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Adherence of pathogenic bacteria is often an essential first step in the infectious process. The ability of bacteria to adhere to one another, or to coaggregate, may be an important factor in their ability to colonize and function as pathogens in the periodontal pocket. Previously, a strong and specific coaggregation was demonstrated between two putative periodontal pathogens, Fusobacterium nucleatum and Porphyromonas gingivalis. The interaction appeared to be mediated by a protein adhesin on the F. nucleatum cells and a carbohydrate receptor on the P. gingivalis cells. In this investigation, we have localized the adhesin activity of F. nuceatum T18 to the outer membrane on the basis of the ability ofF. nuckatum T18 vesicles to coaggregate with whole cells of P. gingivalis T22 and the ability of the outer membrane fraction of F. nuckatum T18 to inhibit coaggregation between whole cells ofF. nucleatum T18 and P. gingivalis T22. Proteolytic pretreatment of the F. nucleatum T18 outer membrane fraction resulted in a loss of coaggregation inhibition, confirming the proteinaceous nature of the adhesin. The F. nucleatum T18 outer membrane fraction was found to be enriched for several proteins, including a 42-kDa major outer membrane protein which appeared to be exposed on the bacterial cell surface. Fab fragments prepared from antiserum raised to the 42-kDa outer membrane protein were found to partially but specifically block coaggregation. These data support the conclusion that the 42-kDa major outer membrane protein of F. nuceatum T18 plays a role in mediating coaggregation with P. gingivalis T22.

Bacterial adherence is a key factor in the colonization of the oral ecosystem, yet little is known about the mechanisms by which the pathogen Bacteroides gingivalis adheres in the periodontal environment. We examined the ability of strains of B. gingivalis to coaggregate with selected microorganisms isolated from the subgingival microbiota of the cynomolgus monkey. A strong interaction was demonstrated between strains of B. gingivalis and Fusobacterium nucleatum, whereas less pronounced or no interaction was observed with other oral isolates. Electron microscopic examination of coaggregates revealed large masses of bacteria, in which the fusiform F. nucleatum T18 and coccobacillary B. gingivalis T22 cells formed a woven pattern. To investigate this interaction and the nature of the bacterial cell surface molecules involved, we used a microcoaggregation assay. Galactose and galactose-related sugars blocked coaggregation, in contrast with the lack of effect of glucose or glucose-related sugars. The ability of F. nucleatum T18 cells to coaggregate was diminished by pretreatment with pronase. Pretreatment of B. gingivalis T22 cells with pronase resulted in an inhibition of coaggregation, whereas pretreatment with sodium metaperiodate completely abolished coaggregation. These data suggest that the coaggregation between B. gingivalis T22 and F. nucleatum T18 represents a carbohydrate-lectin interaction, mediated by a galactose-containing carbohydrate on B. gingivalis T22 and a protein on F. nucleatum T18.

In this investigation, the penicillin-resistant and beta-lactamase-producing subgingival microbiota associated with adult periodontitis was identified, and the impact of a recent exposure to penicillin on the recovery of resistant organisms from this microbiota was assessed. Subjects with adult periodontitis were examined clinically and microbiologically. Twenty-one subjects had a documented history of penicillin therapy within the previous 6 months whereas an additional 21 subjects had no history of antibiotic use within 1 year. Subgingival plaque samples were cultured anaerobically on nonselective and penicillin-containing elective media. MICs and beta-lactamase production were determined for the isolates from the elective medium. The penicillin-resistant microbiota consisted primarily of gram-negative organisms, including Bacteroides, Veillonella, Haemophilus, Eikenella, and Capnocytophaga species. The prevalence (P < 0.05) and proportions (P < 0.005) of both penicillin-resistant pigmented Bacteroides and Veillonella species were significantly greater in subjects with recent penicillin exposure. Of the penicillin-resistant genera identified, beta-lactamase production was detected in species of pigmented Bacteroides, Capnocytophaga, and Streptococcus. The prevalence of beta-lactamaseproducing Bacteroides species was significantly greater in subjects with recent penicillin exposure (P < 0.05). Of the antibiotics examined, no single agent was uniformly effective against all of the penicillin-resistant strains, but metronidazole and clindamycin were active against all of the penicillin-resistant pigmented Bacteroides strains.

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