|Year : 2011 | Volume
| Issue : 2 | Page : 59-68
|Use of antibiotics: From preceding to contemporary
Ruchi Tiwari, Gaurav Tiwari
Department of Pharmaceutical Sciences, Pranveer Singh Institute of Technology, Kalpi Road, Bhauti, Kanpur (Uttar Pradesh), India
|Date of Web Publication||11-Aug-2012|
Pranveer Singh Institute of Technology, Kalpi road, Bhauti, Kanpur-208020 (U.P.)
Source of Support: None, Conflict of Interest: None
| Abstract|| |
As with any public health problem, the evolution of antibacterial resistance must be viewed from a perspective of risk, and analyzed in terms of probabilities within the populations. It is necessary to be able to predict the risk of antibacterial resistance in the future, and two main strategies have recently been developed in mathematical models that may help to evaluate these risks. It is also important to understand how antibiotics are used and how their use affects the evolution of antibacterial resistance. Understanding the epidemiology of antibacterial resistance will enable us to develop preventive strategies to limit existing resistance and to avoid the emergence of new strains of resistant bacteria. Furthermore, resistance development in pathogens became a major problem, which is still with us today. In addition, new pathogens are continually emerging and there still are bacteria that are not eliminated by any antibiotic, e.g., Pseudomonas aeruginosa. In addition to these problems, many of the major pharmaceutical companies have abandoned the antibiotic field, leaving much of the discovery efforts to small companies, new companies, and the biotechnology industries. Despite these problems, development of new antibiotics has continued, albeit at a much lower pace than in the last century.
Keywords: Antibiotics, bacterial resistance, mechanism of action, natural antibiotic sources
|How to cite this article:|
Tiwari R, Tiwari G. Use of antibiotics: From preceding to contemporary. Scho Res J 2011;1:59-68
| Introduction|| |
In 1929, when Alexander Fleming discovered penicillin, there were a number of serious infectious diseases that claimed the lives of hundreds of thousands of people. The introduction of the long awaited miracle drug, "antibiotic", rendered the infections from contagion and trauma seemingly impotent. With their new-found arsenal, doctors slowly began to expand the use of antibiotics to include the treatment of bacterial diseases that were not life-threatening. We then saw the emergence of prophylactic, or preventive, antibiotic prescribing. In cases that were often of viral origin, children were given antibiotics to prevent a secondary bacterial infection. Antibiotics are powerful medicines that fight bacterial infections and save lives. They either kill bacteria or keep them from reproducing.  Antibiotics do not fight infections caused by viruses, such as colds, flu, most coughs and bronchitis, or sore throats, unless caused by Streptococcus pneumoniae. [Table 1] shows the historical discoveries associated with antibiotics.
How do Antibiotics Kill Bacterial Cells but not Human Cells?
In order to be useful in treating human infections, antibiotics must selectively target bacteria for eradication and not the cells of its human host. Indeed, modern antibiotics act either on processes that are unique to bacteria-such as the synthesis of cell walls or folic acid-or on bacterium-specific targets within processes that are common to both bacterium and human cells, including protein or DNA replication. Following are some examples. Most bacteria produce a cell wall that is composed partly of a macromolecule called peptidoglycan, itself made up of amino sugars and short peptides. Human cells do not make or need peptidoglycan. Penicillin, one of the first antibiotics to be used widely, prevents the final cross-linking step, or transpeptidation, in assembly of this macromolecule. The result is a very fragile cell wall that bursts, killing the bacterium. No harm comes to the human host because penicillin does not inhibit any biochemical process that goes on within us. Bacteria can also be selectively eradicated by targeting their metabolic pathways. Sulfonamides, such as sulfamethoxazole, are similar in structure to para-aminobenzoic acid, a compound critical for synthesis of folic acid. All cells require folic acid and it can diffuse easily into human cells. But the vitamin cannot enter bacterial cells and thus bacteria must make their own. The sulfa drugs such as sulfonamides inhibit a critical enzyme-dihydropteroate synthase-in this process. Once the process is stopped, the bacteria can no longer grow.  Another kind of antibiotic-tetracyclines, also inhibits bacterial growth by stopping protein synthesis. Both bacteria and humans carry out protein synthesis on structures called ribosomes. Tetracycline can cross the membranes of bacteria and accumulate in high concentrations in the cytoplasm. Tetracycline then binds to a single site on the ribosome-the 30S (smaller) ribosomal subunit-and blocks a key RNA interaction, which shuts off the lengthening of protein chain. In human cells, however, tetracycline does not accumulate in sufficient concentrations to stop protein synthesis. Similarly, DNA replication must occur in both bacteria and human cells. The process is sufficiently different in each that antibiotics such as ciprofloxacin-a fluoroquinolone notable for its activity against the anthrax bacillus-can specifically target an enzyme called DNA gyrase in bacteria. This enzyme relaxes tightly wound chromosomal DNA, thereby allowing DNA replication to proceed. But this antibiotic does not affect the DNA gyrases of humans and thus, again, bacteria die while the host remains unharmed. Many other compounds can kill both bacterial and human cells. It is the selective action of antibiotics against bacteria that make them useful in the treatment of infections while at the same time allowing the host to live another day. 
