1887

Abstract

To investigate pathogenicity and the evolutionary divergence of the genus, the effect of pathogenic yersiniae on the model organism was studied. Three strains of , including a strain lacking pMT1, caused blockage and death of ; one strain, lacking the haemin storage () locus, caused no effect. Similarly, 15 strains of caused no effect. Strains of showed different levels of pathogenicity. The majority of strains (76 %) caused no discernible effect; 5 % caused a weak infection, 9·5 % an intermediate infection, and 9·5 % a severe infection. There was no consistent relationship between serotype and severity of infection; nor was there any relationship between strains causing infection of and those able to form a biofilm on an abiotic surface. Electron microscope and cytochemical examination of infected worms indicated that the infection phenotype is a result of biofilm formation on the head of the worm. Seven transposon mutants of strain YPIII pIB1 were completely or partially attenuated; mutated genes included genes encoding proteins involved in haemin storage and lipopolysaccharide biosynthesis. A screen of 15 defined mutants identified four where mutation caused (complete) resistance to infection by YPIII pIB1. These mutants, , , and the dauer pathway gene , also exhibit altered binding of lectins to the nematode surface. This suggests that biofilm formation on a biotic surface is an interactive process involving both bacterial and invertebrate control mechanisms.

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2003-11-01
2020-04-10
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