Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics?

Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics?

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Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics, and why don't hospital acquired infections exist elsewhere ?

The infections that are caused in hospitals are usually a result of bacteria that are resistant to multiple antibiotics making them difficult to treat, but why are the bacteria resistant to all these antibiotics? I realize that a lot of antibiotics are used in hospitals but the question that comes to my head whenever I read this is "So?". To make my misconception clearer, I will use MRSA as an example . I mean , for the Staphylococcus aureus bacterium to become resistant , the antibiotic has to be used on it , so how can the antibiotics used to treat different infections in difference people act as a selection pressure for Staphylococcus aureus ( the Bacteria that causes MRSA )?

Hospitals have certain features:

  • They are full of people immunocompromised in some way (old, exposed tissue, on steriods etc.)
  • They are full of people with pathogens
  • They are full of doctors who will give antibiotics to people with pathogenic infections

This is a perfect breeding ground for drug resistance in pathogens, with lots of pathogens, lots of places for them to grow (patients) and quite a lot of exposure to antibiotics. You use Staphylococcus aureus as an example, and it is a good one. We all have some of it on us, but it is not generally exposed to antibiotics so it does not develop resistance, and we do not generally have large areas of exposed flesh that would cause it to be pathogenic. In hospital this is not the case, so we get it causing trouble and developing resistance.

These things do occur outside of hospitals, but it does not tend to be as common or frequent.

Preventing Infections in the NICU

Antibiotic resistance is on the rise in the United States, and, with it, the increased risk of serious infections in hospitals. Unfortunately, infections and antimicrobial resistance pose a profound threat to some of the hospital’s most vulnerable inpatients—newborns. Many patients in the neonatal intensive care unit (NICU) are premature and their immune systems are weak, so we take extra care to protect them.

We keep a detailed database of types of infections, tracking the latest trends and the newest strains. As a result, we're able to use antibiotics in a targeted way.

The Challenge of Antibiotic Resistance

Thanks to Scientific American (March 1998) for acces to this article!

Certain bacterial infections now defy all antibiotics. The resistance problem may be reversible, but only if society begins to consider how the drugs affect "good" bacteria as well as "bad"

by Stuart B. Levy

Last year an event doctors had been fearing finally occurred. In three geographically separate patients, an often deadly bacterium, Staphylococcus aureus, responded poorly to a once reliable antidote--the antibiotic vancomycin. Fortunately, in those patients, the staph microbe remained susceptible to other drugs and was eradicated. But the appearance of S. aureus not readily cleared by vancomycin foreshadows trouble.


Worldwide, many strains of S. aureus are already resistant to all antibiotics except vancomycin. Emergence of forms lacking sensitivity to vancomycin signifies that variants untreatable by every known antibiotic are on their way. S. aureus, a major cause of hospital-acquired infections, has thus moved one step closer to becoming an unstoppable killer.

The looming threat of incurable S. aureus is just the latest twist in an international public health nightmare: increasing bacterial resistance to many antibiotics that once cured bacterial diseases readily. Ever since antibiotics became widely available in the 1940s, they have been hailed as miracle drugs--magic bullets able to eliminate bacteria without doing much harm to the cells of treated individuals. Yet with each passing decade, bacteria that defy not only single but multiple antibiotics--and therefore are extremely difficult to control--have become increasingly common.

What is more, strains of at least three bacterial species capable of causing life-threatening illnesses (Enterococcus faecalis, Mycobacterium tuberculosis and Pseudomonas aeruginosa) already evade every antibiotic in the clinician's armamentarium, a stockpile of more than 100 drugs. In part because of the rise in resistance to antibiotics, the death rates for some communicable diseases (such as tuberculosis) have started to rise again, after having declined in the industrial nations.

How did we end up in this worrisome, and worsening, situation? Several interacting processes are at fault. Analyses of them point to a number of actions that could help reverse the trend, if individuals, businesses and governments around the world can find the will to implement them.

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 surfaces 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 the millions) and damage tissues or otherwise cause illness. The benign competitors can be important allies in the fight against antibiotic-resistant pathogens.

People should also realize that although antibiotics are needed to control bacterial infections, they can have broad, undesirable effects on microbial ecology. That is, they can produce long-lasting change in the kinds and proportions of bacteria--and the mix of antibiotic-resistant and antibiotic-susceptible types--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.

A Bad Combination

Although many factors can influence whether bacteria in a person or in a community will become insensitive to an antibiotic, the two main forces are the prevalence of resistance genes (which give rise to proteins that shield bacteria from an antibiotic's effects) and the extent of antibiotic use. If the collective bacterial flora in a community have no genes conferring resistance to a given antibiotic, the antibiotic will successfully eliminate infection caused by any of the bacterial species in the collection. On the other hand, if the flora possess resistance genes and the community uses the drug persistently, bacteria able to defy eradication by the compound will emerge and multiply.

Antibiotic-resistant pathogens are not more virulent than susceptible ones: the same numbers of resistant and susceptible bacterial cells are required to produce disease. But the resistant forms are harder to destroy. Those that are slightly insensitive to an antibiotic can often be eliminated by using more of the drug those that are highly resistant require other therapies.

To understand how resistance genes enable bacteria to survive an attack by an antibiotic, it helps to know exactly what antibiotics are and how they harm bacteria. Strictly speaking, the compounds are defined as natural substances (made by living organisms) that inhibit the growth, or proliferation, of bacteria or kill them directly. In practice, though, most commercial antibiotics have been chemically altered in the laboratory to improve their potency or to increase the range of species they affect. Here I will also use the term to encompass completely synthetic medicines, such as quinolones and sulfonamides, which technically fit under the broader rubric of antimicrobials.


