Characteristics of an avirulent Campylobacter jejuni strain and its virulence-enhanced variants

Abstract

Summary. The virulence of Campylobacter jejuni for 1 1 -day-old chick embryos is associated with the ability to invade the chorio-allantoic membrane, to resist phagocytosis and to survive and proliferate in vim. The pathogenicity of a well characterised avirulent C. jejuni strain was enhanced by passaging it intravenously and chorio-allantoically through chick embryos. The resulting isogenic variants had greatly increased ability to survive in vim. In this study, the morphological and cell-surface characteristics of the avirulent parental strain were compared with those of the more virulent variants to determine whether pathogenicity was associated with one or more cell-surface constituents. Changes associated with the increased virulence of the two variants included alterations in cultural and cellular morphology, loss of flagella, expression of a new outer-membrane protein, alterations in cell-surface carbohydrates and decreases in cell-surface hydrophobicity.

Peptidoglycan-Modifying Enzyme Pgp1 Is Required for Helical Cell Shape and Pathogenicity Traits in Campylobacter jejuni

“…For instance, some C. jejuni flagellar mutants appeared to have a straight morphology [68]–[70]; however, other mutants with lesions in the same flagellar genes remained helical ([71], [72]; E. Frirdich and E. C. Gaynor, unpublished). Two reports also cited that passage through the chicken gut or chick embryos resulted in straight C. jejuni isolates [65], [73]. Conversely, laboratory passage has led to the isolation of poorly colonizing rod-shaped C. jejuni and C. coli strains [74], [75].…”

Genetic and biochemical evidence of a Campylobacter jejuni capsular polysaccharide that accounts for Penner serotype specificity

“…The capsular polysaccharide‐negative mutants generated in this study will be invaluable in future animal studies to determine the role of the capsular polysaccharide in virulence. C. jejuni strains with enhanced virulence were obtained from avirulent strains by passage through chick embryos, and such strains were shown to have a decreased cell surface hydrophobicity relative to their avirulent parent strain (Field et al ., 1993). An obvious candidate molecule for conferring increased hydrophilicity (or decreased hydrophobicity) on the cell surface is the capsular polysaccharide.…”

“…The surface hydrophobicity of wild‐type and mutant strains was examined using a modification of the method of Field et al . (1993).…”

“…The surface hydrophobicity of wild-type and mutant strains was examined using a modification of the method of Field et al (1993). Disposable plastic columns were packed with Octyl Sepharose CL-4B to a height of 2 cm and washed with 10 ml of 0.2 M ammonium sulphate in 10 mM sodium phosphate buffer, pH 6.8 (buffer A).…”

The flagellar master operon flh DC is a pleiotropic regulator involved in motility and virulence of the fish pathogen Yersinia ruckeri

“…For example, Yersinia pestis is thought to have evolved relatively recently from Yersinia pseudotuberculosis and in evolving from a food-borne to vector-borne pathogenic lifestyle has gained and lost many functions including the loss of flagellar motility (Parkhill et al 2001). Other pathogens that have similarly lost motility include Bordetella species (Leigh et al 1993), Campylobacter jejuni (Field et al 1993), E. coli (Monday et al 2004), Shigella sp. (Tominaga et al 2005), Salmonella enterica (Yim et al 2011) and the fish pathogen Aeromonas salmonicida subsp.…”