Current Issues in Medicine and Antibiotics
One of the foremost concerns in modern medicine is antibiotic resistance. Simply put, if an antibiotic is used long enough, bacteria will emerge that cannot be killed by that antibiotic. The existence of antibiotic-resistant bacteria creates the danger of life-threatening infections that don't respond to antibiotics.  There are several reasons for the development of antibiotic-resistance in bacteria. One of the most important is antibiotic overuse. This includes the common practice of prescribing antibiotics for the common cold or flu. Even though antibiotics do not affect viruses, many people expect to get a prescription for antibiotics when they visit their doctor. Although the common cold is uncomfortable, antibiotics do not cure it, nor change its course. Each person can help reduce the development of resistant bacteria by not asking for antibiotics for a common cold or flu. 
Bacterial Mechanisms of Antibiotic Resistance
Several mechanisms have evolved in bacteria, which confer them with antibiotic resistance. These mechanisms can chemically modify the antibiotic, render it inactive through physical removal from the cell, or modify the target site so that it is not recognized by the antibiotic. The most common mode is enzymatic inactivation of the antibiotic. An existing cellular enzyme is modified to react with the antibiotic in such a way that it no longer affects the microorganism. An alternative strategy used by many bacteria is the alteration of the antibiotic target site. These and other mechanisms are shown in the [Figure 1] and accompanying [Table 2] below. 
The Acquisition and Spread of Antibiotic Resistance in Bacteria
The development of resistance is inevitable following the introduction of a new antibiotic. Initial rates of resistance to new drugs are normally of the order of 1%. However, modern uses of antibiotics have caused a huge increase in the number of resistant bacteria. In fact, within 8-12 years after wide-spread use, strains resistant to multiple drugs become widespread. Multiple drug resistant strains of some bacteria have reached such a proportion that virtually no antibiotics are available for treatment.  Antibiotic resistance in bacteria may be an inherent trait of the organism (e.g., a particular type of cell wall structure) that renders it naturally resistant, or it may be acquired by means of mutation in its own DNA or acquisition of resistance-conferring DNA from another source.
Inherent (Natural) Resistance
Bacteria may be inherently resistant to an antibiotic. For example, an organism lacks a transport system for an antibiotic; or an organism lacks the target of the antibiotic molecule; or, as in the case of Gram-negative bacteria, the cell wall is covered with an outer membrane that establishes a permeability barrier against the antibiotic. 
Several mechanisms are developed by bacteria in order to acquire resistance to antibiotics. All require either the modification of existing genetic material or the acquisition of new genetic material from another source. 
Vertical Gene Transfer
The spontaneous mutation frequency for antibiotic resistance is of the order of about 10 -8 -10 -9 . This means that one in every 10 8 -10 9 bacteria in an infection will develop resistance through the process of mutation. In E. coli, it has been estimated that streptomycin resistance is acquired at a rate of approximately 10 -9 when exposed to high concentrations of streptomycin. Although mutation is a very rare event, the very fast growth rate of bacteria and the absolute number of cells attained means that it doesn't take long before resistance is developed in a population. 
Once the resistance genes have developed, they are transferred directly to all the bacteria's progeny during DNA replication. This is known as vertical gene transfer or vertical evolution.  The process is strictly a matter of Darwinian evolution, driven by principles of natural selection: a spontaneous mutation in the bacterial chromosome imparts resistance to a member of the bacterial population. In the selective environment of the antibiotic, the wild type (non mutants) is killed and the resistant mutant is allowed to grow and flourish. ,
Horizontal Gene Transfer
Another mechanism beyond spontaneous mutation is responsible for the acquisition of antibiotic resistance [Figure 2]. Lateral or horizontal gene transfer (HGT) is a process whereby genetic material contained in small packets of DNA can be transferred between individual bacteria of the same species or even between different species. There are at least three possible mechanisms of HGT, equivalent to the three processes of genetic exchange in bacteria. These are transduction, transformation, and conjugation. 
