Abstract
Bacteria can become resistant to antibiotics by mutation, transformation, and/or acquisition of new genes which are normally associated with mobile elements (plasmids, transposons, and integrons). Mobile elements are the main driving force in horizontal gene transfer between strains, species, and genera and are responsible for the rapid spread of particular elements throughout a bacterial community and between ecosystems. Today, antibiotic resistant bacteria are widely distributed throughout the world and have even been isolated from environments that are relatively untouched by human civilization. In this review macrolides, lincosamides, streptogramins, and tetracycline resistance genes and bacteria will be discussed with an emphasis on the resistance genes which are unique to environmental bacteria which are defined for this review as species and genera that are primarily found outside of humans and animals.
Highlights
The first macrolide, erythromycin, was discovered in 1952 and since macrolides have had an important role in treating infectious diseases (Kirst, 2002)
For most bacteria acquisition of new genes coding for; (a) rRNA methylases which generally results in resistance to macrolides, lincosamides, and streptogramin B antibiotics (MLSB); (b) two types of efflux pumps which pump the drug(s) out of the cell; or (c) one of four types of inactivating enzymes which chemically modify the antibiotic preventing it from binding to the ribosome that is the most important way they become MLS resistant (Table 1)
Antibiotic resistant bacteria are widely distributed throughout the world and have been isolated from deep subsurface trenches, in waste water, surface and ground water, sediments, and soils
Summary
The first macrolide, erythromycin, was discovered in 1952 and since macrolides have had an important role in treating infectious diseases (Kirst, 2002). Macrolides, lincosamides, and streptogramins (MLS), though chemically distinct, are usually considered together because most share overlapping binding sites on the 50S subunit of the ribosome and many bacteria carry acquired resistance genes which confer resistance to more than one drug within this group (Sutcliffe and Leclercq, 2003). These antibiotics inhibit protein synthesis by binding within the exit tunnel, adjacent to the peptidyl transferase center, and inhibit translation by preventing progression of the nascent chain inducing peptidyl-tRNA drop off (Auerbach et al, 2010; Starosta et al, 2010). If unusual results occur, such as finding the Gram-negative tet(B) gene in a Gram-positive bacterium, this should be further verified
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