No abstract

The loci encoding the porcine intestinal receptors for Escherichia coli K88ab and K88ac (K88abR and K88acR) were firmly assigned to chromosome 13 by linkage analysis using a three-generation pedigree. The linear order of these loci and seven other markers on chromosome 13 was determined by multipoint analyses. The K88abR and K88acR loci were tightly linked (theta = 0.01, zeta = 41.06) with the K88abR locus localized 7.4 cM (sex average) proximal to the transferrin locus. The results, together with previous reports from two other groups, provide an unequivocal assignment of the K88 receptor loci to chromosome 13, and reject a previous assignment to chromosome 4. Pigs possessing the receptor had a slightly higher specific IgG response to the K88 antigen after an intramuscular immunization with an E. coli vaccine.

Methods The effects of 4 days of oral administration of different doses of two drugs, an enkephalinase inhibitor (the antisecretory agent, racecadotril) and a μ‐receptor agonist (loperamide), on intestinal growth of a bacterial nonpathogenic strain (Escherichia coli E 404) and on the central nervous system (CNS) were compared in newborn gnotobiotic piglets. Results The E. coli content of the proximal jejunum (segment S1) and the E. coli ratio of stomach:segment S1 were similar in the racecadotril (20 mg/kg b.d., n = 5) and control groups. In contrast, in the loperamide group (1 mg/kg b.d., n = 4), the E. coli content of segment S1 and the E. coli ratio stomach:S1 were both significantly higher than with racecadotril or control (P = 0.04 and 0.005, respectively, for E. coli content; P = 0.05 and 0.03, respectively, for stomach:S1). There were no clinical signs of neurotoxicity and no deaths with racecadotril given orally at a high dose of 130 mg/kg b.d. (n = 5) – nearly 60 times the paediatric dosage. In contrast, an equivalent high dose of loperamide (5 mg/kg b.d.) resulted in death in three out of four piglets. Conclusions In contrast to loperamide, racecadotril did not induce bacterial overgrowth and did not produce central neurotoxicity.

We have observed that antagonisms occur between isogenic strains of Escherichia coli associated with gnotobiotic mice. The strains differed in the carriage of plasmids or in chromosomal mutations. The plasmid-free strains, in general, inhibited the establishment of plasmid-bearing strains in the gastrointestinal tract of mice. The outcome of the interactions between isogenic pairs, however, depended on the order in which the strains were introduced into the mice. Maintaining the bacterial strains in monoassociation with gnotobiotic mice resulted in the "adaptation" of the bacteria to their host. Thus, in all cases, "adapted" strains became the dominant population in the feces of mice, regardless of whether the adapted strains was introduced into mice before or after its isogenic partner which had been cultured in vitro. The ecological advantage disappeared when the adapted strain was cultured in broth. Ultrastructural differences in cell morphology were observed between strains maintained in vivo and in vitro.

Staphylococcus pyogenes PS54, the propagating strain of the group III staphylococcal typing phage 54, manifests no lipase activity on egg yolk medium. This strain was found to harbor at least two prophages. One of these, designated as L54a, was demonstrated to be capable of suppressing lipase production by lysogenic conversion of strains of Staphylococcus pyogenes previously manifesting lipase activity.Suspensions of typing phage 54 were also found to contain substrains of phage having the same conversion property, with respect to lipase activity, as L54a. These converting phages differed from L54a with respect to their ultrastructure and their lytic spectra. They may have arisen by means of recombination between non-converting typing phage 54 and the prophage L54a carried in the propagating strain of Staphylococcus.