According to the Centers for Disease Control, antibiotic-resistant infections impact more than two million people every year and tens of thousands die as a result of ineffective treatments. Recently, a team of researchers from The Scripps Research Institute in Florida uncovered a drug resistance mechanism in Streptomyces platensi bacteria which could help with the development of new antibiotic candidate drugs. Streptomyces platensis comes from a family of bacteria which produce antibiotics as a defense mechanism against other bacterium. In fact, two thirds of the naturally occurring antibiotics used in clinical practice today come from this family. The question remains, how are these antibacterial compounds – platensimycin and platencin – produced so that they are capable of killing other bacteria while leaving the host Streptomyces platensis undamaged?
The recent study found that platensimycin and platencin function as antibacterial agents due to their interference in fatty acid synthesis - fatty acids are required for the construction and maintenance of bacterial cell walls. It turns out that Streptomyces platensis has two complementary mechanisms which confer resistance to platensimycin and platencin. A pair of complementary genes drastically simplify fatty acid biosynthesis, subsequently conferring antibacterial resistance.Ultimately, such an understanding of this self-protective mechanism might allow us to assess how similar drug resistant characteristics occur and may be transferred to other bacteria.
Reference:
The Scripps Research Institute. (2014, February 20). "Scientists uncover drug resistance mechanism that could impact development of two antibiotic drug candidates." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/272903.
Reference:
The Scripps Research Institute. (2014, February 20). "Scientists uncover drug resistance mechanism that could impact development of two antibiotic drug candidates." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/272903.