Abstract

The bacterium Aggregatibacter actinomycetemcomitans is associated with aggressive forms of periodontitis and with systemic diseases, such as endocarditis. By assessing a Ghanaian longitudinal adolescent cohort, we earlier recognized the cagE gene as a possible diagnostic marker for a subgroup of JP2 and non-JP2 genotype serotype b A. actinomycetemcomitans strains, associated with high leukotoxicity as determined in a semi-quantitative cell assay. This group of A. actinomycetemcomitans is associated with the progression of attachment loss. In the present work, we used conventional polymerase chain reaction (PCR) and quantitative PCR to perform the cagE genotyping of our collection of 116 selected serotype b A. actinomycetemcomitans strains, collected over a period of 15 years from periodontitis patients living in Sweden. The A. actinomycetemcomitans strains carrying cagE (referred to as cagE+; n = 49) were compared to the cagE-negative strains (n = 67), present at larger proportions in the subgingival plaque samples, and were also much more prevalent in the young (≤35 years) compared to in the old (>35 years) group of patients. Our present results underline the potential use of cagE genotyping in the risk assessment of the development of periodontal attachment loss in Swedish adolescents.

Highlights

  • Aggregatibacter actinomycetemcomitans is a Gram-negative opportunistic pathogen associated with rapidly progressing periodontitis and with extra-oral diseases, such as endocarditis [1,2,3]

  • Carriers of the JP2 serotype b-specific genotype of A. actinomycetemcomitans are at higher risk of development of attachment loss (AL) compared to carriers of a non-JP2 genotype of A. actinomycetemcomitans

  • In our previous work, delineating the role of cagE as a potential diagnostic marker, we studied a collection of A. actinomycetemcomitans strains collected from a prospective cohort of Ghanaian adolescents [19]

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Summary

Introduction

Aggregatibacter actinomycetemcomitans is a Gram-negative opportunistic pathogen associated with rapidly progressing periodontitis and with extra-oral diseases, such as endocarditis [1,2,3]. Several longitudinal studies have demonstrated that adolescents colonized with A. actinomycetemcomitans, as compared to those that are not, have a significantly increased risk of the development of periodontal attachment loss (AL) [4,5,6,7]. A. actinomycetemcomitans species has been found, and seven different serotypes (a–g) exist, representing genetically divergent lineages [11,12,13]. A. actinomycetemcomitans genotypes can have extensively different pathogenic potentials [5,14,15]. Carriers of the JP2 serotype b-specific genotype of A. actinomycetemcomitans are at higher risk of development of AL compared to carriers of a non-JP2 genotype of A. actinomycetemcomitans. Typical for JP2 genotype strains is the deletion of 530 base pairs (bp) in the promoter region of the ltxCABD gene operon, which encodes leukotoxin (LtxA), and Pathogens 2019, 8, 153; doi:10.3390/pathogens8030153 www.mdpi.com/journal/pathogens

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