Whatever their monikers, antibiotics, by inhibiting bacterial growth, give a host's immune defenses a chance to outflank the bugs that remain. The drugs typically retard bacterial proliferation by entering the microbes and interfering with the production of components needed to form new bacterial cells. For instance, the antibiotic tetracycline binds to ribosomes (internal structures that make new proteins) and, in so doing, impairs protein manufacture penicillin and vancomycin impede proper synthesis of the bacterial cell wall.

Certain resistance genes ward off destruction by giving rise to enzymes that degrade antibiotics or that chemically modify, and so inactivate, the drugs. Alternatively, some resistance genes cause bacteria to alter or replace molecules that are normally bound by an antibiotic--changes that essentially eliminate the drug's targets in bacterial cells. Bacteria might also eliminate entry ports for the drugs or, more effectively, may manufacture pumps that export antibiotics before the medicines have a chance to find their intracellular targets.

My Resistance Is Your Resistance

Bacteria can acquire resistance genes through a few routes. Many inherit the genes from their forerunners. Other times, genetic mutations, which occur readily in bacteria, will spontaneously produce a new resistance trait or will strengthen an existing one. And frequently, bacteria will gain a defense against an antibiotic by taking up resistance genes from other bacterial cells in the vicinity. Indeed, the exchange of genes is so pervasive that the entire bacterial world can be thought of as one huge multicellular organism in which the cells interchange their genes with ease.

Bacteria have evolved several ways to share their resistance traits with one another [see "Bacterial Gene Swapping in Nature," by Robert V. Miller Scientific American, January]. Resistance genes commonly are carried on plasmids, tiny loops of DNA that can help bacteria survive various hazards in the environment. But the genes may also occur on the bacterial chromosome, the larger DNA molecule that stores the genes needed for the reproduction and routine maintenance of a bacterial cell.

Often one bacterium will pass resistance traits to others by giving them a useful plasmid. Resistance genes can also be transferred by viruses that occasionally extract a gene from one bacterial cell and inject it into a different one. In addition, after a bacterium dies and releases its contents into the environment, another will occasionally take up a liberated gene for itself.

In the last two situations, the gene will survive and provide protection from an antibiotic only if integrated stably into a plasmid or chromosome. Such integration occurs frequently, though, because resistance genes are often embedded in small units of DNA, called transposons, that readily hop into other DNA molecules. In a regrettable twist of fate for human beings, many bacteria play host to specialized transposons, termed integrons, that are like flypaper in their propensity for capturing new genes. These integrons can consist of several different resistance genes, which are passed to other bacteria as whole regiments of antibiotic-defying guerrillas.

Many bacteria possessed resistance genes even before commercial antibiotics came into use. Scientists do not know exactly why these genes evolved and were maintained. A logical argument holds that natural antibiotics were initially elaborated as the result of chance genetic mutations. Then the compounds, which turned out to eliminate competitors, enabled the manufacturers to survive and proliferate--if they were also lucky enough to possess genes that protected them from their own chemical weapons. Later, these protective genes found their way into other species, some of which were pathogenic.

Regardless of how bacteria acquire resistance genes today, commercial antibiotics can select for--promote the survival and propagation of--antibiotic-resistant strains. In other words, by encouraging the growth of resistant pathogens, an antibiotic can actually contribute to its own undoing.

How Antibiotics Promote Resistance

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 inevitably outcompete all others.


Promoting resistance in known pathogens is not the only self-defeating activity of antibiotics. When the medicines attack disease-causing bacteria, they also affect benign bacteria -- innocent bystanders -- in their path. They eliminate drug-susceptible bystanders that could otherwise limit the expansion of pathogens, and they simultaneously encourage the growth of resistant bystanders.Propagation of these resistant, nonpathogenic bacteria increases the reservoir of resistance traits in the bacterial population as a whole and raises the odds that such traits will spread to pathogens. In addition, sometimes the growing populations of bystanders themselves become agents of disease.

Widespread use of cephalosporin antibiotics, for example, has promoted the proliferation of the once benign intestinal bacterium E. faecalis, which is naturally resistant to those drugs. In most people, the immune system is able to check the growth of even multidrug-resistant E. faecalis, so that it does not produce illness. But in hospitalized patients with compromised immunity, the enterococcus can spread to the heart valves and other organs and establish deadly systemic disease.

Moreover, administration of vancomycin over the years has turned E. faecalis into a dangerous reservoir of vancomycin-resistance traits. Recall that some strains of the pathogen S. aureus are multidrug-resistant and are responsive only to vancomycin. Because vancomycin-resistant E. faecalis has become quite common, public health experts fear that it will soon deliver strong vancomycin resistance to those S. aureus strains, making them incurable.

The bystander effect has also enabled multidrug-resistant strains of Acinetobacter and Xanthomonas to emerge and become agents of potentially fatal blood-borne infections in hospitalized patients. These formerly innocuous microbes were virtually unheard of just five years ago.

As I noted earlier, antibiotics affect the mix of resistant and nonresistant bacteria both in the individual being treated and in the environment. When resistant bacteria arise in treated individuals, these microbes, like other bacteria, spread readily to the surrounds and to new hosts. Investigators have shown that when one member of a household chronically takes an antibiotic to treat acne, the concentration of antibiotic-resistant bacteria on the skin of family members rises. Similarly, heavy use of antibiotics in such settings as hospitals, day care centers and farms (where the drugs are often given to livestock for nonmedicinal purposes) increases the levels of resistant bacteria in people and other organisms who are not being treated--including in individuals who live near those epicenters of high consumption or who pass through the centers.

