Hospital-Acquired Methicillin- Resistant Staphylococcus ......ospital-acquired/health care–...

623RADIOLOGIC TECHNOLOGY, July/August 2014, Volume 85, Number 6

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Amy Jacobs, MS

Hospital-acquired/health care–associated infection (HAI) is of tremendous concern to health care providers as HAI is

ranked as one of the top 5 causes of death in the United States.1 The Centers for Disease Control and Prevention (CDC) estimate that 1 in 20 hospital-ized patients will contract an HAI.2 The World Health Organization estimates, on average, 8.7% of hospitalized patients worldwide have HAIs at any one time, with the highest frequencies being reported in the Eastern Mediterranean and Southeast Asia regions (11.8% and 10.0%, respectively).3 In the United States, HAIs are contracted by an esti-mated 1.7 million patients annually, accounting for nearly 99 000 deaths4 and imposing additional health care costs of $35.7 to $45 billion.5

HAIs, also known as nosocomial infections, are infections acquired by a patient upon admittance to a hospital that were not present in the patient prior to hospitalization. Infection is said to occur within 48 to 72 hours of admittance or within 10 days of dis-charge from the hospital.6 HAIs can be caused by viral, bacterial, or fungal pathogens and can occur in adults and children.7 The most frequent HAIs are those involving infections of surgi-cal wounds, bloodstream infections, urinary tract infections, and lower respiratory tract infections, with the highest prevalence of HAIs occurring in intensive care units (ICUs) and in acute surgical and orthopedic wards.3 Patients with lowered immune system function-ing, the elderly, and those with underly-ing disease are the most susceptible to

After completing this article, the reader should be able to:Discuss MRSA and its role in hospital-acquired/health care–associated infections (HAIs).Identify the mechanisms of antimicrobial resistance in bacteria generally and

MRSA specifically.Explain how bacteria acquire resistance.Describe how MRSA is identified. List the signs and symptoms of MRSA infection and its risk factors.State the transmission mechanisms for MRSA.Summarize current epidemiological data on MRSA infection.Discuss treatment options for MRSA, including antibacterials, microphages, and

topical honey.Outline techniques for preventing MRSA infection, such as hand washing and the use of

hydrogen peroxide vapor and antimicrobial copper.

Methicillin-resistant Staphylococcus aureus (MRSA) has been a pathogen of serious concern to both the health care and public health communities since the 1960s. This article focuses on the most serious strains of MRSA, hospital-acquired/health care–associated MRSA. Signs and symptoms of MRSA infection are described, in addition to the modes of transmission, laboratory techniques for identifying MRSA, and treatment options. Global MRSA rates are presented and prevention technologies are discussed. Finally, multiagency suggestions for eradicating MRSA are presented, such as strict adherence to standard contact precautions and hand hygiene practices within the medical community.

Hospital-Acquired Methicillin-Resistant Staphylococcus aureus: Status and Trends

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624 RADIOLOGIC TECHNOLOGY, July/August 2014, Volume 85, Number 6


HAIs.3 The use of invasive devices such as catheters and certain procedures increase the risk of acquiring an infectious disease during hospital treatment. Infections associated with these invasive devices include central line–associated bloodstream infections, catheter-associ-ated urinary tract infections, and ventilator-associat-ed pneumonia.8 These types of infections account for an estimated two-thirds of all HAIs.8

Although many pathogenic microorganisms cause HAIs, increasingly to blame are microorganisms resistant to the antimicrobials traditionally used to treat them.9 In fact, 16% of all HAIs are caused by antimicrobial-resistant pathogens.9 Not only are these infectious agents resistant to a single antimicrobial drug, but some also are resistant to multiple drugs or even entire classes of antimicrobial drugs.10 This makes these pathogens of particular interest to clinicians and public health agen-cies, as the pathogens pose significant treatment and transmission challenges, particularly in health care settings.10 An HAI of significant concern for more than 50 years is methicillin-resistant Staphylococcus aureus (MRSA).11 Staphylococcus aureus (S aureus) ranks as the leading causative agent of HAIs, with a high proportion of these being caused by MRSA.12

What Is MRSA?MRSA is a bacterium labeled a “superbug” because

of its acquired resistance to a multitude of antibiot-ics. MRSA is resistant to antibiotics in the class beta-lactams (-lactams), which include, but are not limited to, methicillin, penicillin, and amoxicillin.13 -lactams work by inhibiting bacterial cell wall synthesis and are among the most widely used antibiotics globally.13

By the late 1950s, approximately 10% of S aureus isolates had become resistant to penicillin yet remained susceptible to penicillinase-stable penicillins, in particu-lar oxacillin and methicillin.14 However, S aureus strains began turning up that were no longer susceptible to oxa-cillin and methicillin. Shortly after methicillin’s intro-duction as a treatment option, MRSA was identified.14

While methicillin has been replaced by oxacillin for the treatment of MRSA, the acronym MRSA still is used and is interchangeable with oxacillin-resistant Staphylococcus aureus (ORSA).15 Each year in the United States, approximately 126 000 people are hospi-talized with MRSA infections and 19 000 deaths result;

86% of these are from hospital-acquired/health care–associated MRSA (HA-MRSA).16 More deaths occur from MRSA than from HIV.16,17

StaphylococcusStaphylococcus is a genus of gram-positive bacteria

comprising 40 species, of which most are harmless, asymptomatic colonizers of the skin and mucus mem-branes of numerous organisms, including humans.18 However, some Staphylococcus species are opportu-nistic pathogens that produce complex toxins, lead-ing to severe infections that can sometimes be fatal.18 As an evolutionary adaptation, they also can exhibit frequent and multiple resistance to antimicrobials.18 Staphylococcus aureus is the foremost representative of the staphylococci and is among the most ubiquitous bacteria on earth (see Figure 1).19 This ubiquity might be the result of S aureus’ ability to resist an array of adverse environmental conditions, such as complete drying and high salt concentrations. These abilities also might explain why S aureus is such an effective colo-nizer of nasal and mucosal membranes.19

Staphylococcus aureus grows in grapelike clusters termed cocci and frequently is found in the human axil-la, groin, nose, and throat.16 It is estimated that approxi-mately 1 in 3 people are colonized by S aureus (ie, they are carriers with no signs or symptoms of infection). Staphylococcus aureus causes staph infections, which

Figure 1. This colorized electron micrograph (magnification 4780) shows multiple clumps of methicillin-resistant Staphylococcus aureus bacteria. Public domain image courtesy of the Centers for Disease Control and Prevention.

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cultures of bacteria are routinely subjected to antibiotic susceptibility tests in which an agar plate containing a bacterial culture (ie, E coli) receives applications of various antimicrobials to determine their effect on that specific bacteria. If a bacteria is susceptible to a particu-lar antibiotic, the application area and a reaction zone (often termed a halo) will be voided of bacteria on the agar plate (see Figure 2). However, if a bacteria is resis-tant to the applied antibiotic, there will be no effect on its growth pattern and no halo will be present.

Bacterial resistance is of tremendous concern to both the health care and public health communities because resistant bacteria are both prevalent and pervasive within health care facilities as well as in the community. Resistant bacteria make treatment difficult and often ineffective and sometimes lead to “superbugs” that are unresponsive to most common treatment options. Antimicrobial resistance also increases health care costs. Patients infected by an antimicrobial-resistant pathogen incur costs $6000 to $30 000 higher than

vary in severity and can range from simple skin boils to life-threatening infections.20 The difference in severity depends on the bacteria’s strength, rate of spread, depth of colonization, and treatability with antibiotics.21

Among people colonized with S aureus, fewer than 2% are colonized with MRSA, usually in the nose.20 In a large portion of colonized people, the bacterium does not cause disease. Disease manifests only when there is damage to the skin or another injury that allows bacte-ria to overcome the body’s defense mechanisms, thus leading to infection.16

People who are not colonized with S aureus still can become infected through external contact with the bac-teria as a result of touching a contaminated person or item, such as sharing towels in a locker room with a per-son who has an actively draining or weeping skin infec-tion.16 Staphylococcus aureus causes infection by produc-ing several different enzymes and toxins. For example, proteolytic enzymes break down proteins, resulting in pus production. Enterotoxins cause vomiting, diarrhea, and shock. Exfoliative toxin protein causes skin disrup-tion and blistering. And exotoxin TSST-1 induces toxic shock syndrome.16

Microbiology of Antibiotic ResistanceAntimicrobial agents operate by 1 of 5 mechanisms:

interference with cell wall synthesis (eg, -lactams, van-comycin); inhibition of protein synthesis (eg, clindamy-cins, tetracyclines); interference with nucleic acid syn-thesis (eg, f luoroquinolones, rifampin); inhibition of a metabolic pathway (eg, sulfonamides); and disruption of bacterial membrane structure (eg, polymixins).22,23

Almost as soon as antimicrobials were discovered, penicillin being the first in the late 1920s,24 bacteria began manifesting various forms of resistance against antimicrobials. And as drug development progressed, bacteria’s resistance mechanisms evolved. When anti-biotics were introduced, scientists assumed that the evolution of antibiotic resistance was unlikely because mutation rates were believed to be negligible.25 The abil-ity of bacteria to interchange genes was quite unexpect-ed, and it was later discovered that bacterial resistance had actually begun even before penicillin was used in medical treatment, with the discovery of a -lactamase in Escherichia coli (E coli).26, 27 In order to determine a bacteria’s resistance or susceptibility to antibiotics,

Figure 2. A Mueller-Hinton agar culture plate used in an antibi-otic susceptibility test (AST). Each of the small, labeled discs con-tained an antibiotic cocktail. Each of the light halos surrounding the discs are called reaction zones and represent the bacteria on the agar’s surface that did not survive because of their sensitivity to the antibiotics that had been applied to the discs. This form of AST is known as the Kirby-Bauer method. Public domain image courtesy of the Centers for Disease Control and Prevention.

