Stricter Precautions, Active Surveillance Can Beat MRSA and VRE


Stricter Precautions, Active Surveillance Can Beat MRSA and VRE

By Kelly M. Pyrek

Faced with escalating multi-drug resistance and the continued supremacy of "superbugs" such as methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE) and penicillin-resistant Streptococcus pneumoniae (PRSP), healthcare facilities are pondering the effectiveness of the infection-fighting precautions they are following. Cost-conscious hospital administrators are citing a recent study by Duke University researchers that confirmed nosocomial infections created longer hospital stays and generated costs three times greater than normal. However, many of them are unwilling to foot the bill for costs incurred by stricter contact precautions instead of standard precautions.

Administrators are not the only ones puzzling over the dilemma; risk managers, materials managers, infection control practitioners and epidemiologists are asking themselves if this switch in precautions can reduce the morbidity, mortality and costs associated with these powerful nosocomial infections.

The unequivocal answer is, yes, according to noted infectious disease expert Barry M. Farr, MD, hospital epidemiologist for the University of Virginia Health System. He is a vocal and widely published proponent of active surveillance, isolation of infected and heavily colonized patients, use of personal protective equipment such as gowns and gloves, and thorough environmental cleaning and disinfection. Farr says the literature provides solid evidence that this slate of preventive measures can make a significant difference in the fight against MRSA and VRE.

In a study published in 2001, Farr and colleagues1 discuss a three-year facility-wide outbreak of MRSA that accounted for about 40 percent of all nosocomial Staphylococcus aureus bloodstream infections (BSIs) and 49 percent of surgical site infections (SSIs). Active surveillance of cultures was successful in identifying colonized patients so that healthcare workers (HCWs) could engage in contact precautions. The study reported that MRSA was thoroughly controlled in the facility.

Historically, healthcare facilities created infection control programs that were designed to control antibiotic-resistant nosocomial infections, Farr says, but the number of infections continued to rise. Antibiotic control worked initially, but bacteria began to develop resistant strains and multiply quickly. He says that while studies of antibiotic restriction, substitution and cycling have been promising, more definitive data is needed. Increased hand hygiene compliance is unlikely to control the problem, experts say, and continued environmental contamination poses significant challenges. In the meantime, Farr says, using active surveillance to detect the reservoir for transmission and implementing contact precautions go a long way in curbing the prevalence of infections triggered by resistant organisms.

To grasp more complicated aspects of the issue, clinicians must understand the basic tenets of the chain of infection. Pathogens require a reservoir (a place to live) and a vector (a way to get around) in order to move from patient to HCW to patient again. Farr believes understanding this simple chain is the first step in combating MRSA and VRE.

"Pathogens have to live somewhere," said Farr in a recent teleclass, "MRSA and VRE: Is It Important to Control the Reservoir?" hosted by Webber Training, Teleclass Education for Healthcare Professionals.2 "With most infectious processes, if you have any kind of outbreak, it's coming from somewhere and you need to do something about that reservoir so it doesn't spread."

And that's where the implementation of contact precautions comes into the picture. Contact precautions, as recommended by the Centers for Disease Control and Prevention (CDC) for the past 17 years, are used when an infectious agent (a bacteria or a virus) can be spread either by skin-to-skin contact or by contact with contaminated surfaces. Contact precautions include appropriate patient isolation according to CDC guidelines; glove use; handwashing, gown use (if HCWs will be in contact with the patient, the environmental surfaces or other contaminated items in the room); appropriate patient transport according to CDC guidelines; and dedicated use of non-critical equipment or adequate cleaning and disinfection of shared equipment.

