Susceptibility of phenotypic variants of haemophilus influenzae type b to serum bactericidal activity: Relation to surface lipopolysaccharide

Janet R. Gilsdorf, Patricia Ferrieri

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18 Scopus citations

Abstract

After three serial passages of Haemophilus influenzae type b strain Fuju in rats, we recovered a variant, which differed in colonial morphology, serum sensitivity, and lipopolysaccharide configuration from the parent strain. The parent organism (Fuju) appeared iridescent and transparent on Levinthal agar, and the rat-passaged variant (rat, Fuju) appeared iridescent and opaque. The transparent, parent strain Fuju was sensitive to the complement-mediated bactericidal activity of normal rat serum, and the opaque, ratpassaged strain rat, Fuju was serum resistant. Serum killing of the serum-sensitive strain appeared to be mediated by the classic complement pathway. Both serum-resistant and serum-sensitive strains were killed equally well by immune rat and human serum. These two strains did not differ in the amount of capsular polysaccharide that they elaborated nor in their major outer membrane protein patterns on SDS-PAGE. Lipopolysaccharide isolated from these two strains demonstrated different electrophoretic mobility patterns. Furthermore, the organisms showed different reactivities with two monoclonal antibodies directed against determinants of Hib lipopolysaccharide. Thus, the difference in susceptibility to complement-mediated bactericidal activity of normal rat serum displayed by these two strains is associated with their phenotypes, appears to be unrelated to differences in major outer membrane proteins or in the amounts of capsular polysaccharide elaborated, and is associated with differences in surface lipopolysaccharides.

Original languageEnglish (US)
Pages (from-to)223-231
Number of pages9
JournalJournal of Infectious Diseases
Volume153
Issue number2
DOIs
StatePublished - Feb 1986

Bibliographical note

Funding Information:
Received for publication 3 May 1985, and in revised form 30 August 1985. This research was supported by training grant AI-07054 from the National Institute of Allergy and Infectious Diseases. Dr. Ferrieri was supported in part by grant AI-13926 from the National Institute of Allergy and Infectious Diseases. We would like to thank Drs. Dan Granoff (Washington University, St. Louis) and Eric Hansen (Southwestern Medical School, Dallas) for their generous assistance. Please address requests for reprints to Dr. Janet Gilsdorf, F7828, C. S. Mott Children's Hospital, Box 066, University of Michigan Medical Center, Ann Arbor, Michigan 48109.

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