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Commensal Flora
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Poor dental hygiene is a risk factor for periodontitis involving bacteria such as Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. Aggregatibacter actinomycetemcomitans has been linked to highly aggressive periodontitis. Transient bacterial translocation from oropharynx into the bloodstream is common. Poor dental hygiene and dental procedures are known contributors. Although often asymptomatic, in the presence of an abnormal heart valve, such bacteraemia can cause endocarditis. Common causes of endocarditis are viridans streptococci and bacteria from the HACEK group, all of which are part of the oropharyngeal commensal flora.
Infection-driven periodontal disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas E. Van Dyke, Mike Curtis
The relationship of specific periodontal bacteria and the host response is complex, and how these bacteria evade clearance by the inflammatory/immune response is an area of significant interest. Much of the focus has been given to the putative pathogen Porphyromonas gingivalis because of its frequent association with periodontal disease lesions and its capacity as a keystone pathogen, as described earlier. Evasion of the host response takes many forms and, from a natural selection standpoint, benefits the oral organisms by promoting chronic inflammation that produces abundant sources of collagen peptides and heme-containing compounds. Proposed mechanisms that have been demonstrated in vitro or in animal models include inhibition of leukocyte recruitment by Porphyromonas gingivalis lipopolysaccharide (LPS) binding to host adhesion molecules (ICAM-1, E-selectin), inhibition of IL-8 production by intracellular dephosphorylation of serine 536 on the p65 subunit of nuclear factor (NF)-κB, degradation of FMLP and C5a peptides by gingipains that directly disrupt a chemotactic gradient, and PI3K activation and inhibition of RhoA GTPase. LPS and lipid A have been shown to delay neutrophil apoptosis through toll-like receptor (TLR)2 signaling. LPS of Porphyromonas gingivalis displays significant structural heterogeneity that is mediated by lipid A phosphatases produced by the organism. It is postulated that the lipid A remodeling by the organism is necessary for colonization and contributes to the initiation of commensal organism dysbiosis.
Gatifloxacin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
James Owen Robinson, Keryn Christiansen
Activity against Gram-negative anaerobes, Bacteroides fragilis, other Bacteroides spp., Prevetella spp., Porphyromonas spp., and Fusobacterium spp. have been studied in vitro by a number of authors (Ackermann et al., 2000; Peric et al., 2004; Ednie et al., 1998; Schaumann et al., 1999; Kato et al., 1997; Dubreuil et al., 2003; Sheikh et al., 2015). As there are no CLSI breakpoints for these organisms, determining percentage susceptibility is difficult. For Bacteroides fragilis, MIC90 data are unhelpful, with values in different studies ranging from 1 to 16 μg/ml. If the only established CLSI breakpoints (trovafloxacin susceptible ≤ 2.0 μg/ml, intermediate 4.0 μg/ml, and resistant ≥ 8 μg/ml) are applied, percentage susceptibility ranges from 83% at 1.56 μg/ml (Kato et al., 1997), 90% at breakpoint ≤ 1 μg/ml (Schaumann et al., 1999), and 94% at 4 μg/ml (Dubreuil et al., 2003). Most strains of Porphyromonas spp., Fusobacterium spp., and Prevotella spp. were susceptible (Kato et al., 1997). In general, activity is similar to or slightly less than that of moxifloxacin or garenoxacin (Appelbaum, 1999; Schaumann et al., 2013).
Omadacycline in treating community-based infections: a review and expert perspective
Published in Expert Review of Anti-infective Therapy, 2023
George Sakoulas, Michael Nowak, Matthew Geriak
Omadacycline displays modest in vitro activity against anaerobic bacteria, including Bacteroides fragilis (MIC90 4 µg/mL), Bacteroides thetaiotaomicron (MIC90 4 µg/mL), Bacteroides vulgatus (MIC90 1 µg/mL), Prevotella spp. (MIC90 2 µg/mL), and Peptostreptococcus spp. (MIC90 1 µg/mL)[34]. Omadacycline displays in vitro activity against anaerobic pathogens commonly implicated in human infections due to animal bites [35]. The MIC90 values of Bacteroides pyogenes, Fusobacterium spp., Porphyromonas spp., and Prevotella spp. have been reported to all be ≤0.25 µg/mL [35–38]. The in vitro activity of omadacycline against Clostridioides difficile isolates has been reported in numerous studies. In a study including 250 isolates across various ribotypes, omadacycline displayed potent activity (MIC90 0.031 µg/mL) with no observed differences stratified by ribotype, disease severity, or vancomycin susceptibility [38].
Prevotella species as oral residents and infectious agents with potential impact on systemic conditions
Published in Journal of Oral Microbiology, 2022
Eija Könönen, Dareen Fteita, Ulvi K. Gursoy, Mervi Gursoy
Progressing caries lesions eventually reach the dental pulp, leading to pulpitis and pulpal necrosis. In Brazilian children, P. intermedia (96.9%), P. nigrescens (56.2%), and P. denticola (53.1%) were among the most prevalent species in primary teeth exhibiting pulp necrosis [147]. The microbiome of infectious root canals in their apical portions was primarily characterized as having Prevotella (17.9%) and Bacteroidaceae G-1 (14.3%), P. oris being the most numerous species [148]. Interestingly, elevated levels of Prevotella and Porphyromonas were found in symptomatic cases. In addition, P. baroniae, P. intermedia, P. multisacchariavorax, and A. tannerae predominate in apical periodontitis [149,150], and P. buccae and P. intermedia in radicular and residual cysts [151].
Is there a link between genetic defects in the complement cascade and Porphyromonas gingivalis in Alzheimer’s disease?
Published in Journal of Oral Microbiology, 2020
Over the years several pathogens of bacterial, viral and fungal origin have been shown to be associated with AD brains [16]. However, the etiologic role of these microbes in AD pathogenesis is still in question. Recent studies have proposed that the putative keystone periodontal pathogen Porphyromonas gingivalis can be a risk factor that contributes to AD development in some individuals [17]. Periodontitis is a chronic inflammatory disease affecting the tooth supporting tissues, caused by polymicrobial dysbiosis [18,19]. It has been proposed that imbalance in complement activity may influence dysbiosis of host microbiomes [20]. Pathogens adopt and adapt to survival and utilization of longstanding inflammatory environments as demonstrated by the presence of P. gingivalis in the subgingival crevice (as commensal and pathogen) and at distant sites (heart, placenta, and perhaps brain) with inflammatory components for the development of systemic diseases [21].