Thursday, September 29, 2016

Antimicrobial Resistance: Part 1

Why Be Concerned?

The CDC conservatively estimates that more than 2 million people in the U.S. become sick with antibiotic-resistant infections every year. At least 23,000 people die from those infections. Antimicrobial resistance isn’t just a national problem, it’s a global emergency.

We’re sitting on an explosive situation, and we’re running out of time. We must find a way to stop this explosion of antimicrobial resistance before people once again start dying from infections that were untreatable before the advent of antibiotics. If allowed to continue, a simple cut on the finger could turn life-threatening. No one wants to step back into that time.

How Antimicrobial Resistance Happens

From the very birth of antibiotics, it was realized that the “miracle” drug could turn sour. Alexander Fleming, the British bacteriologist who discovered penicillin, warned that misuse could result in mutant forms of penicillin-resistant bacteria. By the 1950s, approximately 30 years after penicillin came into use, about half of Staphylococcus aureus strains already were resistant to penicillin. It wasn’t particularly concerning then. Science was diligently searching for new antibiotics and could keep up with emerging resistant strains. In the early 1980s, with approximately 100 antibiotics available, there appeared to be an abundance. Pharmaceutical companies’ research and development programs turned their attention elsewhere.

It’s frightening how easily resistance develops. In some bacteria, the ability to resist may be present on the cell’s chromosome but is not normally active. A spontaneous mutation may change that. Although it can happen in multiple ways, the process often starts with transference of genes from one bacterium to another.

Within bacteria are bits of supplemental genetic information, separate from the chromosome itself. Plasmids, these independent genetic elements, are self-duplicating and can carry from 3 to 300 different additional genes. Plasmids multiply within bacteria and change constantly. Plasmids can lose, acquire, or exchange genes, empowering them to develop ways to help its bacterial host do things it could not have done alone, such as acquiring new ways to prevent the bacterium’s death. Plasmids can carry genes for antibiotic resistance, enabling the bacterial host to resist death by antibiotic. These traits can then be transferred to other bacteria. They don’t even have to be the same kind of bacteria.

Here’s one way it happens: A bacterium with the plasmid containing the antibiotic-resistance gene sidles up to another bacterium. It extends a pilus, which reaches out to the other bacterium and draws the two together. The first bacterium makes a copy of its plasmid, or plasmids, and transfers it to the other. Now, both contain a copy of the resistance plasmid. This transference creates a new resistant strain and a new bacterium capable of passing the resistance plasmid on to other, perhaps very different, kinds of bacteria.

Philip M. Tierno, Jr, PhD, in his book The Secret Life of Germs: Observations and Lessons from a Microbe Hunter, noted the speed with which this can happen. “Gene exchange between two germs can take less than an hour. The forty-to-sixty hour cycle of human digestion leaves ample time for this to occur in the human intestinal tract.” These newly resistant bacteria can travel with their hosts to new environments, such as from the gastrointestinal tracts of humans to animals. They can cross country borders—carried by humans, animals, and food—circling the world rapidly.

“Modern Medicine Is Running Out of Magic Bullets”

Virtually all of us unwittingly contribute to the problem of antimicrobial resistance, because each person taking an antibiotic potentially contributes to the pool of resistant bacteria in the environment. We shed, excrete, and otherwise spread bacteria wherever we go. Resistant bacteria easily can move to family and others. Tierno explained, “The more antibiotics are used in a particular environment—a person’s body, a household, a hospital, or the world at large—the more they will upset the natural competitive balance among germs in favor of resistant strains. For example, if a teenager takes antibiotics regularly for acne, the other members of the household will soon come to harbor high concentrations of antibiotic-resistant skin germs simply by ordinary person-to-person contact.”

In his book The Antibiotic Paradox: How Miracle Drugs Are Destroying the Miracle, Stuart B. Levy, MD, noted, “Intermittent and repeated antibiotic use . . . creates an environment not only of microorganisms resistant to the drug being used, but also of bacteria that are resistant to many different antibiotics. . . . The net result is that many previously powerful, nontoxic, inexpensive, and often lifesaving antibiotics can become useless quickly.”

Tierno had more chilling words for us. “The world’s antibiotic use has been a fifty-year experiment in self-sabotage. . . . the selective toxicity of antibiotics has bred more and more dangerous germs. Wonder drugs have produced super bugs. . . . Modern medicine is running out of magic bullets.”

Taking Action

Much of the burden of quelling the spread of antimicrobial resistance will rest on medical-related industries. Companies like Seal Shield rise to meet such challenges with innovation and advanced technology.

One action that can be taken is exploring different avenues of controlling spread of infection. The less infectious disease, the less need there is for antibiotics. Use of Seal Shield products can reduce the risk of cross-transmission of antimicrobial-resistant pathogens in the environment. The antimicrobial impregnated in Seal Shield products, such as their medical keyboards and mice, is inorganic. It is incapable of breeding resistance while it destroys pathogens. Seal Shield’s UVC products effectively kill antimicrobial-resistant pathogens on items such as cell phones and tablets.

Human transmission plays a large role in antimicrobial resistance, but plant and animal care are heavily involved as well, perhaps even more so in the larger picture. In our next blog, we will talk more about all of these elements in the spread of antimicrobial resistance.

Susan Cantrell, ELS 
Infection Control Corner
Contributor Writer

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