The same bacteria that almost disappeared are now resistant to penicillin, ampicillin, erythromycin, vancomycin, fluoroquinolones all the weapons that were supposed to have vanquished them. These bacteria have evolved and pose tremendous new challenges, however man and mans technology can also steadily advance to effectively mitigate the emerging bacterial threats only a vast new impetus to research is needed. Not too long ago, people in the Western countries tended to think of deadly infectious diseases as old-fashioned afflictions that belonged to pre-modern times (or to the present-day Third World).
Since the end of the Second World War, classical sexual diseases like syphilis and gonorrhea virtually disappeared in almost all the industrialized countries (Mode, Sleeman 16). The sexual revolution in the 1970s was encouraged by the confidence that sexually transmitted diseases were merely a temporary inconvenience that penicillin could cure. And then there appeared AIDS. As if that is not enough, just when we thought at least our old enemies were gone, to our dismay we find them all staring in our face, more ferociously than ever. E.
coli, staphylococci and many other pathogens are evolving in scary ways. The more researchers investigate, the more fast-changing microbes they find. As a result of this evolution, many bacteria are learning to resist more and more of the antibiotics we humans use to fight them. Drugs that have once so effectively countered many deadly are losing their power. Without the help of these once magical drugs, even people who have robust immune systems can be seriously sickened or killed by virulent germs, and people with compromised immune systems face a significant chance of dying.
A bacteria can mutate any time it reproduces, and all of that bacterias offspring will bear that mutation. Because bacteria replicate so often, random genetic mutations are common, and some of those mutations create genes that arm bacteria with drug resistance. A change in even just one gene can give a new strain of bacteria the ability to fend off a given antibiotic, maybe even all of the antibiotics in a large class of drugs. Such resistance genes provide bacteria with remarkable defense mechanisms. Resistance can begin in a single person when bacteria are only partially challenged by medication.
This can occur when a patient is given too low a dosage of a drug, or stops taking it when he feels better, without completing the full course of treatment. Sometime children spit out half of the medicine they are given because of the taste. These conditions allow a pathogen to develop ways to fend off the chemical warriors. Then its descendents mutate in a way that makes them more capable of surviving higher doses of the same drug. Successive generations, which can occur in a matter of days if not hours, possess an ever-growing ability to beat the medication, ultimately creating pathogens that become completely resistant to the drug.
Most antibiotics are broad spectrum, meaning they attack any and all bacteria in the patients body. When a person takes an antibiotic for a staph infection, for example, the drug molecules will kill the invaders but also destroy harmless/helpful bacteria, in a situation of collateral damage. Normally, healthy bacteria occupy most of the places in the stomach and intestines guarding against harmful bacteria percolating into bloodstream. The helpful bacteria also consume a large portion of nutrients available to bacteria, thus keeping the pathogenic bacteria at bay and keeping us from getting sick more often.
But after antibiotics have attacked, they become thinned out, leaving the harmful bacteria which may have randomly mutated and acquired drug resistance to be free, feed and multiply. The healthy bacteria will reestablish themselves, but the drug-resistant pathogens will settle among them in greater numbers. And they will have evolved to better resist the same antibiotic when it comes the next time. Moreover, bacteria also develop new traits by exchanging genes with one another.
A staphylococcus bacteria one of the most common pathogens could be handed a new resistance gene by a different kind of resistant bacteria that happens to be close by, or by special viruses that infect bacteria and can take genes with them to their next host. Otherwise harmless bacteria inhabiting our gut or skin could become reservoirs of drug-resistance genes, passing them on to visiting pathogens. Most importantly, when an organism becomes resistant to one drug, say penicillin, it is also likely to resist related drugs such as ampicillin and amoxycillin.
Finding new molecular structures of this family of drugs cannot provide any long-term advantage, because in a few years the organism will become resistant to the whole family again. An entirely new type of drug, or better, a wholly new approach to combat disease is needed ” which, in practical terms, translates to massive research on unprecedented levels. Despite several obvious ominous trends for decades now, only three new classes of antibiotics oxazolidinones, streptogramins, and daptomycin have been developed in the past three decades (Galanter et al., 500).
This pace of research is completely inadequate. We now face a near crisis situation. The reappearance of TB and the increase in cases of antibiotic-resistant pneumonia and meningitis leave little room for complacency in the search for new drugs, if we are to continue to enjoy our lives that are relatively free of bacterial infections. Man will be successful, as he has been since the observations of Pasteur, in finding or creating new antibiotics ” if he gives his mind a vast new scope to pursue knowledge and discovery in the new millennium.
References: Mode, Charles J. , Sleeman, Candace K. Stochastic Processes in Epidemiology: HIV/AIDS, Other Infectious Diseases and Computers. Singapore : World Scientific Publishing Co. , 2000 Galanter, Joshua Mark; Golan, David E. ; Tashjian, Armen H. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy Baltimore, MD : Lippincott Williams & Wilkins, 2005 Krasner, Robert I. The Microbial Challenge: Human Microbe Interactions. Washington, DC : ASM (American Society for Microbiology) Press, 2002