Active surveillance of cultures is the other component of Farr's suggested measures to help fight resistant strains. Surveillance involves the detection and tracking of all patients who are asymptomatically colonized with MRSA and VRE. Colonization means the microorganism is present in or on the body but does not cause illness. A HCW who has been colonized can become a carrier and spread infection to other HCWs and patients. Infection means the organism is present and disease has been caused. Risk factors for increasing the chance of colonization and infection include:3

  • Severity of illness

  • Previous exposure to antibiotics and antimicrobial products

  • Underlying diseases and conditions

  • Invasive procedures and presence of invasive devices such as catheters

  • Repeated contact with or presence in a healthcare facility

  • Previous colonization by a multi-drug resistant organism

Wake Forest University Baptist Medical Center is one facility that has heeded Farr's pleas for hospitals to adopt surveillance measures and contact precautions in a concerted infection control program. The facility, which implemented its active surveillance program for MRSA and VRE last April, performs weekly culturing of all patients in the adult ICUs, adult intermediate care unit and the pediatric and neonatal ICUs. It also plans to use surveillance culturing of patients that are at high risk for colonization of MRSA and VRE in all areas of the hospital. The new initiative was kicked off with a prevalence sweep, wherein all inpatients were cultured for MRSA and VRE. The cultures were collected from the nose and wounds (if present) for MRSA and from the perirectal area for VRE.

In its policy, Wake Forest explains that isolation precautions are instituted for patients that have been identified as infected or colonized with MRSA or VRE, which involves the use of gloves, gowns, cohort nursing and enhanced handwashing to minimize the spread of these pathogens to other patients.

Which leads to the question of the role hand hygiene and personal protective equipment (PPE) play in the prevention of MRSA and VRE. Farr says hand hygiene cannot control MRSA or VRE, but is quick to add, "I am all for hand hygiene. My hospital was ahead of its time in going to alcohol; in 1987 the CDC recommended universal precautions that dictated hand-hygiene principles. In 1996 the name was changed to standard precautions and they began to say hand hygiene before, after and between patient care. It was explicit instruction, yet hand-hygiene compliance rates had not changed. In fact, a Midwest hospital that installed more handwashing facilities still had hand-hygiene rates that had sunk to single-digit ranges. You can't have contact precautions and surveillance without hand hygiene because you need simultaneous implementation."

"We did a study comparing hand hygiene vs. gloves and cover gowns," says Jay Sommers, PhD, director of scientific and clinical affairs for Kimberly-Clark Professional. "Both were effective in reducing the incidence of infection but gowns and gloves usage was significant in reducing infection rates. I think PPE and hand hygiene go hand in hand. If you are going to wear a cover gown, gloves and a mask you need to practice good hygiene. If you are going to be diligent you have to do the whole thing. If not, you are going to compromise the effectiveness of your investment in infection control measures."

When it comes to PPE, a search of the literature reveals a number of interesting facts revealed in various studies:

  • One study reported the containment of VRE in several outbreaks when gloves and gowns were used, but not when only gloves were used.

  • A study said VRE is only mildly controlled when a handwashing compliance rate of 80 percent is achieved.

  • One study documented the contamination of gloves, gowns and stethoscopes after contact with patients colonized or infected with VRE.

  • Another study said that while the HCW's clothes were protected, gowns frequently become contaminated after caring for patients with MRSA or VRE.

  • Several studies have confirmed surface and equipment contamination in hospital rooms occupied by patients with MRSA and VRE.

The protective properties of cover gowns isn't lost on Sommers, who says several years ago, when noted researcher John Boyce was at Brown University, Boyce conducted a study in which cover gowns were used to stop an outbreak of VRE, MRSA and ampicillin-resistant enteroccoci.

"The argument for and against cover gowns is, if you don't have an outbreak it's not going to do anything for you," Sommers says. "If you have an outbreak and you follow the CDC guidelines -- wearing a gown and gloves during patient care and leaving them in the room with the contaminated patient, you can stop the outbreak. Boyce not only wanted to control the outbreak, he wanted to find out the vector of transmission of the organisms throughout the hospital. So he had HCWs wear our SMS (triple-layer) gowns and gloves when they cared for patients. He found out that the outside of the gown became contaminated with these three organisms. Then he cultured the under side of the gown and the HCWs' clothing underneath and found the organisms did not penetrate the material. He also found had the nurses wash their gloved hands; he cultured them and they were negative. Then he had them touch the outside of their gowns and they became positive. So Boyce is saying, 'The organisms are residing on the outside of the gown and by reinforcing the CDC guidelines of leaving the gowns and the gloves in the room, you won't be tracking the organisms throughout the hospital.' That's key to controlling nosocomial pathogens."