Mechanisms of Horizontal Gene transfer (HGT) in Bacteria
The combined effects of fast growth rates to large densities of cells, genetic processes of mutation and selection, and the ability to exchange genes account for the extraordinary rates of adaptation and evolution that can be observed in the bacteria. For these reasons, bacterial adaptation (resistance) to the antibiotic environment seems to take place very rapidly in evolutionary time. Bacteria evolve fast. 
The First Signs of Antibiotic Resistance
There has probably been a gene pool in nature for resistance to antibiotic as long as there has been for antibiotic production, because most microbes that are antibiotic producers are resistant to their own antibiotic. In retrospect, it is not surprising that resistance to penicillin in some strains of staphylococci was recognized almost immediately after introduction of the drug in 1946. Likewise, very soon after their introduction in the late 1940s, resistance to streptomycin, chloramphenicol, and tetracycline was noted. By 1953, during a Shigella outbreak in Japan, a strain of the dysentery bacillus (Shigella dysenteriae) was isolated, which was multiple drug resistant, exhibiting resistance to chloramphenicol, tetracycline, streptomycin, and the sulfonamides.  Over the years, and continuing into the present, almost every known bacterial pathogen has developed resistance to one or more antibiotics in clinical use. Evidence also began to accumulate that bacteria could pass genes for drug resistance between strains and even between species. For example, antibiotic-resistance genes of staphylococci are carried on plasmids that can be exchanged with Bacillus, Streptococcus, and Enterococcus, providing the means for acquiring additional genes and gene combinations. Some are carried on transposons, segments of DNA that can exist either in the chromosome or in plasmids. In any case, it is clear that genes for antibiotic resistance can be exchanged between strains and species of bacteria by means of the processes of HGT. 
Multiple Drug Resistant Organisms
Multiple drug resistant organisms are resistant to treatment with several, often unrelated, antimicrobial agents as described above in Shigella. Some of the most important types of multiple drug resistant organisms that have been encountered include: methicillin/oxacillin-resistant Staphylococcus aureus (MRSA) vancomycin-resistant enterococci (VRE) extended-spectrum betalactamases (ESBLs) (which are resistant to cephalosporins and monobactams), and PRSP - penicillin-resistant Streptococcus pneumoniae.
MRSA and VRE are the most commonly encountered multiple drug resistant organisms in patients residing in non-hospital healthcare facilities, such as nursing homes and other long-term care facilities.  PRSP are more common in patients seeking care in outpatient settings such as physicians' offices and clinics, especially in pediatric settings. ESBLs are most often encountered in the hospital (intensive care) setting, but MRSA and VRE also have a significant nosocomial ecology. 
Methicillin-resistant Staph aureus. MRSA refers to "methicillin-resistant Staphylococcus aureus," which are strains of the bacterium that are resistant to the action of methicillin, and related beta-lactam antibiotics (e.g., penicillin and cephalosporin). MRSA have evolved resistance not only to beta-lactam antibiotics, but to several classes of antibiotics. Some MRSA are resistant to all but one or two antibiotics, notably vancomycin-resistant. But there have been several reports of VRSA (Vancomycin-resistant Staphylococcus aureus) that are troublesome in the ongoing battle against staph infections.
MRSA are often sub-categorized as Hospital-Associated MRSA (HA-MRSA) or Community-Associated MRSA (CA-MRSA), depending upon the circumstances of acquiring disease. Based on current data, these are distinct strains of the bacterial species.
HA-MRSA occurs most frequently among patients who undergo invasive medical procedures or who have weakened immune systems and are being treated in hospitals and healthcare facilities such as nursing homes and dialysis centers.  MRSA in healthcare settings commonly causes serious and potentially life-threatening infections, such as bloodstream infections, surgical site infections, or pneumonia. In the case of HA-MRSA, patients who already have an MRSA infection or who carry the bacteria on their bodies but do not have symptoms (colonized) are the most common sources of transmission. The main mode of transmission to other patients is through human hands, especially healthcare workers' hands. Hands may become contaminated with MRSA bacteria by contact with infected or colonized patients. If appropriate hand hygiene, such as washing with soap and water or using an alcohol-based hand sanitizer is not performed, the bacteria can be spread when the healthcare worker touches other patients.  MRSA infections that occur in otherwise healthy people who have not been recently (within the past year) hospitalized or had a medical procedure (such as dialysis, surgery, catheters) are categorized as CA-MRSA infections. These infections are usually skin infections, such as abscesses, boils, and other pus-filled lesions. About 75% of CA-MRSA infections are localized to skin and soft tissue and usually can be treated effectively. However, CA-MRSA strains display enhanced virulence, spread more rapidly, and cause more severe illness than traditional HA-MRSA infections, and can affect vital organs leading to widespread infection (sepsis), toxic shock syndrome, and pneumonia. It is not known why some healthy people develop CA-MRSA skin infections that are treatable whereas others infected with the same strain develop severe, fatal infections.
