Evolution of MDRs
The introduction of antibiotics for treating infectious diseases in the twentieth century led to an incredible reduction in the death rate of humans. However, the emergence of resistance to antibiotics in bacteria rendered these resistant organisms an ability to rise up against these magic bullets. Though antibiotic resistance is ancient, the indiscriminate use of antibiotics created an immense selective pressure on the bacteria facilitating the faster evolution of resistant bugs. This evolution process was mediated by the pivotal role of various factors like mutations in the antibiotic target sites, efflux pumps and acquisition of resistance genes by horizontal gene transfer. Bacteria exposed to multiple antibiotic environments were endowed with resistance mechanisms to multiple drugs which eventually increased the treatment complication. The selective pressures in health care and community settings spawned multidrug resistance (MDR) as evidenced by the emergence of methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Staphylococcus aureus (VRSA), extended-spectrum-beta-lactamase (ESBL)-producing bacteria and quinolone resistant bacteria. As new drugs also end up with the same fate in this never-ending war between multidrug-resistant bugs and humans, most of the pharmaceutical industries have withdrawn their efforts in seeking new antibiotics. Thus, the present scenario made a compulsion on mankind to search for alternative antibacterial therapies. In this chapter, representative but not comprehensive descriptions are given for various genetic and non-genetic elements that have contributed to the evolution of MDR.
KeywordsHorizontal Gene Transfer West Nile Virus Efflux Pump Antibiotic Resistance Gene Quinolone Resistance
The laboratory is supported by the grants from the Department of Biotechnology (DBT), Ministry of Science and Technology, Government of India (No. BT/PR/11634/INF/22/104/2008), Gujarat State Biotechnology Mission (GSBTM), Department of Science and Technology, Government of Gujarat (No. GSBTM/MD/PROJECTS/SSA/1535/2013–14) and Indian Council of Medical Research, New Delhi, India (No. AMR/49/11-ECDI). K. Vinothkumar is a JRF in the above-mentioned GSBTM grant. The authors are grateful to Dr. Amit Ghosh, Dr. T. Ramamurthy and Dr. S. K. Niyogi, National Institute of Cholera and Enteric Diseases (NICED), Kolkata, India, for their support and advice. The authors thankfully acknowledge the Puri Foundation for Education in India for providing infrastructure facilities and Ms. Neha Rajpara, Mr. Priyabrata Mohanty, Mr. Braj M. R. N. S. Kutar and Ms. Aneri Shah for their invaluable help, advice and support.
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