Envelope protein changes, autoagglutination, sensitivity to hydrophobic agents and a conditional division lesion in Escherichia coli strains carrying ColV virulence plasmids

Rowbury, R. J.; Deeney, Caroline M. M.; Reakes, C. F. L.; Rossouw, F.T.; Smith, D. G.; Tewari, Rupinder

doi:10.1016/s0769-2609(85)80035-1

Cited by 23 publications

(13 citation statements)

References 14 publications

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“…Several phenotypic traits other than colicin production per se may contribute to the virulence associated with ColV plasmids, including autoagglutination and hypomotility at 37°C (which may impede phagocytosis) (464,542,543), enhanced survival in the mouse peritoneum (419), increased adherence to mouse intestinal cells and increased fimbriation (65), aerobactin production (see above), impaired phagocytosis (9), and increased serum resistance (9,29,30,259,373,498,540,541). pColV, I-K94 (a well-studied ColV plasmid) also confers increased acid susceptibility (72).…”

Section: Plasmid-associated Proteins In Serum Resistancementioning

confidence: 99%

Virulence factors in Escherichia coli urinary tract infection

1991

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Uropathogenic strains of Escherichia coli are characterized by the expression of distinctive bacterial properties, products, or structures referred to as virulence factors because they help the organism overcome host defenses and colonize or invade the urinary tract. Virulence factors of recognized importance in the pathogenesis of urinary tract infection (UTI) include adhesins (P fimbriae, certain other mannose-resistant adhesins, and type 1 fimbriae), the aerobactin system, hemolysin, K capsule, and resistance to serum killing. This review summarizes the virtual explosion of information regarding the epidemiology, biochemistry, mechanisms of action, and genetic basis of these urovirulence factors that has occurred in the past decade and identifies areas in need of further study. Virulence factor expression is more common among certain genetically related groups of E. coli which constitute virulent clones within the larger E. coli population. In general, the more virulence factors a strain expresses, the more severe an infection it is able to cause. Certain virulence factors specifically favor the development of pyelonephritis, others favor cystitis, and others favor asymptomatic bacteriuria. The currently defined virulence factors clearly contribute to the virulence of wild-type strains but are usually insufficient in themselves to transform an avirulent organism into a pathogen, demonstrating that other as-yet-undefined virulence properties await discovery. Virulence factor testing is a useful epidemiological and research tool but as yet has no defined clinical role. Immunological and biochemical anti-virulence factor interventions are effective in animal models of UTI and hold promise for the prevention of UTI in humans.

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Section: Plasmid-associated Proteins In Serum Resistancementioning

confidence: 99%

Virulence factors in Escherichia coli urinary tract infection

1991

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“…Such a LPS change is also suggested by the marked changes in inhibitor sensitivity observed in ColV,I-K94 + strains (Rowbury et al, 1985;Davies et al, 1986).…”

Section: Discussionmentioning

confidence: 65%

“…* ColV,I-K94 and ColV-K30 are both from clinical E. coli isolates (Hardy, 1975). Both confer derepressed transfer properties and encode the VmpA protein and colicin V; ColV,I-K94 also encodes colicin Ia (Hardy, 1975;Rowbury et aL, 1985). The aerobactin iron chelation system is encoded by ColV-K30 but not by ColV,I-K94 (Williams, 1979 Phage P1 attachment to E. coli ColV, I-K94 + 1787…”

Section: Phage Plvir Fails To Form Plaques On Colv1-k94 + E Coli Stmentioning

confidence: 99%

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Altered Phage P1 Attachment to Strains of Escherichia Coli Carrying the Plasmid ColV,I-K94

Goodson

Rowbury

1987

Journal of General Virology

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“…Assessment of motility, clumping (autoagglutination), and mucoid phenotype of clinical ColV+ isolates was done according to Rowbury et al (1985) and Tewari et al (1986).…”

Section: Assessment Of Other Colv-encodedpropertiesmentioning

confidence: 99%

Suppression by the ColV,I-K94 plasmid of inhibitor sensitivities in ompA mutants of Escherichia coli

Reakes¹,

Deeney²,

Goodson³

et al. 1988

Can. J. Microbiol.

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A series of ompA mutants derived from Escherichia coli K12 strains showed increased sensitivity (compared with the ompA+ parents) to aminoglycoside antibiotics and to other cationic agents including polymyxin B. One tested mutant also showed increased sensitivity to nafcillin and fusidic acid, but not to the hydrophilic ampicillin. All these inhibitor sensitivities in the ompA mutants were suppressed by ColV, I-K94 and by certain other ColV plasmids, but not by any of the other tested large plasmids. Suppression correlated with the production of the VmpA protein, but transfer and colicin components were not needed for suppression. Further comparison of the ompA and vmpA genes and their products was made and it indicated that there is little if any homology between the genes, that the synthesis of their products is regulated by quite different mechanisms, and that regions of these gene products exposed at the cell surface show different susceptibility to protease attack after denaturation.

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Envelope protein changes, autoagglutination, sensitivity to hydrophobic agents and a conditional division lesion in Escherichia coli strains carrying ColV virulence plasmids

Cited by 23 publications

References 14 publications

Virulence factors in Escherichia coli urinary tract infection

Virulence factors in Escherichia coli urinary tract infection

Altered Phage P1 Attachment to Strains of Escherichia Coli Carrying the Plasmid ColV,I-K94

Suppression by the ColV,I-K94 plasmid of inhibitor sensitivities in ompA mutants of Escherichia coli

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