Studies have shown that rates of CA-MRSA infection are growing fast.  One study of children in south Texas found that cases of CA-MRSA had a 14-fold increase between 1999 and 2001. CA-MRSA skin infections have been identified among certain populations that share close quarters or experience more skin-to-skin contact. Examples are team athletes, military recruits, and prisoners. However, more and more CA-MRSA infections are being seen in the general community as well, especially in certain geographic regions. Also, CA-MRSA are infecting much younger people. In a study of Minnesotans published in The Journal of the American Medical Association, the average age of people with MRSA in a hospital or healthcare facility was 68. But the average age of a person with CA-MRSA was only 23. ,
More people in the U.S. now die from MRSA infection than from acquired immune deficiency syndrome (AIDS). Methicillin-resistant Staphylococcus aureus was responsible for an estimated 94,000 life-threatening infections and 18,650 deaths in 2005, as reported by CDC in the Oct. 17, 2007, issue of The Journal of the American Medical Association. The national estimate is more than double the invasive MRSA prevalence reported 5 years earlier. That same year, roughly 16,000 people in the U.S. died from AIDS, according to CDC. , While most invasive MRSA infections could be traced to a hospital stay or some other health care exposure, about 15% of invasive infections occurred in people with no known healthcare risk. Two-thirds of the 85% of MRSA infections that could be traced to hospital stays or other health care exposures occurred among people who were no longer hospitalized. People over age 65 were four times more likely than the general population to get an MRSA infection. Incidence rates among blacks were twice that of the general population, and rates were lowest among children over the age of 4 and teens. ,
Extended-spectrum beta-lactamase-producing Gram-negative bacteria ESBLs are plasmid-associated beta lactamases that have recently been found in the Enterobacteriaceae. ESBLs are capable of hydrolyzing penicillins, many narrow-spectrum cephalosporins, many extended-spectrum cephalosporins, oxyimino-cephalosporins (cefotaxime, ceftazidime), and monobactams (aztreonam). Beta-lactamase inhibitors (e.g., clavulanic acid) generally inhibit ESBL-producing strains. ESBL-producing isolates are most commonly Klebsiella ssp, predominantly Klebsiella pneumoniae, and E. coli, but they have been found throughout the Enterobacteriaeae. Because ESBL enzymes are plasmid mediated, the genes encoding these enzymes are easily transferable among different bacteria.  Most of these plasmids not only contain DNA encoding ESBL enzymes but also carry genes conferring resistance to several non-ß-lactam antibiotics. Consequently, most ESBL isolates are resistant to many classes of antibiotics. The most frequent co-resistances found in ESBL-producing organisms are aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and sulfamethoxazole-trimethoprim. Treatment of these multiple drug-resistant organisms is a therapeutic challenge.
