Interbacterial adherence between Actinomyces viscosus and strains of Streptococcus pyogenes, Streptococcus agalactiae, and Pseudomonas aeruginosa.
Interbacterial adherence was sought between strains of Actinomyces viscosus indigenous to the human mouth and strains of Streptococcus pyogenes, Streptococcus agalactiae, and Pseudomonas aeruginosa. Six of nine strains of S. pyogenes, three of five strains of S. agalactiae, and two of four strains of P. aeruginosa were found to coaggregate with each of five strains of A. viscosus tested. Some coaggregation reactions were inhibited by 0.05 M lactose and were dependent upon heat- and protease-sensitive Actinomyces components. Such reactions appear to involve the galactosyl-binding adhesin previously described in type 2 fimbriae on A. viscosus. Other coaggregation reactions were dependent upon heat- and protease-sensitive components of the pathogen. That such pathogen strains possessed an adhesin(s) was further suggested by the observation that they agglutinated human erythrocytes. The ability of coaggregation-positive and -negative strains of S. pyogenes and S. agalactiae to adhere to Actinomyces-coated agarose beads was also studied. Coaggregation-positive streptococcal strains attached in higher numbers to the Actinomyces-coated beads than did strains which were coaggregation negative. Lactose (0.05 M) inhibited the attachment of those streptococcal strains which coaggregated with A. viscosus in a lactose-sensitive manner. The adherence of those streptococcal strains whose coaggregation appeared to depend upon the galactosyl-binding adhesin of A. viscosus was also reduced by components of human saliva. Crude sonic extracts of coaggregation-positive streptococci or of P. aeruginosa were also effective in aggregating Actinomyces cells. The effect of lactose and of salivary components on this extract-induced aggregation of Actinomyces cells generally paralleled that observed in other assays. The apparent prevalence and diversity of adherent reactions between the pathogens studied and indigenous strains of A. viscosus suggest that some may affect host susceptibility to these infectious agents.
D000190:Actinomyces / Q000502:physiology*; D001426:Bacterial Proteins / Q000502:physiology*; D006384:Hemagglutination; D006358:Hot Temperature; D006801:Humans; D007785:Lactose / Q000494:pharmacology; D010447:Peptide Hydrolases / Q000494:pharmacology; D011550:Pseudomonas aeruginosa / Q000502:physiology*; D012463:Saliva / Q000502:physiology; D013010:Sonication; D013292:Streptococcus agalactiae / Q000502:physiology*; D013297:Streptococcus pyogenes / Q000502:physiology*
D001426:Bacterial Proteins; D010447:Peptide Hydrolases; D007785:Lactose