Antibiotic resistance occurs when bacteria change in some way that reduces or eliminates the effectiveness of drugs, chemicals, or other agents designed to cure or prevent infections. The bacteria survive and continue to multiply causing more harm. Bacteria can do this through several mechanisms.
Antibiotic resistance occurs when bacteria change in some way that reduces or eliminates the effectiveness of drugs, chemicals, or other agents designed to cure or prevent infections. The bacteria survive and continue to multiply causing more harm.
Bacteria have developed different mechanisms to make the antibiotics used against them ineffective. The genes that encode these defense systems are placed in the bacterial chromosome or in plasmids. They are transmitted from generation to generation: this is the principle of vertical gene transfer. Genetic elements, like plasmids, can also be exchanged among bacteria of different taxonomic affiliation, this is the principle of horizontal gene transfer. Horizontal gene transfer by conjugation is common in nature, and in technical systems, where the density of bacteria is high. Studies carried out on WWTP treatment mechanisms show that the bacteria present often appear to be multidrug-resistant, this fact hardly depending on the input effluent.
Indiscriminate use of antibiotics for relieving oneself of of all kinds of pain when there is no need for the administration of any kind of antibiotics has been regarded as one of the main causes of making antibiotics resistant to bactria.
All living things want to survive. When antibiotics are used to kill the bacteria, they want to survive in this stressed situation. They mutate a few of their genes to become resistant since they have plasmid containing resistance genes as well. They acheive multi drug resistance too.
Dear Dr. Farhana Rumzum Bhuiyan Thanks a lot for your comment and contribution, really thanks. I agree with you misuse and abuse of antimicrobials lead to this phenomenon, not only plasmid but now transposon (jumping gene) play a significant role in the transmission of resistance through bacterial populations.
Dear Dr. Reza Biria Thanks a lot for your comment and contribution, really thanks. I agree with you misuse and abuse of antimicrobials lead to this phenomenon.
Dear all thanks a lot for comments and contributions and I would like to add that the bacteria become resistant in several ways: some bacteria can “neutralize” an antibiotic by changing it in a way that makes it harmless such as by releasing enzymes such as the resistance against b- lactam through the production of B- lactamase. Others have learned how to pump an antibiotic back outside of the bacteria before it can do any harm. Some bacteria can change their outer structure through changing the cellular membrane permeability so the antibiotic has no way to attach to the bacteria it is designed to kill. After being exposed to antibiotics, sometimes one of the bacteria can survive because it found a way to resist the antibiotic. If even one bacterium becomes resistant to antibiotics, it can then multiply and replace all the bacteria that were killed off. That means that exposure to antibiotics provides selective pressure making the surviving bacteria more likely to be resistant. Bacteria can also become resistant through mutation of their genetic material.
As Dr. Evens Emmanuel explained, there are horizontal and vertical genetic transfer mechanisms. Bacteria try to survive either through mutations in their chromosomes and if one bacterium becomes resistant it survives and reproduces and transmits the resistance to the second generation.
Horizontal transfer occurs via three mechanisms ( transformation, transduction, and conjugation). Transformation occurs when bacteria lyses and the bacterial chromosome transmits to other, transduction occurs via the transmission of resistant genes by bacteriophages, conjugation can occur among varies spp. of bacteria, it is believed that environmental bacteria which contain a various resistant gens to different antimicrobials such as Enterococci ( vancomycin-resistant Enterococci) transmit resistant to other intestinal pathogens through conjugation.
These organisms are trying to survive, during my work on these microorganisms. I admired them so much how they protect each other and support each other, so we see that bacteria have resisted and lived for millions of years. These microorganisms when faced a danger are divided into three groups, the first is in the face of danger and most likely dies. The second is sublethally damaged and third survived, to maintain the type. Sometimes they resort to the formation of the biofilm, not necessarily with the same type, because when we defined biofilm, we say that there are several bacterial communities ( more than one bacterial population) and sometimes bacteria with protozoa. This biofilm can also protect them from the influence of antibiotics and the influence of chemicals and disinfectants. They may resort to forming spores, as it minimizes their metabolic activities to a minimum and reduces the water content, and surrounds itself with a coating to preserve the species. All they do is to survive where they support each other and protect each other because they do not know hate and hatred, which only exist in humans.
