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Role of Indigenous Microbial Community in Bioremediation
Published in Vineet Kumar, Vinod Kumar Garg, Sunil Kumar, Jayanta Kumar Biswas, Omics for Environmental Engineering and Microbiology Systems, 2023
Bhupendra Pushkar, Pooja Sevak
The cellular membrane of the microbes separates the outside environment from the cytoplasm. The transport of various pollutants across the microbial cell membrane influences the rate of bioremediation. Cellular membrane plays a key role in the bioavailability of nutrients as well as pollutants for metabolism. Degradation of pollutants mostly takes place in the cytoplasm due to the localization of degrading enzymes in the cytoplasm. Therefore, the target pollutant should be transported inside for active bioremediation (Hua and Wang, 2014). The pollutants are transported inside the cell via different pathways. For example, phenols at higher concentrations enter the cell of bioremediating microbes by passive transport. However, at lower concentrations of phenol, microbes take up phenol using an active transport system (Hua and Wang, 2014). The active or passive uptake rate of pollutants has a major effect on bioremediation. Energy-dependent transport of the pollutants across the cell membrane in microbes determines the biotransformation rate (Chen et al., 2019). The microbial membrane also performs efflux mechanisms, in which the toxic compounds are moved out of the cell into the surrounding or in periplasm after its detoxification inside the cytoplasm. Efflux is widely used for heavy metal bioremediation in microbes. Besides bioremediation, efflux is employed for different functions such as cell homeostasis and resistance to antibiotics, heavy metals, and salts, which enable microbes to survive under extreme conditions (Pushkar et al., 2021).
Odour Control or Inhibition Using Antimicrobial Finishing
Published in G. Thilagavathi, R. Rathinamoorthy, Odour in Textiles, 2022
Rosie Broadhead, Laure Craeye, Chris Callewaert
The antimicrobials used today for textile finishing bring up several concerns. First, antibiotic resistance is a global problem that humanity faces today (Morais, Guedes, and Lopes 2016; Shahidi and Wiener 2012). Gaining resistance is an evolutionary process that occurs within microbial cells. Microorganisms acquire genes, leading to antibiotic resistance mechanisms, such as the development of efflux pumps, for instance, to avoid antimicrobials entering the cell. As such, MRSA is not sensitive to quaternary ammonium compounds (Tischer et al. 2012). Moreover, resistance is a trait that can be interchanged between cells. Besides resistance against QACs, a lot of resistance against silver particles is reported, too. This means that antimicrobials are losing their efficiency in killing microorganisms, and therefore, in the context of antimicrobial finishing, lose their ability in reducing odour (Morais, Guedes, and Lopes 2016).
Microbial Biofilms-Aided Resistance and Remedies to Overcome It
Published in Bakrudeen Ali Ahmed Abdul, Microbial Biofilms, 2020
Efflux pumps are membrane-bound proteins that give particular bacteria a status of multidrug resistance by throwing antimicrobial substances such as antibiotics out of the cells. They can be divided into substrate-specific pumps and non-substrate-specific pumps that throwback different substances out of the cells (Webber & Piddock 2003). The genes for these pumps are present on chromosomes as well as mobile genetic elements and plasmids (Marquez 2005). Till date, five superfamilies of these efflux pumps have been reported which are multidrug and toxin extrusion (MATE), small multidrug resistance (SMR), major facilitator superfamily (MFS), ATP-binding cassette (ABC), and resistance-nodulation division (RND) (Jack et al. 2001, Kuroda & Tsuchiya 2009, Lubelski et al. 2007, Nikaido & Takatsuka 2009, Pao et al. 1998). Except for ABC, all other pumps utilize energy from sodium/potassium motive force. Besides making cells harsh toward antibiotics, they also involved in different bacterial phenotypes such as QS, biofilm formation, and virulence expression.
