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Antibiotic Resistance

Antibiotic Resistance

Antibiotic resistance is the ability of a bacterium or other microorganism to survive and reproduce in the presence of antibiotic doses that were previously thought effective against them. Examples of microbe resistance to antibiotics dot the countryside, plaguing humankind. For instance, in February 1994 dozens of students at La Quinta High School in southern California were exposed to the pathogenic (disease-causing) agent, Mycobacterium tuberculosis, and eleven were diagnosed with active tuberculosis. Many strains of this bacterium are multi-drug resistant (MDR). As for the sexually transmitted pathogen Neisseria gonorrhea, which causes gonorrhea, the antibiotics penicillin and tetracycline that were used against it in the 1980s can no longer be the first lines of defense, again because of antibiotic resistance. If only 2 percent of a N. gonorrhea population is antibiotic resistant, a community-wide infection of this persistent strain can occur.

Mechanisms of Resistance

Antibiotics, whether made in the laboratory or in nature by other microbes, are designed to hinder metabolic processes such as cell wall synthesis, protein synthesis, or transcription, among others. If humans are to prosper against microbial disease, it is necessary to understand how and why bacteria are able to mount their clever defenses. Aided with the knowledge of the genetics and mechanisms of resistance, scientists can discover new ways to combat the resistant bacteria.

The phenomenon of antibiotic resistance in some cases is innate to the microbe. For instance, penicillin directly interferes with the synthesis of bacterial cell walls. Therefore, it is useless against many other microbes such as fungi, viruses, wall-less bacteria like Mycoplasma (which causes "walking pneumonia"), and even many Gram negative bacteria whose outer membrane prevents penicillin from penetrating them. Other bacteria change their "genetic programs," which allows them to circumvent the antibiotic effect. These changes in the genetic programs can be in the form of chromosomal mutations, acquisition of R (resistance) plasmids , or through transposition of "pathogenicity islands."

An example of a chromosomal mutation is the increasing number of cases of penicillin-resistant Neisseria gonorrhae. This bacterium mutated the gene coding for a porin protein in its outer membrane, thereby halting the transport of penicillin into the cell. This is also termed "vertical evolution," meaning that the spread occurs through bacterial population growth. The most common method by which antibiotic resistance is acquired is through the conjugation transfer of R plasmids, also termed "horizontal evolution." In this method the bacteria need not multiply to spread their plasmid. Instead the plasmid is moved during conjugation. These plasmids often code for resistance to several antibiotics at once.

The third method is transfer due to transposable elements on either side of a "pathogenicity island," which is group of genes that appear on the DNA 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.

Finally, bacteria may mutate the gene for the target macromolecule 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.

Resistance and Public Health

The effects of antibiotic resistance are reflected in the agriculture, food, medical, and pharmaceutical industries. Livestock are fed about half of the antibiotics manufactured in the United States as a preventative measure, rather than in the treatment of specific diseases. Such usage has resulted in hamburger meat that contains drug-resistant and difficult-to-treat Salmonella Newport, which has led to seventeen cases of gastroenteritis including one death. Some MDR-tuberculoid strains arise because patients are reluctant to follow the six-months or more of treatment needed to effectively cure tuberculosis. If the drug regimen is not followed, less sensitive bacteria have the chance to multiply and gradually emerge into resistant strains. In other cases the "shotgun" method of indiscriminately prescribing/taking several antibiotics runs the risk of creating "super MDR-germs." Moreover, millions of antibiotic prescriptions are written by physicians each year for viral infections, against which antibiotics are useless. The patient insists on a prescription, and many doctors willingly go along with the request.

Because global travel is common, the potential of creating pandemics is looming. In many Third World countries, diluted antibiotics are sold on the black market. The dosage taken is often too low to be effective, or the patient takes the drug for a very short time. All these behaviors contribute to the development of resistant strains of infectious organisms. If humans are to gain the upper hand against MDR bacteria, it is the responsibility of these industries and the public to educate themselves and to engage in careful practices and therapy.

see also Conjugation; Eubacteria; Mutagen; Plasmid; Transposable Genetic Elements.

Paul K. Small

Bibliography

Garrett, Laurie. The Coming Plague. New York: Farrar, Strauss, Giroux, 1996.

Ingraham, John, and Caroline Ingraham. Introduction to Microbiology, 2nd ed. Pacific Grove, CA: Brooks/Cole, 2000.

Nester, Eugene W., et al. Microbiology: A Human Perspective, 3rd ed. Boston: McGraw Hill, 2001.

Schaechter, Moselio, et al. Mechanisms of Microbial Disease, 3rd ed. Baltimore: Williams and Wilkins, 1998.

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antibiotic resistance

antibiotic resistance Resistance to antibiotic drugs acquired by many bacteria and other pathogens. Because some bacteria survive while non-resistant strains die, they pass their resistance to their progeny and resistance increases in the population. Some bacteria have the ability to pass the genes for antibiotic resistance to other organisms of different species on plasmids (small lengths of DNA). Spread of resistance is accelerated by routine prescription of antibiotics to humans and unregulated application to farm animals for the purpose of disease prevention rather than cure. An inadequate dose or failure to complete a course of antibiotics increases the chances of resistant microorganisms surviving to breed. This may lead to the return of epidemics of untreatable infectious disease, and can create a cycle in which the development of more advanced, powerful antibiotics are constantly needed.

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