. Winter, Infect. Immun. 35:979-989, 1982). However, the amino acid sequence predicted from the cloned B. abortus gene did not reveal significant homology with either OmpA sequences from different members of the family Enterobacteriaceae or other known protein sequences.

Amino Acid Sequence↗
PubMed1994

Sequences related to the major subunit gene fedA of F107 fimbriae in porcine Escherichia coli strains that express adhesive fimbriae.

Porcine Escherichia coli strains isolated from cases of postweaning diarrhea or edema disease were analysed for the presence of fedA, the major subunit gene of F107 fimbriae. The E. coli isolates were known to contain colonisation factor '8813', or to express F107, 2134P or other fimbriae, different from F4, F5, F6, and F41. PCR with fedA-specific primers, restriction enzyme digestion of the PCR product, and nucleotide sequence analysis demonstrated that 2134P pili, colonisation factor '8813' and fimbriae identified on Australian strains of the O141 serotype belong to one family of F107 fimbrial antigens.

Amino Acid Sequence↗
PubMed1994

Prevalence of F107 fimbriae on Escherichia coli isolated from pigs with oedema disease or postweaning diarrhoea.

The study comprises fifty 4 to 12 weeks old pigs that died from oedema disease or severe diarrhoea. Smears were prepared from the mucosa of duodenum, jejunum and ileum, and by immunofluorescence F107 fimbrial antigens were detected. E. coli strains were isolated from the intestines and were characterised by slide agglutination (serogroup and F107 fimbriae production), by their cytotoxicity for Vero cells, and by gene amplification (genes coding for the major F107 subunit FedA, the toxin causing oedema disease SLT-IIv, and enterotoxins LTI, STIa and STII). F107 fimbriae were demonstrated in association with E. coli of serogroups O139:K12 and O141:K85a,b but not of serogroup O149:K91:F4a,c. Expression in culture of F107 fimbriae by some isolates gave additional evidence for production of these fimbriae by ETEC strains. The genetic determinant of SLT-Ilv was found in association with F107, and could not be detected in serogroup O149:K91:F4a,c. Gene fedA was demonstrated in two isolates which were devoid of SLT-IIv. Most isolates from cases of oedema disease belonged to serogroup O139:K12 and did not contain enterotoxin genes. Isolates from pigs that suffered from diarrhoea were serotyped O141:K85a,b or O149:K91:F4a,c, and carried at least two enterotoxin genes in their genomes. In a small proportion of the cases F107 antigens were demonstrated in intestinal smears although gene fedA was not detected in the corresponding isolates. The results confirm the importance of F107 fimbriae as virulence factor in oedema disease E. coli strains, but also demonstrate that F107 fimbriae can be found in association with postweaning diarrhoea isolates. In these latter strains enterotoxins were always demonstrated, irrespective of the presence of toxin SLT-IIv.

Animals↗
PubMed1994

Specific DNA probes to detect Escherichia coli strains producing cytotoxic necrotising factor type 1 or type 2.

Cytotoxic necrotising factors type 1 (CNF1) and type 2 (CNF2) are produced by many Escherichia coli strains isolated from man and animals with intestinal or extra-intestinal colibacillosis. In most laboratories, CNF-producing strains are detected by a cell cytotoxicity assay and confirmed with a neutralisation assay or a mouse footpad assay. In this study, we sought to determine whether DNA probes could detect clinical isolates of E. coli producing CNF2 or CNF1, or both, without the need for cell cultures or animal assays. Two internal fragments of the gene encoding CNF2 were used as DNA probes: a 875-bp XhoI-PstI DNA fragment and an adjacent 335-bp PstI-ClaI fragment. A positive response with both DNA probes was associated with CNF2-producing strains, whereas a positive response with only the 335-bp probe was associated with CNF1-producing strains. Results of colony hybridisation experiments with 185 clinical isolates of E. coli demonstrated that these DNA probes detected CNF2-producing strains with a sensitivity and specificity of 100% and CNF1-producing strains with a sensitivity and specificity of 99%. These two DNA probes should greatly facilitate epidemiological studies to assess the importance of CNF-producing strains as agents of diarrhoea and septicaemia.

Animals↗
PubMed1994

F17-like fimbriae from an invasive Escherichia coli strain producing cytotoxic necrotizing factor type 2 toxin.

