Plasmids were first discovered in Japan just after World War II, inhabiting the bacterium Shigella, which causes dysentery. The type of dysentery due to bacteria was originally treated with sulfonamides, the earliest type of antibiotic. Suddenly, strains of Shigella appeared that were resistant to sulfonamide treatment. The genes for resistance to sul-fonamide proved to reside on plasmids, rather than the bacterial chromosome. Plas-mids that confer antibiotic resistance are called R-plasmids or R-factors (Fig. 16.10).
Worse, the plasmids carrying the sulfonamide resistance genes were able to transfer copies of themselves from one bacterial cell to another. Consequently, the sulfon-amide resistance spread rapidly from Shigella to Shigella. Although the resistance plasmid allowed the Shigella to survive, transferable antibiotic resistance is highly dangerous from the human medical viewpoint. By 1953, the year Watson and Crick discovered the double helix, 80 percent of the dysentery-causing Shigella in Japan had become resistant to sulfonamides. By 1960,10% of the Shigella in Japan was resistant to four antibiotics, sulfonamides, chloramphenicol, tetracycline and streptomycin, and
R-plasmid or R-factor Plasmid that carries genes for antibiotic resistance
Many plasmids carry genes that are beneficial to their host cells, but only under certain environmental conditions.
R-plasmids make bacteria resistant to antibiotics.
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