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Infect Immun. 1993 January; 61(1): 204-212

Genetic structure of populations of Porphyromonas gingivalis associated with periodontitis and other oral infections.

B G Loos, D W Dyer, T S Whittam and R K Selander

Department of Oral Biology, School of Dental Medicine, State University of New York, Buffalo 14214.

ABSTRACT

One hundred isolates of the oral pathogenic bacterium Porphyromonas gingivalis were genetically characterized by determining the electrophoretic mobilities of 16 metabolic enzymes and the presence or absence of catalase activity. A total of 78 distinct electrophoretic types (ETs), representing multilocus genotypes, were identified, and cluster analysis placed them in three major phylogenetic divisions. Division I (71 ETs) included all 88 human isolates examined, most of which had been recovered from patients with periodontitis, together with 4 monkey isolates. The strains in division II (four ETs) and division III (three ETs) are strongly differentiated from those in division I and apparently represent two previously unclassified (cryptic) species. The mean genetic diversity per enzyme locus among the 92 isolates of division I (P. gingivalis, strict sense) was 0.321, and the strains were distributed among 14 phylogenetic clusters and single-ET lineages. The population structure is basically clonal, with some clonal genotypes being widespread, and even global, in distribution. There was no evidence of association between specific genetic lineages or clusters of ETs and the type of disease (periodontitis or root canal infections), invasive potential, serogroup, or fimbrial restriction fragment length polymorphism group. The finding that dental patients are infected by strains of a wide variety of chromosomal genotypes suggests that interstrain variation in pathogenicity is small. On the basis of the observed genetic structure of natural populations of P. gingivalis, we hypothesize that the role of this microorganism in the pathogenesis of periodontitis and other dental infections is largely opportunistic.

Infect Immun. 1993 January; 61(1): 204-212




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