Given that antibiotics and other antimicrobials, such as fungicides, affect the kinds of bacteria in the environment and people around the individual being treated, I often refer to these substances as societal drugs -- the only class of therapeutics that can be so designated. Anticancer drugs, in contrast, affect only the person taking the medicines.

On a larger scale, antibiotic resistance that emerges in one place can often spread far and wide. The ever increasing volume of international travel has hastened transfer to the U.S. of multidrug-resistant tuberculosis from other countries. And investigators have documented the migration of a strain of multidrug-resistant Streptococcus pneumoniae from Spain to the U.K., the U.S., South Africa and elsewhere. This bacterium, also known as the pneumococcus, is a cause of pneumonia and meningitis, among other diseases.

Antibiotic Use Is Out of Control

For those who understand that antibiotic delivery selects for resistance, it is not surprising that the international community currently faces a major public health crisis. Antibiotic use (and misuse) has soared since the first commercial versions were introduced and now includes many nonmedicinal applications. In 1954 two million pounds were produced in the U.S. today the figure exceeds 50 million pounds.

Human treatment accounts for roughly half the antibiotics consumed every year in the U.S. Perhaps only half that use is appropriate, meant to cure bacterial infections and administered correctly--in ways that do not strongly encourage resistance.

Notably, many physicians acquiesce to misguided patients who demand antibiotics to treat colds and other viral infections that cannot be cured by the drugs. Researchers at the Centers for Disease Control and Prevention have estimated that some 50 million of the 150 million outpatient prescriptions for antibiotics every year are unneeded. At a seminar I conducted, more than 80 percent of the physicians present admitted to having written antibiotic prescriptions on demand against their better judgment.

In the industrial world, most antibiotics are available only by prescription, but this restriction does not ensure proper use. People often fail to finish the full course of treatment. Patients then stockpile the leftover doses and medicate themselves, or their family and friends, in less than therapeutic amounts. In both circumstances, the improper dosing will fail to eliminate the disease agent completely and will, furthermore, encourage growth of the most resistant strains, which may later produce hard-to-treat disorders. In the developing world, antibiotic use is even less controlled. Many of the same drugs marketed in the industrial nations are available over the counter. Unfortunately, when resistance becomes a clinical problem, those countries, which often do not have access to expensive drugs, may have no substitutes available.


The same drugs prescribed for human therapy are widely exploited in animal husbandry and agriculture. More than 40 percent of the antibiotics manufactured in the U.S. are given to animals. Some of that amount goes to treating or preventing infection, but the lion's share is mixed into feed to promote growth. In this last application, amounts too small to combat infection are delivered for weeks or months at a time. No one is entirely sure how the drugs support growth. Clearly, though, this long-term exposure to low doses is the perfect formula for selecting increasing numbers of resistant bacteria in the treated animals--which may then pass the microbes to caretakers and, more broadly, to people who prepare and consume undercooked meat.

In agriculture, antibiotics are applied as aerosols to acres of fruit trees, for controlling or preventing bacterial infections. High concentrations may kill all the bacteria on the trees at the time of spraying, but lingering antibiotic residues can encourage the growth of resistant bacteria that later colonize the fruit during processing and shipping. The aerosols also hit more than the targeted trees. They can be carried considerable distances to other trees and food plants, where they are too dilute to eliminate full-blown infections but are still capable of killing off sensitive bacteria and thus giving the edge to resistant versions. Here, again, resistant bacteria can make their way into people through the food chain, finding a home in the intestinal tract after the produce is eaten.

The amount of resistant bacteria people acquire from food apparently is not trivial. Denis E. Corpet of the National Institute for Agricultural Research in Toulouse, France, showed that when human volunteers went on a diet consisting only of bacteria-free foods, the number of resistant bacteria in their feces decreased 1,000-fold. This finding suggests that we deliver a supply of resistant strains to our intestinal tract whenever we eat raw or undercooked items. These bacteria usually are not harmful, but they could be if by chance a disease-causing type contaminated the food.

The extensive worldwide exploitation of antibiotics in medicine, animal care and agriculture constantly selects for strains of bacteria that are resistant to the drugs. Must all antibiotic use be halted to stem the rise of intractable bacteria? Certainly not. But if the drugs are to retain their power over pathogens, they have to be used more responsibly. Society can accept some increase in the fraction of resistant bacteria when a disease needs to be treated the rise is unacceptable when antibiotic use is not essential.

Reversing Resistance

A number of corrective measures can be taken right now. As a start, farmers should be helped to find inexpensive alternatives for encouraging animal growth and protecting fruit trees. Improved hygiene, for instance, could go a long way to enhancing livestock development.

The public can wash raw fruit and vegetables thoroughly to clear off both resistant bacteria and possible antibiotic residues. When they receive prescriptions for antibiotics, they should complete the full course of therapy (to ensure that all the pathogenic bacteria die) and should not "save" any pills for later use. Consumers also should refrain from demanding antibiotics for colds and other viral infections and might consider seeking nonantibiotic therapies for minor conditions, such as certain cases of acne. They can continue to put antibiotic ointments on small cuts, but they should think twice about routinely using hand lotions and a proliferation of other products now imbued with antibacterial agents. New laboratory findings indicate that certain of the bacteria-fighting chemicals being incorporated into consumer products can select for bacteria resistant both to the antibacterial preparations and to antibiotic drugs.