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costs for patients with infections caused by antimicrobial-susceptible pathogens.28 The CDC suggested that in the United States, antibiotic resistance accounts for an additional $20 billion in health care costs, $35 million in societal costs, and an additional 8 million days spent in hospitals each year.29

Microbes such as bacteria, viruses, fungi, and para-sites evolve over time by adjusting to their environmen-tal conditions, just as other organisms do. However, microbes evolve much more rapidly than more complex organisms such as humans. This is a consequence of their short generation time, which in some species is on the order of minutes, as in E coli (20 minutes) and S aureus (30 minutes). Short generation times allow for significant genetic changes to occur with each new generation. In the exponential or logarithmic (log) phase of bacte-rial growth, cells replicate rapidly. Initially, growth is doubled, followed by a logarithmic (exponential) mul-tiplying.30 The time it takes for bacterial cells to double in number defines the generation time. To further illustrate bacterial replication rates, imagine that a single S aureus bacterial cell gets into an open skin wound. In 10 generations, that single bacterial cell will have grown into a colony of more than 1000 cells (210 1024).30 Add another 10 generations and that colony will have grown to more than 1 million cells (220 1 048 576).30 Considering the generation time of about half an hour, it takes only 12 hours for a single original cell to grow into a colony of more than 1 million.30

Bacteria manifest resistance to antimicrobial drugs through an assortment of methods.22 Some bacterial species are innately resistant to more than one class of antibacterial drugs, and in these cases all strains within the species are resistant to all antimicrobials within that class. The more distressing resistance is acquired resistance, in which bacteria that are susceptible to antibiotics are exposed to an antimicrobial or class of antimicrobials, and resistance develops during treat-ment with that antimicrobial.22 This form of resistance is acquired through a variety of mutation, selection, and genetic transfer (horizontal gene transfer) mechanisms. For example, the bacterium might acquire a gene or genes that encode an enzyme or enzymes targeted to destroy the antimicrobial before it has an effect. Or, the bacterium might acquire eff lux pumps that eradicate

the antimicrobial agent from the bacterial cell before it has an effect. Another possibility is that several genes might be acquired that alter cell wall membranes and exclude antimicrobial binding sites. Also, the bacte-rium might acquire mutations, either spontaneously or through horizontal gene transfer, that limit access of antimicrobial agents to the target site within the cell.22,26

Resistance conferred through chromosomal muta-tion, selection, or both is termed vertical evolution, while resistance conferred through the acquisition of genetic material from another organism is termed horizontal evolution.22 Genetic transfers can occur between the same or different species or even genera of bacteria.22,31 Transposons, classes of genetic elements that can “jump” to different places within the genome, facilitate genetic transfer between organisms.22,32 Resistance genes can be conferred upon the bacterium’s genome or into plasmids (circular DNA molecules in bacte-rial cells that replicate independently)33 and can occur through conjugation, transduction, or transformation.22 The mechanism of conjugation differs between gram-negative and gram-positive bacteria. Gram-negative bacteria transfer resistance genes, contained on plas-mids, through an elongated protein structure called a pilus that joins the bacteria during genetic transfer. In gram-positive bacteria, donor and recipient organisms produce sex pheromones that join the 2 organisms during genetic transfer.22 Transduction, a rather rare event, involves the use of an intermediary, a bacterio-phage or bacterial virus, during the genetic transfer. Transformation, on the other hand, involves bacteria incorporating genetic elements found within their envi-ronment that have been released from other bacterial cells that have been destroyed.22

New mutations in bacteria lead to resistance in a variety of ways. For example, mutations can alter a tar-get protein or proteins to which the antimicrobial binds through changes in the protein binding site. Mutations also can result in adding genes that encode for enzymes that disable the antimicrobial by altering the outer cell membrane (protein channel) that the antimicrobial uses to enter the cell, thereby disrupting drug entry. Finally, mutations can up-regulate mechanisms that expel the antimicrobial from the bacterial cell.22,31

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in U.S. intensive care units (ICUs) are identified as methicillin-resistant, according to the CDC.45,46 The mortality rate associated with MRSA infections in U.S. hospitals is estimated at 20%.47

Mechanism of ResistanceResistance to methicillin in S aureus occurs from the

acquisition of the mecA gene that codes for a modified penicillin-binding protein (PBP2a), which confers resis-tance to methicillin and other semisynthetic penicillin-ase-resistant -lactams.34,41,48 To be defined as methicillin-resistant, S aureus must possess this gene sequence. The mecA gene is absent in susceptible strains and present in resistant strains.49,50 The mecA gene is part of a larger Staphylococcus cassette chromosome (SCC)mec gene configuration, of which there are several variations, and it is this gene (mecA) that determines whether MRSA is hospital-acquired/health care–associated (HA-MRSA) or community-acquired/community-associated (CA-MRSA) in origin.51-53 CA-MRSA is caused by new strains of MRSA found in community settings such as locker rooms, soldiers’ barracks, prisons, and child-care and long-term care facilities.54

The SCC element is a genomic island that captures foreign DNA segments that are ubiquitous within staphylococci.55 All methicillin-resistant S aureus possess the determinant for methicillin-resistance, mecA, making the SCC element SCCmec. Sequencing of numerous SCCmec elements has revealed that ele-ments possess structural differences, which are used in epidemiological studies to discern MRSA strains.55 HA-MRSA bacteria possess types I, II, and III of the SCCmec gene, while CA-MRSA bacteria possess type IV or V of the SCCmec gene.56,57 Types I, II, and III are large genes with additional elements on the gene that impart resistance to other antibiotic classes, such as macrolides, lincosamides, aminoglycosides, f luoro-quinolones, tetracyclines, and sulfonamides.58 Types IV and V, on the other hand, are smaller genes with fewer additional resistance features. This distinction between SCCmec types might explain the susceptibility of CA-MRSA to some antibiotics to which HA-MRSA is unresponsive.59 HA-MRSA genetic elements, because of their large size, cannot be incorporated into a bacterio-phage intermediary; therefore, transfer of genetic material

Mechanism of Antimicrobial Resistance in Staphylococcus aureus

The genome of S aureus was first sequenced in 2001.34 Since then, there have been at least 18 annotated whole-genome sequences and many more partially sequenced strains of S aureus, with more expected to be deposited in GenBank,35 a database of publicly available DNA sequences.36 The S aureus genome can essentially be broken down into 3 components: a highly ( 97%) conserved set of core genes; a group of more than 700 core variable (CV) genes spread throughout the conserved core genes that are variably distributed and whose distribution pattern defines S aureus lineages; and the mobile genetic elements (MGEs), which show frequent genetic transfer and, on occasion, recombina-tion.35,37,38 Traits that confer antimicrobial resistance in staphylococci are most commonly located on MGEs on the genome.38,40-42 MGEs are large pieces of discrete DNA that encode mobilization functions and can medi-ate their own transfer to new host (bacterial) cells as well as mediate their own replication autonomously or via integration with host DNA.18,39 MGEs constitute more than 20% of the S aureus genome and encode many recognized virulence factors and antimicrobial resistance elements.18 Horizontal gene transfer of MGEs in S aureus results in strains with increasing pathogen-esis, a higher level of antibiotic resistance, and a wider range of hosts.18 Selective pressure from the environ-ment pushes for attainment and propagation of specific genes that promote fitness and survival in organisms, therefore making MGEs especially valuable in terms of their ability to enhance survival of the bacterium. MGEs thus provide an element of plasticity to the bac-terium, allowing adjustment to new niches and chang-ing environmental factors.18

Microbiology of MRSAEtiology

The first case of antibiotic (methicillin) resistance in S aureus was identified in 1961 in the United Kingdom shortly after methicillin was introduced into clinical treatment.43 Seven years later, in 1968, after its emer-gence in Japan, Europe, and Australia, the United States had its first case of MRSA at Boston City Hospital in Massachusetts.44 Three-quarters of S aureus infections

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cannot occur via transduction.58 It has been suggested that these larger genetic elements might impair the growth and fitness of HA-MRSA, and it is only the selective pressure of antibiotics that makes HA-MRSA viable and sustaining.58 In contrast, CA-MRSA SCCmec types IV and V are small enough to be transferred effi-ciently by bacteriophage or transposon into methicillin-susceptible Staphylococcus aureus (MSSA) strains, leading to bacteria that were once only susceptible to -lactams but are now resistant to -lactams.58

Empirical evidence confirms the transfer of resistance from another bacterial genera to S aureus. In 2002, a strain of MRSA resistant to vancomycin was cultured from a dialysis patient’s foot ulcer.60 This strain was examined, and it was later determined that resistance to vancomycin was conferred upon this S aureus strain through transfer of genetic resistance material on the plasmid of another bacteria, namely Enterococcus faecalis.60

Evolution of ResistanceAntibiotic resistance in S aureus began in the mid-

1940s, with increasing numbers of infections caused by penicillin-resistant S aureus in hospitals.61,62 Penicillin-resistant S aureus strains produced a plasmid encoding penicillinase, an enzyme that hydrolyzes the -lactam ring of penicillin, rendering the antibiotic ineffective.61,62 Penicillin-resistant strains, mainly S aureus clone phage-type 80/81,63-65 then became prevalent in the community, leading to widespread infection by the early 1950s and 1960s.61,62 The emergence of penicillin-resistant S aureus led to the development of methicillin for treatment.26

Staphylococcus aureus phage-type 80/81 infections became inconsequential with the introduction of methicillin.66

Shortly after the introduction of methicillin, S aureus isolates were documented as resistant to this antibiotic as well.43 The mechanism of resistance to methicillin is different from that of penicillin resistance in that penicillin resistance is narrow in its spectrum, only act-ing on penicillin itself, whereas methicillin resistance is more broadly based and includes resistance to the entire -lactam class of antibiotics.61 These strains circulated through hospitals in Europe throughout the 1970s,67 but by the 1980s they disappeared for unknown rea-sons.61 Emerging strains appeared in U.S. hospitals

in the late 1970s and were endemic worldwide by the mid-1980s.68,69 They still are present today.61 Although endemic, MRSA was confined to hospitals and health care facilities. As a last resort, vancomycin was intro-duced as the final line of defense against MRSA.70 The widespread use of vancomycin to treat burdensome MRSA infections in hospitals and health care facilities provided selective pressure for vancomycin-intermediate (VISA) and vancomycin-resistant (VRSA) strains.

