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Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative, facultative anaerobic, nonmotile bacterium that is often found in association with localized aggressive periodontitis, a severe infection of the periodontium. It is also suspected to be involved in chronic periodontitis.[1] Less frequently, A. actinomycetemcomitans is associated with nonoral infections such as endocarditis. Its role in aggressive periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry and microbiology at the University of Southern California School of Dentistry.
'Bacterium actinomycetem comitans' was first described by Klinger (1912) as coccobacillary bacteria isolated with Actinomyces from actinomycotic lesions in humans. It was reclassified as Actinobacillus actinomycetemcomitans by Topley & Wilson (1929) and as Haemophilus actinomycetemcomitans by Potts et al. (1985). The species has attracted attention because of its association with localized aggressive periodontitis.[2]
Nomenclature
Recent studies have shown a phylogenetic similarity of A. actinomycetemcomitans and Haemophilus aphrophilus, H. paraphrophilus, and H. segnis, suggesting the new genus Aggregatibacter for them.
Importance
It is one of the bacteria that might be implicated in destructive periodontal disease. Although it has been found more frequently in localized aggressive periodontitis,[3] prevalence in any population is rather high. It has also been isolated from actinomycotic lesions (mixed infection with certain Actinomyces species, in particular A. israelii). It possesses certain virulence factors that enable it to invade tissues, such as the pore-forming toxin leukotoxin A. It has also been isolated from women with bacterial vaginosis and as an etiologic agent in endocarditis.[4] The pore-forming toxin LtxA of A. actinomycetemcomitans may be a trigger of the autoimmune disease rheumatoid arthritis due to its ability to stimulate protein citrullination, a post-translational protein modification targeted by autoantibodies in this disease.
Virulence factors
- Leukotoxin A: kills granulocytes, monocytes, and other white blood cells expressing integrin beta-2 (CD18)
- Cytolethal distending toxin
- Immunosuppression factors that inhibit blastogenesis, antibody production, and activate T-suppressor cells
- Inhibition of granulocyte functions
- Resistant to complement-mediated killing
- Lipopolysaccharides
- Surface antigens
- Heat shock proteins
- Antimicrobial resistance
A. actinomycetemitans serotypes
- a strain, for example ATCC 29523, frequently in oral cavity, variable leukotoxin expression
- b strain Y4, most frequently in localized aggressive periodontitis, high leukotoxin expression; of the b subset, clone Jp2 is particularly leukotoxic[7]
- c strain ATCC 33384, low leukotoxin expression
- serotypes d, e, f, g
- within each serotype, leukotoxin expression can be highly variable between strainse
