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and carry the codes for several factors which make the infection more successful. These transposable elements allow the genes to jump from bacteria to bacteria or simply from chromosome to plasmid within the organism.

The "road blocks" that bacteria have evolved which result in antibiotic resistance employ several mechanisms. One strategy is simply to destroy or limit the activity of the antibiotic. The beta-lactamases are enzymes which render the penicillin-like antibiotics dysfunctional by cleaving a vital part of the molecule. Some bacteria can deactivate antibiotics by adding chemical groups to them; for instance, by changing the electrical charge of the antibiotic through the addition of a phosphate group. Other bacteria accomplish a similar effect by bulking themselves up with the addition of an acetyl group.

Still other bacteria acquire resistance by simply not allowing the antibiotic to enter the cell. The bacterium mentioned above, Neisseria gonorrhea, has altered porin proteins, thereby stopping uptake of the antibiotic. Some bacteria acquire intricate pumping mechanisms to expel the drug when it gains entry to their cell.

macromolecule large Finally, bacteria may mutate the gene for the target macromolecule molecule such as a pro- with which the antibiotic is supposed to bind. For example, tetracycline binds to and inhibits ribosomes, so a mutation in the ribosomal genes may cause conformational alterations in the ribosomal proteins that prevent tetracycline from binding but still allow the ribosome to function.

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