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Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
The report section discusses the risk of each pathogen based on virulence factors. Longitudinal studies have shown the potential risk for each of these pathogens. This gives the clinician information to “target” pathogens with the goal of elimination, suppression or alteration in the composition of pathogens associated with disease. Knowing which pathogens are present and their concentrations yields a suggestion of a specific antibiotic regimen that most effectively targets the taxa of the pathogens detected. This allows selection of antibiotics based on the actual causative agent(s) rather than the indiscriminate use without objective data.
Infectious Diseases
Published in Lyle D. Broemeling, Bayesian Analysis of Infectious Diseases, 2021
Bacteria inflict damage in a different way than viruses by multiplying so rapidly they crowd out the host tissues and destroy their routine function. Often, they kill cells outright, but sometimes they produce toxins that can paralyze, destroy metabolic pathways, or generate a massive immune response that in itself is toxic. Drug-resistant bacteria sometimes manufacture an enzyme that can destroy antibiotics and eliminates them altogether. Special virulence factors enable bacteria to penetrate cells, gather nutrients for growth and survival, and evade the host’s defenses by evading the immune response. In addition, bacteria do not attack until their numbers are sufficiently high to establish an infection. This is a communication system called “quorum sensing”, that enables the microbes to coordinate their activities. The bacteria that join together in the slimy biofilms such as dental plaque assume individual specialized tasks. Despite these feints and stratagems, bacteria are easier to treat than viruses. Because they are independent and because their morphology differs from that of mammalian cells, they are more susceptible to drugs delivered via the blood stream.
Role of Plant-Based Bioflavonoids in Combating Tuberculosis
Published in Megh R. Goyal, Durgesh Nandini Chauhan, Assessment of Medicinal Plants for Human Health, 2020
Alka Pawar, Yatendra Kumar Satija
Pyrazinamide (PZA) is an analogue of nicotinamide. It is a prodrug, which requires conversion to pyrazinoic acid by enzyme MTB pyrazinamidase.85 It possesses an in vivo-enhanced lesion cleansing action and interferes in the production of virulence factors that highlight powerful antibacterial activity. PZA mainly attacks the cell membrane of mycobacteria. Ribosomal protein SA (RpsA), which encodes for ribosomal protein S1 (an essential protein implicated in protein translation as well as in the ribosome-sparing process of trans-translation), has been reported as the cellular target of PZA.67 Over-expression of RpsA has been correlated with PZA resistance in MTB.
Mechanisms of Porphyromonas gingivalis to translocate over the oral mucosa and other tissue barriers
Published in Journal of Oral Microbiology, 2023
Caroline A. de Jongh, Teun J. de Vries, Floris J. Bikker, Susan Gibbs, Bastiaan P. Krom
Next to C. albicans, there is also evidence that the bacterium Fusobacterium nucleatum is involved in the ability of P. gingivalis to invade the tissue. F. nucleatum is also commonly found in subgingival plaque and is considered to be part of the ‘orange complex’ in the pyramid of Socransky [6]. The influence of F. nucleatum on cell invasion by P. gingivalis was observed using antibiotic protection assays, as described previously in this review. In this study, the cell line Ca9–22 was used as a model for the gingival epithelium and Human aorta endothelial cells (HAEC) were used as a model for the endothelium. Invasion into both cell types by P. gingivalis was significantly enhanced in the presence of F. nucleatum. It is suggested that coaggregation of the two bacterial species may influence the expression of virulence factors. However, the exact molecular mechanism of how F. nucleatum enhances P. gingivalis invasion into gingival epithelial and endothelial cells remains to be elucidated.
Understanding the genetic basis of immune responses to fungal infection
Published in Expert Review of Anti-infective Therapy, 2022
Samuel M. Gonçalves, Cristina Cunha, Agostinho Carvalho
In recent years, the identification of factors involved in antifungal immunity has contributed to an improved understanding of the pathogenesis of fungal infections. However, like many other infectious diseases, fungal infections are characterized by significant interindividual variability in their onset, progression, and outcome. While virulence factors and mechanisms of adaptation of the pathogen contribute to infection, a dominant role for heritable host factors has also been emphasized [7–9]. Our current knowledge of the genetic basis of fungal infection has stemmed primarily from the investigation of patients with rare monogenic defects and from cohort-based studies that identified common single nucleotide polymorphisms (SNPs) associated with infection [10]. In addition, fundamental studies comparing profiles of susceptibility between inbred mouse strains have provided support to the concept of genetic susceptibility to fungal infection [11].
Bacteriophages for ESKAPE: role in pathogenicity and measures of control
Published in Expert Review of Anti-infective Therapy, 2021
Amrita Patil, Rajashri Banerji, Poonam Kanojiya, Santosh Koratkar, Sunil Saroj
Simultaneously, several findings suggest the role of bacteriophage in initiating or enhancing the pathogenicity of ESKAPE pathogens by several mechanisms like horizontal gene transfer. Studies have provided evidence that bacteriophage can disseminate virulence factors coding for adhesion, invasion, and immune evasion due to the horizontal gene transfer mechanism. The inter-relation of bacterial virulence genes with bacteriophages might indicate evolutionary changes, a research gap that needs to be explored. Such a dual role of bacteriophage may grave a threat globally. Therefore, it is crucial to assure safety by unraveling the basic mechanism of bacteriophage therapy and bacteriophage pathogenicity. A better understanding of the interactions between bacteriophage, bacteria, and humans, before implementing bacteriophage therapy, is an urgent need.