The F17b fimbriae encoded by the transmissible virulence plasmid Vir, also coding for cytotoxic necrotizing factor type 2, were characterized. A 5.7-kb region of Vir mediates in vitro N-acetylglucosamine-sensitive adhesion to calf intestinal villi. Sequence analysis revealed that this region codes for a structural subunit and an adhesin closely related to the F17-A and F17-G proteins encoded by the F17 fimbrial gene cluster. The F17b-A gene presents an open reading frame of 540 bp encoding a polypeptide of 180 amino acids with a putative signal peptide of 21 residues. The mature protein shows an identity of 74% with the F17-A structural subunit. This 20-kDa protein is recognized by antiserum directed against F17 fimbriae. The F17b-G gene shows an open reading frame of 1,029 bp encoding a polypeptide of 343 amino acids with a putative signal peptide of 22 residues. The F17b-G polypeptide exhibits 95% identity with the F17-G adhesin. The functional homology of the gene products was further confirmed by demonstrating that mutants in the F17-A gene can be complemented by the F17b-A gene and vice versa. These results prove that fimbriae belonging to the F17 family are also found on pathogenic Escherichia coli strains other than enterotoxigenic isolates producing heat-labile or heat-stable enterotoxin.

Adhesins, Escherichia coli↗
PubMed1993

Inhibition of adhesion of enterotoxigenic Escherichia coli cells expressing F17 fimbriae to small intestinal mucus and brush-border membranes of young calves.

Enterotoxigenic Escherichia coli strains expressing F17 fimbriae bind to the intestinal mucosa of young calves. F17 fimbriae recognize receptors present in the mucus layer and the brush-border membranes from duodenum, jejunum and ileum. The adhesion of E. coli F17 can be inhibited by several glycoproteins. Adhesion is also inhibited by pretreatment of mucus and brush-border membranes with sodium metaperiodate. The use of glycoconjugates as potential adhesion-blockers is further discussed.

Adhesins, Escherichia coli↗
PubMed1993

Replicon typing characterization of plasmids encoding resistance to gentamicin and apramycin in Escherichia coli and Salmonella typhimurium isolated from human and animal sources in Belgium.

Escherichia coli and salmonella strains with plasmids conferring resistance to gentamicin and apramycin have been isolated with increasing frequency both from cattle and hospital patients in Belgium. The apramycin-gentamicin resistance plasmids were characterized in recipient strains by their profiles and molecular weights using agarose gel electrophoresis, by their antimicrobial resistance patterns and by replicon typing using a series of DNA probes specific for the genes controlling their systems of replication. Overall, most of the plasmids differed in their DNA electrophoretic patterns. Seventeen different antimicrobial resistance profiles were observed, and there were six different types of replicons. However, two replication genes predominated and had a preferential distribution in different bacterial species. The rep FIC.a plus rep Q multireplicon was found mainly in plasmids recovered from gentamicin- and apramycin-resistant E. coli while replicon of the type rep FIC.b largely prevailed in S. typhimurium. Identical replication genes were found in most animal and human strains, hence suggesting a high homology between apramycin-gentamicin plasmids in these communities. Finally, our results indicate that the rapid spread of apramycin-gentamicin-resistance in several species of Enterobacteriaceae isolated from animals and from humans in Belgium is not due to a single plasmid, but rather that the gene encoding AAC(3)-IV is carried by various replicons.

Animals↗
PubMed1993

Escherichia coli producing CNF1 and CNF2 cytotoxins in animals with different disorders.

Two DNA probes were used for the detection of CNF1- and CNF2-positive E coli strains in a collection of 553 E coli isolates from cattle, sheep, goats, pigs, horses, dogs, cats and poultry. CNF-positive E coli were frequently associated with septicaemia in cattle, dogs, and cats, with diarrhoea in calves, cats and dogs, and with abortion in bovine and porcine species. CNF2-positive strains were observed among adult healthy cattle. They were also found in cases of pneumonia, metritis, mastitis in cattle and in 1 case of metritis of a mare. The physiopathology induced by CNF-positive E coli strains remains to be elucidated. However, the impact of CNF strains on veterinary pathology is clear and the diagnosis of CNF-producing E coli should become routine in veterinary practice.

Animals↗
PubMed1992

The pathogenesis of edema disease in pigs. A review.

Edema disease is known to cause important losses in the period shortly after weaning. Although the disease is known for many decades, intensive studies with bacterial lysates of pathogenic E. coli, followed by biotechnological research the last ten years, has led to a better understanding of its pathogenesis. Especially the impact of the toxin is clearly established. Evidence also exists that adhesion factors play a crucial role in the pathogenesis of edema disease.

