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Confronting Multidrug ResistanceA Role for Each of Us
Stuart B. Levy, MD
JAMA. 1993;269(14):1840-1842.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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SCIENTIFIC journals, an Institute of Medicine study, newspapers, and magazines report the reappearance of "old" pathogens as major clinical problems worldwide.1-3 In particular, Mycobacterium tuberculosis and Plasmodium falciparum have been cited. In fact, this reemergence includes a diverse group of infectious organisms that have a common feature— multidrug resistance.
Soon after penicillin was introduced into clinical practice, physicians became keenly aware that the bacteria being attacked, namely the staphylococci, were not going to succumb easily to this antibiotic and, in retrospect, to many others. Their "resistance" was linked to a gene that coded for an enzyme, penicillinase, which destroyed penicillin. To complicate matters, the gene was not carried on the chromosome, as was expected, but instead, resided on a self-replicating extrachromosomal DNA unit—what we now call a plasmid. Plasmids are not novel elements limited to only certain bacteria. They are common components of the total genetic composition of most,
. . . [Full Text PDF of this Article]
Author Affiliations
From the Center for Adaptation Genetics and Drug Resistance, Departments of Molecular Biology and Microbiology and of Medicine, Tufts University School of Medicine, and the New England Medical Center, Boston, Mass.
Footnotes
Reprints not available.
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