“Antibiotics are substances produced by microorganisms that kill or inhibit other microorganisms. Antibiotics are products of the earth, more specifically of soil; they are byproducts of cellular metabolism; antibiotics are “all natural.”1
There is one key factor in controlling major antibiotic resistance. This does not occur within the lab, either. It is a growing problem among the population of people who take antibiotics, and even some that do not. Staphylococcus aureus is probably the most trouble-causing bacteria, yet. It has mutated to make itself resistant to a number of once helpful antibiotics. It has been fairly recent since S. aureus has become resistant (at least in some mutated strains) to the drug vancomycin, which we used in our project. They have found that many strains of S. aureus are already resistant to most all antibiotics except vancomycin. So, this definitely presents a problem to those trying to fight these bacteria and keep people alive.
One might ask how these bacteria can “outsmart” our lifesaving drugs. The answer is not all figured out and completely understood yet. “Bacteria aquire genes for resistance in three ways. 1.In spontaneous mutation, bacterial DNA may change spontaneously. Drug resistant tuberculosis arises this way. 2.In a process called transformation, one bacterium may take up DNA from another. Penicillin-resistant gonorrhea results from transformation. 3.Most frightening, however, is resistance acquired from a small circle of DNA called a plasmid. Plasmids can flit between bcteria of various types—and carry multiple resistance. In 1968, 12,500 Guatemalans died in an epidemic of Shigella diarrhea, caused by a microbe harboring a plasmid that conferred resistances to four antibiotics! But bacteria do something much more clever than just mutating. That’s chancy, so bacteria prefer to share biochemical secrets—resistance genes—that enable them to resist or destroy antibiotics. This diabolical bartering can occur in a couple of ways. 1.Some bacteria share plasmids—small chunks of DNA, like mini-chromosomes—that exist outside the main chromosomes. This sharing can leap broad divions in bacterial phylogeny. It’s almost as if a cow could lend a crow a gene and teach it to grow teeth.
2.Gene cassettes are genes that can be spiced in the chromosomes. While the mechanism is kind of complex, it can be compared to an expedition to a shopping mall. Genes called integrons code for enzymes called integrases that can splice those cassettes into chromosomes or other genetic material where they become functional. That makes the integrons function something like a shopping cart.”2
“The selection process is fairly straightforward. When an antibiotic attacks a group of bacteria, cells that are highly susceptible to the medicine will die. But cells that have some resistance from the start, or that acquire it later (through mutation or gene exchange), may survive especially if too little drug is given to overwhelm the cells that are present. Those cells, facing reduced competition from susceptible bacteria, will then go on to proliferate. When confronted with an antibiotic, the most resistant cells in a group will inevitable outcompete all others.”3
Penicillin has proven to be an extremely powerful drug. It was one of the first antibiotics discovered, and it is unfortunate and slightly scary that the bacteria are becoming resistant. “Penicllin G, the first modern antibiotic to come into widespread use, is still the safest, most effective, and cheapest antibiotic. The ratio between toxic and clinically effeactive doses is several hundred to a thousandfold except in newborn infants and persons with poor kidney function, or when the antibiotic is applied directly th brain tissue. Penicillin G can be administered by mouth, but absorption is limited, and it may be destroyed by the acid in the stomach. Penicillin G is abactericidal, anrrow-spoectrum antibiotic that is highly effective against gram-positive bacteria, especially staphylococci, which cause boils, osteomyelitis, wound infections, and infections of the heart and blood vessesl; streptococci, which cause ‘strep’ throat, predispose to rheumatic fever and acute glomerulonephritis, infect abrasions and wounds, and cause blood poisoning and childbed fever; pneumococci, which cause the most common form of bacterial pneumonia; and against the bacteria that cause syphilis, gonorrhea, and common forms of bacterial meningitis. Nevertheless, penicillin G has several shortcomings. It is destroyed by stomach acid and by enzymes (penicillinases) produced y several microorganisms, its spectrum of activity is limited, and it frequently causes allergic reactions.”4 Unfortunately, there is now a bigger problem with penicillin G: resistance. “Bacteria evolve resistance to penicillin by using beta-lactamase (an enzyme that breaks down penicillin). The gene for beta-lactamase is carried on a separate self-replicating bit of DNA called a plasmid. Plasmids travel from one bacterium to another and from one kind of bacterium to another. Widespread use of antibiotics allowed the beta-lactamase plasmid to be incorporated in most of the bacteria that live in humans. Plasmids that allow resistance to many antibiotics are now common. Even worse, some plasmids confer resistance to several types of antibiotics.”5