ESBL-producing strains have been isolated from abscesses, blood, catheter tips, lung, peritoneal fluid, sputum, and throat cultures. They apparently have a world-wide distribution. Rates of isolation vary greatly worldwide and within geographic areas and are rapidly changing over time. In the United States, between 1990 and 1993, a survey of the intensive care units of 400 hospitals recorded an increase from 3.6% to 14.4% in ESBL-producing strains of Klebsiella. In 1994, the CDC reported that 8% of Klebsiella spp from a few large centers produced ESBLs. , In Europe, as of 1995, ESBLs occurred in 20-25% of Klebsiella pneumoniae from patients in ICUs, although they were found in patients up to 30-40% frequency in France. Known risk factors for colonization and/or infection with organisms harboring ESBLs include admission to an intensive care unit, recent surgery, instrumentation, prolonged hospital stay, and antibiotic exposure, especially to extended-spectrum beta-lactam antibiotics. Use of extended-spectrum antibiotics exerts a selective pressure for emergence of ESBL-producing strains. The resistance plasmids can then be transferred to other bacteria, not necessarily of the same species, conferring resistance to them. The lower GI tract of colonized patients is the main reservoir of these organisms. Gastrointestinal carriage can persist for months. In some cities in the United States, nursing homes may be an important reservoir of ESBL-producing strains.  Nursing home patients are more likely to be treated empirically with antibiotics, and thus on admission to a hospital to be more likely to possess an ESBL-producing strain. Patient-to-patient transmission of ESBL-producing organisms occurs via the hands of hospital staff. It is known that ESBL-producing strains can survive in the hospital environment. Nosocomial infections in patients occur through the administration of extended-spectrum beta-lactam antibiotics or via transmission from other patients via healthcare workers who become colonized with resistant strains via exposure to patients or other healthcare workers. Spread of ESBL-producing strains can be minimized by good infection control practices, especially by good hand washing technique.  Staphylococcus aureus (MRSA) and Gram negative bacterial infections such as Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas aeruginosa, and, finally, emerging infections such as the 2009 H1N1 influenza virus and bacteria containing the newly emerging New Delhi metallo -beta-lactamase (NDM- 1) enzyme that makes them resistant to a broad range of antibacterial drugs. Although comparator agents that have been previously approved for the specific indication under study have traditionally been used in noninferiority studies, the increasing prevalence of MDR (multidrug-resistant) and XDR (extensively drug-resistant) pathogens makes the selection of an appropriate comparator in Hospital-Acquired Bacterial Pneumonia (HABP) and Ventilator-Associated Bacterial Pneumonia (VABP) studies increasingly difficult. For the treatment of infection with XDR pathogens that are resistant to all other options, it may be necessary to allow use of comparator treatments that do not have an approved indication for the treatment of HABP and/or VABP (e.g., colistin and tigecycline). 
Societal, Medical, and Agricultural Practices that Lead to Antibiotic Resistance
In the face of a microbe's inherent ability to develop antibiotic resistance, many societal, medical, and agricultural practices contribute to this process, foremost of which are discussed below. ,
Antibiotics in Food and Water
Prescription drugs are not the only source of antibiotics in the environment. In the United States, antibiotics can be found in beef cattle, pigs, and poultry. The same antibiotics then find their way into municipal water systems when the runoff from housing facilities and feedlots contaminates streams and groundwater.  So, it's a double hit: we get antibiotics in our food and drinking water, and we meanwhile promote bacterial resistance. Routine feeding of antibiotics to animals is banned in the European Union and many other industrialized countries. Maybe they know something we don't. ,
Indiscriminate Use of Antibiotics in Agriculture and Veterinary Practice
The non-therapeutic use of antibiotics in livestock production makes up at least 60% of the total antimicrobial production in the United States. Irresponsible use of antibiotics in farm animals can lead to the development of resistance in bacteria associated with the animal or with people who eat the animal. Such resistance can then be passed on to human pathogens by mechanisms of HGT. Of major concern is the use of antibiotics as feed additives given to farm animals to promote animal growth and to prevent infections (rather than cure infections). The use of an antibiotic in this way contributes to the emergence of antibiotic-resistant pathogens and reduces the effectiveness of the antibiotic to combat human infections. ,
Antibiotic Resistance in Genetically Modified Crops
Antibiotic-resistance genes are used as "markers" in genetically modified crops. The genes are inserted into the plant in early stages of development in order to detect specific genes of interest, e.g., herbicide-resistant genes or insecticidal toxin genes. The antibiotic-resistance genes have no further role to play, but they are not removed from the final product. This practice has met with criticism because of the potential that the antibiotic-resistance genes could be acquired by microbes in the environment. In some cases, these marker genes confer resistance to front-line antibiotics such as the beta-lactams and aminoglycosides. 
Inappropriate Use of Antibiotics in the Medical Environment
One problem is the casual use of antibiotics in medical situations where they are of no value. This is the fault of both healthcare workers and patients. Prescribers sometimes thoughtlessly prescribe "informed" demanding patients with antibiotics. This leads to use of antibiotics in circumstances where they are of not needed, e.g., viral upper respiratory infections such as cold and flu, except when there is serious threat of secondary bacterial infection. Another problem is patient failure to adhere to regimens for prescribed antibiotics. Patients and doctors need to realize their responsibility when they begin an antibiotic regimen to combat an infectious disease.  There are several measures that should be considered. Patients should not take antibiotics for which there is no medical value (corollary: doctors should not prescribe antibiotics for which there is no medical value). Patients should adhere to appropriate prescribing guidelines and take antibiotics until they have finished. Patients should be give combinations of antibiotics, when necessary, to minimize the development of resistance to a single antibiotic (as in the case of TB). Patients need to be given another antibiotic or combination of antibiotics if the first is not working. 