The first VISA MRSA strain was documented in 1996 in an infant aged 4 months,71 and in 2002 the first VRSA MRSA strain was documented.60,72 Both have since been documented worldwide.73 Fortunately, the number of occurrences still is comparatively low. From 2002 to 2006 only 7 cases of VRSA were reported in the United States74 and, as of October 2010, all VISA and VRSA isolates have been susceptible to other anti-microbials recommended by the U.S. Food and Drug Administration (FDA).75

HA-MRSA vs CA-MRSAMRSA is divided into 2 subcategories, depending on

where the infection was acquired. If the infection was obtained in a hospital or health care facility while a per-son was a patient, this form of MRSA is termed hospital-acquired/health care–associated MRSA (HA-MRSA). If the infection was obtained outside of a hospital or health care facility, this type of MRSA is labeled community-acquired/community-associated MRSA (CA-MRSA). Since its discovery in 1961 and into the mid-1990s, MRSA was almost exclusively found in health care settings (HA-MRSA).76,77 By the mid-1990s, however, MRSA infections began appearing in individuals who had no previous health care–related associations or risk factors.76,77 Around this same time, reports of CA-MRSA also began emerging in other countries, such as Canada, Australia, and New Zealand, primarily in the form of necrotizing pneumonia and skin and soft-tissue infec-tions among native peoples, athletes, and prisoners.57,76,78,79

CA-MRSA isolates differ in many ways from HA-MRSA isolates. One difference is that while CA-MRSA isolates are resistant to the actions of -lactams and erythromycin, they are susceptible to many non--lactam antibiotics. HA-MRSA iso-lates, on the other hand, are typically multidrug

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care facilities, making it increasingly difficult to discern strain origins.88,89 Outbreaks of CA-MRSA occur world-wide with similar epidemiology, and clones continually emerge that vary with geography. However, CA-MRSA genotypes still are affected by antibiotics that are inef-fective on HA-MRSA strains.14,61

MRSA has even become an emerging problem in animals, affecting livestock, horses, and household pets.90 Transmission of MRSA between humans and animals is a concern, and evidence indicates that children in households with cats, dogs, or both have become infected with CA-MRSA. However, whether the infection was transmitted from human to animal or vice versa is unclear.90,91

Necrotizing Fasciitis MRSA is one of the bacteria considered to be “f lesh-

eating,” although the bacteria do not actually eat the f lesh of infected individuals. So-called f lesh-eating bacteria produce and emit toxins that destroy (or necro-tize) the tissue they infect. Medically, this condition is known as necrotizing fasciitis (NF), a “severe bacterial infection of the fascia, the tissues that line and separate muscles, that causes extensive tissue death.”92 NF is a rare but serious bacterial infection that can be caused by several bacteria, including group A Streptococcus, Klebsiella, Clostridium, E coli, S aureus, and Aeromonas hydrohila.93 While MRSA infection can lead to NF, MRSA is not the most common causative agent of this type of infection. NF is most commonly caused by group A Streptococcus.93 However, more cases are being reported in which MRSA is the causative agent. For example, during a 5-year period from 2001 to 2006 at a large urban hospital, there were 74 reported and investi-gated cases of NF, of which 39% were caused by MRSA that resulted in a 15% mortality rate.94

Most cases of NF result from bacteria entering the body through a break in the skin, and NF often is asso-ciated with other health problems that tend to weaken the body’s immune system.93 Most healthy people have a very low probability of contracting NF.93 Once a person is infected, NF spreads rapidly, often within hours of contact with the infectious agent, infecting the fascia (layers of connective tissue surrounding muscles, nerves, fat, and blood vessels).93

resistant, particularly to the action of all -lactams as well as many non--lactams, including erythromycin, clindamycin, and tetracycline.14 MRSA strains that show partial or full resistance to vanomycin have been reported since 1996.14 CA-MRSA isolates also are dif-ferent in that they contain the SCCmec type IV or V genetic elements and numerous toxins, such as the exotoxin Panton-Valentine leukocidin (PVL), which causes leukocyte destruction and tissue necrosis, while HA-MRSA carries SCCmec type I-III genetic elements and does not typically produce toxins.80,81 In addition, CA-MRSA exhibits a different pulsed-field gel electro-phoresis pattern than HA-MRSA isolates.56 Growth rates also differ between HA-MRSA and CA-MRSA, with CA-MRSA exhibiting much more rapid growth than HA-MRSA. This difference might confer a selec-tive advantage to CA-MRSA, allowing it to spread globally.58 Evidence from molecular typing indicates CA-MRSA strains evolved spontaneously, rather than transferring from hospitals to communities.81 Some of the earliest cases of CA-MRSA occurred in the 1990s in aboriginal populations in western Australia.82-84 The first well-documented CA-MRSA cases in the United States occurred from 1997 to 1999 in healthy children with no known health issues who died from their infec-tions.85 Despite the susceptibility of these particular CA-MRSA strains to antibiotics, they were resistant to -lactams, which these patients were initially treated with. The delay in treatment with antibiotics that their infections were susceptible to might have contributed to the children’s deaths.85 Even though these children lost their lives to their infections, CA-MRSA strains were susceptible to most antibiotics.85

When CA-MRSA emerged within communities, the genotypes were unrelated to those of HA-MRSA.85 For example, in the United States, the predominant CA-MRSA causative strains were USA 300 and USA 400, with USA 400 most prevalent until 2001,85 when USA 300 became dominant.86 Data from a multistate study indicated that 59% of purulent skin and soft-tissue infections were caused by MRSA, and 97% of these infections were due to CA-MRSA strain USA 300.87

The epidemiology of MRSA has become quite com-plex because of the intermingling of HA-MRSA and CA-MRSA infections in the community and health

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Symptoms of NF can be confusing and often lead infected patients to delay seeking medical treatment. Often, the infected person complains of pain or sore-ness similar to a pulled muscle. The skin might be red, swollen, and warm to the touch. Pain at the infection site might be severe and out of proportion to the appear-ance of the infected area. A black spot often appears on the skin, with ulcers or blisters at or near the infection site.93 Treatment involves immediate antibiotic therapy as well as surgical removal of dead tissues because anti-biotics might not effectively reach all infected tissue.93 Techniques for preventing NF include covering open wounds with clean, dry bandages until healed; prompt-ly seeking first aid for even minor, noninfected wounds, including minor breaks in the skin; avoiding hot tubs, swimming pools, and whirlpools if you have an open wound (even if it is contained); and washing hands often with soap and water or an alcohol-based cleaner when soap and water are unavailable.93

Clinical IdentificationDetecting MRSA is complicated by several factors

that necessitate rapid, accurate, and sensitive testing methods in routine diagnostic laboratories.95 One of these factors is that methicillin/oxacillin resistance is heterogeneous in most strains of S aureus, meaning that susceptible cells and highly resistant cells reside within a MRSA isolate.96

Clinicians use several conventional laboratory tests to determine whether an S aureus infection is in fact MRSA. Microbiological tests include the cefoxitin disk screen test, the latex agglutination test for PBP2a, and a Mueller-Hinton agar plate supplemented with oxacillin.14 When used correctly, broth- and agar-based screening methods usually can detect MRSA, with the cefoxitin disk test available for additional verification.14 Oxacillin rather than methicillin is used as a screen-ing agent for several reasons. First, methicillin is no longer commercially available as a treatment agent in the United States.14 Second, the integrity of oxacillin’s antimicrobial action when maintained under storage is greater than that of methicillin.14 Third, oxacillin is a better detecting agent for heteroresistant strains.14

In recent years, molecular-based screening methods have become the gold standard for MRSA detection.

