Our constant struggle with bacteria has yielded many resistant species over the last decades. Our antibiotics have become less effective because, due to natural selection, bacteria undergo genetic changes that give rise to resistance. The most well-known resistant species is probably MRSA, which is short for methicillin-resistant Staphylococcus aureus. It is also known as the hospital bug, because it frequently infects hospitalized patients. While we do have antibiotics to kill the resistant form of S. aureus, evolution does not stop: lately, some MRSA strains have acquired resistance for our last-resort drugs, that are only used when everything else fails. Harvard scientists have discovered the mechanism behind this change, providing clues about how we can develop new strategies, to stay one step ahead of the bacteria.
Mutation
In order to acquire new characteristics, MRSA needs genetic mutations. Modification of genes results in changes in protein construction, which might just prevent our drugs from asserting their deadly effect. Over the last couple of years, some S. aureus strains managed to develop resistance against vancomycin, an antibiotic used as a last resort. According to Harvard scientists, they get the required mutation in a remarkable way: they copy genetic code from another resistant bacterial species, belonging to the Enterococcus family. MRSA gets the required genetic code by simultaneously infecting a patient, and it appears they have found a way to cooperate, despite being totally different species.
Transposon
The scientists found the genetic part that made MRSA resistant to vancomycin by unravelling its entire genetic code. Underlying the newfound ability to gather abilities from other bacteria were certain properties that made them more 'social'. This explains why they were able to borrow genetic material from the already vancomycin-resistant Enterococcus strain. Social MRSA were able to acquire a genetic component known as Tn1546, a piece of genetic code that is able to insert itself into the genome: these genetic structures are known as transposons. Also called 'jumping genes', transposons function in similar fashion to viruses, that implant their own genetic material into ours after infection.
New antibiotics
In order to become more social, MRSA had to mutate and acquire certain characteristics. According to the Harvard scientists, this also created new weaknesses that can be exploited by new drugs. Therefore, even though MRSA acquired vancomycin resistance, we may still be one step ahead in the rat race, despite the fact that developing new antibiotics will take a while. There are other initiatives already underway, including the use of nanoparticles, certain prehistoric proteins, or by simply finding other targets.
Overcoming resistance
While vancomycin resistance by itself is not new, it does become a problem if all other antibiotics do not work either. When it comes to the already quite resistant MRSA species, losing the deadly effect of vancomycin becomes a big problem, as we need to have at least one functioning antibiotic to be able to rid patients of infections. Because of evolutionary mechanisms such as natural selection and survival of the fittest, we will be in a constant rat race with bacteria. It is of paramount importance to stay one step ahead, because if we cannot keep up, spread of lethal bacteria could severely threaten mankind.
Mutation
In order to acquire new characteristics, MRSA needs genetic mutations. Modification of genes results in changes in protein construction, which might just prevent our drugs from asserting their deadly effect. Over the last couple of years, some S. aureus strains managed to develop resistance against vancomycin, an antibiotic used as a last resort. According to Harvard scientists, they get the required mutation in a remarkable way: they copy genetic code from another resistant bacterial species, belonging to the Enterococcus family. MRSA gets the required genetic code by simultaneously infecting a patient, and it appears they have found a way to cooperate, despite being totally different species.
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| MRSA as observed by a scanning electron microscope. |
The scientists found the genetic part that made MRSA resistant to vancomycin by unravelling its entire genetic code. Underlying the newfound ability to gather abilities from other bacteria were certain properties that made them more 'social'. This explains why they were able to borrow genetic material from the already vancomycin-resistant Enterococcus strain. Social MRSA were able to acquire a genetic component known as Tn1546, a piece of genetic code that is able to insert itself into the genome: these genetic structures are known as transposons. Also called 'jumping genes', transposons function in similar fashion to viruses, that implant their own genetic material into ours after infection.
New antibiotics
In order to become more social, MRSA had to mutate and acquire certain characteristics. According to the Harvard scientists, this also created new weaknesses that can be exploited by new drugs. Therefore, even though MRSA acquired vancomycin resistance, we may still be one step ahead in the rat race, despite the fact that developing new antibiotics will take a while. There are other initiatives already underway, including the use of nanoparticles, certain prehistoric proteins, or by simply finding other targets.
Overcoming resistance
While vancomycin resistance by itself is not new, it does become a problem if all other antibiotics do not work either. When it comes to the already quite resistant MRSA species, losing the deadly effect of vancomycin becomes a big problem, as we need to have at least one functioning antibiotic to be able to rid patients of infections. Because of evolutionary mechanisms such as natural selection and survival of the fittest, we will be in a constant rat race with bacteria. It is of paramount importance to stay one step ahead, because if we cannot keep up, spread of lethal bacteria could severely threaten mankind.
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