Loss of lectin-like activity in aberrant type 1 fimbriae of Escherichia coli.
Growth of a streptomycin-resistant strain of Escherichia coli (VL-2) in the presence of 30 microgram of streptomycin per ml resulted in the production by these bacteria of structurally altered, nonfunctional type 1 fimbriae. This strain, when grown in this subinhibitory concentration of streptomycin, became incapable of producing mannose-sensitive hemagglutination (<1% of that of the control). Adhering ability to epithelial cells and human leukocytes was also diminished (42 and 7% of that of the control, respectively). Although these streptomycin-treated bacteria were as heavily fimbriated as untreated bacteria, their fimbriae were significantly longer. Furthermore, in contrast to the fimbriae of the untreated bacteria, those isolated from the drug-treated bacteria were found to lack mannose binding activity as measured by hemagglutination. It appears, therefore, that streptomycin can cause even resistant bacteria to produce an aberrant fimbrial protein, possibly by causing misreading of messenger RNA. These studies indicate that the use of sublethal doses of certain antibiotics whose mode of action is well known may shed light on the genetic and chemical modulation of bacterial factors involved in mucosal colonization.
D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics / Q000276:immunology / Q000648:ultrastructure*; D010861:Fimbriae, Bacterial / Q000276:immunology*; D037102:Lectins; D008362:Mannosides; D009154:Mutation; D013302:Streptomyces / Q000187:drug effects
D037102:Lectins; D008362:Mannosides