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ABSTRACT: Strains of Escherichia coli isolated from documented cases of disease in pigs and belonging to a wide range of pathogenic serotypes were tested for their ability to produce a heat labile verotoxin (VT). The strains isolated from oedema disease all produced VT, indicating that the cytotoxin detected by the vero-cell assay was identical to "oedema disease principle". Strains belonging to the serotypes associated with enterotoxic diarrhoea were VT-. Not all the strains belonging to the recognised oedema disease serotypes (O141:K85, O139:K82 and O138:K81) produced VT, but the VT- strains were not associated with outbreaks of clinical disease.
Journal of Medical Microbiology 01/1988; 24(4):359-62. · 2.50 Impact Factor
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ABSTRACT: To assess the importance of aerobactin-mediated iron uptake as a bacterial virulence determinant in animal infections, a total of 576 strains of Escherichia coli isolated from cattle, chickens, sheep and pigs were screened by colony hybridization to determine the presence of the aerobactin genetic determinants, and by a bioassay to detect aerobactin secretion in iron-limited conditions. Results obtained by the two complementary methods correlated well. The incidence of the aerobactin system was very high among septicaemia isolates, particularly those from cattle and chickens, an observation that strongly suggests an important role for this mechanism of iron assimilation in pathogenesis. On the other hand, the incidence of the aerobactin system among mastitis strains was not significantly higher than among faecal isolates from healthy animals. No classical enterotoxigenic E. coli strains tested carried the aerobactin genetic determinants. Although most strains that produced aerobactin were also able to make colicin V, the fact that the two characteristics existed separately in a significant minority of isolates suggested that colicin testing alone could not be reliably used to determine the presence of the aerobactin system.
Journal of general microbiology 05/1987; 133(4):835-42.
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ABSTRACT: Mucosal antibodies in vivo and in vitro interfere with the stability of plasmids coding for important virulence determinants in porcine enteropathogenic E. coli (EEC), such as the adhesion determinants K88ab and K88ac. The effector antibody is not directed against K88 antigens and is not serotype specific, but an antigen common to K88+ strains is implicated. Further lack of pathogen specificity is exemplified by antibody elimination of the more recently discovered K88ad plasmid. Antibodies that interfere with K88 plasmids do not affect K99, which now appears as an alternative adhesion factor in porcine enteropathogenic E. coli. This plasmid can be eliminated, however, by antibodies having K99 specificity. In extending the studies to drug-resistance plasmids, further evidence has emerged that mucosal antibodies may assist in host control of the reservoir of R factors in the intestinal microflora. A major effector mechanism is that secretory IgA and IgM antibodies from orally immunized pigs can block the transfer of R factors between donor and recipient strains of E. coli.
Annals of the New York Academy of Sciences 07/1983; 409:564-79. · 3.15 Impact Factor
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Journal of Infection 04/1983; 6(2):111-21. · 4.13 Impact Factor
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ABSTRACT: Transfer of an Hly plasmid determining production of alpha haemolysin to a non-haemolytic strain of Escherichia coli increased the virulence of the strain for mice. Injections of non-toxic amounts of alpha haemolysin, phenylhydrazine, haemoglobin, iron or manganese salts simulated the effect of the Hly plasmid by stimulating bacterial growth. Active or passive immunisation against alpha haemolysin protected mice on challenge with haemolytic E. coli by inhibiting in-vivo proliferation of the strain. Protection was eliminated by administration of iron salts at the time of challenge. The Hly plasmid probably acts as a virulence factor by enabling haemolytic strains of E. coli to obtain iron for growth from the lysed erythrocytes of infected animals.
Journal of Medical Microbiology 03/1982; 15(1):23-30. · 2.50 Impact Factor
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ABSTRACT: The heat-labile K88 antigen, a virulence determinant coded for by a transmissible plasmid, was eliminated from enteropathogenic strains of Escherichia coli by passage through media containing antibodies to the heat stable antigens of an Abbotstown (O149:K91,K88ac) strain. The plasmid-curing activity of O149 antisera was not O-antigen specific as O149, O45, O8 and O138 strains of E. coli could be 'cured' of their K88 plasmids by this technique. The curing activity was differentiated from the O-antibody by gel filtration, the O149 antibodies were eluted in the IgM peak while the curing activity was found in the IgG peak. In view of the lack of O-specificity and the absence of K88 antibodies it appears that antibodies to a common heat-stable antigenic determinant were involved in this phenomenon.
Immunology 10/1979; 38(1):123-7. · 3.32 Impact Factor
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ABSTRACT: The heat labile K88 antigen which is a product of an episomal gene, was eliminated from a pocrine enteropathogen by passage through media containing sow colostrum antibodies raised against heart stable antigens of E. coli. In consequence the porcine enteropathogen lost its ability to adhere to and aggluinate chicken erythrocytes, and model system for piglet intestinal adhesion and virulence.
Immunology 08/1978; 35(1):125-7. · 3.32 Impact Factor
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ABSTRACT: It was found that oral immunisation of pigs with heat stable Escherichia coli antigens resulted in a decrease in the sensitivity of the porcine intestine to both the heat stable (ST) and the heat labile (LT) and the heat labile (LT) form of the enterotoxin produced by enterotoxigenic strains. Antitoxic factors capable of neutralising LT, but not ST, could be passively transferred in the intestinal secretions of the immunised animals.
Research in Veterinary Science 08/1978; 25(1):113-5. · 1.65 Impact Factor
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ABSTRACT: 1) Although virulence of enteropathogenic E. coli in the pig is essentially associated with the K88 adhesion determinant, protection of the neonate and weanling is not necessarily dependent upon antibodies to this surface antigen. 2) Modification of the surface antigenic characteristics of enteropathogens occurs in the presence of antibody, suggesting an immune mechanism of induced loss of the genetic elements responsible for the synthesis of K88. 3) Antibodies directed against the K88 antigen do not seem to participate in the elimination of the K88 antigen. These observations provide a new concept that antibody mediated mechanisms of host defense include elimination of virulence determinants, a feature vital to maintaining the balance of the host pathogen relationship favorable to the host.
Advances in experimental medicine and biology 02/1978; 107:133-42. · 1.09 Impact Factor
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Journal of Medical Microbiology 06/1972; 5(2):243-50. · 2.50 Impact Factor
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Journal of Medical Microbiology 12/1971; 4(4):487-93. · 2.50 Impact Factor
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Journal of Medical Microbiology 12/1971; 4(4):467-85. · 2.50 Impact Factor
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Journal of Medical Microbiology 09/1971; 4(3):301-5. · 2.50 Impact Factor
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Journal of general microbiology 09/1970; 62(3):287-99.