Molecular nucleic acid amplification testing methods involve isolation of the mecA gene through polymerase chain reaction (PCR). As discussed previously, the mecA gene confers oxacillin/methicillin resistance in S aureus.14

In 2011 the FDA approved the use of a rapid-detection method for MRSA and methicillin-sensitive S aureus (MSSA).97 The KeyPath MRSA/MSSA Blood Culture Test (MicroPhage Inc) is a phenotypic test of cefoxi-tin susceptibility and resistance98 and can distinguish between MRSA and MSSA in a blood sample within 5 hours after bacterial growth is first detected in the sample with 98.9% and 99.4% accuracy, respectively.97 A 2013 study compared performance of the KeyPath MRSA/MSSA BC test to conventional identifica-tion and susceptibility methods and found that the KeyPath MRSA/MSSA BC test produced diagnostic results a median of 30 hours faster than conventional methods.99

In June 2013 the FDA approved another rapid blood culture testing method, the Xpert MRSA/SA Blood Culture (BC) test (Cepheid) for use in the rapid detection and identification of MRSA and MSSA.100 Cepheid’s Xpert MRSA/SA BC test is a molecular-based test that allows for identification of MRSA or MSSA in a blood culture determined to be gram-posi-tive cocci clusters or singles within 1 hour of culturing. This approval comes 3 years after a class I recall was issued by the FDA to Cepheid regarding false negatives generated by the Xpert MRSA/SA BC test.101

Clinical Signs and SymptomsBecause MRSA is a form of staph infection, the signs

and symptoms of MRSA are similar to those for other types of staph infection. MRSA infections can start as small red bumps that resemble pimples, boils or spider bites.102-104 The infected area might be red, swollen, pus-filled, warm to the touch, extremely painful (more painful than would be expected for the minimal appearance of the sore) or a combination of these (see Figure 3).102 MRSA skin infections can occur anywhere on the body but are commonly found on the back of the neck, the legs, groin, or buttocks.104 As the infection continues, fever might develop and the infection might spread from the origi-nal site. If not addressed soon after symptoms develop,

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early stages, MRSA infections can become severe and complications such as sepsis, necrotizing fasciitis, and death can ensue.105

Risk FactorsBecause HA-MRSA and CA-MRSA infections

occur in different settings, the risk factors associated with each are different.106 However, a person does not need to be infected to transmit either type; people who are colonized and thus are carriers also can transmit the infection.106

HA-MRSAThe risk of developing HA-MRSA is a concern in

most hospitals because of the vulnerability of hospital-ized patients. HA-MRSA risk increases in the elderly and people with weakened immune systems.106 Risk of infection also increases if a patient has a medical device inserted into his or her body, such as a catheter or intra-venous line.106 HA-MRSA also is prevalent in long-term care facilities such as nursing homes because of the close person-to-person contact between patients and the declining health status of most patients, who might have impaired immune systems.106

CA-MRSAAccording to epidemiological data, groups at highest

risk of contracting CA-MRSA in the United States are those in areas with high concentrations of people where risk of cross-infection is high, such as schoolchildren, poor and homeless young adults, military personnel, athletes, and day-care center personnel and clients.39,81 Athletes are at risk of infection from close contact with others while participating in sports as well as contact in locker rooms and shower facilities.106

TransmissionHospital Settings

MRSA is transmitted to patients via human hands, mainly those of health care personnel, according to the CDC.107 If appropriate hand hygiene is not practiced, either through the use of soap and water or an alcohol-based hand cleaner, MRSA bacteria can spread from health care personnel to patients, resulting in serious infection.107 Transmission also can occur when invasive

the infection can turn into deep, painful abscesses that require surgical draining or even subcutaneous tissue removal at the infected area.103 If MRSA infects the lungs, it can cause pneumonia and the infected person might experience shortness of breath, fever, and cough.102 Other possible signs and symptoms include chills, head-ache, joint pain, low blood pressure, and a rash that cov-ers most of the body.105 Because MRSA also can be an invasive infection and can occur in any organ of the body or the bloodstream, these signs and symptoms require immediate medical attention. If not addressed in the

Figure 3. A. Cutaneous abscess caused by MRSA on the knee. B. Cutaneous abscess caused by MRSA on the hip that began to drain spontaneously. Public domain images courtesy of the Centers for Disease Control and Prevention.

A

B

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medical devices are used that have been in contact with MRSA, either through direct contact with an infected or colonized person or from contact with a contami-nated surface or person who has not appropriately sani-tized his or her hands.107

Skin InfectionsMRSA skin infections can be transmitted from per-

son to person if there is close skin-to-skin contact where there are openings in the skin tissue such as abrasions, cuts, lesions, or boils. MRSA also can contaminate sur-faces outside the body when someone with an infection touches that surface with contaminated hands or other body parts where the bacteria reside.108 Once MRSA enters the body, it can spread to the blood, joints, bones, or any other organ.109

BiofilmA biofilm is a community of microbial cells that can

include MRSA. The cells adhere to each other and to a surface material that is embedded into an extracel-lular polymeric substance (EPS) matrix that protects the MRSA from antibiotics and host immune defenses (see Figure 4).110 Dr Timothy Lu, a leading biofilm researcher, likened a biofilm to “fruit Jell-O,” in which

pieces of fruit represent microbial cells and the gelatin is like the protective EPS-type matrix.111 Biofilms form on both biotic (living) and abiotic (nonliving) surfaces, such as catheters and implanted medical devices, and can persist and form infection that is difficult to eradi-cate.111 Biofilms might prolong the duration of MRSA infections and promote colonization.110

EpidemiologySurveillance

Since 1995, the CDC Emerging Infections Program (EIP) has used active bacterial core surveillance (ABCs) to track invasive bacterial pathogens significant to public health.112 This surveillance system uses both laboratory and population-based data to track invasive bacterial pathogens in the populace.112 Each incidence of bacterial infection within the 10 current EIP sites, patient demographic information, and cultures of the infectious agent are provided to the CDC and indepen-dent reference laboratories for analysis.112 Surveillance sites include California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee, with a representation of 41 million people.112 Currently, the CDC tracks 6 patho-gens using group A and group B Streptococcus (GAS, GBS), Haemophilus influenzae, Neisseria meningitis, Streptococcus pneumoniae, and MRSA.112

Among its many accomplishments, ABCs has contributed to the development and implementation of a program designed to assist state and local health departments in tracking MRSA occurrence.112 ABCs has shown that the proportion of health care–associated Staphylococcal infections due to MRSA has increased since the 1970s, with 2% in 1974, 36% in 1992, and 64% in 2003 (3% increase annually).113 However, more recent estimates have revealed a downward trend in MRSA infections since the 2000s: Central line–associated MRSA bloodstream

infections decreased 50% to 70% between 2001 and 2007.114

All MRSA-related bloodstream infections decreased 34% between 2005 and 2008.10

Invasive MRSA infections acquired in hospitals declined 54% from 2005 through 2011.10,115

Data from 2011 show a decrease of 25.92% in MRSA infections overall, including both

Figure 4. This electron micrograph (magnified 2363) depicts a biofilm of Staphylococcus aureus cells found on the luminal surface of an indwelling catheter. The sticky substance woven between the bacterial cells protects the bacteria against attacks from the patient’s immune system and from antibiotics. Public domain image courtesy of the Centers for Disease Control and Prevention.

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those hospitalized with AIDS and influenza combined in each of the last 3 years of the survey (ie, 2006, 2007, and 2008).17

A study published in 2011 analyzing changes in the epidemiology of HA-MRSA bloodstream infections (MRSA-BSI) at a tertiary 900-bed university hospi-tal from 1990 through 2008 noted that 524 patients developed HA-MRSA-BSI.119 Investigators divided this 19-year study into 4 consecutive periods: 1990-1994, 1995-1999, 2000-2004, and 2005-2008. While no signifi-cant trend in infection rate was observed over the 19-year period, investigators did identify significant upward trends in patient age and comorbidities, health care–associated acquisition of MRSA, and nonintravascular catheter sources between the 4 periods.119 The first and second periods were dominated by one type of MRSA clone (ST247/SSCmecI), while the third and fourth periods were dominated by a clonal complex (ST125/SCCmecIV and ST228/SCCmecI).119 No significant dif-ferences were found in regard to mortality rates across the 4 periods, with mortality reaching about 29% for all patients after 30 days of infection throughout the 19-year period.119

Global OccurrenceThe global status of HA-MRSA differs widely

among regions and even between countries within a region, according to epidemiological data from various health agencies and medical laboratories.110 In East Asia, Southeast Asia, North America, and South America, the situation is rather severe, and within these regions, the situation differs from country to country.110 In East Asia, for example, prevalence rates in Japan and Korea are more than 50%, whereas rates are 25% to 50% in other East Asian countries.110 In Southeast Asia, Indonesia and Singapore have the lowest prevalence rates at 25% to 50%, while rates in other Southeast Asian countries are greater than 50%.110 In Western Europe, most countries report prevalence rates of 10% to 25%, although Spain, Great Britain, Italy, and Portugal’s rates are 25% to 50%.110 In North America, the majority of the United States has rates greater than 50%, except for Alaska, where rates are 25% to 50%. In Canada the rate is 5% to 10%, and in Mexico it is 10% to 25%.110 Most South American countries also exhibit

community- and health care–associated types, from a baseline established in 2007 to 2008.116

MRSA infections also are monitored at participating hospitals through the National Nosocomial Infections Surveillance System and the National Healthcare Safety Network (NHSN). The CDC’s NHSN is the most widely used HAI tracking system in the United States and provides data to national, state, and local organizations, including health care facilities, to help measure progress in prevention efforts and identify problem areas in HAI prevention.117 The NHSN also aids health care facilities in tracking blood safety errors and health care personnel infection control adherence rates. Currently, more than 11 000 medical facilities use NHSN.117

