scholarly journals Current methods for inhibiting antibiotic resistant bacteria by targeting bacterial cell metabolism and disrupting antibiotic elimination through the AcrAB-Tolc efflux pump

Author(s):  
Tatiana Hillman

Bacteria have a complex and lengthy evolutionary history of antibiotic resistance. For millions of years, bacteria have evolved a gene pool filled with multiple drug resistant genes. However, for the past 50 years, bacteria have been mutating and evolving vigorously and rapidly. Those 50 years predate to the time of the first use of antibiotic drugs in the 1940s. Since the 1940s, with the wide-spread use of the first antibiotic, penicillin, bacteria have effectively developed resistance to multiple antibiotic drugs. Bacteria develop antibiotic resistance after acquiring antibiotic resistant genes from conjugation and a horizontal transfer of those genes. Bacteria also have innate properties, structure, and functions that can increase their resistance of antibiotics. Bacteria cells can mutate its genes and block the binding of antibiotic drugs to its DNA. If the bacteria effectively impede the activity of an antibiotic through a DNA mutation, then the same mutation is shared with other bacterial cell strains through horizontal transfer. Antibiotics can be expelled from bacteria cells by efflux pumps called AcrBC-Tolc channels from the resistance-nodulation division (RND) family. Targeting the cell metabolism or the expression of efflux pumps may deter or impede the proliferation of antibiotic resistance. Researchers cultured E. tarda with glucose and alanine, and the uptake of kanamycin increased, eliminating approximately 3,000 times the amount of MDR bacterial cells compared to the cells only treated with kanamycin. Another researcher named Dr. Li mutated a gene of the AcrAB-Tolc binding site, forming a replacement for the highly non-polar phenylalanine amino acid residue with an alanine. His mutagenesis of the efflux pumps binding sites for AcrAB-Tolc inhibited the exit of antibiotics through the AcrAB-Tolc efflux pumps. Therefore, the review serves to discuss the new, novel, and current methods for reducing the spread of antibiotic resistant bacteria by targeting bacterial cell metabolism and its antibiotic resistant genes.

2019 ◽  
Author(s):  
Tatiana Hillman

Bacteria have a complex and lengthy evolutionary history of antibiotic resistance. For millions of years, bacteria have evolved a gene pool filled with multiple drug resistant genes. However, for the past 50 years, bacteria have been mutating and evolving vigorously and rapidly. Those 50 years predate to the time of the first use of antibiotic drugs in the 1940s. Since the 1940s, with the wide-spread use of the first antibiotic, penicillin, bacteria have effectively developed resistance to multiple antibiotic drugs. Bacteria develop antibiotic resistance after acquiring antibiotic resistant genes from conjugation and a horizontal transfer of those genes. Bacteria also have innate properties, structure, and functions that can increase their resistance of antibiotics. Bacteria cells can mutate its genes and block the binding of antibiotic drugs to its DNA. If the bacteria effectively impede the activity of an antibiotic through a DNA mutation, then the same mutation is shared with other bacterial cell strains through horizontal transfer. Antibiotics can be expelled from bacteria cells by efflux pumps called AcrBC-Tolc channels from the resistance-nodulation division (RND) family. Targeting the cell metabolism or the expression of efflux pumps may deter or impede the proliferation of antibiotic resistance. Researchers cultured E. tarda with glucose and alanine, and the uptake of kanamycin increased, eliminating approximately 3,000 times the amount of MDR bacterial cells compared to the cells only treated with kanamycin. Another researcher named Dr. Li mutated a gene of the AcrAB-Tolc binding site, forming a replacement for the highly non-polar phenylalanine amino acid residue with an alanine. His mutagenesis of the efflux pumps binding sites for AcrAB-Tolc inhibited the exit of antibiotics through the AcrAB-Tolc efflux pumps. Therefore, the review serves to discuss the new, novel, and current methods for reducing the spread of antibiotic resistant bacteria by targeting bacterial cell metabolism and its antibiotic resistant genes.


Antibiotics ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 575
Author(s):  
Emi Nishimura ◽  
Masateru Nishiyama ◽  
Kei Nukazawa ◽  
Yoshihiro Suzuki

Information on the actual existence of antibiotic-resistant bacteria in rivers where sewage, urban wastewater, and livestock wastewater do not load is essential to prevent the spread of antibiotic-resistant bacteria in water environments. This study compared the antibiotic resistance profile of Escherichia coli upstream and downstream of human habitation. The survey was conducted in the summer, winter, and spring seasons. Resistance to one or more antibiotics at upstream and downstream sites was on average 18% and 20%, respectively, and no significant difference was observed between the survey sites. The resistance rates at the upstream site (total of 98 isolated strains) to each antibiotic were cefazolin 17%, tetracycline 12%, and ampicillin 8%, in descending order. Conversely, for the downstream site (total of 89 isolated strains), the rates were ampicillin 16%, cefazolin 16%, and tetracycline 1% in descending order. The resistance rate of tetracycline in the downstream site was significantly lower than that of the upstream site. Furthermore, phylogenetic analysis revealed that many strains showed different resistance profiles even in the same cluster of the Pulsed-Field Gel Electrophoresis (PFGE) pattern. Moreover, the resistance profiles differed in the same cluster of the upstream and the downstream sites. In flowing from the upstream to the downstream site, it is plausible that E. coli transmitted or lacked the antibiotic resistance gene.


Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1841
Author(s):  
Thanaporn Chuen-Im ◽  
Korapan Sawetsuwannakun ◽  
Pimmnapar Neesanant ◽  
Nakarin Kitkumthorn

Antibiotic resistance of microorganisms is a serious health problem for both humans and animals. Infection of these bacteria may result in therapy failure, leading to high mortality rates. During an early intervention program process, the Sea Turtle Conservation Center of Thailand (STCCT) has faced high mortality rates due to bacterial infection. Previously, investigation of juvenile turtle carcasses found etiological agents in tissue lesions. Further determination of sea water in the turtle holding tanks revealed a prevalence of these causative agents in water samples, implying association of bacterial isolates in rearing water and infection in captive turtles. In this study, we examined the antibiotic resistance of bacteria in seawater from the turtle holding tank for a management plan of juvenile turtles with bacterial infection. The examination was carried out in three periods: 2015 to 2016, 2018, and 2019. The highest isolate numbers were resistant to beta-lactam, whilst low aminoglycoside resistance rates were observed. No gentamicin-resistant isolate was detected. Seventy-nine isolates (71.17%) were resistant to at least one antibiotic. Consideration of resistant bacterial and antibiotic numbers over three sampling periods indicated increased risk of antibiotic-resistant bacteria to sea turtle health. Essentially, this study emphasizes the importance of antibiotic-resistant bacterial assessment in rearing seawater for sea turtle husbandry.


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