Plasmids multiple drug resistance

The spread of multiple drug resistance has serious implications because of its persistence. Plasmid-mediated resistance to lincosamides and macrolides is the result of methylation of the shared receptor site on the 50S subunit of the bacterial ribosome. Plasmid transferable resistance has recently been reported for fluoroquinolones (Martinez-Martinez et ah, 1998). 

Kruse, H. and Sorum, H. (1994) Transfer of multiple drug resistance plasmids between bacteria of diverse origins in natural microenvironments. Applied Environmental Microbiology, 60, 4015 1021. 

The present state of research increasin y strengthens the emerging concept that, like the multiple drug resistance markers both in enteric and other pathogenic bacteria, the metabohc versatiUty of soil bacteria, with few exceptions, is determined totally, or partly, by Ihe resident plasmids [75]. 

Plasmid-mediated resistance to tetracyclines is widespread. Tetracycline-resistant organisms show decreased intracellular accumulation of the drugs. Resistance mechanisms include decreased activity of the uptake systems and the development of mechanisms (efflux pumps) for active extrusion of tetracyclines. Plasmids that include genes involved in the production of efflux pumps for tetracyclines commonly include resistance genes for multiple antibiotics. 

Gentamicin resistance is usually due to the multiplication of plasmid (R-factor, epi-some) coding for the production of at least 4 enzymes which inactivate the antibiotic, and often also inactivate such related ones as sisomicin and tobramycin (3, 5 ). Since amikacin is usually not affected by these enzymes, it is the drug of choice for the treatment of gentamicin-resistant Gram-negative bacterial infections in those cases where therapy is a necessity. 

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