Characterization of an inducible bacteriophage from a leukotoxic strain of Actinobacillus actinomycetemcomitans

Stevens, R. H.; Hammond, Benjamin F.; Lai, Chung-Sheng

doi:10.1128/iai.35.1.343-349.1982

Cited by 46 publications

(27 citation statements)

References 41 publications

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“…&Aa is a temperate bacteriophage that infects strains of Actinobacillus actinomycetemcomitans [1], an oral microorganism that is considered to be the etiologic agent of Localized Juvenile Periodontitis (for review see [2]). Subsequent to our discovery of phage 4~Aa, other A. actinomycetemcomitans phages have been identified [3][4][5][6], and in 1987, we reported an association between the presence of A. actinomycetemcomitans phages and periodontal disease activity [5,6].…”

Section: Introductionmentioning

confidence: 99%

Prevalence and distribution of bacteriophage φAa DNA in strains of Actinobacillus actinomycetemcomitans

Stevens¹

1994

FEMS Microbiology Letters

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phi Aa is a bacteriophage that was originally isolated by induction of a lysogenic strain of the oral bacterium Actinobacillus actinomycetemcomitans. Since the discovery of phage phi Aa, additional phages infecting several other strains of A. actinomycetemcomitans have been identified. To determine the prevalence of phi Aa or phi Aa-related temperate phages in this species, a phi Aa-specific DNA probe was prepared to screen for homologous sequences among 42 strains of A. actinomycetemcomitans. Fourteen (33%) of the 42 strains examined contained DNA sequences that hybridized with the phage phi Aa probe. A bacteriophage designated phi Aa33384 was isolated by induction from one of the strains (ATCC 33384) that contained a sequence that hybridized with the phi Aa probe. The phi Aa probe hybridized with the DNA extracted from bacteriophage phi Aa33384. The distribution of the phage phi Aa sequence among A. actinomycetemcomitans serotypes was 5/13 (38%) of the serotype a strains, 0/16 (0%) of the serotype b strains, and 9/13 (69%) of the serotype c strains. The results of this investigation suggest that the target sequence prepared from the phage phi Aa genome is fairly common in the A. actinomycetemcomitans chromosome, and that the sequence is distributed among the A. actinomycetemcomitans serotypes in a seemingly nonrandom manner.

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Section: Introductionmentioning

confidence: 99%

Prevalence and distribution of bacteriophage φAa DNA in strains of Actinobacillus actinomycetemcomitans

Stevens¹

1994

FEMS Microbiology Letters

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“…Both in Corynehaclerium diphtheria causing diphtheria and ^-haemolytic streptococci causing scarlatina, the toxins responsible for disease are coded for by a phage genome. However, there are only a few reports on phages able to infect oral bacteria (Shimizu 1968, Totsuka 1976, Brady et al 1977, Higuchi et al 1977, Stevens et al 1982, Tylenda et ai. 1985, The significance of phage in dental plaque is therefore obscure.…”

Section: Discussionmentioning

confidence: 99%

“…1985, The significance of phage in dental plaque is therefore obscure. A prophage has been detected in one strain of A. aclinomycetemcomi' lan.s isolated from localized juvenile periodontitis (Stevens et al 1982). This prophage coded for a bacteriophage of group A.…”

Section: Discussionmentioning

confidence: 99%

The presence of phage‐infected Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients

Preus

Olsen

1987

J Clinic Periodontology

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Electron microscopy revealed 2 different types of bacteriophages isolated from Actinobacillus actinomycetemcomitans colonizing exclusively diseased sites in 4 patients with localized juvenile periodontitis (LJP). All sites infected with phage were undergoing periodontal destruction, as judged from consecutive routine radiographs. The phages isolated had a wide host range as assessed from their ability to infect a series of reference strains of A. actinomycetemcomitans. A 5th patient harboured non-infected A. actinomycetemcomitans in a surgically treated site which had undergone no bone destruction during the last 12 months. The present findings suggested that the pathogenic potential of A. actinomycetemcomitans in LJP may increase due to phage infection.

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“…In 1982, Stevens et al 26 reported that a double-stranded phage called <I>Aa could be isolated after mitomycin C induction of A. actinomycetemcomitans strain 651. Most of the other 11 strains they tested also appeared to carry the phage since they were resistant to infection by <I>Aa.…”

Section: Bacteriophagementioning

confidence: 99%

Molecular Genetics and the Analysis of Leukotoxin in A. actinomycetemcomitans

Kolodrubetz¹

1996

Journal of Periodontology

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The primary pathogen involved in certain forms of early‐onset periodontitis is A. actinomycetemcomitans. Among its numerous potential virulence factors is a leukotoxin that kills certain host defense cells. In order to analyze the regulation and in vivo function of leukotoxin and other virulence factors in A. actinomycetemcomitans, molecular genetic approaches are being established. Although there has been significant progress in developing plasmids and bacteriophage as E. colilA. actinomycetemcomitans shuttle vectors, more work needs to be done. Tn5‐based transposon mutagenesis has been shown to work in this organism. Targeted mutagenesis is now possible in A. actinomycetemcomitans; exogenously introduced DNA recombines efficiently with the homologous chromosomal locus. These techniques have been applied to studies of leukotoxin. Targeted mutagenesis has been used to construct leukotoxin negative mutants that are otherwise isogenic with their leukotoxin‐producing parent strain. These mutants can be tested in animal models to ascertain the in vivo role of leukotoxin in A. actinomycetemcomitans pathogenesis. Gene targeting has also been used to make strains in which the leukotoxin promoter is regulating the synthesis of a β‐galactosidase reporter gene. Such strains have been used to show that leukotoxin synthesis increases in cells grown anaerobically, but that several other environmental changes had little effect on leukotoxin synthesis. Finally, plasmid shuttle vectors with leukotoxin promoters from various strains of A. actinomycetemcomitans fused to reporter genes have been used in cis/trans tests to show that leukotoxin promoter sequences and strain‐specific trans‐acting factors are important in determining why different strains of A. actinomycetemcomitans produce different levels of leukotoxin. J Periodontol 1996;67:309–316.

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Characterization of an inducible bacteriophage from a leukotoxic strain of Actinobacillus actinomycetemcomitans

Cited by 46 publications

References 41 publications

Prevalence and distribution of bacteriophage φAa DNA in strains of Actinobacillus actinomycetemcomitans

Prevalence and distribution of bacteriophage φAa DNA in strains of Actinobacillus actinomycetemcomitans

The presence of phage‐infected Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients

Molecular Genetics and the Analysis of Leukotoxin in A. actinomycetemcomitans

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