ABSTRACT
Human dental plaque samples were screened for the presence of bacteriophage for Actinomyces viscosus and Streptococcus sanguis. None of the 336 samples yielded phage for S. sanguis, but 10 contained virulent actinomyces phage. A high host cell specificity was observed in that one phage isolate infected only A. viscosus T14V, eight phage isolates infected only A. viscosus MG-1, and one infected both strains. None was capable of productively infecting various other actinomyces strains that represented the six actinomyces coaggregation groups. Because phage-containing samples occurred randomly in this survey, no correlation between the individual collecting the samples, dental clinic, or type of patient and the presence of phage in the sample was noted. Examination of one of the samples that yielded phage for the presence of a natural host strain for that particular phage resulted in the isolation of two strains which were identified as A. viscosus serotype II and Actinomyces naeslundii serotype I. This is the first report of an A. naeslundii host strain and actinomyces bacteriophage of human dental plaque origin. The finding of both phage and host strains in the same dental plaque sample along with the observation of high host cell specificity by these phage provide indicators that support an active role for actinomyces bacteriophage in oral microbial ecology. The use of these freshly isolated phage as probes to study actinomyces coaggregation properties is discussed.
Subject(s)
Actinomyces/genetics , Bacteriophages/isolation & purification , Dental Plaque/microbiology , Actinomyces/pathogenicity , Adhesiveness , Bacteriophages/ultrastructure , Humans , Microscopy, Electron , Sewage , Species Specificity , Virus ReplicationSubject(s)
Muramidase/analysis , Parotid Gland/enzymology , Saliva/enzymology , Adult , Female , Humans , MaleABSTRACT
Lysozyme and total protein concentrations in parotid saliva were measured in 17 patients with primary Sjögren's syndrome, in six patients with Sjögren's syndrome secondary to hyperlipoproteinemia and in 14 age- and sex-matched healthy control subjects. Increased lysozyme concentrations were found only in patients with primary Sjögren's syndrome and correlated well with the presence of parotid gland enlargement. The total protein concentration in the saliva of patients with Sjögren's syndrome was not different from that of the control subjects. Parotid saliva lysozyme determination may be useful as an early adjunctive diagnostic test of primary Sjögren's syndrome.