Abscess Forming Ability of Streptococcus milleri Group: Synergistic Effect with Fusobacterium nucleatum

Abstract

The abscess forming abilities of "Streptococcus milleri" strains (Streptococcus constellatus, Streptococcus anginosus, 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 .

Community surveillance enhances Pseudomonas aeruginosa virulence during polymicrobial infection

“…The clinical significance of these infections is profound because they are often more severe and recalcitrant to therapeutic intervention than monoculture infections (2,6,7,(9)(10)(11)(12)(13)(14). One of the most prevalent opportunistic pathogens found in polymicrobial infections is P. aeruginosa, and there is evidence that P. aeruginosa enhances virulence during coinfection with Gram-positive bacteria (10,22,23).…”

“…Indeed, microbes within polymicrobial infections often display synergy, defined as the cooperative interaction of two or more microbes to produce a result not achieved by the individual bacterium acting alone (8). Synergistic interactions can result in enhanced pathogen persistence in the infection site, increased disease severity, and increased antimicrobial resistance (2,6,7,(9)(10)(11)(12)(13)(14).…”

Biofilm Models of Polymicrobial Infection

“…In biofilms and biofilm-related infections, these 'effects' include increased growth, antimicrobial tolerance, virulence and persistence, and enhanced production of exopolysaccharide (EPS) [17][18][19][20][21][22][23][24][25][26][27][28]. Another classic cooperative interaction is metabolic cross-feeding, or syntrophy, where one species makes a metabolic byproduct which enhances the growth of a neighbor [29].…”

Real-time monitoring of the adherence of Streptococcus anginosus group bacteria to extracellular matrix decorin and biglycan proteoglycans in biofilm formation

“…Whilst present in low numbers in dental plaque, SAGs are frequently isolated from polymicrobial infections; they are predominant components of a number of orofacial infections, including dento-alveolar and periodontal abscesses, and are frequently associated with failed root canal treatment (Jacobs et al, 2003;LedezmaRasillo et al, 2010;Lewis et al, 1986;Schuman and Turner, 1999;Siqueira et al, 2002;Okayama et al, 2005;Whiley et al, 1992). It has been proposed that SAGs are present early in the pathogenic process and may actually initiate infection, thereafter preparing the environment for subsequent colonisation by anaerobic species (Aderhold et al, 1981;Gossling, 1988;Nagashima et al, 1999;Shinzato and Saito, 1994). As microaerophilic bacteria, SAGs can proliferate in regions of low oxygen tension, further reducing both the oxygen concentration and redox potential to favour the growth of strict anaerobes.…”