In addition to federal tracking of MRSA cases, many state health departments also track the occur-rence of MRSA in health care facilities. However, tracking and reporting vary among states. For exam-ple, the Texas Department of State Health Services reported that 55% of S aureus infections occurring in Texas in 2012 were sensitive to oxacillin/methicillin, (45% of MRSA cases were not susceptible to oxacillin/methicillin)108 while the Mississippi State Department of Health simply reported that it has not found a significant increase or an unusual number of MRSA cases in the state.118

A study published in 2012 by researchers at the University of Chicago Medicine (UCM) and the University Healthcare Consortium (UHC) esti-mated that rates of MRSA in U.S. academic medical centers doubled between 2003 and 2008.17 This con-tradicts CDC findings that show MRSA infections in hospitals are declining.17 This might be because the CDC looked only at invasive infections (those found in the blood, spinal f luid, or deep tissue) and excluded skin infections, which the UCM-UHC study included.17 The UCM-UHC results estimated that hospitalizations for MRSA increased from 21 out of every 1000 patients in 2003 to 42 out of every 1000 patients in 2008.17 Researchers attributed this overall increase to CA-MRSA infections, while also not-ing that HA-MRSA cases generally are declining.17 Interestingly, the UCM-UHC researchers reported that the number of MRSA-infected patients far exceeded

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rates greater than 50%, with the exception of Paraguay, Panama, and Columbia, where rates are 25% to 50%.110 Australia and Africa (North and South Africa only; Middle Africa epidemiological data is absent) have prevalence rates of 25% to 50%; the Middle East is at 10% to 25%; and Northern Europe has the lowest rate at less than 5%.110 The lower rate in Northern Europe might be the result of strict surveillance measures, anti-biotic control, and eradication measures.110

MRSA in the EnvironmentStaphylococcus aureus has been reported in marine

environments since the early 1990s.120 It is well known that S aureus is not susceptible to the action of salts, owing to its ability to survive in natural fresh and salt-water environments. While MRSA has been identified in environmental waters, the reported incidence is low. An analysis of MRSA in seawater and sand samples during summer months at 3 Southern California beaches showed a low incidence of MRSA in both seawater (1.6%) and sand (2.7%) samples.120 Another study showed that of 350 seawater samples collected at a recreational subtropical beach, 22 MRSA isolates were identified, 17 of which were clonally related to CA-MRSA strain USA 300.121 A study examining the survivability of HA-MRSA and CA-MRSA isolates in pool, seawater, and river water showed that all HA-MRSA and CA-MRSA survived in the seawater and river water inoculations but were unculturable after 24 hours in the pool water, indicating that both seawater and river water can be reservoirs for both HA-MRSA and CA-MRSA if they become contaminat-ed.122 The CDC reported that there are no known cases of people being infected with MRSA from recreational waters at facilities; however, they caution that MRSA can be spread at recreational water facilities through direct and indirect contact with people, infected objects, or surfaces.123

TreatmentAntimicrobials

While vancomycin still is used to treat MRSA infections, many other FDA-approved drug alterna-tives to vancomycin are used. These include antimi-crobials such as linezolid, daptomycin, tigecycline,

quinupristin/dalfopristin,124 ceftaroline,125 and tela-vancin.126 Investigational compounds not yet approved by the FDA that exhibit in vitro action against MRSA include ceftobiprole, dalbavancin (currently in phase III clinical trial),127 oritavancin (also in phase III clinical trial),128 and iclaprim.124,129

With antibiotic-resistant organisms on the rise, medical researchers and drug companies are racing to develop the next antibiotic to treat serious infec-tions. Researchers at the University of Illinois and the University of California San Diego are investigating the use of undecaprenyl diphosphate synthase (UPPS) inhibitors as a new form of antibacterial drug.130 UPPS is an enzyme essential in early-stage cell wall synthesis. Because humans do not make UPPS (human cells do not contain cell walls), it is a potential target for new drug development.131

In 2011, the Infectious Diseases Society of America provided new recommendations on treatment options and antibiotic dosing requirements to treat various types of MRSA.80 The management of clinical syn-dromes presented by MRSA infection is discussed, as are recommendations to physicians and other health care providers regarding usage and dosing with vanco-mycin, as well as the use of alternate therapies for treat-ing MRSA infections caused by vancomycin-resistant strains and strains treated with vancomycin that have failed to respond favorably.80

BacteriophagesWhile antibiotics are the historical treatment for

bacterial infections, they are not the only treatment option. Many novel treatment approaches have been suggested to overcome antibiotic resistance. The devel-opment, mass-production, and wide availability of anti-biotics are crowning achievements of the 20th century; however, over the past 30 years, we have seen a serious decline in the number of newly approved antibiotics in the United States.132,133

We now recognize many inherent problems in the use of antibiotics beyond the development of antibiotic-resistant microbes. For example, broad-spectrum antibi-otics can have a deleterious effect on the human body’s natural communities of beneficial bacteria,134 which are essential to health135 and immunity.136 Economic factors

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pathogen must be identified for effective phage use) and possible development of bacterial resistance against phag-es.138 Attendees at the conference cited regulatory hurdles and development costs as high for the medical applica-tion of phages.138 While Western countries are hesitant to approve phage therapy, other countries have been using phage therapy as a treatment option for decades.

Phages are similar to antibiotics in that both have remarkable antimicrobial activity via lysis (cell break-down), but phages possess several therapeutic advan-tages over antibiotics.140 For example, treatment with phages results in fewer, if any, adverse effects compared with antibiotics.140 Also, because of phage specificity, only the target bacteria are affected, thus eliminating or reducing the risk of secondary infection.141 Phages rep-licate at the site of infection, making them more avail-able as treatment progresses.142 Phage-resistant bacteria remain susceptible to other phages with the same host target range, and selection of new phages is fast, often taking days or weeks.140 Finally, phages have been more successful than antibiotics in treating certain infections in humans.143

A 2003 review of 30 years’ worth of studies (1966-1996) using phage therapy in treatment revealed success rates of 80% to 95% with few adverse effects, as well as several studies showing significant effectiveness of phages against many multidrug-resistant bacteria, including S aureus.144

Topical HoneyHoney, specifically honey produced by Apis mellifera

(the Western or European honeybee145), has been used to treat infection for centuries.146 Modern research-ers have reported that natural, nonheated honey has broad-spectrum antibacterial action against pathogenic bacteria.147 The antibacterial activity in most types of honey is the result of the enzymatic production of hydrogen peroxide. However, a honey that has been found to be very effective in the treatment of MRSA infections, manuka honey, is considered a nonperoxide honey, meaning it maintains its antibacterial activity even in the absence of hydrogen peroxide.148 Manuka honey is derived from honeybees consuming nectar from the New Zealand f lowering plant Leptospermum scoparium.149

also make developing new antibiotics unprofitable, time-consuming, and therefore undesirable in a free market. These problems with antibiotics have led to a need for alternative treatments.

One such alternative treatment that has been in use for more than 90 years globally is phage therapy.137 Phage therapy is the use of viruses as a biological con-trol agent against pathogenic or invasive bacteria.138 Phages are viruses that only attack bacteria and specifi-cally attack only the types of bacteria they are capable of infecting, which is called their host range.139

Phages were discovered by Felix Twort in 1915 and then, independently, by Felix d’Hérelle in 1917.139 D’Hérelle is credited with the discovery because he pur-sued investigation into the nature of bacteriophages and their use as anti-infective agents.139 D’Hérelle first used phage therapy in 1919 to cure a young boy of dysentery; however, phage therapy was not used by other practi-tioners until the late 1920s or early 1930s.132,139 Even then, its use was short-lived once antibiotics came onto the scene.132 Most likely, the decline in phage therapy was the result of misuse of phages by practitioners who had a poor understanding of phage biology and lacked expertise in administering them.132

Bacteriophage therapy is proving to be an important alternative to antimicrobial treatment in the face of invasive, multidrug-resistant pathogenic bacteria such as MRSA. However, in the Western world, we are still far from using phages as viable treatment mechanisms. An opinion article, based on a scientific meeting on viruses of microbes in Europe and appearing in a spe-cial issue of the journal Virology, addressed the current status of and hurdles to phage therapy in the West, as well as the need for a coordinated effort within the public health sector to evaluate the use of phage therapy as an adjunct to antibiotics.138 According to this article, the FDA supports use of phage therapy, has stated its interest in phage therapy as a treatment option, and favors developing regulatory guidance for using phages. However, this is not a new development.138 The FDA cited specific advantages to using phages for treatment, noting phages’ specificity, ability for high-purification, nontoxicity, and effectiveness where other treatments have failed.138 The FDA also cited negative aspects to using phages, including phages’ specificity (the bacterial

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A 2012 study to identify the antimicrobial activity of manuka honey showed that treatment with this type of honey resulted in a significant decrease in the bacterial growth rate and the down-regulation and up regulation of several proteins.149 These results indicate a novel mode of action and the potential of manuka honey as an antimicrobial treatment option.149 Another study reported that fewer proteins were identified in MRSA cells treated in the lab with manuka honey for 4 hours than cells left untreated and that one of the missing proteins, FabL, a protein necessary for fatty acid bio-synthesis, might explain the mode of action of manuka honey against MRSA.150

Microbial resistance to honey has never been reported, making it extremely promising as a treat-ment in the new era of antimicrobial resistance.151 Presently, the use of honey as an antimicrobial treat-ment is limited in the United States to an FDA-approved topical wound and burn treatment (MediHoney, Derma Sciences) for management of light-to-moderately exuding wounds and treatment of first- and second-degree burns.152 Most honey treat-ment in the United States is used only in an alternative medicine branch called apitherapy.146