Physicians, for their part, can take some immediate steps to minimize any resistance ensuing from required uses of antibiotics. When possible, they should try to identify the causative pathogen before beginning therapy, so they can prescribe an antibiotic targeted specifically to that microbe instead of having to choose a broad-spectrum product. Washing hands after seeing each patient is a major and obvious, but too often overlooked, precaution.

To avoid spreading multidrug-resistant infections between hospitalized patients, hospitals place the affected patients in separate rooms, where they are seen by gloved and gowned health workers and visitors. This practice should continue.

Having new antibiotics could provide more options for treatment. In the 1980s pharmaceutical manufacturers, thinking infectious diseases were essentially conquered, cut back severely on searching for additional antibiotics. At the time, if one drug failed, another in the arsenal would usually work (at least in the industrial nations, where supplies are plentiful). Now that this happy state of affairs is coming to an end, researchers are searching for novel antibiotics again. Regrettably, though, few drugs are likely to pass soon all technical and regulatory hurdles needed to reach the market. Furthermore, those that are close to being ready are structurally similar to existing antibiotics they could easily encounter bacteria that already have defenses against them.

With such concerns in mind, scientists are also working on strategies that will give new life to existing antibiotics. Many bacteria evade penicillin and its relatives by switching on an enzyme, penicillinase, that degrades those compounds. An antidote already on pharmacy shelves contains an inhibitor of penicillinase it prevents the breakdown of penicillin and so frees the antibiotic to work normally. In one of the strategies under study, my laboratory at Tufts University is developing a compound to jam a microbial pump that ejects tetracycline from bacteria with the pump inactivated, tetracycline can penetrate bacterial cells effectively.

Considering the Environmental Impact

As exciting as the pharmaceutical research is, overall reversal of the bacterial resistance problem will require public health officials, physicians, farmers and others to think about the effects of antibiotics in new ways. Each time an antibiotic is delivered, the fraction of resistant bacteria in the treated individual and, potentially, in others, increases. These resistant strains endure for some time -- often for weeks -- after the drug is removed.

The main way resistant strains disappear is by squaring off with susceptible versions that persist in--or enter--a treated person after antibiotic use has stopped. In the absence of antibiotics, susceptible strains have a slight survival advantage, because the resistant bacteria have to divert some of their valuable energy from reproduction to maintaining antibiotic-fighting traits. Ultimately, the susceptible microbes will win out, if they are available in the first place and are not hit by more of the drug before they can prevail.

Correcting a resistance problem, then, requires both improved management of antibiotic use and restoration of the environmental bacteria susceptible to these drugs. If all reservoirs of susceptible bacteria were eliminated, resistant forms would face no competition for survival and would persist indefinitely.

In the ideal world, public health officials would know the extent of antibiotic resistance in both the infectious and benign bacteria in a community. To treat a specific pathogen, physicians would favor an antibiotic most likely to encounter little resistance from any bacteria in the community. And they would deliver enough antibiotic to clear the infection completely but would not prolong therapy so much as to destroy all susceptible bystanders in the body.

Prescribers would also take into account the number of other individuals in the setting who are being treated with the same antibiotic. If many patients in a hospital ward were being given a particular antibiotic, this high density of use would strongly select for bacterial strains unsubmissive to that drug and would eliminate susceptible strains. The ecological effect on the ward would be broader than if the total amount of the antibiotic were divided among just a few people. If physicians considered the effects beyond their individual patients, they might decide to prescribe different antibiotics for different patients, or in different wards, thereby minimizing the selective force for resistance to a single medication.

Put another way, prescribers and public health officials might envision an "antibiotic threshold": a level of antibiotic usage able to correct the infections within a hospital or community but still falling below a threshold level that would strongly encourage propagation of resistant strains or would eliminate large numbers of competing, susceptible microbes. Keeping treatment levels below the threshold would ensure that the original microbial flora in a person or a community could be restored rapidly by susceptible bacteria in the vicinity after treatment ceased.

The problem, of course, is that no one yet knows how to determine where that threshold lies, and most hospitals and communities lack detailed data on the nature of their microbial populations. Yet with some dedicated work, researchers should be able to obtain both kinds of information.

Control of antibiotic resistance on a wider, international scale will require cooperation among countries around the globe and concerted efforts to educate the world's populations about drug resistance and the impact of improper antibiotic use. As a step in this direction, various groups are now attempting to track the emergence of resistant bacterial strains. For example, an international organization, the Alliance for the Prudent Use of Antibiotics (P.O. Box 1372, Boston, MA 02117), has been monitoring the worldwide emergence of such strains since 1981. The group shares information with members in more than 90 countries. It also produces educational brochures for the public and for health professionals.

The time has come for global society to accept bacteria as normal, generally beneficial components of the world and not try to eliminate them -- except when they give rise to disease. Reversal of resistance requires a new awareness of the broad consequences of antibiotic use -- a perspective that concerns itself not only with curing bacterial disease at the moment but also with preserving microbial communities in the long run, so that bacteria susceptible to antibiotics will always be there to outcompete resistant strains. Similar enlightenment should influence the use of drugs to combat parasites, fungi and viruses. Now that consumption of those medicines has begun to rise dramatically, troubling resistance to these other microorganisms has begun to climb as well.

Further Reading


DRUG RESISTANCE: THE NEW APOCALYPSE. Special issue of Trends in Microbiology, Vol. 2, No. 10, pages 341-425 October 1, 1994.

