The phenomena of antibiotic resistance cannot be reduced to a few elementary deductions. The study of it has revealed a large number of mechanisms by which genetic material and hence, fitness benefits, can be transferred, acquired, or appropriated by both benign and pathogenic organisms. While we have known that microbes could become drug resistant for over half a century, we seem to be more at a loss as to what to do about than ever.

> Most bacterial genomes that have been sequenced contain a large proportion of DNA that have been relatively recently acquired from other sources. This horizontally acquired DNA usually encodes functions that are of selective advantage to the organism such as antibiotic resistance, virulence and biodegradation pathways. There are a number of different DNA elements described transferring antibiotic resistance: self replicating plasmids (that can be self transmissible by conjugation or brought into the cell by tranformation or transduction), prophages, transposons, integrons and resistance islands. -- Evolution and spread of antibiotic resistance. Journal of Internal Medicine 2002; 252: 91–106

> Tetracycline resistance in most bacteria is due to the acquistion of new genes, often associated with mobile elements. These genes are usually associated with plasmids and/or transposons. It is unlikely that overall use of tetracyclines will change in the near future, especially in North America where tetracyclines are still used as growth promoters. Thus the trends discussed in this review will most likely show continued increases in the number of genera TCR [tetracycline resistance] and the percent of bacterial populations no longer susceptible to tetracyclines. -- Update on acquired tetracycline resistance genes. FEMS Microbiology Letters 245 (2005)

> Minimizing the spread of antibiotic resistance is arguably the most pressing applied goal of evolutionary biology. The widespread use of antibiotics has markedly improved public health over the past 60 years. However, the efficacy of antibiotic treatment is rapidly decreasing as a result of the continual increase in the frequency of bacteria that have evolved resistance to antibiotics. Despite efforts from a range of disciplines, our ability to predict and combat the evolution of antibiotic resistance in pathogenic bacteria is limited. It is unclear if we will ever be able to combat the spread of antibiotic resistance, but taking a more integrative approach will almost certainly help.-- NATURE REVIEWS | Genetics	Volume 11 | june 2010

Peter Loring Borst
Ithaca NY USA
peterloringborst.com

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