Subacute bacterial endocarditis due to actinobacillus actinomycetemcomitans

Serra, P; Tonato, Maurizio

doi:10.1016/0002-9343(69)90174-0

Cited by 42 publications

(10 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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“…For example, A.a. may cause bacterial endocarditis (Overholt, 1966;Page and King, 1966;Serra and Tonato, 1967) as well as thyroid abscesses (Burgher et al, 1973). The black-pigmented oral Bacteroides can cause serious infections of the head and neck, and Capnocytophaga strains are known to cause septicemia, especially in immunocompromised patients.…”

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1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease

et al. 1986

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Major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of localized juvenile periodontitis (LJP). Several lines of evidence suggest that LJP is an infectious process closely associated with Actinobacillus (Haemophilus) actinomycetemomitans as a causative agent, although other organisms may also participate. The immunologic profile of LJP patients suggests that a cell-associated neutrophil locomotory dysfunction is a key underlying immunodeficiency resulting in increased susceptibility to periodontal infection. In addition, LJP patients often exhibit cervical lymphadenopathy and IgG-hypergammaglobulinemia, and a markedly elevated antibody response to the infecting organism, A. actinomycetemcomitans, is found in the serum and crevicular fluid of most patients. Evaluation of the locomotory properties of LJP neutrophils shows that random migration and chemokinesis are normal; however, about 70% of the LJP patients suffer from a defect in chemotaxis, with their neutrophils responding poorly to bacterial chemotactic factors, synthetic chemotactic peptides, and complement fragments (C5a). Depressed chemotaxis of LJP neutrophils is paralleled by their reduced capacity to bind the synthetic chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP), as well as C5a. Furthermore, there is a reduction in the amount of glycoprotein 110, a neutrophil membrane matrix component and differentiation antigen which is associated with FMLP- and possibly also C5a-mediated chemotaxis. Reduction of C5a and of FMLP ligand binding, decreased expression of GP-110, and reduced neutrophil chemotaxis are consistent with a stem cell maturation error in LJP patients. This is further supported by studies demonstrating increased expression of CR2, the C3d/EBV receptor, on peripheral blood neutrophils of LJP patients. CR2 receptors are normally present on immature human neutrophils but are lost during the maturation process. These alterations in neutrophil surface components and their reduced chemotaxis may result from a genetically determined abnormality. Studies demonstrating the familial nature of both the neutrophil chemotactic disorder and the clinical entity represented by localized juvenile periodontitis point to a strong role for genetic determinants in the disease which affect neutrophil surface receptors.

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“…Cases of A. actinomycetemcomitans endocarditis which were not resolved by penicillin (2,12,15,16) or which followed a tooth extraction with penicillin prophylaxis (13) have also been reported. A. actinomycetemcomitans endocarditis has responded favorably to combinations of antibiotics, including ampicillin, chloramphenicol, erythromycin, and streptomycin, but fatal cases in which such therapeutic regimes were used have also been reported (2,16,19,27), raising doubt concerning the universal efficacy of these combinations.…”

Section: Slots Et Almentioning

confidence: 99%

“…no. 244,1980), endocarditis (6,16,19,27), vertebral osteomyelitis (14), brain abscess (12), thyroid gland abscess (4), and urinary tract infection (26). A. actinomycetemcomitans is often a constituent of mixed bacterial infections, but it can also be the sole infecting agent (25,28).…”

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In Vitro Antimicrobial Susceptibility of Actinobacillus actinomycetemcomitans

1980

Antimicrob Agents Chemother

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The agar dilution technique was used for determination of the antibiotic susceptibilities of 57 oral isolates and 2 nonoral isolates of Actinobacillus actinomycetemcomitans. Tetracycline, minocycline, and chloramphenicol inhibited more than 96% of the strains tested at a concentration of c2 Atg/ml; 89% of the strains were inhibited by 2 ug of carbenicillin per ml. The other antimicrobial agents tested were less active. Approximately 10% of the A. actinomycetemcomitans strains were resistant to ampicillin, erythromycin, and penicillin G at concentrations of 32 to 64 ug/ml. These data suggest that tetracycline and minocycline may be valuable drugs in the treatment ofA. actinomycetemcomitans infections.Actinobacillus actinomycetemcomitans is a facultative, gram-negative bacterium of clinical importance. It has been isolated from actinomycosis (3, 5, 9, 10), periodontitis (24; J. Slots, H. S. Reynolds, P. M. Lobbins, and R. J. Genco, J. Dent. Res., 59: 328, Special Issue A, Am. Assoc. Dent. Res., abstr. no. 244, 1980), endocarditis (6, 16, 19, 27), vertebral osteomyelitis (14), brain abscess (12), thyroid gland abscess (4), and urinary tract infection (26). A. actinomycetemcomitans is often a constituent of mixed bacterial infections, but it can also be the sole infecting agent (25, 28). A. actinomycetemcomitans can be a part of the indigenous oral microflora (9), and the portal of entry of this organism is often assumed to be-the oral cavity and the upper respiratory tract.A. actinomycetemcomitans strains vary in in vitro susceptibilities to penicillin, ampicillin, and other commonly used antibiotics (8,11,16). Evidence that this diversity affects therapy is suggested by the fact that a given antibiotic has been effective in certain cases of A. actinomycetemcomitans infection, but has failed in others (2,16,27 All strains utilized carbohydrates fermentatively, were capnophilic, decomposed H202, reduced nitrate, and were benzidine positive. None of the strains required X (hemin) and V (nicotinamide adenine dinucleotide) growth factors or hydrolyzed esculin, gelatin, starch, or urea, and none produced acetylmethylcarbinol, decarboxylases, H2S, oxidase, or indole. All strains produced acid from glucose, fructose, and mannose but not from adonitol,

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Subacute bacterial endocarditis due to actinobacillus actinomycetemcomitans

Cited by 42 publications

References 14 publications

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

1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease

In Vitro Antimicrobial Susceptibility of Actinobacillus actinomycetemcomitans

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