Antibiotic resistance is an inevitable result of the use of antibiotics, and is not a new concept. Even in the 1940’s, when penicillin was first mass-produced, resistant bacteria were recognized. But misuse and overuse of antibiotics both create added pressure for the development and spread of resistant bacteria, resulting in reservoirs of resistance that threaten treatment success in all regions of the world.
Acquired antibiotic resistance is the result of a genetic mutation that changes the way a microbe responds to a drug made to eradicate it. These responses vary greatly – for example, some genetically resistant bacteria have altered binding sites so that prevent antibiotic molecules from attaching to cell walls, others have mechanisms to pump out antibiotics when they do get inside.
Even before an antibiotic is administered, a portion of a bacterial population may be genetically resistant to that antibiotic. But adding a drug to the mix puts selective pressure on the community, killing those bacteria that are susceptible but allowing resistant bacteria to survive and multiply. This is especially a risk when antibiotics are administered at low doses not strong enough to wipe out whole populations, or when antibiotic therapy is initiated but then terminated before it can run its full course of wiping out an infection. This leaves lingering populations of bacteria that have been exposed to the drug and given the opportunity to develop resistance. Without susceptible bacteria to compete with, antibiotic-resistant bacteria can quickly multiply and develop into an infection that is no longer treatable by the usual drugs, requiring more aggressive treatment or sometimes leaving doctors with no options – especially in developing nations, where drug access is often limited.
Acquired antibiotic resistance is the result of a genetic mutation that changes the way a microbe responds to a drug made to eradicate it. These responses vary greatly – for example, some genetically resistant bacteria have altered binding sites so that prevent antibiotic molecules from attaching to cell walls, others have mechanisms to pump out antibiotics when they do get inside.
Even before an antibiotic is administered, a portion of a bacterial population may be genetically resistant to that antibiotic. But adding a drug to the mix puts selective pressure on the community, killing those bacteria that are susceptible but allowing resistant bacteria to survive and multiply. This is especially a risk when antibiotics are administered at low doses not strong enough to wipe out whole populations, or when antibiotic therapy is initiated but then terminated before it can run its full course of wiping out an infection. This leaves lingering populations of bacteria that have been exposed to the drug and given the opportunity to develop resistance. Without susceptible bacteria to compete with, antibiotic-resistant bacteria can quickly multiply and develop into an infection that is no longer treatable by the usual drugs, requiring more aggressive treatment or sometimes leaving doctors with no options – especially in developing nations, where drug access is often limited.
Diagram credit: http://microvet.arizona.edu/Courses/MIC438/decker/AntibioticRes/AntibioticResistance.html
Genes conferring antibiotic resistance can also propagate in commensal (non-disease causing) bacteria, which are native to all humans, and then be transferred to pathogenic bacteria through conjugation. Both commensal and pathogenic resistant bacteria can be spread through the food supply (e.g. Escherichia coli), or between humans in clincal or community settings (e.g. methicillin-resistant Staphylococcus aureus, or MRSA). These resistant strains are an increasing medical and economic concern - MRSA alone kills 19,000 Americans every year, and one recent study found that antibiotic-resistant infections cost the U.S. healthcare system more than $20 billion annually. The CDC and WHO both rank antibiotic resistance as one of the top three public health concerns worldwide.
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