"Boyce's study says that gowns work to protect clothes from contamination," Farr says. "Two thirds of the time, white coats were contaminated and 3 out of 11 times he got positive hand cultures when touching the white coat. Gown, glove and stethoscope all had contamination, whether the patient was colonized or infected."

Sommers says that despite Boyce's study and others like it that advocate the wearing of cover gowns and following contact-precautions protocol, healthcare facilities don't heed the advice.

"Unfortunately, a lot of hospitals are reluctant to use more cover gowns because they think they will spend too much money," Sommers says. "Boyce wanted everyone in the hospital to start wearing cover gowns, but they couldn't afford it. It is a cost-effective strategy but how do you convince someone to reprioritize and spend $10,000 to save $100,000, especially in today's economic environment? If SARS becomes prevalent here, people will start wearing all kinds of protective apparel all the time. It's bad because it indicates an increase in resistant organisms but it's good because at least people know what they can wear to try to protect themselves."

"The cost benefits are plenty yet many facilities don't take the contact precautions and surveillance approach because they assume it will be more costly," Farr says. "If you are using an evidence-based approach, what are you using if you don't acknowledge cost studies? Studies show the cost of resistant infections is $1 million to $3 million, which is far more than (the cost of) using contact precautions."

Farr was one of four investigators in a study of the cost-effectiveness of active survillance cultures and contact precautions for the control of MRSA.4 The study looked at the estimated costs of surveillance cultures and isolation measures used during a MRSA outbreak at the researchers' hospital compared to the estimated attributable excess costs of methicillin resistance for bacteremias occurring during a MRSA outbreak not controlled at another hospital. The study was set in the neonatal ICUs of two tertiary-care hospitals. The estimated costs of controlling the 10.5-month outbreak in the neonatal ICU that resulted in 18 colonized and four infected infants ranged from $48,617 to $68,637. The estimated attributable excess cost of 75 MRSA bacteremias in a second neonatal ICU outbreak that resulted in 14 deaths and lasted 51 months was $1.3 million. Weekly active surveillance cultures and isolation of patients with MRSA halted an outbreak at the researchers' hospital and cost 19- to 27-fold less than the attributable costs of MRSA bacteremias in another outbreak that was not promptly controlled.

In another cost-associated study,5 Farr and four other investigators acknowledged that several hospitals opting not to use active surveillance cultures to identify carriers of VRE have reported that adoption of other parts of the CDC guideline for controlling VRE has had little to no impact. Because use of surveillance cultures and contact isolation controlled a large outbreak at the investigators' hospital, their costs were estimated for comparison with the excess costs of VRE bacteremias occurring at a higher rate at a hospital not employing these measures.

In this study of two university hospitals, inpatients deemed at high risk for VRE acquisition at the University of Virginia Health System (UV) underwent weekly perirectal surveillance cultures. Estimated costs of cultures and resulting isolation during a two-year period were compared with the estimated excess costs of more frequent VRE bacteremias at another hospital of similar size and complexity not using surveillance cultures to control spread throughout the hospital. Of 54,052 patients admitted, 10,400 had perirectal swabs taken. Cultures and isolation cost an estimated $253,099. VRE culture positivity was limited to 193 (0.38 percent) and VRE bacteremia to 1 (0.002 percent) as compared with 29 bacteremias at the comparison hospital. The estimated attributable cost of VRE bacteremia at the comparison hospital of $761,320 exceeded the cost of the control program at UV by threefold. The investigators concluded that the excess costs of VRE bacteremia may justify the costs of preventive measures. The costs of VRE infections at other body sites, of deaths from untreatable infections, and of dissemination of genes for vancomycin resistance also help to justify the costs of implementing an effective control program.

Sommers believes the case for contact precautions and other preventive measures will win out in the long run.