MRSA PreventionThe CDC provides recommendations to health

care providers to help prevent MRSA infections (see Box 1).153 Epidemiologists and researchers agree that HAIs, including MRSA, can be prevented through proper hand-washing practices, medical equipment sterilization, and eliminating the use of unnecessary catheter lines in patients.154

Breaking the Chain of Infection The chain of infection is the mode of transmis-

sion of infectious disease from one person or object to another. In this chain, there are many links that must be intact and in sequential order for infection to be transmitted.155 While many factors make the chain of infection difficult to break, it is not impossible. Health care professionals, including radiologic technologists, can prevent tens of thousands of infections annually by breaking a single link.156 Radiologic technologists and other health care workers must be diligent in following

standard precautions and hand hygiene, and these must be used for every patient in the health care facil-ity. Standard precautions also include proper cleaning and disinfection of hospital equipment before use on every patient. In the radiology suite, pieces of equip-ment used daily and on multiple patients are of par-ticular importance for proper disinfection, as each can be a source of infection transmission.156 These include examination tables, x-ray tubes, the upright Bucky, and exposure switch.156

Hand WashingAlthough it might seem like common sense that

hand washing is the most effective tool in the medical toolbox to prevent infection, too many health care pro-fessionals still do not adhere to proper hand-washing guidelines (see Figure 5).154 For decades, hand hygiene

Box 1

Top CDC Recommendations for Preventing MRSA Infections107,153

Strictly adhere to CDC hand hygiene guidelines. Practice contact precautions:

If possible, patients with MRSA should be placed in their own room or share a room with someone else who has MRSA.

All health care personnel and visitors in contact with a known MRSA-infected patient shall wear gloves and a gown, which are removed upon exiting the room.

All persons who have been in contact with MRSA-infected patients should thoroughly clean their hands.

A patient on contact precautions should be asked to remain in his or her room as much as possible to prevent spreading the infection.

Recognize patients previously infected or colonized with MRSA.

Report MRSA testing results immediately. Educate health care providers on MRSA infections.

Also consider: Facility participation in active surveillance testing. Patient decolonization. Chlorohexidine bathing of MRSA-infected patients.

Abbreviations: CDC, Centers for Disease Control and Prevention; MRSA, methicillin-resistant Staphylococcus aureus.

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The link between hand washing and infection con-trol was made by a Hungarian physician more than 165 years ago.168,169 The physician, Ignaz Semmelweis, noticed that mortality rates between 2 clinics within a maternity hospital were significantly different.154,169 In the clinic that had the higher mortality rate, he noticed that personnel went from autopsy rooms to the delivery suite without washing their hands.154,169 He theorized the physicians and medical students were carrying germs from the cadavers to mothers and their newborn infants.154,169 The physicians began washing their hands with a chlorinated lime solution, and the mortality rate plummeted.154,169 The CDC and the World Health Organization provide resources for health care professionals on the proper hand-washing technique (see Box 2).

Alcohol-Based Hand SanitizersWhen soap and water are not available, as in some

emergency situations, the CDC recommends using an alcohol-based hand sanitizer containing at least 60% alcohol.171 It also advises that not all germs are killed with hand sanitizers, and when hands are visibly dirty these rubs are not as effective.171 The FDA reported some hand sanitizer and antiseptic product manufac-turers are falsely claiming that their products prevent MRSA infections. These claims are unproven, as the FDA has not approved any over-the-counter products for preventing MRSA.172

has been known to reduce HAIs,157-161 yet report after report illustrates the failure of health care professionals to practice consistent hand-washing behavior,162-164 despite efforts to improve hand hygiene.165 Our hands are populated with millions of bacteria (see Figure 6). The Minnesota Department of Health reported that on 1 cm2 of skin, there are roughly 1500 bacterial cells.166 A study published in 2011 examining the effect of hand washing on the presence of bacteria of fecal origin on hands revealed that 23% of samples contained bacteria when only water was used during hand washing vs 8% of samples when soap and water were used.114

A report in the Annals of Internal Medicine found that adherence to hand hygiene practices among health care professionals, including physicians, averaged 57% but varied widely across medical specialties.167 Another study, published in 2012, analyzed hand hygiene com-pliance during a hand hygiene awareness campaign over a 3-year period at a teaching hospital in rural New Hampshire and found that hand hygiene compliance increased significantly, from 41% to 87%, during the campaign period.165 This was coupled with a signifi-cant and sustained decline in the HAI rate, from 4.8 to 3.3 per 1000 patient days, further substantiating that improving hand hygiene compliance contributes to infection reduction.165

Figure 5. The CDC recommends that people spend at least 20 seconds scrubbing their hands together while washing their hands. To count the time, you can hum the tune “Happy Birthday” all the way through twice. Public domain image courtesy of the Centers for Disease Control and Prevention.

Figure 6. Hand hygiene awareness poster for use in hospital settings. Image courtesy of the Centers for Disease Control and Prevention.

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Targeted vs Universal DecolonizationResults published in the New England Journal of

Medicine in 2013 from the REDUCE MRSA trial, funded by the Department of Health and Human Services, evaluated the effectiveness of 3 MRSA preven-tion practices in ICUs: routine care, use of germ-killing soap and ointment on patients infected with MRSA (targeted decolonization), and use of germ-killing soap and ointment on all ICU patients (universal decoloniza-tion).46 Patients receiving universal decolonization were bathed daily for the duration of their stay in the ICU with chlorhexidine soap and had mupirocin ointment applied to the insides of their nasal passages for 5 days.46 The study found that universal decolonization reduced the rate of bloodstream infections by up to 44% and sig-nificantly reduced the presence of MRSA in ICUs.46

Hydrogen Peroxide VaporDecontamination of the hospital environment is

as essential as health care personnel decontaminating themselves before and after coming into contact with patients, particularly patients colonized or infected with MRSA. Several pathogens linked to HAI can survive for extended periods of time on surfaces173 and might not be eradicated effectively with conventional cleaning

methods.174 Hydrogen peroxide vapor can be used proactively, to prevent infection, or reactively, to stop outbreaks in the hospital setting. It can be scaled for use in single rooms or used hospital-wide.175 Hydrogen peroxide vapor currently is used in hospitals worldwide to reduce the transmission of multidrug resistant organ-ism infections.175 In addition to use in hospital rooms, it also can be used to decontaminate mobile equipment, fixed equipment in high-risk areas, and for prevention in low-risk areas.175 When hydrogen peroxide vapor was first introduced in the United States, the equipment required specialists to operate it; however, now hospital personnel can be trained on its operation.175

Hydrogen peroxide vapor fills the room uniformly, even reaching around corners and behind obstructions, with what ultimately becomes a surface-deposited microcondensation layer of hydrogen peroxide, provid-ing a full 3-D, rapid killing of all microorganisms.175

Several studies have examined the impact of hydro-gen peroxide vapor decontamination on hospital facili-ties.174,176,177 A 2004 study showed a significant difference in MRSA contamination between rooms cleaned using only conventional methods (66% of sample swabs contained MRSA) and those decontaminated with hydrogen peroxide vapor (1.2% of sample swabs con-tained MRSA).174 In 2013, Johns Hopkins researchers published results showing significant reduction in con-traction of multidrug-resistant organism infections for newly admitted patients when rooms were disinfected with hydrogen peroxide vapor, despite having previ-ously housed patients with multidrug-resistant organ-ism infections.176 Hydrogen peroxide vapor consistently yields higher levels of decontamination than conven-tional cleaning methods.

Antimicrobial CopperCopper has long been known to possess sanitizing

properties and might be useful for environmental con-trol in health care facilities for preventing HAIs.178 Hard surfaces in health care facilities can be contaminated with microorganisms responsible for HAIs, such as MRSA, and these surfaces serve as ongoing sources of contamination to patients, either through direct con-tact or indirect contact via health care providers.178,179 To reduce hard surfaces as sources of contamination,

Box 2

Resources for Hand-Washing Instruction170

The Centers for Disease Control and Prevention has developed an interactive educational course titled “Welcome to Hand Hygiene & Other Standard Precautions to Prevent Healthcare-Associated Infections.” This course is available online at http://www.cdc.gov/handhygiene/training/interactive education/frame.htm.

The World Health Organization lists “Your 5 Moments for Hand Hygiene”: 1. Before touching a patient.2. Before a clean or aseptic procedure.3. After body fluid exposure risk.4. After touching a patient.5. After touching patient surroundings.

A downloadable poster is available at http://www.who.int /gpsc/5may/Your_5_Moments_For_Hand_Hygiene_Poster.pdf.

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However, by skipping one simple but important action, a radiologic technologist could unknowingly create an envi-ronment favorable for infection transmission. All health care professionals also must understand the simplicity behind infection transmission to help stop transmission.156

The eradication of HA-MRSA begins with each health care provider and facility. By adhering to hand hygiene and surface decontamination protocols, the radiologic technologist plays a valuable role in eradicat-ing not only MRSA but also other HAIs.