ANTIBIOTIC RESISTANCE: ORIGINS, EVOLUTION, SELECTION AND SPREAD. Edited by D. J. Chadwick and J. Goode. John Wiley & Sons, 1997.

STUART B. LEVY is professor of molecular biology and microbiology, professor of medcine and director of the Center for Adaptation Genetics and Drug Resistance at the Tufts University School of Medicine. He is also president of the Alliance for the Prudent Use of Antibiotics and president-elect of the American Society for Microbiology.

Contact : Washington State Department of Health/ Romesh Gautom, Public Health Laboratory, 206/361-2885
Matt Ashworth, Communication Office, 360/753-3237

Invitational EU Conference

Health of the Population : Strategies to prevent and control the emergence and spread of antimicrobial-resistant microorganisms.

Copenhagen, 9-10 September 1998.

(Workshops, 7-8 September 1998).

How common are such infections?

Infections linked to Cryptococcus or Mucor are relatively rare - but "Staph" infections are much more common.

Staphylococcus aureus accounts for about 110 infections every month at Scottish hospitals.

Bacteria, viruses or other micro-organisms that cause disease are collectively known as pathogens - and there are a lot of them. Other common varieties found in hospitals are:

  • Escherichia coli - better known as E. coli. It's a bacteria found in the intestines of humans and animals. It can be spread through contaminated food, touching animals or poor hygiene. Some strains such as E. coli O157 produce toxins that can make people very ill but most people get better without medical treatment. There are nearly 400 cases a month reported at Scottish hospitals.
  • Clostridioides difficile - previously known as Clostridium difficile and abbreviated to C. diff. A very common type of bacteria, particularly prevalent in the soil which can cause a bowel infection and diarrhoea. It can particularly affect people who have been treated with antibiotics or who have been in hospital for a long time. Nearly 350 cases are reported a month on average at Scottish hospitals.

Standard precautions in hospitals are work practices that provide a basic level of infection control for the care of all people, regardless of their diagnosis or presumed infection status.

These precautions should be followed in all hospitals and healthcare facilities and include:

  • good personal hygiene, such as hand washing before and after patient contact and the appropriate use of alcohol-based hand rub solutions
  • the use of barrier equipment such as gloves, gowns, masks and goggles
  • appropriate handling and disposal of sharps (for example, needles) and clinical waste (waste generated during patient care)
  • aseptic (sterile) techniques.

Implementing standard precautions minimises the risk of transmission of infection from person to person, even in high-risk situations.

Evaluation of an S. aureus infection involves evaluation of clinical signs and symptoms as well as the history and physical findings. In many cases, routine cultures will reveal the diagnosis (i.e., blood, sputum) however, RT-PCR (real-time PCR) for 16S rRNA genes may be necessary in some cases. Drug susceptibility testing often is required to guide treatment. If patient samples are collected for pathogen identification in the microbiology laboratory, caution must be exercised as the presence of S. aureus in the skin or mucous membrane does not necessarily indicate infection because these organisms are frequently members of the normal flora.[4]

Treatment of S. aureus infections depends largely on the type of infection as well as the presence or absence of drug resistant strains.[6] When antimicrobial therapy is needed, the duration and mode of therapy are largely dependent on the infection type as well as other factors.[6] In general, penicillin remains the drug of choice if isolates are sensitive (MSSA, or methicillin sensitive S. aureus strains) and vancomycin for MRSA strains.[3] In some cases, alternative therapy is necessary for addition to antimicrobial therapy.[6] For example, fluid-replacement management is often required for toxin-mediated illness and removal of foreign devices for prosthetic value endocarditis or catheter-associated infections. Because many MRSA strains are resistant to multiple antibiotics, MRSA infections are emerging as serious pathogens in both the hospital and the community settings.[3][5]

Healthcare-Associated Infections (HAIs)

Healthcare-associated infections (HAIs) are complications of healthcare and linked with high morbidity and mortality. Each year, about 1 in 25 U.S. hospital patients is diagnosed with at least one infection related to hospital care alone additional infections occur in other healthcare settings. Many HAIs are caused by the most urgent and serious antibiotic-resistant (AR) bacteria and may lead to sepsis or death. CDC uses data for action to prevent infections, improve antibiotic use, and protect patients.

  • 50 percent decrease in central line-associated bloodstream infections (CLABSI) between 2008 and 2014 3
  • 36 percent decrease in healthcare-associated invasive MRSA, 2008&ndash2014. In addition, National Healthcare Safety Network (NHSN) data reported a 13% decrease (2011 &ndash 2014) for hospital-onset MRSA bacteremia bloodstream infections, confirming overall trends.
  • 17 percent decrease in select surgical site infections (SSI)
  • 8 percent decrease in hospital-onset Clostridium difficile (C. difficile) infections between 2011 and 2014
  • 24 percent decrease in CAUTI in acute care hospital wards, 2009 &ndash 2014, and 16 percent increase in CAUTI in hospital intensive care units. 4

Progress in Healthcare-Associated Infections

SIR for central line-associated bloodstream infections declined sharply

National and State Healthcare-associated Infections Progress Report, published January 2016, based on 2014 data

Trends in catheter-associated urinary tract infections (CAUTI) in hospitals 2009 &ndash 2014 4

Source: CDC&rsquos National Healthcare Safety Network (NHSN)

3 CLABSI data reflect progress in acute-care hospitals only.
4 CAUTI data reflect progress in acute-care hospitals only. Although 2009 &ndash 2014 data show no change in overall CAUTI SIRs, specific hospital units showed major
changes in CAUTI SIRs: 24% decrease in hospital wards and 16% increase in hospital intensive care units (ICUs).

