The concept of antibiotic immunity is a misnomer that can lead people to believe that they may become "immune" or "resistant" to an antibiotic if they take it too frequently or inappropriately. This notion stems from a misunderstanding in the general public of the concept of antibiotic resistance.
It is not people who become immune or resistant to an antibiotic. Rather it is the bacteria responsible for infections that become resistant. The purpose of an antibiotic is to kill--or at least inhibit the growth of--bacteria to quell an infection. Bacteria have been around for thousands of years and have had to survive in hostile environments. As a result, they are able to adapt and have a number of mechanisms for survival, one of which is the development of resistance to antibiotics.
Misuse or overuse of antibiotics selects for resistant bacteria. In a bacterial infection, billions of bacteria are present. Taking an antibiotic will kill or inhibit those bacteria that are susceptible to its effects and leave behind a subpopulation of bacteria that are resistant to the antibiotic. These remaining bacteria can survive and continue to grow. If they then spread from person to person, they may become the norm, and all future infections caused by these resistant bacteria will withstand the original antibiotic, rendering it useless for treatment. For many infections, patients often begin to feel better before all the bacteria have been eliminated. But it is important to complete a full course of antibiotics, even if ones symptoms have improved, to ensure that as many bacteria as possible are destroyed.
Bacteria have a variety of mechanisms by which they become resistant to antibiotics, depending on the particular antibiotic (or class of antibiotic) and the type of bacteria involved. Because antibiotics work differently to attack an essential function of bacteria, it is necessary to consider both the phenotypic mechanism of resistance and the underlying genotypic mechanism of resistance.
From a physical or biochemical perspective, there are a number of factors that contribute to antiobiotic resistance. First, the cell wall of a bacterium can be altered so that an antibiotic cannot penetrate it. Second, some bacteria produce enzymes that can destroy antibiotics before they can work. Third, certain bacteria have developed mechanisms known as efflux pumps, which are able to "eject" antibiotics from the bacterial cell before they have a chance to exert any effect. Finally, the antibiotic target site within the bacteria can be altered. In this situation, when an antibiotic enters the bacterial cell it must bind to its intended target in order to have an effect on the bacteria. If the target within the bacteria has been changed to make this binding impossible, the bacteria will be resistant to the medicines effects.
Underlying the phenotypic mechanisms of antibiotic resistance are the genetics of antibiotic resistance. Bacteria, like other living organisms, possess DNA that codes for the proteins and enzymes it requires for survival. Changes to the DNA can result in alterations in the final proteins or enzymes, which in turn can lead to antibiotic resistance. A common genetic mechanism for the development of antibiotic resistance is the acquisition of tiny fragments of DNA known as plasmids or transposons. Transposons may code for a specific antibiotic-inactivating enzyme, which, when produced by the bacteria, destroys an incoming antibiotic before it has an opportunity to work. These tiny fragments may be passed directly from one bacterium to another by a process known as conjugation. Alternatively, small viruses may attack certain bacteria and inject DNA fragments by a process known as transduction.
Another genetic mechanism of antibiotic resistance is the acquisition and accumulation of resistance genes from neighboring bacteria through a process known as transformation. A good example of this is the pneumococcus bacterium, which is a common cause of pneumonia, bacterial sinusitis, middle ear infections and even meningitis. When penicillin first became available for clinical use in the 1940s, the pneumococcus bacterium was 100 percent susceptible to penicillin. After decades of use, a portion of pneumococcal bacteria have accumulated small pieces of genetic material that they have scavenged from other bacteria, rendering them resistant to the effects of penicillin. Finally, a fourth genetic mechanism by which bacteria can develop antibiotic resistance is through mutations in their DNA. Every time a bacterium multiplies and grows, it may develop a mutation in its DNA. If the mutation occurs in a part of the DNA that codes for a protein or substance that is the target of an antibiotic, the bacteria may become resistant to that drug.
There is nothing stopping a bacterium from becoming resistant to more than one antibiotic. In fact, for some bacteria and antibiotics, cross resistance is common, which creates a new problem. The more drugs a bacterium is resistant to, the more difficult it becomes to treat an infection. Although many alternative antibiotics are currently available for use and new ones continue to be developed, there is a concern that doctors may run out of options for treating some highly resistant bacterial infections. Newer antibiotics may also be more costly than older ones and could come with side effects that make them more difficult to take. Ultimately the biggest concern with antibiotic resistance is that a patient will be treated for a potentially life threatening infection such as meningitis with an antibiotic to which the underlying bacteria is resistant. By the time the resistance is recognized through laboratory testing the patient may have suffered severe consequences.
The hope is that with more appropriate use of antibiotics and thus a reduction in antibiotic selection pressure, we can stem the tide of resistance and maintain a useful armamentarium of antibiotics for treating all types of bacterial infections. Patients should thus avoid taking antibiotics for things such as the common cold (which is caused by viruses and not bacteria), complete their courses of antibiotics as prescribed and not share their antibiotics with others.
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