Methicilin-resistant S. aureus were originally resistant to Methicilin but later on develop resistance to many other antibiotics. Similarly, vancomycin resistant Enterococci (VRE) also develop multi-drug resistance. Why it is so often that bacteria develop multiple resistance? How do they acquire the multiple resistance?
Resistance determinants can be transferred between bacteria, for example on plasmids. Bacteria can also develop resistance through additional mutations, leading to changes such as overexpression of multidrug efflux transporters, target mutations, target overexpression, down-regulation of porins or other routes of drug uptake, and changes to membrane structure.
The reason that these strains tend to develop multiple resistances is that we "select" for these strains. A simple example: One patient comes in with a S. aureus infection. He gets treated with Methicilin. Due to bad luck or wrong treatment (the therapy is cancelled directly after the symptons disappear) a few partially Methicilin-resistant S. aureus survive, multiply and get transferred to another patient. This patient gats also treated with Methicilin and by the process repeats itself until you have a MRSA strain resisting Methicilin treatment. Thus, the next antibiotic is used, until the strain gets resistant also to the second one. Rinse and repeat until you get a strain resistant to all available ABs.
As to the how: Either by the selection process mentioned above or by horizontal gene transfer from a strain already resistant to the second AB. The resistance genes often end up on or adjacent to mobile genetic elements and/or plasmids.
In addition to mutation and gene transfer, mentioned previously, some resistance mechanisms that develop against one drug, may affect other drugs, to which the microorganism was never exposed, as well. For example an eflux pump aimed a removing one drug may remove other drugs too. Or, the entry restriction of one drug, for example by modifying pore size, may inhibit the entry of several other drugs as well.
All the previous answers are correct, and also very clearly explained. We have only consider, in addition, the reason of sublethal contact of bacteria with antibiotic, and strongly work avoiding non rational treatment of deseases except when really necessary, and also avoid to use the in veterinary, food or other areas.
I think you mean "What and /or how does human activity trigger MDR in microorganisms. Read these two articles and they will help you clear what exactly is there that you wish to find out.
Always keep focused on terms like sublethal dosage, unnecessary antibiotic therapy and local susceptibility data reports.
The reasons are already explained by previous researchers. Prokaryotes are one of the most successful forms of life ever evovled on earth and this is to a great extend due to their capability and adaptability to changing environmental conditions. Gene transfer among prokaryotes are known to exist even inter generic and various mechanisms such as transformation, transduction, conjugation, bacteriophage mediated gene transfer as well as transposon mediated mechanisms help them acquire new capabilities. This includes drug resistance genes too. Since the usage rather misuse of antibiotics is very high, especially in developing and third world countries, that selection pressure for resistant forms are high and emergence of multidrug resistant forms are very frequent. Could be tackled only through wise and restrained use of antibiotics in humans and animal production systems.
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