"I think hospitals will become more willing to go to contact precautions when they need them," he says, "as opposed to saying unilaterally, 'We don't need them and we're not going to do them.' I think they are becoming more open to them because they see what the outcomes are and they listen to people like Barry Farr."

More than 1,000 people were doing just that on March 12, 2003 when Farr presented a teleclass on finding the reservoirs of MRSA and VRE. He traced the arrival of resistant strains in the 1940s, when the introduction of penicillin first caused resistance rates to soar in just a few years thereafter. He says resistance occurred first in healthcare facilities, then spreading to the community, which indicates the classic mechanism of transmission.

"In 1859 we were exposed to Darwin's theory of natural selection," Farr said. "Antibiotic use is very high in the U.S. and nearly all patients in the ICU are on them. It doesn't take Einstein to figure out that resistance will mutate, proliferate and spread."

Indeed. According to Farr, MRSA infection rates doubled in a decade, representing half of all Staphylococcus aureus infections. He relates how his facility battled with MRSA.

"It arrived in 1978, grew in 1979 and by 1980, half of our BSIs and SSIs were due to the same strain," Farr says. "Despite knowing MRSA was present, we didn't bother to put patients in isolation. When we started doing surveillance and saw it was spread to people asymptomatically colonized, we put patients in isolation and the outbreak was controlled. What had been killing patients was eradicated in one and a half years and it was done with no antibiotic control effort."

In a 1999 study,6 Farr said the source of the spread of antibiotic-resistant microbes can be likened to an iceberg, with clinically obvious infections representing the tip of the iceberg and most of the spread coming from clinically inapparent colonized patients who represent most of the reservoir for transmission. He said surveillance cultures to identify this reservoir are important to the control of spread with effective barrier precautions. Such precautions have been shown to reduce the spread of MRSA 15.6-fold compared with standard precautions.

Farr explains that active surveillance gets past the tip of the iceberg and can help detect the formidable chunk of the iceberg that hides underwater -- those asymptomatically colonized with MRSA or VRE.

"Patients who are recognized by clinical microbiology represent the tip of the iceberg," Farr says. "All others are asymptomatic and are far more important in the evolution of an epidemic. The hospital thinks it will deal with it when they get an outbreak, get the results from clinical microbiology and put (infected) patients in isolation. The majority of colonized patients will not be identified with that approach."

Farr adds, "Many studies report surveillance works in controlling VRE infections. A few studies suggest it doesn't work but these studies (were conducted with) very small samples. If the study is on a small scale, it only focuses on the tip of the iceberg. The most important factor (in combating resistant strains) is, how many other people have it?"

Farr points to northern European hospitals that are vigilant about employing contact precautions and conducting active surveillance; these facilities boast exceedingly low or virtually non-existent rates of MRSA and VRE, including less than 1 percent of incidence in Denmark.

A recent study by investigators at a Norwegian hospital 7 documented a MRSA outbreak where staff and patients were screened immediately after detection of the first MRSA isolate. Colonized and infected patients were nursed using contact precautions, and the staff members were not allowed to work until three nose samples were MRSA-negative. Colonized persons were treated with topical administration of mupirocin to the nostrils and a chlorhexidine body wash. The outbreak affected seven patients and five healthcare workers. Pulsed-field gel electrophoresis proved all isolates to be of the same type, and the MRSA phage type was M3. There was no sign of transmission of MRSA after contact precautions were implemented. MRSA was eradicated in four of the patients and all HCWs. One patient died and one was still colonized three years after onset of the outbreak. Contact precautions proved to be sufficient to prevent transmission of MRSA.

"In European hospitals, everyone with a resistant strain is caught when coming into the facility," Sommers says. "They isolate them right away and the resistant strains can be controlled more effectively. Maybe we need to go to that model. By not being proactive, we have let (resistant strains) get the upper hand."

"If we choose to look the other way it will spread like crazy," Farr says, acknowledging the increase in community-acquired MRSA and VRE.

In a study with two other investigators 8 Farr acknowledges that carriage of MRSA among persons without healthcare-associated risks has increased.

