Beware the Bug!

The discovery of penicillin in 1928 began the dawn of a new medical era. From the 1940s to the 1970s, a golden age flourished, and more than 100 new antibiotics were discovered. For the first time in human history, diseases such as tuberculosis and pneumonia could be easily cured, and the average life expectancy around the world increased by 10 years.

For awhile, there was hope that many infectious diseases might be eliminated permanently. However, in a phenomenon known as antibiotic resistance, bacteria soon learned to survive our biochemical attacks. In the 1940s, shortly after penicillin came into widespread use, one strain of Staphylococcus aureus became resistant. Drug companies developed new versions of penicillin, such as methicillin and flucloxacillin, but the bacteria quickly became resistant to those as well. Fast-forward to the present, and antibiotic-resistant superbugs are making headlines around the world. Our early successes against infectious diseases were only the first battles in an ongoing war, and there is still no guarantee of who will prevail in the end.

Evolution in Action

Antibacterial resistance is an example of evolution in action. Whenever an antibiotic is used, there is always the chance that some of the bacteria will survive. Compared to the bacteria that were killed off, the survivors have genes that make them more resistant to the drug. Since bacteria reproduce asexually, all of the offspring produced by the surviving bacteria will be equally resistant to the drug, helping them to survive antibiotic treatment. Bacteria can also acquire resistance genes in a process called conjugation, where bits of DNA called plasmids are passed from one bacterium to another. This gene-swapping procedure can occur between bacteria of the same species or related species.

Bacteria use many strategies to escape death, such as making enzymes to inactivate antibiotics or changing the structure of their cell walls to make themselves less vulnerable to attack. Although there are more than 150 antibiotics, most of them belong to one of 15 different classes. Antibiotics that belong to the same class work in a similar way, so once a strain of bacteria becomes resistant to one antibiotic, it can also quickly become resistant to other antibiotics from the same class.

And since bacteria multiply rapidly and can produce a new generation in as little as 20 minutes, their resistance genes can spread quickly throughout the population. Eventually the drug-resistant bacteria become predominant, and can be killed only with more powerful antibiotics.

In addition to bacteria, other disease-causing agents (such as viruses, parasites, and fungi) can also become drug-resistant. The HIV virus and the Plasmodium protozoans that cause malaria are two examples of drug-resistant microbes.

Overprescription, Underuse, and Misuse of Antibiotics

Whenever antibiotics are used, the targeted bacteria must either adapt or die. If antibiotics are used inappropriately, then there is a much greater chance that the bacteria will adapt, survive, and pass on their resistance genes.

Have you ever gone to the doctor for a cold or flu, and insisted on getting an antibiotic "just in case?" The common cold and the flu are caused by viruses, not bacteria, so antibiotics are completely useless. The overprescription of antibiotics in such cases has played a large role in the rise of antibiotic-resistant bacteria. Using antibiotics for too short a time, at too low a dose, or at the wrong potency will also lead to the development of drug-resistant strains.

Ironically, the underuse of antibiotics also favors the development of drug resistance. This is a major concern in developing countries, where patients may not be able to afford the entire dosage needed, and sometimes have access only to expired or substandard drugs. Once again, these conditions increase the likelihood that resistant bacteria will survive and spread.

The antibacterial soaps, disinfectant wipes, and other germ-killing products in your home may also be contributing to antibiotic resistance. For example, triclosan is a powerful microbicide used to stop the spread of hospital infections. It can also be found in numerous household products ranging from soaps and cosmetics to plastic cutlery and socks. Triclosan-resistant bacteria are currently rare, but there are concerns that its widespread use could eventually make the antibiotic much less effective. Furthermore, antibacterial household products may kill off too many of the "good bacteria" that naturally live on our skin and in our guts, and increase the likelihood that the "bad bacteria" will become overabundant.

Half of all antibiotics sold each year are used on farm animals, whether to treat sick animals, or at a constant low dose to prevent disease and promote growth. These conditions favor the development of antibacterial resistance, and resistant bacteria may be transferred from animals to people through meat consumption, direct contact with farm animals, or when bacteria from animal excreta seeps into the groundwater. The rise of antibiotic-resistant strains of Salmonella, Campylobacter, and Enterococcus bacteria have all been linked to the use of antibiotics in agriculture.

With the advent of global trade and travel, antibiotic resistance has become a worldwide concern. A resistant bacterial strain that develops in one region of the world can be quickly transported to other regions, thus greatly increasing the risk of outbreaks and epidemics.