ConclusionOverall, the rate of HA-MRSA infections in the

United States is declining.115 Results from a CDC study published in 2010 showed that invasive (ie, life-threat-ening) MRSA infections declined 28% between 2005 and 2008, with bloodstream MRSA infections declin-ing even further.10 NHSN results found that MRSA bloodstream infections in hospitals decreased nearly 50% during the 10-year period from 1997 to 2007.185

Although these reports are promising for HA-MRSA and many HAIs, infections caused by Clostridium dif-ficile, another HAI agent, are rising rapidly. In fact, they have tripled within the past decade.186 Further incentive to reduce and eliminate HAIs such as MRSA comes from the new federal health care law in which hospitals with infection rates that exceeded national averages will lose 1% of their Medicare funding beginning in 2015. Although this might not seem like much, consider that $563 billion in Medicare claims were paid last year in support of 49 million Medicare patients.154

The decrease in HA-MRSA is certainly good news for both the health care and public health communities; however, the risk of developing infectious MRSA with-in a health care setting is still present. More remains to be done to eradicate this disease, and health care work-ers must remain vigilant in their fight.115 Radiologic technologists must do their part with frequent and proper hand washing and implementation of standard precautions to break the chain of MRSA infection.

Amy Jacobs, MS, received a master of science degree in biology, a bachelor of science in marine biology from the University of West Florida, and a bachelor of science

copper has been suggested as a surface coating because of its sanitizing properties.180 The mechanism of copper’s antimicrobial properties has not been fully explained, but it has been suggested that copper ions in contact with cell walls and membranes trigger struc-tural damage, resulting in DNA fragmentation.181

One study evaluated the effect of antimicrobial cop-per implementation on the microbial f lora found in an ICU and the use of antibiotics over a nonsequential 1-year period.182 There was a 95% reduction overall in the microbial f lora concentration (measured as colony-forming units per milliliter or CFU/mL), a reduction in the use of antimicrobial drugs (per day per patient) by 30%, and a reduction in hospitalization time and cost per patient.182 A separate study conducted by the same authors examined the effect of antimicrobial copper on microbial f lora in a neonatal ICU and found similar results, with a 90% reduction in microbial f lora concen-tration measured in colony-forming units per milliliter, including reductions in S aureus.183

A literature review of 37 studies analyzing the reduc-tion in microbial f lora from copper (both pure copper and copper alloys) showed that all but one examination identified significant reductions in microorganisms when placed in contact with copper, with pure copper providing the best results.180 The reductions were sig-nificant, especially when compared with other metals such as stainless steel, the metal most commonly used in health care facilities because of its anticorrosive prop-erties and its appearance of cleanliness.180 Studies have shown that microorganisms persist on stainless steel surfaces for long periods of time.181 In fact, the transmis-sion of infection-causing microbes in hospitals occurs most commonly through health care workers’ direct contact with surfaces. Health care workers then pass the bacteria on to their patients.184

The Radiologic Technologist’s Role in Preventing MRSA

Like other health care providers, radiologic technolo-gists learn about standard precautions during their pro-fessional education.156 It is imperative that they remain vigilant and keep implementation of standard precautions at the forefront of their daily activities. It is easy to become complacent about activities that become second nature.

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in psychology from Florida State University. She has an extensive background in molecular microbiology and currently works as an ecologist and freelance science writer. Her work has been published in numerous scientific journals, and she has served as a journal manuscript reviewer throughout her career. She is a new contributor to Radiologic Technology.

Reprint requests may be mailed to the American Society of Radiologic Technologists, Communications Department, at 15000 Central Ave SE, Albuquerque, NM 87123-3909, or e-mailed to [email protected].

© 2014 American Society of Radiologic Technologists

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139. Carlton RM. Phage therapy: past history and future pros-pects. Arch Immunol Ther Exp (Warsz). 1999;47(5):267-274.

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141. Chopra I, Hodgson J, Metcalf B, Poste G. The search for antimicrobial agents effective against bacteria resistant to multiple antibiotics. Antimicrob Agents Chemother. 1997;41:497-503.

142. Smith HW, Huggins MB. Successful treatment of experi-mental Escherichia coli infections in mice using phages: its general superiority over antibiotics [abstract]. J Gen Microbiol. 1982;128:307-318. http://www.ncbi.nlm.nih.gov /pubmed/7042903. Accessed July 21, 2013.

143. Smith WH, Huggins MB. Successful treatment of experimental Escherichia coli infections in mice using phage: its general superiority over antibiotics. Microbiol. 1982;128(2):307-318.

144. Mathur MD, Vidhani S, Mehndiratta PL. Bacteriophage therapy: an alternative to conventional antibiotics [abstract]. J Assoc Physicians India. 2003;51:593-596. http://www.ncbi.nlm.nih.gov/pubmed/15266928. Accessed July 24, 2013.

145. Species-Apis mellifera-honey bee. Bug guide Web site. http://bugguide.net/node/view/3080. Accessed July 29, 2013.

146. Mandal MD, Mandal S. Honey: its medicinal prop-erty and antibacterial activity. Asian Pacific J Trop Med. 2011;1(2):154-160.

147. Lusby PE, Coombes AL, Wilkinson JM. Bactericidal activ-ity of different honey against pathogenic bacteria. Arch Med Res. 2005;36:464-467.

148. Tan HT, Rahman RA, Gan SH, et al. The antibacterial prop-erties of Malaysian tualang honey against wound and enteric microorganisms in comparison to manuka honey. BMC Complement Alternat Med. 2009;9:34. doi:10.1186/1472 -6882-9-34.

149. Packer JM, Irish J, Herbert BR, et al. Specific non-peroxide antibacterial effect of manuka honey on the Staphylococcus aureus proteome [abstract]. Int J Antimicrob Agents. 2012;40(1):43-50. http://www.ncbi.nlm.nih.gov/pubmed /22580031. Accessed July 29, 2013.

150. Society for General Microbiology. How manuka honey helps fight infection. ScienceDaily. http://www.sciencedaily .com/releases/2009/09/090907013759.htm. Published September 10, 2009. Accessed July 29, 2013.

151. Dixon B. Bacteria can’t resist honey. Lancet Infect Dis. 2003;3(2):116. doi:10.1016/S1473-3099(03)00524-3.

152. Shah S. FDA clears new MediHoney hydrogel for treating burns. Med Gadget Web site. http://www.medgadget .com/2011/08/fda-clears-new-medihoney-hydrogel-for -treating-burns.html. Published August 3, 2011. Accessed July 29, 2013.

153. Healthcare-associated infections. Top CDC recommenda-tions to prevent healthcare-associated infections. Centers for Disease Control and Prevention Web site. http://www.cdc .gov/HAI/prevent/top-cdc-recs-prevent-hai.html. Reviewed April 12, 2011. Updated March 23, 2012. Accessed July 21, 2013.

154. Braunstein GD. Hospital-acquired infections: A costly, lethal scourge that we must labor to wash our hands of. Huffington Post Web site. http://www.huffingtonpost .com/glenn-d-braunstein-md/hospital-acquired -infections_b_1422371.html. Published April 23, 2012. Accessed July 29, 2013.

155. Infection control for nursing students. Chain of Infection: Diagram & Explanation. Truman College Web site. http://faculty.ccc.edu/tr-infectioncontrol/chain.htm. Accessed July 29, 2013.

156. Schmidt JM. Stopping the chain of infection in the radiology suite. Radiol Technol. 2012;84(1):31-51.

157. Semmelweiss IP. The Etiology, the Concept and the Prophylaxis of Childbed Fever. Pest, Hungary: CA Hartleben’s Verlag-Expedition, 1861. (Translation by FP Murphy, republished Classics of Medicine Library, Birmingham:1981).

158. Mortimer EA Jr, Lipsitz PJ, Wolinsky E, et al. Transmission of staphylococci between newborns: importance of the hands to personnel [abstract]. Am J Dis Child. 1962;104(3):289-295. http://archpedi.jamanet-work.com/article.aspx?articleid=500351. Accessed July 29, 2013.

159. Larson E. A causal link between handwashing and risk of infection? Examination of the evidence [abstract]. Infect Control Hosp Epidemiol. 1988;9(1):28-36. http://www.ncbi .nlm.nih.gov/pubmed/19722934?dopt=Abstract. Accessed July 29, 2013.

160. Pittet D, Hugonnet S, Harbarth S, et al. Effectiveness of a hospital-wide program to improve compliance with hand hygiene [summary]. Lancet. 2000;356(9238):1307-1312. http://www.scien cedirect.com/science/article/pii /S0140673600028142. Accessed July 29, 2013.

161. Pittet D, Allegranzi B, Sax H, et al. Evidence-based model for hand transmission during patient care and the role of improved practices [summary]. Lancet Infect Dis. 2006;6(10):641-652. http://www.sciencedirect.com /science/article/pii/S1473309906706004. Accessed July 29, 2013.

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Jacobs

174. French GL, Otter JA, Shannon KP, Adams NM, Watling D, Parks MJ. Tackling contamination of the hospital envi-ronment by methicillin-resistant Staphylococcus aureus (MRSA): a comparison between conventional terminal cleaning and hydrogen peroxide vapour decontamination [abstract]. J Hosp Infect. 2004;57(1):31-37. http://www.ncbi .nlm.nih.gov/pubmed/15142713. Accessed July 29, 2013.

175. Hodgson M. The role of hydrogen peroxide vapor systems in infection control. Infection Control Today Web site. http://www.infectioncontroltoday.com/articles/2010/11/the-role -of-hydrogen-peroxide-vapor-systems-in-infection-control.aspx. Published November 30, 2010. Accessed July 29, 2013.

176. Passaretti CL, Otter JA, Reich NG, et al. An evaluation of environmental decontamination with hydrogen per-oxide vapor for reducing the risk of patient acquisition of multidrug-resistant organisms [abstract]. Clin Infect Dis. 2013;56(1):27-35. http://www.ncbi.nlm.nih.gov/pubmed /23042972. Accessed July 29, 2013.