The investigators looked at studies reporting prevalence of community-acquired MRSA (CA-MRSA) among MRSA isolates from hospitalized patients and the prevalence of MRSA colonization among community members. The CA-MRSA prevalence among hospital MRSA was 30.2 percent in 27 retrospective studies and 37.3 percent in five prospective studies. The pooled MRSA colonization rate among community members was 1.3 percent, but there was significant heterogeneity among study populations. Community members from whom samples were obtained in healthcare facilities were more likely to be carrying MRSA than were community members from whom samples were obtained outside of the healthcare setting. Among studies that excluded persons with healthcare contacts, the MRSA prevalence was 0.2 percent. Moreover, most persons with CA-MRSA had > or =1 healthcare-associated risk, which suggests that the prevalence of MRSA among persons without risks remains low (less than or equal to 0.24 percent). The investigators concluded that effective control of dissemination of MRSA throughout the community will require effective control of nosocomial MRSA transmission.

"We are starting to see a lot of community-acquired MRSA," Sommers agrees. "For years we only saw those pathogens in the hospital. Now you see MRSA in the outside world and that's a bad sign. Serving as infectious reservoirs and vectors are people who have been in the hospital who go home without being cured and they carry the organisms. Or it's HCWs that are very highly colonized with MRSA in their nares and are spreading it. Part of the problem is the hospitals don't really control it to the extent that they should. When you look at SARS, health officials didn't do anything to stop the outbreak early. They just let it go, so it was spread to the whole community. We will see more of that. For the first time we saw two cases of vancomycin resistant Staphylococcus aureus (VRSA) in the U.S.; for years it only existed in a test tube at the CDC. Both patients lived, but it took a lot of antibiotics. It's a trend we'll probably see more of."

VRE is doing as much damage as MRSA, Farr reports, saying that it exploded onto the scene in the same decade as MRSA, going from 0 percent to 25 percent of all enterococcal infections.

Farr says that a patient who died of bacteremia got the attention of his healthcare facility, which started implementing active surveillance cultures for VRE. "We detected many infections by looking for them," Farr said. "It was the same iceberg phenomenon and same method of control. VRE is an epidemic of colonization. If you control colonization, infections disappear. Some people think if you give a patient enough antibiotics you will turn their own enterococcus against VRE. Microbiologists will laugh in your face. Patients get this by the spread of the bacteria one to another. At 100 percent compliance with surveillance and contact precautions, (the rate of) VRE (incidence) goes down."

Farr said his facility, after learning some hard lessons, has become a role model in the use of contact precautions and active surveillance to help reduce incidences of VRE and MRSA. He remembers that in 1980, half of the BSIs at his hospital were MRSA related, and that's where many hospitals' MRSA rates are now. He says his facility is a model to follow because of surveillance, "not because we have mildly ill patients; we have patients that are in the top 1 or 2 percent in terms of acuity of illness. We have the sickest patients yet one of the lowest rates of antibiotic resistant infections. Yet UVA was leading the nation in VRE two decades ago."

Farr says that environmental contamination also must be addressed when attempting to control and eliminate MRSA and VRE infections. He points to a study showing that 42 percent of nurses' hands were contaminated when nurses touched surfaces only, not patients.

"After the patient with MRSA or VRE has been discharged, if the room has not been properly disinfected, a study has shown 16 percent of surfaces are still contaminated," Farr says. He favors a bucket method over a spray for cleaning MRSA and VRE contaminated surfaces and equipment. "A thin film of disinfectant won't kill resistant strains, and it's hard to tell if surface areas have been missed with a spray. When you do environmental cleaning, if it is not rigorous, it won't work. The volume of the disinfectant and the amount of elbow grease is important."

It's an approach that is working well to eradicate TB, yet many facilities are still loath to follow contact precautions and active surveillance. "With antibiotic resistance we are taking a 'don't ask, don't tell' approach to the epidemiology of colonization, which drives the epidemic of infections. We are choosing not to take the approach that is working in northern Europe."

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