There are two main ways that bacterial cells can acquire antibiotic resistance. One is through mutations that occur in the DNA of the cell during replication. The other way that bacteria acquire resistance is through horizontal gene transfer.
Antibiotics stop working because bacteria come up with various ways of countering these actions, such as:
Preventing the antibiotic from getting to its target When you really don't want to see someone, you might find yourself doing things like hiding from them or avoiding their phone calls. Bacteria employ similar strategies to keep antibiotics at bay. One effective way to keep a drug from reaching its target is to prevent it from being taken up at all. Bacteria do this by changing the permeability of their membranes or by reducing the number of channels available for drugs to diffuse through. Another strategy is to create the molecular equivalent of a club bouncer to escort antibiotics out the door if it gets in. Some bacteria use energy from ATP to power pumps that shoot antibiotics out of the cell.
Changing the target Many antibiotics work by sticking to their target and preventing it from interacting with other molecules inside the cell. Some bacteria respond by changing the structure of the target (or even replacing it within another molecule altogether) so that the antibiotic can no longer recognize it or bind to it.
Destroying the antibiotic This tactic takes interfering with the antibiotic to an extreme. Rather than simply pushing the drug aside or setting up molecular blockades, some bacteria survive by neutralizing their enemy directly. For example, some kinds of bacteria produce enzymes called beta-lactamases that chew up penicillin.
Antibiotic resistance occurs when bacteria change in some way that reduces or eliminates the effectiveness of drugs, chemicals, or other agents designed to cure or prevent infections. The bacteria survive and continue to multiply causing more harm. Bacteria can do this through several mechanisms.
The genetic potential of a bacterium consists of the chromosome and one or more optional genephores and extra-chromosomal, the plasmids. Genes are also carried by transposable genetic elements and by integrons. A bacterium can thus acquire resistance to antibiotics by two great genetic mechanisms. One supports chromosome and defines chromosomal resistance, the other supports plasmids or transposable elements and they define extra-chromosome resistance.
Chromosome resistance results from a mutation. It’s a rare phenomenon. It is not caused by the presence of the antibiotic. But the antibiotic reveals the resistance mutation by selecting the mutant resistant bacteria (or more precisely, by destroying the other bacteria of the species, those which have remained sensitive to the action of the antibiotic).
The plasmid resistance is linked to the synthesis of additional proteins and not to a modification of the normal constituents of the bacteria. Furthermore, many resistance plasmids are conjugative or mobilizable which allows horizontal transfer; these transfers are at the origin of a very important dissemination of the resistance within the bacterial populations, which qualifies the plasmid resistance of "contagious or infectious".
I would like to add that these microorganisms have smart strategies to maintain survival. Every drug has a specific working mechanism. Just that we use this medicine, these organisms will try to find an anti-mechanical mechanism, for example, changing the permeability of the cellular membrane in the event of anti-tetracycline, or trying to disrupt the drug’s action such as secretion of enzymes like penicillinase by Staphylococcus aureus to disrupt Penicillins. People modified these drugs with semi-synthetic penicillins (methicillin), where they inhibit certain proteins (PBP) important for the synthesis of the cell wall. As a counter-strategy, the bacteria transformed these proteins to (PBP2a) where methicillin is not binding to them by the acquisition of Mec A gene from environmental and commensal bacteria so they change the binding site, bacteria can also adapt to new determinants, for example, to membrane-embedded antibiotic efflux pumps, by rearranging membrane structures in such a way that they will be compatible and interact with the new acquisition or a number of other genes may need to change in order to effect full expression of a new gene, e.g. mecA in Staphylococci. etc. ... so all we used a certain way these microorganisms are trying to find a way to counter it. Also, resistance can be acquired by the formation of biofilm with different bacterial populations. So, they sense the danger and works to find the means to resist this danger ( chorom sensing mechanisms) not only medications but against heat, high salinity, ph, cold, and freezing through the production of shock proteins. So, really they have smart strategies to maintain survival.
