[Federal Register Volume 59, Number 94 (Tuesday, May 17, 1994)]
[Unknown Section]
[Page 0]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 94-11913]


[[Page Unknown]]

[Federal Register: May 17, 1994]


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Part V





Department of Health and Human Services





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Centers for Disease Control and Prevention



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Preventing the Spread of Vancomycin Resistance--Report From the 
Hospital Infection Control Practices Advisory Committee; Comment Period 
and Public Meeting; Notice
DEPARTMENT OF HEALTH AND HUMAN SERVICES

Centers for Disease Control and Prevention

 

Preventing the Spread of Vancomycin Resistance--A Report From the 
Hospital Infection Control Practices Advisory Committee Prepared by the 
Subcommittee on Prevention and Control of Antimicrobial-Resistant 
Microorganisms in Hospitals; Comment Period and Public Meeting

AGENCY: Centers for Disease Control and Prevention (CDC), Public Health 
Service (PHS), Department of Health and Human Services (DHHS).

ACTION: Notice.

-----------------------------------------------------------------------

SUMMARY: This notice is a request for review and comment of the draft 
document, Preventing the Spread of Vancomycin Resistance--A Report From 
the Hospital Infection Control Practices Advisory Committee (HICPAC) 
Prepared by the Subcommittee on Prevention and Control of 
Antimicrobial-Resistant Microorganisms in Hospitals. The draft document 
was prepared in collaboration with the National Center for Infectious 
Diseases (NCID), CDC, and representatives of the American Hospital 
Association, American Society for Microbiology, Association for 
Professionals in Infection Control and Epidemiology, Infectious 
Diseases Society of America, Society for Healthcare Epidemiology of 
America, and Surgical Infection Society.

DATES: Written comments on the draft document must be received on or 
before July 18, 1994.

ADDRESSES: Comments on this document should be submitted in writing to 
the Centers for Disease Control and Prevention (CDC), Attention: VRE 
Report Center, Mailstop A-07, 1600 Clifton Road, NE., Atlanta, Georgia 
30333. The Federal Register containing this draft document may be 
viewed and photocopied at most libraries designated as U.S. Government 
Depository Libraries and at many other public and academic libraries 
that receive the Federal Register throughout the country. In addition, 
copies of this Federal Register notice document can be obtained by 
calling (404) 332-2569.

FOR FURTHER INFORMATION CONTACT: The VRE Report Center, telephone (404) 
332-2569.

SUPPLEMENTARY INFORMATION: A public meeting for an open discussion of 
the draft document will be held at the CDC, Atlanta, Georgia, on June 
15, 1994. Details about the meeting will be announced in a forthcoming 
issue of the Federal Register.

    Dated: May 11, 1994.
Claire V. Broome,
Acting Deputy Director, Centers for Disease Control and Prevention 
(CDC).

Appendix--Preventing the Spread of Vancomycin Resistance-- A Report 
from the Hospital Infection Control Practices Advisory Committee 
Prepared by the Subcommittee on Prevention and Control of 
Antimicrobial-Resistant Microorganisms in Hospitals

Executive Summary

    This document contains recommendations for the prevention and 
control of the spread of vancomycin resistance, with special focus on 
vancomycin-resistant enterococci (VRE).
    A rapid increase in the incidence of infection and colonization 
with VRE has been reported from U.S. hospitals in the last 5 years. 
This increase poses several problems, including (a) the lack of 
available antimicrobial(s) for therapy of infections due to VRE, since 
most VRE are also resistant to multiple other drugs, e.g., 
aminoglycoside and ampicillin, previously used for treatment of 
infections due to these organisms; and (b) the possibility that the 
vancomycin-resistance genes present in VRE may be transferred to other 
gram-positive microorganisms such as Staphylococcus aureus.
    An increased risk of VRE infection and colonization has been 
associated with previous vancomycin and/or multi-antimicrobial therapy, 
severe underlying diseases or immunosuppression, and cardio-thoracic or 
intraabdominal surgery. Because enterococci can be found in the normal 
gastrointestinal or female genital tracts, most enterococcal infections 
have been attributed to endogenous sources within the individual 
patient. However, recent reports of outbreaks and endemic infections 
due to enterococci, including VRE, have shown that patient-to-patient 
transmission of the microorganisms can occur either via direct contact 
or indirectly via hands of personnel or contaminated patient-care 
equipment or environmental surfaces.
    Prevention and control of the spread of vancomycin resistance will 
require concerted effort from various departments of the hospital, and 
can only be achieved if each of the following elements is addressed: 
(1) Education of hospital staff regarding the problem of vancomycin 
resistance, (2) early detection and prompt reporting of vancomycin 
resistance in enterococci and other gram-positive microorganisms by the 
hospital microbiology laboratory, (3) implementation of appropriate 
infection-control measures to prevent person-to-person transmission of 
VRE, and (4) prudent vancomycin use by clinicians.

