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Infectious diseases have long been a scourge of mankind. Some kinds of infections are caused by bacteria, microscopically small forms of life able to take up from their environment the nutrients they need for growth and reproduction.

When bacteria infect a susceptible host they can multiply rapidly, damaging or destroying the host. With the discovery of the first antibiotic drugs -- penicillin, the sulfonamides, streptomycin -- came the hope of the end of bacterial infections. At first this goal seemed realistic as new antibiotics capable of attacking more and more types of bacteria were discovered. Then quietly at first, but soon with increasing ferocity, the bacteria began to strike back in the mid 1950s.

In some patients being treated with antibiotics a few bacteria were able to withstand the lethal effects of the drugs, surviving and multiplying while their antibiotic sensitive relatives were killed. Soon populations of resistant bacteria began to take up residence in hospitals and clinics where antibiotics were being used. This was Darwin's process of natural selection at work.

Another even more serious problem emerged. Bacteria resistant to groups of antibiotics rather than to just a single drug were detected with increasing frequency. In just a few years 60 to 80% of bacteria showed resistance to multiple drugs. In some cases the resistance trait was infectious, that is, in addition to being inherited from generation to generation, it could be passed among related bacteria, coming in contact with each other.

Surprisingly, it was found that the genes responsible for infectious drug resistance were not carried on the chromosomes of the resistant bacteria but instead were due to plasmids, genetic elements that could replicate themselves independently of the chromosome.

How did drug resistant plasmids evolve? What mechanisms did the resistance genes collect on them? How did plasmids reproduce and maintain themselves within populations of bacteria? How were they transferred among bacteria?



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