Trends in Healthcare-Associated Infections Winnable Battle Indicators

Trends in central line-associated blood stream infections (CLABSI) in hospitals, 2006 &ndash 2014 3

Source: CDC&rsquos National Healthcare Safety Network (NHSN)
3 CLABSI data reflect progress in acute-care hospitals only.

Trends in surgical site infections (SSI) in hospitals, 2006 &ndash 2014

Source: CDC&rsquos National Healthcare Safety Network (NHSN)

Trends in catheter-associated urinary tract infections (CAUTI) in hospitals, 2009 &ndash 2014 4

Source: CDC&rsquos National Healthcare Safety Network (NHSN)
4 CAUTI data reflect progress in acute-care hospitals only. Although 2009 &ndash 2014 data show no change in overall CAUTI SIRs, specific hospital units showed major changes in CAUTI SIRs: 24% decrease in hospital wards and 16% increase in hospital intensive care units (ICUs).

Trends in healthcare-associated invasive methilicillin-resistant Staphylococcus aureus (MRSA) infections, 2007 &ndash 2014 5

Source: Emerging Infections Program / Active Bacterial Core Surveillance
5 Starting in 2015, the MRSA data source will be Emerging Infections Program / Healthcare-Associated Infections Component (EIP / HAIC) and National
Healthcare Safety Network (NHSN).

Considerations in Choosing Healthcare-Associated Infections as Winnable Battle

  • CDC had a long history of tracking HAIs as well as developing and promoting evidence-based recommendations for infection prevention and control, but many infections were not being prevented.
  • In the early 2000s, evidence indicated that full adherence to CDC guidelines prevented 70% of CLABSIs in some hospitals however, too many infections were still occurring.
  • In 2009, the federal government added commitment to HAI prevention with the establishment of national prevention goals with the National Action Plan to Prevent Health Care-Associated Infections: Road Map to Elimination external icon using CDC&rsquos National Healthcare Safety Network (NHSN) to track progress. In addition, for the first time, states received limited funding to support developing infrastructure that could promote and assist in HAI prevention efforts.
  • This combination of CDC data, guidelines, national goals, and new state support provided a unique opportunity to make major gains in reducing &mdash and in some cases, eliminating &mdash HAIs.

Challenges / Obstacles

  • We needed to develop a new normal external icon in which HAIs are considered unacceptable and rare events in healthcare.
  • We needed commitment from traditional and new public health and healthcare stakeholders at all levels &mdash federal, state, local, health system, healthcare provider, and patient &mdash as well as public and private sectors to make an impact.
  • There was a need among many stakeholders to embrace more transparency and accountability.

Tennessee has made significant progress preventing HAIs by intensely focusing on using actionable NHSN data to drive improvement in healthcare. Tennessee started in 2008 as one of only two states in the country with a CLABSI SIR significantly higher than the national baseline, and by 2014, the state had reduced CLABSIs to 52% below the national baseline.

The Tennessee Department of Health (TDH) HAI & AR (Antibiotic Resistance) Program achieved this by turning to its data: collecting, verifying, and then acting on hospital data to compare facilities, identify where infections were occurring, and then focus targeted prevention in specific facilities in the state and locations within the facility.

Such aggressive action was not possible without TDH&rsquos strong partnerships. HAI prevention was integrated into work with CMS-funded networks, state hospital associations, and other local partners to establish priorities, set goals, align strategies, and clearly define roles and responsibilities.

&ldquoWe&rsquove embraced the TAP strategy in Tennessee for several reasons. We feel it has the greatest return on investment, by targeting facilities with the potential to prevent the greatest number of infections,&rdquo said Dr. Marion Kainer, TDH HAI Program Director.

TDH is a state leader in HAI / AR prevention. In fact, CDC worked with TDH to adapt this early strategy into CDC&rsquos TAP strategy, now available nationwide with NHSN data tools. TDH is now working to expand its successful approach across the spectrum of healthcare and HAI / AR threats in the state.

CDC Contributions in Healthcare-Associated Infections Winnable Battle

Since 2008, the combination of CDC data systems, evidence-based recommendations, public health-healthcare programs, and partnerships have contributed to significant reductions of HAIs across healthcare settings. CDC focuses its prevention efforts on major device- and procedure-related HAIs, as well as controlling the spread of infections.

Using Data for Action: Transparency and Accountability

CDC promotes the use of HAI / AR data for action to identify gaps in infection prevention, set goals for prevention, and prioritize interventions for public health impact. Partners use CDC&rsquos data systems and data-based tools and resources to drive quality improvement in healthcare.

    CDC&rsquos National Healthcare Safety Network (NHSN) is the nation&rsquos most widely used system to track HAIs. Facilities use NHSN to not only fulfill federal and state reporting requirements, but also act on their NHSN data to monitor and prevent infections within their facilities. In collaboration with CMS and state partners, CDC increased the number of healthcare facilities reporting to NHSN from

Developing Innovative Approaches to Prevention

Wherever CDC works to detect and respond to HAI / AR outbreaks, prevent infections, stop spread of bacteria between patients, and improve antibiotic use, CDC looks to continually improve and develop innovative approaches to maximize public health impact.