Selection and spread of resistance of a certain antibiotic by other antibiotics, i.e. the co-selection process, can also account for the maintenance of resistance to a particular antibiotic, even if its use has been discontinued. Multiple resistance genes are frequently found on the same plasmid or transposon and therefore the use of any of the antibiotics would select for resistance to all the others. Resistance can also be maintained by non-antibiotic selective pressures, but the extent to which these environmental factors impact resistance is not fully known. A multitude of transposons and plasmids code not only for resistance to multiple antibiotics but also for genes mediating heavy metal tolerance, virulence, and metabolic functions. Multidrug resistance transporters such as AcrAB and LmrA, with a broad range of substrate specificities (e.g. antibiotics, amino acids, and sugars) can also impact the stability of resistance traits. Some of these pumps, and other regulatory resistance mechanisms, can be regulated by multiple environmental stress conditions and compounds besides antibiotics, for example iron starvation and the presence of bile salts.
While antibiotics appear to be the central element in selecting resistant bacteria, they are not wholly responsible for the persistence and spread of them once selected. The selection event (forward reaction) is clearly the most important one, which fosters resistant bacteria of different genotypes and phenotypes in the environment. But once selected, the resistant strains can ‘take on a life of their own’ in response to other selection and maintenance factors in the absence of antibiotics. This makes the reversal of resistance (backward reaction) more difficult to achieve. There is a need to create more ingenious ways of reestablishing susceptible flora. This goal may theoretically be accomplished by using bacteria themselves in the form of probiotic formulations. However the potential presence of antibiotic resistance genes in probiotic organisms also needs to be evaluated. Understanding the impact of antibiotics on the evolutionary and ecological flexibility and versatility of the bacterial world is essential for strategically responding to the global problem of antibiotic resistance.
some bacteria can naturally resist certain kinds of antibiotics, others can become resistant if their genes change or they get drug-resistant genes by produce new strains.
Dear Dr. Wisam Thamer Al-Mayah Thanks a lot for your comment and contribution, really thanks. I agree with you, microflora and commensal bacteria mostly have resistance genes, while pathogens tend to acquire these genes via genetic transfer. Thanks
Antibiotic resistant bacteria are bacteria that cannot be fully inhibited or killed by an antibiotic. The antibiotic may have worked effectively before the resistance occurred.
Patterns of antibiotic usage greatly affect the number of resistant organisms which develop. Overuse of broad-spectrum antibiotics, such as second- and third-generation cephalosporins, greatly hastens the development of methicillin resistance. Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, and the use of antibiotics as livestock food additives for growth promotion.
Antibiotics work in several ways; It affects a number of daily vital processes that the bacteria depend on for growth and survival. Among these methods that represent the mechanism of antibiotics:
Impeding the production of the bacterial cell wall, which protects the bacterial cell from the external environment, and thus helps it to live and reproduce.
- Blocking protein formation by preventing the binding of amino acids (the basic unit of protein building) to each other. By preventing the action of the ribosome (the organ responsible for protein synthesis) in the normal way.
Impeding metabolism, such as the manufacture of folic acid, an acid that bacteria need to reproduce and survive.
There are two main ways that bacterial cells can acquire antibiotic resistance. One is through mutations that occur in the DNA of the cell during replication. The other way that bacteria acquire resistance is through horizontal gene transfer .
an increase in temperature leads to an increase in antibiotic resistance rates of Escherichia coli, Klebsiella pneumonia, and Staphylococcus aureus. due to elevated temperatures facilitating horizontal gene transfer of mobile genetic elements of resistance, and increased pathogen growth rates promoting environmental persistence.