Pathogenicity of an Escherichia coli O115:K"V165" mutant negative for F165(1) fimbriae in septicemia of gnotobiotic pigs

Abstract

To evaluate the role of the F1651 fimbrial system in the pathogenesis of septicemia, 2-day-old germfree pigs were inoculated intragastrically with Escherichia coli 0115:K"V165":F165 wild-type strain 5131, its F1651negative TnphoA mutant M48, or E. coli 0115:K(-):F165(-) wild-type strain 862B. Pigs were sacrificed at different times (3,6,12,24,48, and 96 h) postinfection (p.i.). Pigs inoculated with strain 5131 developed clinical signs (anorexia, lameness, reluctance to move, or lack of motor coordination) and were moribund within 48 h p.i., and, at necropsy, infecting bacteria were isolated in various extraintestinal organs. Strain 5131 was isolated as early as 6 h p.i. from the blood of inoculated pigs. Pigs inoculated with mutant M48 developed only mild clinical signs at 96 h p.i. Mutant M48 colonized extraintestinal organs of pigs but to a lesser extent than the parent strain did. In contrast to the parent strain, this mutant was not isolated in the blood of inoculated pigs. Pigs inoculated with strain 862B remained normal during the experiment. All of the strains colonized the mucus layer of the intestine, but no histological changes of intestinal mucosa were observed by either light or electron microscopy. The parent strain, but not the mutant M48, expressed F1651 in vivo. In a competitive study in which the parent strain and its afimbrial mutant were inoculated simultaneously, clinical signs of septicemia developed 24 h after inoculation, and only the parent strain 5131 was isolated from the blood of inoculated pigs. Our results suggest that the F1651 fimbrial system of E. coli 0115:K"V165" strains may play an important role in the ability of the bacteria to survive in the blood and spread systemically through the porcine host.

Administration of Pediococcus acidilactici or Saccharomyces cerevisiae boulardii modulates development of porcine mucosal immunity and reduces intestinal bacterial translocation after Escherichia coli challenge1,2

“…Jejunum brush border vesicles were prepared from all animals (18 pigs per experimental group) and examined for the presence of specific F4 receptors, as described previously (Baker et al, 1997). Adherence tests were performed as described previously (Ngeleka et al, 1993). Obtained from the E. coli laboratory (ECL, Université de Montréal, faculté de médecine vétérinaire, St-Hyacinthe, Québec, Canada), the strain ECL 8559 was used as the positive control for F4 and ECL 3463 (previously called 862B) as the negative control strain.…”

F1651fimbriae of the P fimbrial family inhibit the oxidative response of porcine neutrophils

“…For example, an F165 1 ‐negative mutant of a pathogenic E. coli strain failed to colonize extraintestinal organs and to induce septicemia in experimentally inoculated gnotobiotic piglets. Moreover, an O‐antigen capsule‐negative spontaneous mutant of this pathogenic E. coli strain was serum‐sensitive in vitro and non‐pathogenic in young pigs [14–16].…”

“…Wild‐type E. coli strain 5131 was isolated from the intestinal contents of a diarrheic and septicemic piglet at the Faculté de Médecine Vétérinaire, Université de Montréal, Saint‐Hyacinthe, Que., Canada. This strain is serum‐resistant, induces septicemia in experimentally inoculated piglets, and is resistant to phagocytic killing by pPMNLs [2–16]. Strain HB101 (pCJ7) is a transformant from plasmid pACYC184 in which was inserted a 10‐kb fragment of DNA (from an F165 1 ‐positive wild‐type septicemia‐inducing E. coli strain 4787) into the Bam HI site [15].…”

“…We have reported that the MR fimbrial adhesin F165 1 is associated with porcine septicemia–inducing E. coli [14]. F165 1 is a member of the P fimbrial family with an F11‐like major fimbrial subunit and expresses a class III Prs‐G adhesin (commonly associated with E. coli causing human cystitis) with specificity for the galactose‐ N ‐acetyl‐α‐(1‐3)‐galactose‐ N ‐acetyl (GalNac‐GalNac) moiety [15].…”

Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F1651, a P-like fimbriae

“…F165 1 fimbriae are produced by Escherichia coli 4787, a strain associated with septicemia in pigs, and involved in pathogenesis (Ngeleka et al , 1992, 1993). The F165 1 adhesin from E. coli , encoded by the foo operon, belongs to the family of Pap‐related fimbriae.…”