Combating Antibiotic Resistance
The following are recommendations to combat the development of antibiotic resistance in bacteria and other microorganisms.
Search for New Antibiotics
To combat the occurrence of resistant bacteria, biotechnology and pharmaceutical companies must constantly research, develop, and test new antimicrobials in order to maintain a pool of effective drugs on the market.
Stop the Use of Antibiotics as Growth-Promoting Substances in Farm Animals
Of major concern is the use of antibiotics as feed additives given to farm animals to promote animal growth and to prevent infections rather than cure infections. The use of such antibiotics contributes to the emergence of antibiotic-resistant bacteria that threaten human health and decreases the effectiveness of the same antibiotics used to combat human infections. ,
Use the Right Antibiotic in an Infectious Situation as Determined by Antibiotic Sensitivity Testing, When Possible
Stop Unnecessary Antibiotic Prescriptions
Unnecessary antibiotic prescriptions have been identified as causes for an enhanced rate of resistance development. Unnecessary prescriptions of antibiotics are made when antibiotics are prescribed for viral infections (antibiotics have no effect on viruses). This gives the opportunity for indigenous bacteria (normal flora) to acquire resistance that can be passed on to pathogens. ,
Finish Antibiotic Prescriptions
Unfinished antibiotic prescriptions may leave some bacteria alive or may expose them to sub-inhibitory concentrations of antibiotics for a prolonged period of time. Mycobacterium tuberculosis is a slow-growing bacterium, which infects the lung and causes tuberculosis. This disease kills more adults than any other infectious disease. Due to the slow-growing nature of the infection, treatment programs last for months or even years. This has led to many cases on unfinished prescriptions, and 5% of strains now observed are completely resistant to all known treatments and hence incurable. Several other possible solutions have been proposed or implemented to combat antibiotic resistance. In the pharmaceutical industry, past and current strategies to combat resistance have not been effective. Pharmaceutical companies are seeking new, less costly strategies to develop antibiotics. A decrease in the number of prescriptions for antibiotics, especially in small children, is occurring. Several countries such as the UK have regulations concerning the use of antibiotics in animal feed. Large scale public health education efforts are underway to stress the importance of finishing prescriptions. Indeed, in many places, failure to finish tuberculosis prescriptions can result in jail time. 
Myths About Antibiotics
Among the prevalent myths about antibiotics are the following three:
Antibiotics are responsible for the decline in infectious disease. The truth is that antibiotics are helpful for many infections. However, antibiotics have not resulted in the elimination of infectious diseases by themselves. In fact, we now have antibiotic-resistant diseases that are much more difficult to treat as a direct result of the use of antibiotics such as certain strains of gonorrhea and tuberculosis, as well as many others that are less well known such as MRSA, a resistant strain of Staphylococcus. These cause many deaths, especially in hospitals.
Antibiotics are useful against colds and flu. In truth, antibiotics are only helpful for bacterial infections. However, many physicians continue to prescribe them for viral conditions such as colds and flu. The rationale is to prevent secondary bacterial infection. This would be fine, except for myth 3 below, the dangers of antibiotics. Given the dangers of antibiotics, it is prudent in most cases not to take antibiotics for colds and flus. They can worsen the situation and prolong recovery.
Antibiotics are harmless. This is the most insidious myth. It leads to overprescribing and blinds physicians and the public to the dangers of antibiotics, described in the next section. Meanwhile, safer methods of avoiding and treating infections are ignored on the premise that the antibiotics will take care of everything.
The interaction between antibiotics and other medications should also be noted. In addition to the side effects and cautions described in books, antibiotics present other problems that are described below. ,
Problems with Antibiotics
The list of problems with antibiotics is quite long. Some are common and well known. Others are subtle, but no less important.
