Identification of the major adherence ligand of Klebsiella pneumoniae in the receptor for coliphage T7 and alteration of Klebsiella adherence properties by lysogenic conversion.

We have studied the adherence of both laboratory and wild-type Klebsiella pneumoniae strains, isolated from sputum, urine, and stool samples, to human buccal and intestinal and urinary tract epithelial cells. Of 32 unencapsulated strains, 30 adhered to all epithelial cells tested. Four K. pneumoniae strains lysogenic for AP3, a phage which causes conversion to resistance of coliphages T3, T7, and phi I, were all unable to adhere to epithelial cells. One of these strains was cured from phage infection and became capable of adhering, Spontaneous mutants resistant to coliphage T7, as well as K. pneumoniae K59-sensitive cells preadsorbed with inactivated T7 particles, did not adhere to epithelial cells. All strains capable of adhering were able to adsorb coliphage T7 and T3, whereas all nonadhesive strains were not. AP3-like prophages were induced from 7 of 12 nonadhesive Klebsiella strains. A laboratory strain which was able to adhere was lysogenized with 2 of these phages. In both cases, the strain lost its ability to adsorb coliphages T3, T7, and phi I and to adhere to human epithelial cells. All K. pneumoniae adhesive strains agglutinated yeast cells, whereas the nonadhesive strains did not. Competition studies have shown that D-mannose and concanavalin A prevented adherence to human epithelial cells, yeast agglutination, and adsorption of coliphage T7 to K. pneumoniae cells. It is concluded that in K. pneumoniae adherence to epithelial cells is mediated by the receptor for coliphages T7 (and T3), which in turn recognizes D-mannose in the receptors it binds.