“Methicillin (Staphcillin) resists penicillinase destruction and must be given by injection. It was the first penicillin effective against resistant ‘hospital staphylococcus,’ its only clinical indication. Much less effective than penicillin G against penicillin-G sensitive bacteria, methicillin also first demonstrated that penicillins could be toxic to the kidneys. Oxacillin, cloxacillin, dicloxacillin, and nafcillin are similar to methicillin in that they resist destruction by penicillinase and can be given by mouth.”6
“Obviously, if a bacterial pathogen is able to develop or acquire resistance to an antibiotic, then that substance becomes useless in the treatment of infectious disease caused by that pathogen (unless the resistnace can somehow be overcoe with secondary measures). So as pathogens develop resistance, we must find new (different) antibiotics to fill the place of the old ones in treatment regimes. Hence, natural penicillins have become useless against staphylococci and must be replaced by other antibiotics; tetracycline, having been so widely used and misused for decades, has become worthless for many of the infections that once designated it as a ‘wonder drug’.”7
“More recently, the development of multiple drug resistance by strains of two types of bacteria has resulted in some infections that are essentially untreatable with antibiotics. One of these infections is multiple drug resistant tuberculosis (MDR-TB) and the majority of these cases thus far have occurred in New York among persons with HIV infection, prisoners, and the homeless. The other multiply resistant bacteria, Enterococcus, occurs primarlily in the hospital setting. This resistant strain has been named VRE or vancomycin resistant enterococcus, since vancomycin was formerly the only effective antibiotic for treating this infection. The emergence of multiple antibiotic resistance in strains of the bacterium Streptococcus pneumoniae (SP) signifies that antibiotic resistance is a problem the general population must be concerned about.8
“As if this prospect of bacteria ganging up to defeat antibiotics were not alarming enough, recognize that this generosity extends beyond members of their own species, says Abigail Slayers. ‘Just about any bacterium can get genes from just about any other bacterium.’”9
As the scientists work on finding new cures and treatments, there is one thing that the general population can do to help control this frightening problem. Both overuse and inappropriate use contribute to antibiotic resistance. Many people demand antibiotics from their doctors for things like colds, which cannot be helped by antibiotics anyway. They take these drugs as for anything, and in the amounts that they find desirable. When a doctor prescribes an antibiotic however, people tend to stop taking it as soon as they begin to feel better. This is underuse of antibiotics, and is probably one of the greatest contributing factors. The bacteria are exposed to the antibiotics, but they are not all overpowered and killed, since the person stops taking them. Some of them are, which is why the person feels better, but there are the ones left behind. These are the ones that have the chance to become stronger in the face of an attack with another antibiotic. Then the person becomes sick again, and they are given the same antibiotic, but it no longer works. Now the doctor is faced with a problem, and so is anyone who catches the illness from that person. Another antibiotic must be used, and logically, the person is more likely to stop taking this drug as well. There is something that people can do to control this. They must listen to their doctors and always finish their medication, no matter what.
“One component of the solution is recognizing that bacteria are a natural, and needed, part of life. Bacteria, which are microscopic, single-cell entities, abound on inanimate surefaces and on parts of the body that make contact with the outer world, including the skin, the mucous membranes and the lining of the intestinal tract. Most live blamelessly. In fact, they often protect us from disease, because they compete with, and thus limit the proliferation of, pathogenic bacteria—the minority of species that can multiply aggressively (into millions) and damage tissues or otherwise cause illness. The benign competitors cam be important allies in the fight against antibiotic-resisntant pathogens. People should also realize that although antibiotics are needed to control bacterial infections, they can have broad, undersirable effects on microbial ecology. That is, they can produce long-lasting change in the kinds and proportions of bacteria—not only in the treated individual but also in the environment and society at large. The compounds should thus be used only when they are truly needed, and they should not be administered for viral infections over which they have no power.”10
"Not many people alive today are old enough to remember the dreadful impact of common bacterial infections on otherwise young and healthy people during the pre-antibiotic age. It would be an enormous tragedy if we lost our antibiotic armamentarium in the 21st century and returned to those bleak times."11
This research on antibiotic resistance shows the problem researchers are facing and means of controlling it. It is actually quite frightening to think about what we could face in the future if new and stronger antibiotics are not discovered or created, or if people do not learn to take them correctly. The problem is there, but it is not so big that it cannot be fought.