Brain abscess due to <i>Actinobacillus actinomycetemcomitans</i>

Stepanović, Srdjan; Tošić, Tanja; Savić, Branislava; Jovanović, Milica; K'ouas, Guylène; Carlier, Jean‐Philippe

doi:10.1111/j.1600-0463.2005.apm1130312.x

Cited by 21 publications

(12 citation statements)

References 15 publications

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“…Arguably, these lesions could serve as the primary infective focus for the dissemination and subsequent seeding of bacteria into an end organ site. For a majority of episodes, the absence of other detectable infective foci led researchers to conclude that the oral cavity, by default, is the primary source of infection (57,61,63,67,86,88,114,126,139). However, these studies, mainly case reports, suggest a relationship between pyogenic CNS infections and an oral origin of bacteria such as Abiotrophia spp., Dalister pneumosintes, Streptococcus intermedius, S. oralis, Streptococcus constellatus, Fusobacterium spp., F. nucleatum, Aggregatibacter actinomycetemcomitans, and Porphyromonas gingivalis (57,61,63,67,86,88,114,126,139).…”

Section: Cnsmentioning

confidence: 95%

Microbiology of Odontogenic Bacteremia: beyond Endocarditis

et al. 2009

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SUMMARY The human gingival niche is a unique microbial habitat. In this habitat, biofilm organisms exist in harmony, attached to either enamel or cemental surfaces of the tooth as well as to the crevicular epithelium, subjacent to a rich vascular plexus underneath. Due to this extraordinary anatomical juxtaposition, plaque biofilm bacteria have a ready portal of ingress into the systemic circulation in both health and disease. Yet the frequency, magnitude, and etiology of bacteremias due to oral origin and the consequent end organ infections are not clear and have not recently been evaluated. In this comprehensive review, we address the available literature on triggering events, incidence, and diversity of odontogenic bacteremias. The nature of the infective agents and end organ infections (other than endocarditis) is also described, with an emphasis on the challenge of establishing the link between odontogenic infections and related systemic, focal infections.

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Section: Cnsmentioning

confidence: 95%

Microbiology of Odontogenic Bacteremia: beyond Endocarditis

et al. 2009

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“…We prefer this model for the following reasons. (i) A. actinomycetemcomitans causes extraoral infections, including abscess infections; thus, the model has clinical relevance (17)(18)(19). (ii) The infectious dose is easily controlled and results in a contained infection that has been used to study the pathogenesis of oral bacteria (14,34,35).…”

Section: Resultsmentioning

confidence: 99%

“…A. actinomycetemcomitans is the proposed causative agent of localized aggressive periodontitis (15,16), an acute disease characterized by massive tissue destruction and tooth loss. A. actinomycetemcomitans also causes extraoral infections, including abscess infections (17)(18)(19), and our laboratory has used a murine abscess infection model to characterize A. actinomycetemcomitans genes required for growth in vivo (14). In this study, we used high-resolution transcriptomics to examine the physiology of A. actinomycetemcomitans during growth in the murine abscess.…”

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confidence: 99%

Probing Bacterial Metabolism during Infection Using High-Resolution Transcriptomics

et al. 2013

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A fundamental aspect of most infectious diseases is the need for the invading microbe to proliferate in the host. However, little is known about the metabolic pathways required for pathogenic microbes to colonize and persist in their hosts. In this study, we used RNA sequencing (RNA-seq) to generate a high-resolution transcriptome of the opportunistic pathogen Aggregatibacter actinomycetemcomitans in vivo. We identified 691 A. actinomycetemcomitans transcriptional start sites and 210 noncoding RNAs during growth in vivo and as a biofilm in vitro. Compared to in vitro biofilm growth on a defined medium, ϳ14% of the A. actinomycetemcomitans genes were differentially regulated in vivo. A disproportionate number of genes coding for proteins involved in metabolic pathways were differentially regulated in vivo, suggesting that A. actinomycetemcomitans in vivo metabolism is distinct from in vitro growth. Mutational analyses of differentially regulated genes revealed that formate dehydrogenase H and fumarate reductase are important A. actinomycetemcomitans fitness determinants in vivo. These results not only provide a high-resolution genomic analysis of a bacterial pathogen during in vivo growth but also provide new insight into metabolic pathways required for A. actinomycetemcomitans in vivo fitness.

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“…Aggregatibacter actinomycetemcomitans is a Gram-negative capnophilic bacterium that is regarded as a principal pathogen associated with LAgP (1, 2). This bacterium is also associated with systemic infections that can result in endocarditis (3), meningitis, and brain abscesses (4). A. actinomycetemcomitans has also been detected in atherotic plaques and in placentas of women suffering from preeclampsia, which is a pregnancy complication evoking high blood pressure and endangering both the mother and the fetus (5).…”

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confidence: 99%

Antibiotic susceptibility of Aggregatibacter actinomycetemcomitans JP2 in a biofilm

Oettinger‐Barak

Dashper

Catmull

et al. 2013

Journal of Oral Microbiology

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BackgroundLocalized aggressive periodontitis (LAgP) is an inflammatory disease associated with specific bacteria, particularly Aggregatibacter actinomycetemcomitans, which can result in early tooth loss. The bacteria grow as a biofilm known as subgingival plaque. Treatment includes mechanical debridement of the biofilm, often associated with empirical antibiotic treatment.ObjectiveThe aims of this study were to test in vitro the sensitivity of A. actinomycetemcomitans JP2 during planktonic and biofilm growth to doxycycline and to the combination of metronidazole and amoxicillin, which are two antibiotic protocols commonly used in clinical practice.DesignTwo in vitro biofilm models were used to test the effects of the antibiotics: a static 96-well plate assay was used to investigate the effect of these antibiotics on biofilm formation whilst a flow chamber model was used to examine the effect on established biofilms.ResultsOf the antibiotics tested in this model system, doxycycline was most efficacious with a minimal inhibitory concentration (MIC) against planktonic cells of 0.21 mg/L and minimal biofilm inhibitory concentration (MBIC) of 2.10 mg/L. The most commonly prescribed antibiotic regimen, amoxicillin + metronidazole, was much less effective against both planktonic and biofilm cells with an MIC and MBIC of 12.0 mg/L and 20.2 mg/L, respectively. A single treatment of the clinically achievable concentration of 10 mg/L doxycycline to sparse A. actinomycetemcomitans biofilms in the flow chamber model resulted in significant decreases in biofilm thickness, biovolume, and cell viability. Dense A. actinomycetemcomitans biofilms were significantly more resistant to doxycycline treatment. Low concentrations of antibiotics enhanced biofilm formation.ConclusionA. actinomycetemcomitans JP2 homotypic biofilms were more susceptible in vitro to doxycycline than amoxicillin + metronidazole.

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Brain abscess due to Actinobacillus actinomycetemcomitans

Cited by 21 publications

References 15 publications

Microbiology of Odontogenic Bacteremia: beyond Endocarditis

Microbiology of Odontogenic Bacteremia: beyond Endocarditis

Probing Bacterial Metabolism during Infection Using High-Resolution Transcriptomics

Antibiotic susceptibility of Aggregatibacter actinomycetemcomitans JP2 in a biofilm

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