Famous Superbugs

Staphylococcus aureus: Staphylococcus aureus is normally found on the skin of healthy individuals, and does not cause problems unless it enters the body (e.g., by infecting a wound). S. aureus infections were treatable with penicillin in the 1940s and 1950s, but now almost all strains have become resistant to the drug. Methicillin-resistant Staphylococcus aureus (MRSA) is sometimes called the "hospital superbug," and infects more than 100,000 people a year in the United States. In 2003, a particularly virulent strain of S. aureus began infecting healthy people in the US and Europe. This strain contained a gene called PVL, and was spread through skin contact.

Even more alarming is the fact that some strains of S. aureus have also become resistant to vancomycin, the "last resort antibiotic." In May of 1996, a vancomycin-resistant strain of S. aureus (VRSA) was identified in Japan, followed in 2002 by isolated cases in the US and other countries. It's likely that VRSA acquired its vancomycin-resistance genes from Enterococci, since laboratory experiments had shown that this was possible back in 1992.

Vancomycin-Resistant Enterococci (VRE): Vancomycin is known as a "last resort antibiotic," and is deployed only after other antibiotics have failed. The drug was first introduced in the 1950s, and resistance did not develop until 30 years later. This is because bacteria must synthesize their cell walls in a whole new way in order to survive vancomycin treatment – a process that requires complicated genetic changes. However, vancomycin resistance has become common in a group of bacteria called Enterococci. Enterococci are naturally found in human intestines and normally are harmless. However, they may become dangerous if they infect another part of the body after surgery or injury. Vancomycin-resistant Enterococci (VRE) are extremely difficult to treat. The rise of VRE in humans has been linked to the use of avoparcin, a closely related antibiotic that is used in livestock.

Drug-Resistant Tuberculosis (DR-TB): TB is an old disease that's becoming increasingly hard to treat. Six to 12 months of antibiotic treatment is needed to completely eradicate TB-causing mycobacteria, but many patients fail to complete the full length of the treatment, which favors the development of drug resistance. By 1984, half of US patients with active tuberculosis had a strain that was resistant to at least one antibiotic (DR-TB). In more recent years, coinfection with TB and HIV has also contributed to the rise of drug-resistant TB. Multidrug-resistant TB (MDR-TB) is resistant to both rifampicin and isoniazid, the two most effective first-line drugs for the disease. Extensively drug resistant TB (XDR-TB) is almost untreatable, since these strains are resistant to both first-line and backup medications. The World Health Organization (WHO) first identified XDR-TB in March of 2006, and since then, has confirmed its presence in 27 countries.

Solutions

The WHO and many other groups have issued guidelines on how to combat antibiotic resistance. The consensus is that a multipronged attack is needed, which includes a dramatic change in the way we use antibiotics, better infection control measures, and a constant pipeline of new medications.

The best way to fight antibiotic resistance is to prevent it in the first place, and that requires the general public to become more knowledgeable about antibiotic resistance. People can protect themselves from contagious diseases by practicing good hygiene (e.g., frequent hand washing), through safe food preparation, and by getting recommended vaccinations. Patients on antibiotic treatment need to take the medication exactly as prescribed. Any leftover antibiotics should be brought to a drug recycling program, because drugs that are thrown in the garbage, flushed down the toilet, or poured down the sink will end up in the water table, and may increase the resistance of bacteria in the environment. Consumers should also know that antibacterial cleaning products are unnecessary, and that soap, vinegar, and household bleach are sufficient for most household purposes.

Better infection control practices are needed in hospitals to prevent antibiotic-resistant infections and to contain outbreaks when they occur. In the US, 88,000 deaths a year are attributed to nosocomial infections, and more than 70% of hospital infections are caused by bacteria resistant to at least one antibiotic. Healthcare professionals can greatly reduce the number of infections through simple measures like washing their hands frequently and changing their gloves after each patient treatment.

A constant supply of new antibiotics are needed to fight existing strains of drug-resistant bacteria, and to deal with new strains. To be effective, these new treatments should not simply be variations of existing drugs, but must attack bacteria in new and different ways. A promising approach is combining old antibiotics with a "bodyguard" molecule that blocks the bacteria's resistance mechanisms. Recent advances in genetics offer many new tools to combat antibiotic resistance. Gene mapping has allowed researchers to pinpoint the sections of bacterial DNA responsible for resistance, and thus provides the first step in developing antibiotics to overcome those resistance mechanisms. Using genetic engineering, researchers can get microbes to produce antibiotics in large quantities, and also create variations of existing drugs by changing the biochemical pathways of the antibiotic-producing microbes.

However, it is only a matter of time before bacteria builds up resistance to whatever new drugs are developed. We are in a perpetual arms race against disease-causing bacteria, and constant education, research, and vigilance is required to stay ahead.

Visit the following websites for more information: • US Food and Drug Administration: Antibiotic Resistance • Health Canada: Antibiotic Resistance

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