Marcelo E. Tolmasky

Institute of Molecular Biology and Nutrition, Department of Biological Science, California State University Fullerton, Fullerton, CA

Bacterial infectious diseases have always afflicted human beings accounting for a large percentage of the causes of death. A great triumph over these diseases was the introduction of antibiotics in the mid-1940s. The early treatments of, until then, fatal diseases with penicillin were an extraordinary success. Soon, new antibiotics were discovered providing physicians with a large number of weapons to combat bacterial diseases and they are still the main treatment against bacterial infections. Bacteria responded to the use of antibiotics with ingenious and diverse mechanisms to become a resistant and to share the resistance traits. Today, about 50 years after their introduction no bacterial infectious disease has been completely wiped out, and many diseases are emerging or reemerging. In most cases the causative agents are now resistant to one or more antibiotics. Their widespread use (for the right or wrong reasons) in treatment of a variety of diseases, the increase in number of immunocompromised patients (elders, HIV infected, transplant, other critically ill postsurgical and intensive care unit patients) that need them to control infections, their utilization as animal feed, and their over the counter availability in many parts of the world together with the very active international travel and migration contribute to a rapid raise in the number of antibiotic resistance strains.

The resistance mechanisms include changes in permeability that prevent antibiotics to penetrate inside the cell, presence of efflux mechanisms that pump out the antibiotic, modification or substitution of the target, and chemical modification of the antibiotic molecule. Bacteria also exchange resistance traits at the cellular level utilizing mechanisms such as conjugation, natural transformation or transduction. The resistance genes are also mobilized at molecular levels by transposons and integrons.

The purpose of this special edition is to discuss various aspects of mechanisms of resistance to two groups of antibiotics, aminoglycosides and b -lactams, and some of the mechanisms of dissemination of the resistance genetic determinants. Various chapters discuss the following: aspects of aminoglycoside phosphotransferases (Gerard D. Wright and Paul R. Thompson; and Michael H. Perlin, Scott A. Brown, and Jaydev N. Dholakia), the bifunctional enzyme 6'-N-aminoglycoside acetyltransferase-2"-O-aminoglycoside phosphotransferase (Esther Culebras, and José L. Martínez), the physiological functions and regulation of expression of the chromosomal 2'-N-acetyltransferase (David R. Macinga and Philip N. Rather), inhibitor resistant class A b -lactamases (Robert A. Bonomo and Louis B. Rice), replication of plasmids, extrachromosomal elements that commonly carry genetic determinants for resistance genes (Luis A. Actis, Marcelo E. Tolmasky and Jorge H. Crosa), the role of conjugative transfer in dissemination of b -lactam and aminoglycoside resistance genes (Virginia Waters), and a description of Tn1331, a transposon carrying genes encoding resistance to both b -lactam and aminoglycoside resistance genes, some of them included in a structure resembling the variable portion of integrons (Marcelo E. Tolmasky).