| Aggregatibacter actinomycetemcomitans | |
|---|---|
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Pasteurellales |
| Family: | Pasteurellaceae |
| Genus: | Aggregatibacter |
| Species: | A. actinomycetemcomitans |
| Binomial name | |
| Aggregatibacter actinomycetemcomitans (Klinger 1912) Nørskov-Lauritsen and Kilian 2006 | |
| Synonyms | |
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Aggregatibacter actinomycetemcomitans is aGram-negative, facultative anaerobe, nonmotile bacterium that is often found in association withlocalized aggressive periodontitis, a severe infection of theperiodontium. It is also suspected to be involved inchronic periodontitis.[1] Less frequently,A. actinomycetemcomitans is associated with nonoral infections such as endocarditis. Its role in aggressiveperiodontitis was first discovered byDanish-bornperiodontistJørgen Slots, a professor ofdentistry andmicrobiology at theUniversity of Southern California School of Dentistry.[citation needed]
'Bacterium actinomycetem comitans' was first described by Klinger (1912) as coccobacillary bacteria isolated withActinomyces from actinomycotic lesions in humans. It was reclassified asActinobacillus actinomycetemcomitans by Topley & Wilson (1929) and asHaemophilus actinomycetemcomitans by Pottset al. (1985). The species has attracted attention because of its association with localized aggressive periodontitis.[2]
Recent studies have shown a phylogenetic similarity ofA. actinomycetemcomitans andHaemophilus aphrophilus,H. paraphrophilus, andH. segnis, suggesting the newgenusAggregatibacter for them.[2]
It is one of thebacteria that might be implicated in destructiveperiodontal 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 certainActinomyces species, in particularA. israelii). It possesses certainvirulence factors that enable it to invade tissues, such as the pore-forming toxin leukotoxin A. It has also been isolated from women withbacterial vaginosis and as an etiologic agent in endocarditis.[4] The pore-forming toxin LtxA ofA. actinomycetemcomitans may be a trigger of the autoimmune diseaserheumatoid arthritis due to its ability to stimulate proteincitrullination, a post-translational protein modification targeted by autoantibodies in this disease.[5][6]
In bacteria,small RNAs are involved in gene regulation. Jorth et al. identified 9 sRNA by Northern blotting from computer-predicted candidates in strain VT1169 and 202 sRNA by RNA seq in strain 624.[8][9] A systematic screen by RNA-seq and RT-PCR in HK1651 strain (a clinical isolate from an aggressive periodontitis patient), quantified 70 sRNAs and further identified 17 differentially expressed sRNAs during growth phases.[10] Target prediction indicated possibility of sRNA interaction with several virulence genes.[10] This study confirmed the presence of one of previously identified Fur regulatedsRNAs JA04 identified in strain HK1651.[citation needed]