Overview of methodologies for the culturing, recovery and detection of Campylobacter
Published in International Journal of Environmental Health Research, 2023
Marcela Soto-Beltrán, Bertram G. Lee, Bianca A. Amézquita-López, Beatriz Quiñones
Even though campylobacteriosis is a zoonotic infection, it has been shown that the emergence of Campylobacter resistance in human clinical samples is connected to antimicrobial resistance found in animals. The inappropriate usages of antibiotics in the veterinary medicine and animal production contribute to the increased antimicrobial resistance and the emergence of multidrug resistance profiles. The indiscriminate use of antibiotics in food animal production has been indicated as a catalyst in the development of resistant foodborne or waterborne Campylobacter infecting humans (Wieczorek and Osek 2013; Whitehouse et al. 2018). Additionally, acquisition of genes by horizontal transfer can also provide resistance mechanisms including the enzymatic degradation, alteration of the antimicrobial compound, active efflux of the antimicrobial across the cell membrane, or alteration of the cell membrane to reduce the permeability to the antimicrobial.
Characterization of Burkholderia cepacia complex from environment influenced by human waste
Published in International Journal of Environmental Health Research, 2022
Jasna Hrenovic, Martina Seruga Music, Martina Drmic, Lucija Pesorda, Branka Bedenic
The BCC isolates possess a wide range of intrinsic resistance to antimicrobial agents (CLSI 2019; EUCAST 2021), leaving few antibiotics for the treatment of infected patients such as ceftazidime, meropenem, minocycline, sulfamethoxazole, chloramphenicol. The occurrence of acquired resistance traits make the antimicrobial chemotherapy very challenging for clinicians (Isles et al. 1984; Martina et al. 2020). Therefore, the mechanisms responsible for antibiotic resistance in BCC are extensively studied. The putative β-lactamases of the class A (Pen-like), class C (AmpC) and class D (OXA-like) play a role in antibiotic resistance (Becka et al. 2018; Degrossi et al. 2019). The acquired extended-spectrum β-lactamases (ESBLs) of TEM family with good activity against penicillins and cephalosporins were also reported in some BCC isolates (Maravic et al. 2012). Except the production of specific enzymes, the expression of efflux pumps could be responsible for the resistance to clinically significant antibiotics (Maravic et al. 2012; Podnecky et al. 2015). In addition to numerous antibiotic resistance mechanisms, BCC expresses many virulence traits, such as biofilm production, cell invasion and intracellular survival, responsible for severe infections and poor clinical outcome (Fazli et al. 2015).
Molecular characterization of quinolone resistance and antimicrobial resistance profiles of Klebsiella pneumoniae and Escherichia coli isolated from human and broiler chickens
Published in International Journal of Environmental Health Research, 2022
Mehri Haeili, Hila Salehzeinali, Somayyeh Mirzaei, Zeinab Pishnian, Amin Ahmadi
Quinolones act by inhibiting the activity of two essential bacterial type II topoisomerases, DNA gyrase and topoisomerase IV resulting in impaired DNA replication (at lower concentrations) and cell death (at lethal concentrations) (Redgrave et al. 2014). Resistance to these agents is multifactorial and can occur via a range of mechanisms. Amino-acid substitution within the quinolone resistance-determining region (QRDR) of chromosomal genes encoding the DNA gyrase (gyrA and gyrB) and/or topoisomerase IV (parC and parE) is the most common mechanism of high-level resistance in Enterobacteriaceae (Yoshida et al. 1990). In addition, a number of plasmid-mediated quinolone resistance (PMQR) mechanisms have been described: The first identified PMQR gene was discovered in a clinical isolate of K. pneumoniae in 1998 (Martínez-Martínez et al. 1998) and PMQR genes are increasingly being identified worldwide in several Gram-negative bacteria, including Enterobacteriaceae. To date, three types of PMQR determinants have been described: (i) Qnr peptides (QnrA, QnrB, QnrS, QnrD, and QnrC) which protect type II topoisomerases from quinolone attack; (ii) AAC(6ʹ)-Ib-cr, a variant of aminoglycoside acetyltransferase that modifies ciprofloxacin and norfloxacin (Rodríguez-Martínez et al. 2011); and (iii) efflux pumps QepA and OqxAB (Yamane et al. 2007) (Robicsek et al. 2006a; Strahilevitz et al. 2009; Kim et al. 2009b).