  • With academic applied research partners in CDC&rsquos Prevention Epicenter Program, CDC identifies and tests new strategies for infection prevention and control, as well as clinical practice. For example, CDC worked with Chicago-area long-term acute care hospitals to evaluate a novel intervention bundle designed to stop the spread of CRE external icon , finding it reduced CRE bloodstream infections by 56%. Likewise, the CDC-designed nationwide REDUCE MRSA Trial external icon demonstrated that one strategy reduced bloodstream infections by up to 44% and significantly reduced the presence of MRSA and other pathogens in ICUs. Now, these infection prevention strategies are adopted as best practices in healthcare settings across the nation.
  • CDC communicates and promotes infection prevention measures we know work. For example, the public health community has long recognized that antibiotic use puts patients at risk for C. difficile infection. With historically high C. difficile rates, CDC combined science, policy, and communications to release the Core Elements of Hospital Antibiotic Stewardship Programs to show how hospital CEOs and medical officers can improve antibiotic use and protect patients in their facilities (CDC Vital Signs: Antibiotic Rx in Hospitals: Proceed with Caution, 2014). CDC has since published core elements of antibiotic stewardship in nursing homes (2015) and outpatient settings (2016, pending).
  • To identify gaps and strategies to meet Winnable Battle goals, CDC expanded data analytical techniques to predict HAI / AR trends, identify new interventions, and inform program direction. For example, CDC used mathematical modeling to predict increases in HAI / AR infections and C. difficile over the next five years without immediate, nationwide improvements in infection control and antibiotic prescribing (CDC Vital Signs: Stop Spread of AR, 2015). This led CDC to partner with academic researchers to test interventions within public health-healthcare prevention networks. These partnerships put these findings into practice which, if successful, serve as models for HAI / AR prevention in other areas of the country. This work also provided evidence to support expanding State HAI / AR Prevention Programs to better prevent infections, stop spread, and improve antibiotic use.
  • In response to the complexities of combating HAI / AR across healthcare settings and in the community, CDC is integrating its detection, response, and prevention strategies to better protect patients. CDC urges healthcare personnel to always follow infection control recommendations and stewardship to better protect patients from HAIs caused by AR (CDC Vital Signs: Protect Patients from AR, 2016). Many of the most urgent and serious AR bacteria threaten patients while they are being treated in healthcare facilities for other conditions, and may lead to sepsis or death (CDC Vital Signs: Think Sepsis. Time Matters, 2016).

Expanding Collaborations to Implement What We Know Works

CDC works with diverse public health and healthcare partners to align prevention goals, promote the use of CDC guidelines and data for action, and aggressively work to prevent HAIs and AR infections across the spectrum of care.

  • CDC works with other federal agencies to align national prevention goals and integrate proven prevention strategies and measures into national policies to change infection control practice.
    • CDC and CMS have collaborated closely to include infection prevention and control and antibiotic stewardship programs in revised Conditions of Participation in Medicare and Medicaid programs for acute care hospitals and long-term care facilities. CDC&rsquos NHSN data and prevention tools are also used by CMS-funded Quality Improvement Networks.
    • CDC leads the 2016&ndash2017 HHS Agency Priority Goal (APG) to expand stewardship programs nationwide, and worked closely with the CMS-led APGs to reduce CLABSIs (2012&ndash2013) and CAUTIs (2012&ndash 2015) nationwide.
    • CDC also works with FDA to protect patients and stop outbreaks from spreading in healthcare facilities. Often, these outbreaks result from either failures in infection control practices or contaminated equipment or medications.
    • These partnerships expand HAI / AR prevention and antibiotic stewardship programs to implement proven strategies to prevent infections and transmission across healthcare settings.
    • CDC is also implementing more prevention networks &mdash where public health and healthcare work together &mdash in more states to better prevent infections, stop spread, and improve antibiotic use.

    In fiscal year 2016, Congress appropriated $160 million for CDC to fight AR, a testament to the urgent AR threat and highest levels of support for the ambitious public health actions outlined in the National Action Plan for Combating Antibiotic-Resistant Bacteria (2015). This is a substantial opportunity for state and local public health, academic, healthcare, and veterinary partners to accelerate our efforts to establish the new normal in which HAIs are considered unacceptable and rare events in healthcare.

    Why bacteria's resistance to antibiotics is a problem in a viral pandemic

    Each year, a particular kind of infection kills more than 35,000 people in the United States. Those deaths are caused by antibiotic-resistant bacteria.

    And some scientists are concerned about how the current pandemic might affect such bacteria.

    That’s because hospitalized patients with coronavirus will often be given antibiotics to fight any secondary bacterial infection, not to fight the virus itself.

    Benjamin Kerr is a professor of biology at the University of Washington who studies how bacteria become antibiotic resistant. He spoke to KUOW’s Angela King about antibiotics and the pandemic.

    Benjamin Kerr: So there does appear to be heightened use of antibiotics as a proactive tactic in Covid-19 patients and hospitals to prevent secondary bacterial infections. Similarly, antifungals are being used to prevent secondary fungal infections.

    A recent report in the journal Science suggested that antibiotic use for this purpose was surging both in the U.S. and worldwide. As a consequence, bacteria may be experiencing more exposure to antibacterial compounds generally, antibiotics specifically, which has been shown to favor the evolution of antibiotic resistance. It might seem confusing why antibiotic prescription has increased during a viral epidemic, but actually, in past viral pandemics, the 1918 flu epidemic as well as the 2009 flu epidemic, a large fraction of individuals, the cause of death turned out to be due to secondary bacterial infections.

