You can run, but you cannot hide from bacteria. Within the realm of microbiology there are organisms capable of developing resistance to drug therapy through a variety of different mechanisms. Bacteria serve as one such microorganism and are found abundantly across the globe. Speaking in terms of the human body, beneficial bacteria exist (i.e. normal flora), but the concern is focused more towards those that cause widespread infections and diseases. Whether through intrinsic or extrinsic factors, these microbes harness the ability to develop diverse strains that ultimately resist drug treatment.
In saying this, the misuse of antibiotics is a very common extrinsic feature contributing drug resistance. The concept of patient noncompliance is a prime example of how drugs are not taken properly for the duration of time recommended, thus leading to strains that become more tolerant over time. In regards to intrinsic aspects, the genome of the bacteria is altered in a couple of different ways. First, horizontal gene transfer, generally speaking, is a process seen within the bacteria community where genes are passed from one cell to another cell in order to adjust to a new environment. This increase in fitness allows the microbe to survive and develop immunity to certain types of therapy. In addition, mutations represent another mechanism by which bacteria evolve. Here, the idea is that the pathogen genome is changed in a manner where the drugs become inactivated. Drug therapy ends up killing more of the nonresistant microbes, thereby reducing competition posed by mutants who can now continue to multiply. Bacteria can also develop resistance to drug treatment for reasons like impermeability, or even sometimes by having multidrug efflux pumps that excessively rid the cell of the applied drug.
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Many other microorganisms, such as viruses, fungi, and protists, can also have negative effects on the human body. Because of unique characteristics possessed by each, the level to which they are capable of developing resistance varies. For instance, some viruses are known as retroviruses and induce drug-resistant mutations. Influenza is one such example of a retrovirus that requires antiviral treatment, which also corresponds with patient noncompliance. In comparison with bacteria, I believe viruses can develop immunity easier, based on the fact that doses are often intended to be taken for longer periods of time, therefore making them difficult to follow up on.
Although fungal resistance to drugs is not seen as much as in viruses and bacteria, they still offer significant potential for increased tolerance through similar means, such as horizontal gene transfer previously mentioned. Because fungi are more closely related to humans than bacteria, these organisms also are considered to be much more difficult to treat than bacteria. However, I feel that bacteria are capable of developing drug resistance to a greater extent since they exist in so many different forms. In addition to fungi, protists pose as another microbial threat to humans and exhibit resistance-developing properties as well. Protists might have less of an advantage than bacteria when clinical factors are compared because treatments are often in single, high doses, making compliance by patients that much simpler. On the other hand, protists are the most structurally and functionally diverse than any other microorganism. Because of this, I think that protist group possibly has a greater chance of developing resistance to drug therapy.
Overall, the main point attempted to be driven home is the fact that bacteria have the ability to form new strains through many different methods of resistance development. In comparison with other microorganisms I believe bacteria compete very well in this capacity. However, the fact that viruses like influenza develops into new strains almost on a seasonal basis leads me to believe that it is this category of microbes that are the frontrunners in developing immunity to drugs. Whatever the case may be, it is clearly evident that pathogenic microorganisms as a whole can escape drug treatment in one way or another. Consequentially, drug research continues, along with further studying of these pathogens, in hopes of discovering the secret to halting drug resistance.
- Foster, John W. and Joan L. Slonczewski. Microbiology: An Evolving Science. W.W. Norton & Company. New York, NY. 2009.
- Guan, Yi and Honglin Chen. Resistance to Anti-Influenza agents. Vol. 366, Issue 9294, p1339-1140. 10 October, 2005. EBSCOhost: Academic Search Complete. Accessed on April 4, 2010. <http://web.ebscohost.com/ehost/detail?vid=11&hid=105&sid=92b628da-283c-4105b555bb719d0b9fc%40sessionmgr114&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=a9h&AN=18405045>
- Kontoyiannis, Dimitrios P. and Russell E. Lewis. Antifungal Drug Resistance of Pathogenic Fungi. Vol. 359, Issue 9312, p1135. 30 March, 2002. Academic Search Complete. Accessed on April 4, 2010. <http://web.ebscohost.com/ehost/detail?vid=10&hid=105& sid=92b628da-283c-4105 b55d 5bb719d0b9fc%40sessionmgr114&bdata=JnNpdGU 9Z Whvc3QtbGl2ZQ%3d%3d#db=a9h&AN=6403394 >
- Xian-Zhi, Li and Hiroshi Nikaido. Efflux-Mediated Drug Resistance in Bacteria. Vol. 69, Issue 12. P1555-1632. 2009. EBSCOhost: Academic Search Complete. Accessed on April 4, 2010.<http://web.ebscohost.com/ehost/detail?vid=8&hid=105&sid=92b628da283c41051b55d5bb719d0b9fc%40sessi\onmgr114&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=a9h&AN=44256070>
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