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Abscess forming ability of streptococcus milleri group: synergistic effect with Fusobacterium nucleatum
H Nagashima1, A Takao, N Maeda
1Second Department of Oral and Maxillofacial Surgery, School of Dental Medicine, Tsurumi University, Yokohama, Kanagawa, Japan.
Abstract:
The abscess forming abilities of "Streptococcus milleri" strains (Streptococcus constellatus, Streptococcus anginiosus, and Streptococcus intermedius) isolated from dentoalveolar abscesses and the synergistic effect of Fusobacterium nucleatum co-inoculated with the isolates were examined on a mouse subcutaneous abscess model. Five days after inoculation, all S. milleri strains formed abscesses, which showed less pathological spread to surrounding connective tissues than those formed by Staphylococcus aureus 209P strain and were similar to those by F. nucleatum ATCC25586. When each S. milleri strain and F. nucleatum were co-inoculated, abscess sizes and each bacterial number recovered from abscesses increased in comparison to those treated by bacterial mono-inoculation of each S. milleri strain or F. nucleatum alone. The strongest synergistic effect was observed in the combination of S. constellatus and F. nucleatum. In a time course experiment with this combination, the recovery of S. constellatus subsequently decreased after the decrement of F. nucleatum, and it appeared that the association with F. nucleatum maintained the bacterial number of S. constellatus in the abscess. The cell-free supernatant of F. nucleatum had a tendency to increase the abscess size caused by S. constellatus in this model. When S. constellatus was cultured with F. nucleatum culture supernatant in vitro, growth enhancement in the early phase was observed. Furthermore, the phagocytic killing of S. constellatus by human polymorphonuclear leukocytes (PMNs) was significantly suppressed and the PMN membranes appeared to be injured by addition of the F. nucleatum culture supernatant. These results suggest that the pathogenicity of S. milleri strains in odontogenic infections may be enhanced by the co-existence of F. nucleatum.
Insights
Streptococcus milleri strains form abscesses, but Fusobacterium nucleatum enhances their pathogenicity in odontogenic infections. Co-inoculation increases abscess size and bacterial numbers, with F. nucleatum protecting S. constellatus from immune cells.
Area of Science:
- Microbiology
- Infectious Diseases
- Oral Pathology
Background:
- Dentoalveolar abscesses often involve polymicrobial infections.
- Streptococcus milleri group bacteria are frequently isolated from these abscesses.
- The role of Fusobacterium nucleatum in potentiating S. milleri pathogenicity is not fully understood.
Purpose of the Study:
- To investigate the abscess-forming capabilities of S. milleri strains.
- To examine the synergistic effects of F. nucleatum co-inoculation with S. milleri.
- To elucidate the mechanisms behind F. nucleatum's influence on S. milleri pathogenicity.
Main Methods:
- A mouse subcutaneous abscess model was used to assess abscess formation.
- S. milleri strains (S. constellatus, S. anginiosus, S. intermedius) and F. nucleatum were inoculated alone and in combination.
- In vitro assays evaluated the effect of F. nucleatum supernatant on S. constellatus growth and resistance to human polymorphonuclear leukocytes (PMNs).
Main Results:
- All tested S. milleri strains formed abscesses, with less tissue spread than Staphylococcus aureus.
- Co-inoculation of S. milleri with F. nucleatum significantly increased abscess size and bacterial recovery compared to mono-inoculation.
- F. nucleatum supernatant enhanced S. constellatus in vitro growth and suppressed PMN-mediated killing, suggesting immune evasion.
- The combination of S. constellatus and F. nucleatum showed the strongest synergistic effect.
Conclusions:
- F. nucleatum potentiates the pathogenicity of S. milleri group bacteria in odontogenic infections.
- Synergistic interactions between these bacteria contribute to increased abscess severity.
- F. nucleatum may enhance pathogenicity by promoting bacterial growth and evading host immune responses.