    Angela King: So if bacteria are becoming resistant to the antibiotics we currently have, what’s being done to create new ones that might be more effective?

    Kerr: Many of the pharmaceutical companies have actually abandoned the antibiotic design market in part because these drugs may be less lucrative as they lose efficacy when resistance arises. There are also several university-based labs interested in expanding the arsenal of antibiotics antibacterial compounds more generally.

    King: How do antibacterial ingredients in home products contribute to the problem of drug resistance?

    Kerr: Some cleaning products, detergents, but actually many different items, shampoos, toothpastes, contain antibacterial compounds. Also antibacterial compounds are used in alcohol-free hand sanitizers. The main thing to know is that if a product is advertised as antibacterial, the chances are high that the compounds are not providing any additional protection against something like coronavirus. So if you're checking cleaning products or detergents or again, alcohol-free hand sanitizers, ingredients like triclosan and or benzalkonium chloride or compounds like this, again, if your target is bacteria specifically, there may be some protection there. But with regards to protection for something like coronavirus, you're not getting any additional protection there.

    King: Any products you would suggest or others maybe we should steer clear from?

    Kerr: I would definitely recommend checking with the CDC or EPA websites on any particular product for basic cleaning. A mix of soap and warm water works well through the same principle as good hand hygiene.

    Scientific Studies on Antibiotic Resistance

    Many research groups around the world have concluded that EMF causes several changes to bacteria. And despite the majority of them being harmful for the human population, some of the effects are actually positive.

    In fact, some industries use these positive effects to enhance their production. I’ll discuss this in more depth in the later sections of this post. But for now, it’s important that you understand EMF’s negative effect on your health, which is a more significant threat at the moment.

    Now, like all other EMF-induced problems, this is also a subjective situation. The effects and severity of EMF on bacteria depends on several factors like frequency, exposure time, coherence, bacterial class, growth conditions, and genetic features.

    So, to understand this better, scientists studied EMF’s effects on a few common pathogens, and the results are exactly what we suspected. So, let’s have a look.

    Pseudomonas Aeruginosa & Staphylococcus Epidermis

    Pseudomonas Aeruginosa, or P. aeruginosa, is a type of bacteria that takes advantage of your weakened immune system to create infections and damage tissues.

    You can contract this bacterium from fruit and vegetables, contaminated food, public pools, hot tubs, bathrooms, sinks, and such. It also grows on humidifiers and unclean medical equipment, so there’s a higher risk of P. aeruginosa contraction in hospitals.

    Suppose you come in contact with this bacterium. In that case, you can suffer problems like urinary tract infections (UTI), respiratory system infections, dermatitis, bone and joint infections, soft tissue infections, bacteremia, and gastrointestinal infections.

    On the other hand, Staphylococcus Epidermis, also known as the “accidental pathogen,” transfers from skin-to-skin contact. When contracted, this S. epidermis looks for minor cuts and pimples on your skin to enter through and cause a bigger infection. It’s common for S. epidermis-induced infections to go away after some time, as your immune system is good at killing this bacterium.

    An Iranian research group did a study to see EMF’s effects on Pseudomonas Aeruginosa & Staphylococcus Epidermis. They kept the subjects under the exposure of EMF operating on 900 MHz frequency for 24 hours. For context, this is the same frequency on which the 2G network operates.

    After this, the researchers tried to treat these bacteria with antibiotics. They found that P. aeruginosa gained resistance to all kinds of antibiotics, whereas S. epidermis remained sensitive to piperacillin, ampicillin, and ceftriaxone.

    “According to the obtained results, it can be concluded that the bacterial species used in this study were influenced by the electromagnetic field and responded differently,” conclude the researchers.

    Listeria Monocytogenes and Escherichia Coli

    Just like salmonellosis, the bacteria that cause salmonella, Listeria Monocytogenes, is found in food. L. monocytogenes causes an illness called listeriosis, which has a 20-30% mortality rate, much higher than other food-borne illnesses.

    L. monocytogenes’ symptoms are fever, chills, muscle aches, nausea, diarrhea, confusion or changes in alertness, loss of balance, and convulsions.

    Similarly, Escherichia Coli or E. coli is also found in food. Its effects are somewhat identical to that of L. monocytogenes but far less destructive. Its symptoms are food poisoning, pneumonia, and urinary tract infection (UTI).

    Another group of Iranian researchers exposed these bacteria to WiFi radiation running on 2.4 GHz frequency and cell phone radiation at 900 MHz frequency. The exposure time was 12 hours, and they found that both bacteria became resistant to all antibiotics.

    Lebanese researchers also did a similar research study on L. monocytogenes and E. coli. They said, “WiFi exposure acted on bacteria in a stressful manner by increasing antibiotic resistance and motility of E. Coli, as well as enhancing biofilm formation ability in E Coli, S Aureus, and S Epidermis.” A biofilm is created when bacteria attach and organize themselves into a coordinated functional community.

    Non-bacterial infection

    It is possible for other microbes to cause infections. For example, coughs, colds and the flu are usually caused by viruses and not bacteria. Athletes foot and thrush are caused by fungi.

    While there are treatments for these conditions, antibiotics only work on infections caused by bacteria. That is why doctors often don’t offer antibiotics to some patients, even if they ask for them. If antibiotics are used on viral or fungal infections, they will not help with the illness. Using them incorrectly increases the risk of antibiotic resistance.

    Registered office:
    Antibiotic Research UK
    Genesis 5
    York Science Park
    YO10 5DQ

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