Use of lytic bacteriophage for Actinomyces viscosus T14V as a probe for cell surface components mediating intergeneric coaggregation

Abstract

A lytic bacteriophage for Actinomyces viscosus T14V (the reference strain for actinomyces coaggregation group A) was isolated from raw sewage. This phage, designated BF307, also lysed the T14V-derived nonfimbriated mutant PK455-2 as well as A. viscosus MG-1 and T14AV but not the other serotype 2 or serotype 1 strains of this species that were tested or any of nine Actinomyces naeslundii isolates. Phages BF307 belonged to Bradley morphological group C and was similar in appearance to the A. viscosus MG-1 phages Av-1 and Av-3, which do not productively infect A. viscosus T14V. A. viscosus MG-1 mutants selected for resistance to phage BF307, Av-3, or CT7 (a human dental plaque isolate with the same host range as BF307) were coresistant to the other two phages but sensitive to Av-1. These results indicate that the receptors on A. viscosus MG-1 for phages BF307, Av-3, and CT7 are identical or share a common precursor and that the receptor for phage Av-1 is distinct. Comparison of the genomes of BF307, Av-3, and CT7 revealed that their DNAs were similar in size but distinguishable by restriction analysis. Two altered coaggregation phenotypes were identified among the phage BF307-resistant mutants of strains MG-1, T14V, T14AV, and PK455-2. Class I mutants had lost the ability to interact with coaggregation group 1 streptococci, and class II mutants did not coaggregate with either group 1 or group 2 streptococci. These results are consistent with the proposal that the phage BF307 receptor on these A. viscosus strains is related to one of the structures that mediates coaggregation with oral streptococci. A model to delineate the various coaggregation mediators on the surface of actinomyces coaggregation group A cells is presented, and the use of these phages to probe surface components of human oral actinomyces strains is discussed.

Isolation of bacteriophages from the oral cavity

“…Interest in this approach is increasing as a result of the continuing rise in the incidence of multiple antibiotic-resistant pathogenic bacteria (Chanishvili et al 2001). Bacteriophages have the potential to regulate the oral microflora by lysing sensitive cells, selecting mutants that may have altered properties and by releasing bacterial components with pro-inflammatory activity (Delisle et al 1988); the complex and recalcitrant nature of infections of the oral cavity suggest that bacteriophages could be considered as potential therapeutic tools for the elimination of infectious foci. As bacteriophages that infect exopolysaccharide-producing bacteria frequently carry specific polysaccharide depolymerases that aid viral penetration, bacteriophage may constitute a source of enzymes that can disrupt pathogenetic processes associated with biofilm and exopolysaccharide production (Hughes et al 1998;Hanlon et al 2001) in the oral cavity.…”

“…2001). Bacteriophages have the potential to regulate the oral microflora by lysing sensitive cells, selecting mutants that may have altered properties and by releasing bacterial components with pro‐inflammatory activity (Delisle et al. 1988); the complex and recalcitrant nature of infections of the oral cavity suggest that bacteriophages could be considered as potential therapeutic tools for the elimination of infectious foci.…”

Phages are important unrecognized players in the ecology of the oral pathogenPorphyromonas gingivalis

“…Actinomyces and Streptococcus sp.) [10][11][12][13] . This latter work suggests that negative selection pressure exerted by phages is an integral factor shaping dynamics of oral biofilm development in vivo.…”