They Contribute to Cancer
A 2008 study of 3,000,000 people divided the participants into groups that had taken no antibiotics for the past 2 years, those that had taken 2-5 prescriptions, and those that had taken six or more prescriptions in the same time period. Participants were tracked for 6 years afterwards. Those who had taken 2-5 antibiotic prescriptions had a 27% increase in cancers compared to those who took none. Those who took six or more prescriptions had a 37% increase in cancers. This was a carefully done study on a large group of people and published in a very reputable journal.  Other studies show the same thing. A National Cancer Institute study in a major medical journal found that the incidence of breast cancer doubled among women who took more than 25 antibiotic prescriptions or took antibiotics for more than 500 days over 17 years. ,
I used to worry every time I prescribed penicillin when I was a medical intern. It had been explained that rarely a patient would have a fatal allergic reaction to it. I was taught that if I practiced medicine long enough, someone would die in my office after a shot of penicillin. While this is uncommon, other allergic reactions to antibiotics occur frequently. Not only can the drug cause a reaction, but most antibiotics contain chemical colors, sugar, and other additives that can trigger a reaction in sensitive individuals. ,
Destruction of Beneficial Bowel Flora
Like pesticides, antibiotics kill good bugs along with the bad ones. Wide-spectrum antibiotics are notorious for this. The human intestine has a somewhat delicate ecology in which certain bugs help digest food, produce certain vitamins, and maintain a balance of organisms that prevents harmful bacteria and yeasts from multiplying. Wide-spectrum antibiotics derange the normal ecology of the intestine. This can cause parasitic infection, vitamin deficiencies, loss of minerals through diarrhea, inflammation of the gut, malabsorption syndromes, and development of food allergies due to defects in intestinal function. 
Development of Resistant Species of Micro-Organisms
An article in Science Magazine, August 1992, stated, "Doctors in hospitals and clinics around the world are losing the battle against an onslaught of new drug-resistant bacterial infections including staph, pneumonia, strep, tuberculosis, dysentery, and other diseases that are costly and difficult, if not impossible, to treat." Bacteria have a certain ability to mutate. Antibiotics kill bacteria that are susceptible to their action, but this leaves the field open for mutant strains to multiply even more. It is a case of survival of the fittest. The use of antibiotics actually encourages the development of the mutant, drug-resistant super-bacteria. ,
This may sound odd, as the purpose of antibiotics is presumably to help the immune response. However, evidence indicates that people treated with antibiotics have more repeat infections than those who are not treated. This is especially true of children whose ear infections are treated with antibiotics. Vitamin A and C and the use of simple herbs such as echinacea and astragalus, for example, are much safer and often equally effective.
In fact, antibiotics do not aid the immune system. They replace one of its functions. Antibiotics act by inhibiting certain enzymatic processes of bacteria, and by changing mineral balances. Normal cells, however, are also affected. This may be one reason why antibiotics weaken the immune response. Other toxic effects of antibiotics, such as the effect upon the normal bowel flora, may also be a cause. AIDS research indicates that a risk factor for AIDS is an impaired immune response. This can be due to a history of repeated antibiotic use. Perhaps it is no accident the same group with the highest incidence of AIDS, male homosexuals as of 2009, is also a group that uses more antibiotics than other groups in America. 
Overgrowth of Candida Albicans and Other More Dangerous Intestinal Infections
Normally, Candida albicans, a common yeast, lives peacefully in our intestines and elsewhere, in harmony with other flora that keep the yeast in check. Take an antibiotic and all of this changes. By suppressing the normal flora, Candida takes over and problems begin. In its mild form, the result is diarrhea or a yeast infection. Far more serious is the growing problem of chronic muco-cutaneous yeast infection. This is described in books such as The Yeast Connection and The Yeast Syndrome. It is a major iatrogenic illness today, and a very debilitating and potentially fatal condition. One of the prime risk factors for chronic Candida infection is repeated antibiotic use. 
Even more dangerous is that antibiotic use opens the intestines to infection by other species of pathogenic or disease-causing bugs, parasites, yeasts, and other types of organisms ranging from amebas to far more toxic ones that can cause all types of systemic damage, as well as damage to the intestinal lining and related areas.
Chronic Fatigue Syndrome
This is another "new" health plague. It is associated with chronic viral illness and a weakened immune system. While its exact origins are not clear, one of the major risk factors for chronic fatigue syndrome is repeated antibiotic use.
Nutrient Loss and Resulting Deficiency States
Nutrient loss from antibiotics is in part due to diarrhea, which causes a loss of essential minerals. Destruction of friendly bacteria in the intestines can also impair the synthesis of certain vitamins in the intestines. While not a major cause of malnutrition, antibiotic usage may be another factor contributing to poor nutrition and thus weakened body chemistry.