177. Fu TY, Gent P, Kumar V. Efficacy, efficiency and safety aspects of hydrogen peroxide vapour and aerosolized hydro-gen peroxide room disinfection systems [abstract]. J Hosp Infect. 2012;80(3):199-205. http://www.ncbi.nlm.nih.gov /pubmed/22306442. Accessed July 29, 2013.

178. Rutala WA, Weber DJ, Healthcare Infection Control Practices Advisory Committee (HICPAC). Guideline for disinfection and sterilization in healthcare facilities, 2008. Centers for Disease Control and Prevention Web site. http://stacks.cdc.gov/view/cdc/11560/. Accessed July 13, 2013.

179. Karlin KD. Metalloenzymes, structural motifs and inor-ganic models [abstract]. Science. 1993;261(5122):701-708. http://www.ncbi.nlm.nih.gov/pubmed/7688141. Accessed on July 29, 2013.

180. Leite GC, Padoveze MC. Copper as an antimicrobial agent in healthcare: an integrative literature review. J Infect Cont. 2012;1(2):33-36.

181. Grass G, Rensing C, Solioz M. Metallic copper as an anti-microbial surface. Appl Environ Microbiol. 2011;77(5):1541-1547. doi:10.1128/AEM.02766-10.

182. Efstathiou P, Kouskouni E, Papanikolaou S, et al. P369: Financial benefits after the implementation of antimicrobial copper in intensive care units (ICUs) [poster/abstract]. 2nd International Conference on Prevention and Infection Control (ICPIC 2013). Antimicrob Resistance Infect Control. 2013;2(Suppl 1):P369. http://www.aricjournal.com/content /2/S1/P369. Accessed July 29, 2013.

183. Efstathiou P, Anagnostakou M, Kouskouni E, et al. O068: Implementation of antimicrobial copper in neonatal intensive care unit (NICU) [abstract]. 2nd International Conference on Prevention and Infection Control (ICPIC 2013). Antimicrob Resistance Infect Control.2013;2(Suppl 1).

162. Albert RK, Condie F. Hand-washing patterns in medical intensive-care units. N Engl J Med. 1981;304(24):1465-1466.

163. McGuckin M, Waterman R, Govednik J. Hand hygiene compliance rates in the United States — a one-year multi-center collaboration using product/volume usage measure-ment and feedback. Am J Med Qual. 2009;24(3):205-213. doi:10.1177/1062860609332369.

164. Erasmus V, Daha TJ, Brug H, et al. Systematic review of studies on compliance with hand hygiene guidelines in hospital care. Infect Control Hosp Epidemiol. 2010;31(3):283-294. http://www.jstor.org/stable/10.1086/650451. Accessed July 29, 2013.

165. Kirkland KB, Homa KA, Lasky RA, Ptak JA, Taylor EA, Splaine ME. Impact of a hospital-wide hand hygiene initia-tive on healthcare-associated infections: results of an inter-rupted time series. BMJ Qual Saf. 2012;21(12):1019-1026. doi:10.1136/bmjqs-2012-000800.

166. Hands and bacteria poster. Minnesota Department of Health Web site. http://www.health.state.mn.us/handhy giene/why/handsbacteria.html. Updated November 22, 2010. Accessed July 29, 2013.

167. Pittet D, Simon A, Hugonnet S, Pessoa-Silva CL, Sauvan V, Perneger TV. Hand hygiene among physicians: perfor-mance, beliefs, and perceptions [abstract]. Ann Intern Med. 2004;141(1):1-8. http://annals.org/article.aspx?articleid =717563. Accessed July 29, 2013.

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170. Your 5 moments for hand hygiene [poster]. World Health Organization. May 2009. http://www.who.int/gpsc/5may /Your_5_Moments_For_Hand_Hygiene_Poster.pdf. Accessed April 8, 2014.

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184. Halwani M, Solaymani-Dodaran M, Grundmann H, Coupland C, Slack RJ. Cross-transmission of nosocomial pathogens in an adult intensive care unit: incidence and risk factors. J Hosp Infect. 2006;63(1):39-46.

185. Dudeck MA, Horan TC, Peterson KD, et al. National Healthcare Safety Network (NHSN) report, data summary for 2011, device-associated module. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/nhsn /PDFs/dataStat/NHSN-Report-2011-Data-Summary.pdf. Published April 1, 2013. Accessed June 23, 2013.

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1. What is another name for hospital-acquired/ health care–associated infections (HAIs)?a. beta-lactamsb. nosocomial infectionc. mononucleosisd. necrotizing fasciitis

2. Most frequently, HAIs involve infections of the:1. bloodstream.2. urinary tract.3. lower respiratory tract.

a. 1 and 2b. 1 and 3c. 2 and 3d. 1, 2, and 3

3. The use of invasive devices such as catheters decrease the risk of acquiring an infectious disease during hospital treatment.a. trueb. false

4. According to the article, what HAI has been of significant concern for more than 50 years?a. Escherichia colib. methicillin-resistant Staphylococcus aureus

(MRSA)c. Actinobacter baumanniid. Clostridium difficile

5. Staphylococcus aureus (S aureus) is able to resist an array of adverse environmental conditions including:

1. complete drying.2. high salt concentrations.3. temperatures lower than 10°F.


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RADIOLOGIC TECHNOLOGY, July/August 2014, Volume 85, Number 6



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6. Vertical evolution is the term for resistance conferred:a. through chromosomal mutation and/or selection.b. through circular replication.c. through the acquisition of genetic material from

another organism.d. from a bacterial virus.

7. All of the following are ways in which new mutations in bacteria lead to resistance except:a. altering a target protein.b. altering the inner cell membrane.c. obtaining genes that encode for enzymes.d. upregulation of mechanisms for expulsion of

antimicrobials.

8. Which phrase best describes mobile genetic elements?a. large pieces of discrete DNA that encode

mobilization functionb. bacteriophages used to transfer DNA to bacteriac. genes that travel throughout the body of an

infected person d. elements that transfer core variable genes

9. The estimated mortality rate associated with MRSA infections in U.S. hospitals is ______%.a. 12b. 20c. 39d. 97

10. Community-acquired/community-associated MRSA (CA-MRSA) first appeared in:a. the 1960s.b. the 1990s.c. 2002.d. 2010.

11. Necrotizing fasciitis is a rare but serious bacterial infection that can be caused by S aureus and:

1. Klebsiella.2. Clostridium difficile.3. Escherichia coli.


12. Which of the following tests is not used to detect MRSA?a. cefoxitin disk screen testb. latex agglutination test for PBP2a c. Mueller-Hinton agar plate supplementation with

oxacillin d. Mueller-Hinton agar plate supplementation with

methicillin

13. Which of the following might be the first sign of MRSA?a. fever b. nausea c. diarrhea d. small red bumps

14. Which population is not at high risk for CA-MRSA? a. schoolchildren b. athletes c. the homelessd. hospital inpatients

15. According to the Centers for Disease Control and Prevention (CDC), what is the main way hospital-acquired MRSA (HA-MRSA) is transmitted?a. poor hand hygieneb. nasal cannulasc. dirty hospital gownsd. needles




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21. Which of the following has been used to treat infections for centuries?a. honey b. teac. baking soda d. alcohol

22. Which of the following is not a CDC recommendation for preventing HA-MRSA?a. proper hand washing b. medical equipment sterilization c. eliminating the use of unnecessary catheter lines d. reducing the number of blood test draws

23. The chain of infection is:a. the way the organism enters the body.b. a mechanism of antibacterial resistance

transmission.c. a mode of transmission of infectious disease

from one person or object to another.d. a mode of transmission from 2 or more people to

another person.

24. In the radiology suite, which pieces of equipment are particularly important to disinfect properly because they can be sources of infection transmission?

1. examination table2. exposure switch3. upright Bucky


16. Which is the most widely used HAI tracking system in the United States?a. National Healthcare Safety Networkb. Nosocomial Infections Surveillance System c. University Healthcare Consortiumd. Emerging Infections Program

17. What part of the world has the lowest HA-MRSA rate?a. East Asiab. Northern Europe c. North Americad. the Middle East

18. Which of the following can be reservoirs for MRSA if they become contaminated?

1. pool water2. river water3. seawater


19. Which drug is still used to treat MRSA?a. methicillin b. vancomycin c. oxytocind. alcohol

20. Phage therapy is the use of:a. viruses as biological control agents.b. bacteria as biological control agents. c. antibiotics for treatments. d. antivirals for treatments.



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25. Hungarian physician Ignaz Semmelweis made the connection between hand washing and infection control in a maternity hospital more than 165 years ago. He theorized that hospital staff were transferring germs from ______ to mothers and their newborns. a. porous surfaces b. surgical equipmentc. bed linensd. cadavers

26. What is the lowest percentage of alcohol the CDC recommends for hand sanitizers?a. 10b. 50 c. 60 d. 75

27. What can be used as a proactive or reactive cleaning mechanism in a hospital setting?a. hydrogen peroxide b. alcohol c. hydrogen peroxide vapor d. alcohol vapor

28. Which material has been suggested as an infection preventive surface coating?a. copperb. aluminumc. stainless steel d. carbon fiber

29. Where does the eradication of HA-MRSA begin?1. health care provider 2. health care facility3. patient

a. 1 and 2 b. 1 and 3c. 2 and 3d. 1, 2, and 3

30. By what percentage has life-threatening MRSA infection declined, according to the CDC?a. 10b. 28 c. 49 d. 50

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