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Microbiological Concerns in Non-Sterile Manufacturing
Published in Jeanne Moldenhauer, Disinfection and Decontamination, 2018
An organism capable of causing a disease is referred to as a pathogen. An organism that will cause a disease or set up an infection under certain circumstances is called an opportunistic pathogen. The relative ability of any organism to cause a disease or set up an infection is called virulence. Those characteristics of the organism or condition of the host that facilitate an infection are called virulence factors. Certain microbial disease processes are caused by the organism itself or by some metabolic byproduct of that organism. Humans as well as other animals harbor many different types and species of microorganisms that are necessary for the body’s proper function. This is called a commensal or symbiotic relationship. When these organisms migrate from their “normal” body location to other locations they can and will cause an infection. Other organisms that would be considered normal micro flora can undergo genetic changes or be replaced by a different strain of the same species and become pathogenic. A weed has been described as a plant that is growing in the wrong place. This analogy can be made for resident micro flora. The point of this review is that any microorganism is an unknown regarding its ability to cause harm. The factors that can and should be considered when evaluating the virulence of organisms in a product are: the use of the product: hazard varies according to the route of administration (eye, nose, respiratory tract);the method of application;the intended recipient: risk may differ for neonates, infants, and the debilitated;use of immunosuppressive agents, corticosteroids;presence of disease, wounds, organ damage.
Quorum Sensing
Published in Vineet Kumar, Vinod Kumar Garg, Sunil Kumar, Jayanta Kumar Biswas, Omics for Environmental Engineering and Microbiology Systems, 2023
Archisman Bhunia, Kumar Narayan, Abhilasha Singh, Asmeeta Sircar, Nivedita Chatterjee
The colossal communication within the microbial community has engaged a cooperative approach to survive in antagonistic environments (Kumar et al., 2020, 2021). A bacterium residing within a biofilm generally exhibits resistance to antibiotics and biocides, which also shelters them from environmentally stressed circumstances and invasions by the host immune response. Moreover, the cells lying at close proximity aid in the horizontal gene transfer and exchange of metabolic by-products inside the biofilm. QS promotes the growth of related strains of bacteria referred to as autoinduction. It simultaneously inhibits the proliferation and maturation of other bacterial/fungal strains, and other organisms competing for the same ecological niche. QS gene end products regulate a diverse range of transcriptional mechanisms in bacterium, both in vitro and in vivo. QS systems in organisms contribute to growth potential, biofilm formation, sporulation, antibiotic resistance expression, virulence expression, autolysis, oxidative stress tolerance, metabolic activity, motility, DNA transfer, etc. (Jiang et al., 2019). Biofilms are an omnipresent form of bacterial community. Their formation is an essential requirement adopted for growth, proliferation, and maturation of the microbes, a mean to stretch the existence of the microbial colony. The formation is accompanied with the production of EPS, which leads to foundational switching in the bacterial growth and overall gene expression. The formation of biofilm noticeably reduces the susceptibility of bacteria to antibacterial agents and radiation. Specific QS signaling blockage (quorum quenching) is usually taken into account as a promising measure to avert the formation of biofilms in majority of the pathogens, hence escalating the sensitivity of pathogens to antibacterial agents and surpassing the bactericidal effect of antibiotics (Jiang et al., 2019). But if the signal production is nutrient-finite, then the nutrient-inadequate interior of a biofilm cannot donate to quorum sensing, which restricts the aptness of bacteria to appraise their own population and behave appropriately (Narla et al., 2021). The production of virulence factors helps microbe evade the barriers of immune response and cause pathogenic impacts. A gram-negative bacterium, P. aeruginosa, is proficient in existing within a diverse range of environmental conditions. This organism, being an opportunistic pathogen, is known to remain associated with nosocomial infections and is now among the foremost causes of death in severe respiratory infections (Antunes et al., 2010).
The antibiofilm potential of a heteropolysaccharide produced and characterized from the isolated marine bacterium Glutamicibacter nicotianae BPM30
Published in Preparative Biochemistry & Biotechnology, 2023
C. Trilokesh, B. S. Harish, Kiran Babu Uppuluri
EPS inhibits biofilm and biofilm formation in several ways. Through quorum sensing the pathogenic bacteria can regulate the gene expression for forming biofilms based on the population density. Each strain will have its own quorum sensing related genes.[57] For instance, the quorum sensing gene regulation system of P. aeruginosa consists of three major types namely las, rhl, and pqs.[57] These systems are responsible for the expression of antibiotic resistant genes and the generation of virulence factors such as proteases, exoenzymes, elastases, pyocyanin, rhamnolipids, alginate, and so on. The virulence factors are responsible for causing various infections in the host organism.[57] In the present work after exposure to the EPS, there could be significant downregulation of the quorum sensing genes, virulence factors, and potential anti-swarming effect which results in reduced biofilm formation. Further, the EPS can act as competitive inhibitor for lectin or sugar-binding proteins present in bacterial surfaces and prevents biofilm formation.[58] EPS could block the adhesins in the pilli or fimbriae of the bacteria or modify the physical properties of the cells and the abiotic surfaces and lead to inhibition of the biofilm formation.[58] The EPS in the present work could inhibit biofilm based on any of these possible reasons. Since the present study reports a novel antibiofilm EPS from G. nicotianae BPM30, the exact mode of action was not established. The detailed mechanism of action for the antibiofilm activity for the present EPS is under progress.