Treating Effects, Not Causes
Antibiotics only address the end-stage result of a weakened body chemistry-bacterial invasion. The bacteria may only be there to "mop up" the biological debris that are present because the body is too weak to eliminate the poisons. Fever is one way the body burns up toxic substances. Providing it does not get out of hand, the infectious process can serve a useful purpose. Cutting short the process with antibiotics aborts the cleansing function of a fever and impairs long-term health.  In hundreds of cases, when these imbalances are corrected, the tendency for infections decreases drastically. In other words, healthy people do not get as many infections. Infections do not strike randomly. There is a logic to infections, and the underlying causes can be addressed. This line of reasoning traces back to the famous debate between Pasteur and Beauchamp. Dr. Pasteur insisted that germs are the cause of disease. His colleague, Beauchamp, insisted that the health of the host was more important than the germs. On his death bed, Pasteur was said to have declared that Beauchamp was correct - "the host is everything, the germs are nothing." Orthodox medicine, however, embraced Pasteur's view, and ignored Beauchamp. It is time to focus more on the person, and less on the germs.
While the cost of a single antibiotic prescription may not be extremely high, newer ones are somewhat costly. The costs are high when the side effects are considered, along with the sheer numbers of prescriptions that are written around the world each day, month, and year. Millions of doctor visits and prescriptions for antibiotics add up to a major expense. While penicillin is not expensive, other newer antibiotics are quite costly. 
These newer antibiotics are used more frequently today due to the presence of penicillin-resistant strains of bacteria. We must also include in the cost of antibiotics the cost of allergic reactions, Candida albicans infections, repeat infections, development of resistant organisms, and immune suppression. The cost is justified if life is at stake. However, if less toxic and less costly alternatives can be used, shouldn't these be tried first? Bringing health care costs under control is not just a matter of eliminating waste and inefficiency. We need methods of healing that build up the health of the people, not tear it down. ,
Reducing the Need for Antibiotics
Steps to avoid the need for antibiotics can be divided into two areas:
Preventing infections is a part of taking back control over your life and health. You can do a lot to prevent infections. Much of it involves common sense.
Wash your hands several times daily, wash wounds carefully, dress properly in cold weather, and obtain adequate rest and sleep. Proper hygiene and sanitation are measures we often take for granted.
Diet, Rest, and Sleep
Rest and sleep are of utmost importance to avoid infections of all kinds. In addition, a healthful diet is also most critical. Adequate intake of nutrients including vitamins A, C, E, selenium, and zinc are important for the immune system.
Reduce Toxic Exposure
Reduce or eliminate your exposure to toxic chemicals from food, air, water, or through direct contact with your skin or elsewhere (such as mercury amalgam dental fillings).
Your thoughts and attitudes affect your immune system more than you may imagine. Fears, anger, worries, and resentments tend to weaken the immune system. ,
Other Important Hints for Fighting Infections
Use natural remedies aggressively and faithfully. This is a very important point. Do not skimp on the dosages of vitamins and herbs, for example. Taking a little more will not usually hurt you, but taking less may make them less effective.
Patience and persistence are essential with any serious infection. Of course, each person and each situation is different. It is not a problem, however, if healing an infection naturally takes a week or even two or three, provided you are slowly getting better. It is not necessary or helpful to abandon your methods just for this reason. Drugs may speed up your progress, but leave you weakened and toxic.  Always act quickly with all infections, even a cold. I hear of many people who do not want to take antibiotics or other drug remedies, but who fail to apply the natural remedies quickly or at all. This is not wise as any infection can be very dangerous for one's life, in fact. Start natural treatment at the first sign of infection. This will increase their effectiveness and prevent complications that occur due to waiting. Waiting with infections is always a bad idea, as it can allow the infection to take hold more firmly in the body. You never know when complications will set in quickly and become life threatening. If one method is not working at all after a few days, add another one or two. Also, realize that at times results are slow because it is a serious infection and not because your methods are not working. You may combine all the natural methods, and you may use them along with antibiotics or other medication if you wish, unless told otherwise. The natural methods do not, to my knowledge, interfere with antibiotics and, in fact, will make them more effective by replacing nutrients in the body. If you do not feel better even after couple of days after taking the necessary precautions to reduce infection, its always best to consult a knowledgeable health practitioner. Rarely, an infection will require medical or other intervention. ,,
| Conclusion|| |
Antibiotics are an interesting class of medications that can save lives. However, antibiotics are overprescribed and are toxic. They should be used as a last resort, not the first. Very often, simple, inexpensive natural methods described here work better with far fewer adverse effects. Infections are always serious conditions, even seemingly mild ones. it is advised to take every infection seriously and treat them rapidly with natural remedies that have been proved to cure them fully. Finally, always ask for help if you are not sure how to use simple, natural methods or if an infection is not getting cured even after two or three days.
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[Figure 1], [Figure 2]
[Table 1], [Table 2]
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