Animals↗
PubMed1992

[Virulence factors and phenotypes of sixty-one strains of Escherichia coli of bovine origin, producing cytotoxic necrotising toxin type 1 (CNF 1)].

Virulence factors and phenotypes of 61 strains CNF1+ were investigated. Eighty-nine percent of the strains produced an aerobactin and were resistant to the bactericidal activity of sheep serum, both of which are properties of septicemic strains of E coli. None of the strains reacted either with DNA probes corresponding to the enterotoxins STaP, STb, LT-I and LT-IIa, or to the verotoxins VT-I and VT-II. None produced the adhesins K99, Att25 (FY or F17) and Att111. The great majority (93.4%) of the CNF1+E coli possessed both properties. These properties allow CNF1+ to be distinguished from CNF-E coli.

Animals↗
PubMed1991

Epidemiological study of Salmonella enteritidis strains of animal origin in Belgium.

Since 1987, the number of cases of salmonellosis caused by Salmonella enteritidis has considerably increased in Western Europe. Comparison of endemic animal strains isolated in Belgium from 1976-84 with strains isolated from 1987 on shows that the strains which cause the current epidemic have no features distinguishing them from the previously-isolated strains and that furthermore, they do not constitute a bacterial clone. They belong to 13 different lysotypes and in most cases remain sensitive to antibiotics. Nevertheless, the lysotype 33 (which belongs to the phage type 4 has increased significantly. It encompasses 37% of the animal strains isolated in Belgium from 1987-9, but only 7% of the strains isolated from 1976-84. It is worth noting that the endemic as well as the epidemic strains contain a virulence plasmid sharing sequence similarities with the FIB and FIIA plasmid replicons and with the VirA and VirB virulence regions of the S. typhimurium virulent plasmid: pIP1350.

Animals↗
PubMed1991

Virulence factors associated with cytotoxic necrotizing factor type two in bovine diarrheic and septicemic strains of Escherichia coli.

Forty-three bovine isolates of Escherichia coli producing a second type of cytotoxic necrotizing factor (CNF2) and three K-12 strains carrying different Vir plasmids coding for CNF2 were tested for the presence of several virulence factors. Most of the strains were serum resistant (79%), produced an aerobactin (70%), and adhered to calf villi (53%); some of them produced a colicin (32%) and a hemolysin (9%). These strains were also tested by a colony hybridization assay with gene probes for six toxins (classical heat-stable [STaP and STb] and heat-labile [LT-I and LT-IIa] enterotoxins and Shiga-like toxins [SLT-I and SLT-II]) and five adhesion factors (K99, K88, 987P, F17, and F41). Only two gene probes, LT-IIa (9%) and F17A (53%), hybridized with the CNF2 strains. However, antibodies raised against F17 fimbriae did not agglutinate the strains hybridizing with the F17A probe. In contrast, all except one of these strains adhered to calf villi. Interestingly, these two properties, F17A positivity and adherence to calf villi, were the only ones expressed by the K-12 strains carrying different Vir plasmids. In conclusion, this study confirmed that CNF2-producing strains are unrelated to previously described toxigenic E. coli strains and also demonstrated that in half of the strains the production of CNF2 was associated with an adhesion factor genetically related to, but different from, F17, which is more than likely encoded by Vir plasmids.

Animals↗
PubMed1988

Isolation and nucleotide sequence of the F17-A gene encoding the structural protein of the F17 fimbriae in bovine enterotoxigenic Escherichia coli.

The genetic determinant for production of the fimbrial F17 adhesive antigen was isolated from a bovine enterotoxigenic Escherichia coli strain. The F17-A gene, coding for the structural component of the F17 fimbrial adhesin, was cloned and sequenced. An open reading frame of 540 base pairs encoding a polypeptide of 180 amino acids, of which the NH2-terminal 21 residues are characteristic of a signal sequence, has been characterized. The mature protein lacks histidine, methionine, and tryptophan. A possible promoter and ribosome binding site as well as a possible site for termination of transcription are proposed. An important homology of the F17-A protein with fimA and papA fimbrial proteins was found. The N-terminal sequence of the mature F17-A pilin is extremely similar to the N-terminal sequence of the G fimbriae identified on human pyelonephritogenic E. coli strains.

Amino Acid Sequence↗