Systemic Infection Due to<i>Actinobacillus actinomycetemcomitans</i>

Burgher, Louis W.; Loomis, George W.; Ware, Frederick L.

doi:10.1093/ajcp/60.3.412

Cited by 51 publications

(17 citation statements)

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“…It is a member of the HACEK (Haemophilus aphrophilus, Haemophilus parainfluenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens and Kingella kingae) group of human pathogens responsible for approximately 3 % of endocarditis (el Khizzi et al, 1997;Serra & Tonato, 1969; Steckelberg et al, 1990;Vandepitte et al, 1977) and other extra-oral infections (Burgher et al, 1973;Martin et al, 1967;Muhle et al, 1979;Overholt, 1966;Page & King, 1966). It has also been associated with atheromatous plaques and may play a role in their formation (Haraszthy et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional analysis of the 5' terminus of the flp fimbrial gene cluster from Actinobacillus actinomycetemcomitans

2003

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Fresh isolates of the oral bacterial pathogen Actinobacillus actinomycetemcomitans exhibit a fimbriated, rough colony phenotype. Evidence suggests that the fimbrial subunit gene flp is part of a cluster of 14 genes (flp to tadG) thought to encode proteins involved in the synthesis, assembly and export of these fimbriae. To determine the transcriptional organization of the 59 terminus of this gene cluster, total RNA from rough and smooth phenotype variants of A. actinomycetemcomitans strain 283 were analysed by RT-PCR. Primers designed to amplify regions spanning gene junctions or multiple genes yielded amplicons at each individual gene junction from flp to tadD for both the rough and smooth variants. Semi-quantitative RT-PCR of the rcpA to tadZ amplicon revealed that significantly more mRNA was transcribed from the rough than the smooth variant. Longer amplicons encompassing flp to tadZ (3?9 kb) and tadA to tadD (2?1 kb) were also detected, but only from the rough variant. Rapid amplification of cDNA ends (RACE) was used to identify the 59 end of the mRNA containing flp. Antisense primers located within rcpC, orfB and flp-2 enabled amplification of a RACE product that was subsequently isolated and subcloned into pGEM-T. DNA sequencing indicated that the 59 end of the mRNA was located at a G or T nucleotide 2102 to 2101 nt upstream of flp. Corresponding s 70 consensus sequences were located at 210 (TATAAT) and 235 (TTGCAT) relative to the transcription start site. These data confirm that the flp gene cluster is an operon transcribed as a polycistronic message commencing from a G or T nucleotide located in the intergenic region upstream of flp. Promoter function of the flp upstream region was confirmed using a lacZ reporter gene construct transformed into Escherichia coli. RT-PCR analysis further suggests that although transcription does occur in both the rough and smooth variants, full-length transcripts are rapidly degraded or are significantly downregulated in the smooth variant. INTRODUCTIONThe oral bacterium Actinobacillus actinomycetemcomitans is a Gram-negative coccobacillus most notably associated with localized juvenile periodontitis, an aggressive form of early onset periodontitis affecting children 10 to 17 years old, and some cases of refractory adult periodontitis (Haraszthy et al., 2000;Slots & Dahlen, 1985; Tanner et al., 1979;Zambon, 1985). It is a member of the HACEK (Haemophilus aphrophilus, Haemophilus parainfluenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens and Kingella kingae) group of human pathogens responsible for approximately 3 % of endocarditis (el Khizzi et al., 1997;Serra & Tonato, 1969; Steckelberg et al., 1990;Vandepitte et al., 1977) and other extra-oral infections (Burgher et al., 1973;Martin et al., 1967;Muhle et al., 1979;Overholt, 1966;Page & King, 1966). It has also been associated with atheromatous plaques and may play a role in their formation (Haraszthy et al., 2000). Newer niches are being discovered for A. actinomycetemcomitans, ...

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Section: Introductionmentioning

confidence: 99%

Transcriptional analysis of the 5' terminus of the flp fimbrial gene cluster from Actinobacillus actinomycetemcomitans

2003

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“…Finally, LIP tends to cluster in families, suggesting that predisposition to the disease may be genetically regulated (Jorgenson et al, 1975;Melnick et al, 1976;Saxen, 1980;Saxen and Nevanlinna, 1984;Boughman et al, 1986;Beaty et al, 1987;Hart etal., 1992 (Colebrook, 1920) (Goldsworthy, 1938;King and Tatum, 1962;Pulverer and Ko, 1970;Sneath and Iohnson, 1973;Tanner et al, 1982;Slots, 1982 (Block et al, 1973;Page and King, 1966). A. actinomycetemcomitans has also been associated with meningitis (Page and King, 1966), septicemia (Page and King, 1966), urinary tract infections (Townsend and Gillenwater, 1969), pneumonia (Meyers et al, 1971), and abscesses of the brain (Garner, 1979;Martin et al, 1967), abdomen (Garner, 1979;Martin et al, 1967), and face (Page and King, 1966) as well as other organs and extremities (Burgher et al, 1973;Page and King, 1966 (Shenker et al, 1982a (Shenker et al, 1982b(Shenker et al, , 1990(Shenker et al, , 1999 (Meyer et al, 1991(Meyer et al, , 1996(Meyer et al, , 1997 Tsai et al, 1979). The leukotoxin is a 1 16-kDa protein that was initially detected and purified from A. actinomycetemcomitans strain JP2, an isolate cultured from an eight-year-old boy suffering from generalized alveolar bone loss around his primary teeth …”

Section: (I) Introductionmentioning

confidence: 99%

Beyond the Specific Plaque Hypothesis: Are Highly Leukotoxic Strains of Actinobacillus Actinomycetemcomitans a Paradigm for Periodontal Pathogenesis?

Guthmiller

Lally

Korostoff

2001

Critical Reviews in Oral Biology & Medicine

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“…Endocarditis was considered unlikely because of the absence of clinical signs of endocarditis and the absence of vegetations at echocardiography. A review of the English language literature reveals 12 reports of brain abscesses due to infection with A. actinomycetemcomitans (Martin et al 1967, Burgher et al 1973, Brewer et al 1975, Ingham et al 1978, Garner 1979, Churton & Greer 1980, Kaplan et al 1989, Kuijper et al 1992, Zijlstra et al 1992, Renton et al 1996, Stepanovic et al 2005 (Table 1). All but two reports are of male patients in the age of 19-62 years.…”

Section: Discussionmentioning

confidence: 99%

Brain abscess associated with Aggregatibacter actinomycetemcomitans: case report and review of literature

2011

Br Dent J

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Systemic Infection Due toActinobacillus actinomycetemcomitans

Cited by 51 publications

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Transcriptional analysis of the 5' terminus of the flp fimbrial gene cluster from Actinobacillus actinomycetemcomitans

Transcriptional analysis of the 5' terminus of the flp fimbrial gene cluster from Actinobacillus actinomycetemcomitans

Beyond the Specific Plaque Hypothesis: Are Highly Leukotoxic Strains of Actinobacillus Actinomycetemcomitans a Paradigm for Periodontal Pathogenesis?

Brain abscess associated with Aggregatibacter actinomycetemcomitans: case report and review of literature

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