With our improved healthcare system and increased development of antibiotics, it’s not hard to think for a split second that we are safe from infectious bacteria! However, recent outbreaks of “superbugs” have proved otherwise.
There have been outbreaks of MRSA in the hospitals; this superbug has been found to be resistant to 15 to 30 different antibiotics. That means when it's detected, a doctor has only a very small number of compounds at hand that are able to kill it. Another superbug that is causing a stir is a strain of highly drug-resistant Streptococcus pneumoniae which causes acute ear infections in children. As these superbugs are discovered, other bacteria are continually becoming more and more antibiotic resistant.
When people are infected by bacteria, most people will turn to doctor prescribed antibiotics for help; however, antibiotics will manage to kill most of the bacteria cultures, but not all of them! The bacteria that survive the antibiotic treatments most likely would have had some resistance from the start, or that they would have acquired it through mutation or gene exchange with other bacteria. Those cells that survived now face reduced competition from antibiotic susceptible bacteria, and they will go on to proliferate, therefore becoming increasingly resistant to the drugs that we use. So here’s the question: if bacteria adapt and evolve so fast, is there a way to prevent these bugs from mutating into an even more drug resistant bacteria? Floyd E. Romesberg seems to have found the key (at least a start) to preventing bacteria from developing resistance.
To understand his research, first, you will have to know how bacteria mutation occurs. Durring the 1970s scientists discovered the “SOS response” that occurs in bacteria that take advantage of mutation as a form of self defense (chromosomal mutations). “When bacteria are under extreme stress, they try various means of fixing the damage as an initial step. Then they switch genes whose protein products precipitate a spate of mutations that occur 10,000 times as fast as those arising during normal cell replication. In essence, the cells undergo a quick identity change.” (Stix 82) Romesberg used E. coli in his experiment. He found that by using ciprofloxacin (an antibiotic), it triggers the clipping of a protein called LexA in E. coli, resulting in fast development in resistance. When he and the researchers created a strain of E. coli in which LexA could not be cleaved off, the SOS response didn’t materialize. The group of researchers has also gotten similar results for another antibiotic, rifampicin. As a result of his discoveries, Romesberg has been trying to generate a small molecule that could be administered orally along with antibiotics which would switch off the process of LexA cleavage. His work is only focused on fluoroquinolones (bacterialcidal drug that inhibit DNA replication and transcription of the targeted bacteria) because resistance to them only develops through the chromosomal mutations of bacteria. However, this is not enough, as mentioned before, resistance can also be acquired in bacteria though gene exchange from other species or within the same species.
Nevertheless, Romesberg and his teams’ discoveries and researches will provide us a better option to fight off drug resistant bacteria instead of constantly coming up with new antibiotics. It’s all about tackling the source of the problem. But just as a note, people should stop being so depended on drugs. Don’t always go to the doctor for antibiotics and let your own body produce immunity against the foreign invaders because although antibiotics can be a quick fix to the sickness, and can be used to help those with a weakened immune system to save many lives, drugs can also cause complications between the patient and the bacteria. Also keep in mind that the dose of antibiotic intake during a bacterial infection is not always the more the better!
This is the site where Romesbergs article can be purchased online, sorry I couldn’t find a PDF copy of the article:
However, here’s the magazine reference:
Stix, Gary. “An Antibiotic Resistance Fighter.” Scientific American April 2006: 81-83