Molecular biology has both advanced the state of the science of antibiotics and caused them to present vexing problems. Antibiotics are chemicals that interfere with metabolic processes and inhibit the growth of or kill microbes, especially bacteria. The mechanisms of antibiotics vary. Penicillin and vancomycin, for example, cause lysis in gram-positive bacteria (i.e. they are narrow spectrum) by obstructing their ability to synthesize cell walls. Conversely, tetracyclines affect both gram-positive and gram-negative bacteria (i.e. broad spectrum) by binding to ribosomes, thereby impeding the production of proteins and limiting their activity.1
The dilemma of dual use illustrates the various scientific perspectives involved in a real-world problem. Bacterial resistance to antibiotics is a real and growing problem in the medical community. Tuberculosis, malaria, ear infections and numerous other diseases are becoming increasingly difficult to treat. For example, tuberculosis cases in the developed world were almost completely eliminated shortly after discovery of the pharmaceutical isoniazid in 1940, but the emergence of resistant strains that can only be treated with less effective drugs is very dangerous to public health. The sources are varied. For example, about 2 million patients contract bacterial infections in hospitals each year, known as nosocomial infections. Immunocompromised patients are particularly vulnerable to infections of Staphylococcus aureus, which is commonly found in hospitals, leading to pneumonia and other ailments. Isolated strains of S. aureus are now found to be resistant to previously efficacious antibiotics, including methicillin, oxacillin, penicillin and amoxicillin. Some strains are even resistant to vancomycin, the antibiotic prescribed by physicians after exhausting other options. 2
A gene in Yersinia pestis, the causative agent of the plague, was isolated in 2006 and was found to be similar to an Escherichia coli gene known to cause multiple types of antibiotic resistance.3 This non-virulent strain of Y. pestis that over-expresses the gene is resistant to numerous common antibiotics, including those commonly prescribed to treat plague infection. Spontaneous antibiotic-resistant bacteria have been found to mutate to forms that affect the expression of this gene, indicating a mechanism by which bacteria can acquire resistance. 4
Antibiotic resistance is genetically encoded. Numerous microbes produce antibiotic compounds to protect themselves from other microbes, and as a result, some of these microbes have evolved to be resistant to them. Spontaneous mutations can also produce resistance genes which can be passed on to future generations via genetic exchange processes. For instance, bacteria may transfer a circular strand of DNA (i.e. plasmid) external to its chromosome to another bacterium through conjugation. Bacteria may also get genes that have been released from dead bacteria, incorporating them into their chromosome or plasmid through transformation. A third means is transduction, whereby a bacterial virus (i.e. bacteriophage) invades the bacterial cell and removes genetic material. When the bacteriophage infects another cell, that gene may be incorporated into the other cell’s chromosome or plasmid.