Changes in expression of bacterial surface antigens induced by antibiotics and their influence on host defenses.

Concomitant with the discovery that a number of antibiotics were able to induce profound morphological changes (increased septation, thickened walls, filamentation) at low concentrations their ability to inhibit bacterial protein/polysaccharide synthesis was determined. In particular toxin and extracellular enzyme biosynthesis could be repressed by the lincosamines, fusidic acid, erythromycin and streptomycin in Staphylococcus aureus, Streptococcus pyogenes, Propionibacterium acnes, Pseudomonas aeruginosa and Escherichia coli. Several of these exoproducts act as antigens associated with microbial virulence and are therefore of importance in pathogenicity. Likewise structural components such as fimbriae in Escherichia coli, M protein in Streptococcus pyogenes, protein A in Staphylococcus aureus and capsule in Bacteroides fragilis and Haemophilus influenzae were not synthesised when the producer bacteria were grown in low concentrations of antibiotic. These products, through their importance as impedins of opsonization and subsequent phagocytosis by white blood cells, are important determinants in the host-parasite relationship. By their loss during drug exposure, potentiation of opsonophagocytosis occurred leading to more rapid killing of the pathogen. The immunogenicity of the antibiotic-damaged bacteria was also changed under these circumstances.