Page 335 - AWSAR 2.0

of antibiotics, for most diseases in the recent past. But, the real concern arises from the fact that the microorganisms, which cause these fatal disesases are steadily growing resistant to the antibiotics. The antimicrobial resistance (AMR or AR) is the ability of any microorganism that it may have developed to survive during an antibiotic treatment. These antibiotic resistant strains of micoorganisms are being called “superbugs”. Having witnessedtheeffectofanAMRfirsthand, during the course of my doctoral research, the ability of these pathogens to fight antibiotics deeply concerns me. A colleague of mine was sufferring from severe stomach ache, later resulting in vomiting. She was hospitalized and rightly treated for food poisoning. Six months after her recovery, the symptoms relapsed and it was discovered that the strain which infected her was an AMR. She had to undergo intensive treatment for over a year, and spend thousands of rupees to be completely free
of the strain.
For over a decade,
scientists have been
attempting to understand the
mechanisms of development
of antimicrobial resistance.
Several studies suggested
that stress conditions lead to
change in the deoxyribonucleic
acid (DNA) sequence (genetic
mutation) or transferring the
responsible gene to another
bacteria (horizontal genes
transfer) are the major cause
of de novo development and
clonal spread of antimicrobial
resistant strains. The present
strategy to address the
problem includes overcoming
AMR by chemical modification
of existing drugs or the
discovery of an entirely new class of drugs.
Ms. Debika Ojha || 311
In this regard, certain drugs are already in their 3rd and 4th modification stage and soon may be considered as ineffective. Whereas, the discovery of new drugs requires millions of dollars for pharmaceutical companies. Considering this fact few scientists have suggested that the efficiency of existing drugs can be increased by counter-attack bacterial mechanisms of drug resistance.
Here, comes the importance of Recombinase A protein (RecA). Cells experience DNA breakage for various reasons, which if not repaired immediately, will prove lethal to the cells. RecA is the key regulatory enzyme of homologous recombination (bacterial mesor DNA repair pathway). This protein is present (conserved) in all species. For example, in humans the protein similar RecA protein is called as Rad51. But recently several studies proved that RecA also helps in the evaluation of antibiotic resistance by
participating in an important pathway, “SOS response” (bacterial stress-induced DNA repair mechanism).
There are different groups or classes of antibiotics and they target different cell components or biochemical pathways to kill cells. Here, an important class of antibiotics the “genotoxic class” of fluoroquinolones, such as ciprofloxacin (this antibiotic used against common infectious diseases such as diarrhea, skin infection, typhoid fever, urinary tract infections, and abdominal infection) targets DNA replication enzymes and leads to DNA breakage. During stress condition RecA protein gets activated and leaves LexA repressor and activates
bacteria SOS response which allows repair of
we are aware that modern medicine has come up with cures, in the form of antibiotics, for most diseases in the recent past. But, the real concern arises from the fact that the microorganisms, which cause these fatal disesases are steadily growing resistant to the antibiotics. The antimicrobial resistance (AMR or AR) is the ability of any microorganism that it may have developed to survive during an antibiotic treatment.