Introduction

    From 1989 though 1993, the percentage of nosocomial enterococcal 
infections reported to the CDC National Nosocomial Infections 
Surveillance (NNIS) System that were resistant to vancomycin increased 
from 0.3% to 7.9%.1 The increase was due mainly to the 34-fold 
rise, from 0.4% to 13.6%, of infections due to VRE in intensive-care 
unit (ICU) patients, although a trend towards increased vancomycin 
resistance was also noted in non-ICU patients.1 The occurrence of 
VRE in NNIS hospitals was directly associated with larger hospital size 
(200 beds) and university affiliation.1 Other hospitals 
also have reported increased endemic rates and clusters of VRE 
infection and colonization.2-6 The actual increase in incidence of 
VRE in U.S. hospitals may be larger because vancomycin resistance, in 
particular moderate vancomycin resistance (as manifested in the VanB 
phenotype), is not detected consistently with the automated methods 
used in many clinical laboratories.7,8
    Vancomycin resistance in enterococci has emerged amidst the 
increasing incidence of high-level enterococcal resistance to 
penicillin and aminoglycosides, thus presenting a serious challenge for 
physicians treating patients with infections due to these 
microorganisms.1,4 Treatment options are often limited to 
combinations of antimicrobials or experimental compounds with unproven 
efficacy.9
    The epidemiology of VRE has not been well elucidated; however, 
certain patient populations have been found to be at increased risk for 
VRE infection or colonization; these include critically ill patients or 
those with severe underlying disease or immunosuppression, such as ICU 
patients or patients in the oncology or transplant wards; those who 
have had an intra-abdominal or cardio-thoracic surgical procedure, or 
indwelling urinary or central venous catheter; and those who have had 
prolonged hospital stay or received multi-antimicrobial and/or 
vancomycin therapy.2-6, CDC unpublished data Because enterococci 
are part of the normal flora of the gastrointestinal and female genital 
tracts, most infections with these microorganisms have been attributed 
to the patient's endogenous flora.10 However, recent reports have 
demonstrated that enterococci, including VRE, can spread by direct 
patient-to-patient contact or indirectly via transient carriage on 
hands of personnel11 or contaminated environmental surfaces and 
patient-care equipment.12
    In addition to the existing problem with VRE, the potential 
emergence of vancomycin resistance in clinical isolates of S. aureus is 
a serious public health concern. The vanA gene, which is frequently 
plasmid-borne and confers high-level resistance to vancomycin, can be 
transferred in vitro from enterococci to a variety of gram-positive 
microorganisms,13,14 including Staphylococcus aureus.15 
Although vancomycin resistance in clinical strains of S. epidermidis or 
S. aureus has not been reported, a vancomycin-resistant clinical strain 
of Staphylococcus haemolyticus has been isolated.16
    In response to the dramatic increase in vancomycin resistance in 
enterococci, the Subcommittee on the Prevention and Control of 
Antimicrobial Resistant Microorganisms in Hospitals of the CDC's 
Hospital Infection Control Practices Advisory Committee (HICPAC) held 
meetings on November 14, 1993 and February 18, 1994, with 
representatives from the American Hospital Association, American 
Society for Microbiology, Association for Professionals in Infection 
Control and Epidemiology, Infectious Diseases Society of America, 
Society for Healthcare Epidemiology of America, and Surgical Infection 
Society. The Subcommittee members agreed that prompt implementation of 
control measures is needed and developed recommendations to prevent the 
spread of VRE. The Subcommittee recognizes that data are limited and 
considerable research will be required to elucidate fully the 
epidemiology of VRE and determine cost-effective control strategies, 
and many U.S. hospitals have concurrent problems with other 
antimicrobial-resistant organisms, such as methicillin-resistant S. 
aureus and beta-lactam and aminoglycoside-resistant gram-negative 
bacilli, that may have different epidemiologic features and require 
different control methods.

Recommendations

    Hospital infection control programs, in collaboration with quality 
improvement programs, microbiology laboratories, clinical departments, 
and nursing, administrative, and housekeeping services, should develop 
a comprehensive, institution-specific, strategic plan to detect, 
prevent, and control infection and colonization with VRE. It is 
strongly suggested that the following elements be addressed in the 
plan.

I. Education Program

    Continuing education programs for hospital staff should include 
information concerning the epidemiology of VRE and the potential impact 
of this pathogen on the cost and outcome of patient care. Because 
detection and containment of VRE require a very aggressive approach and 
high performance standards for hospital personnel, special awareness 
and educational sessions may be indicated.

II. Role of the Microbiology Laboratory in the Detection, Reporting, 
and Control of VRE

    The microbiology laboratory is the first line of defense against 
the spread of VRE in the hospital. The laboratory's ability to identify 
enterococci and detect vancomycin resistance promptly and accurately is 
essential in recognizing VRE colonization and infection and avoiding 
complex, costly containment efforts that are required when recognition 
of the problem is delayed. In addition, cooperation and communication 
between the laboratory and the infection control program will 
facilitate control efforts substantially.
    A. Identification of enterococci: Presumptively identify colonies 
on primary isolation plates as enterococci by using the colonial 
morphology, Gram stain, and PYR test. Although identifying enterococci 
to the species level can help predict certain resistance patterns 
(e.g., E. faecium is more resistant to penicillin than E. faecalis) and 
may help determine the epidemiologic relatedness of enterococcal 
isolates, such identification is not essential if antimicrobial 
susceptibility testing is performed.
    B. Antimicrobial susceptibility testing: Determine vancomycin 
resistance as well as high-level resistance to penicillin and 
aminoglycosides\17\ for enterococci isolated from blood, sterile body 
sites (with the possible exception of urine), and other sites as 
clinically indicated. Evaluate the laboratory's method of 
susceptibility testing, whether by automated microdilution or disk-
diffusion technique, for its ability to detect vancomycin resistance by 
using E. faecalis ATCC 51299. This strain has a moderate level of 
vancomycin resistance mediated by the vanB gene, which, unlike high-
level resistance mediated by vanA, is difficult to detect by most 
methods used in clinical laboratories. Laboratories using disk 
diffusion should incubate plates for 24 hours and read zones of 
inhibition by using transmitted light.\17\,\18\ If testing as above 
reveals that the method used by the laboratory is inadequate to detect 
vancomycin resistance, the laboratory should perform either of the 
following:
    1. Streak 1 l of standard inoculum (0.5 McFarland) from an 
isolated colony of enterococci onto BHI agar containing 6 g/ml 
of vancomycin, and incubate the inoculated plate for 24 hours at 35 
deg.C. Consider any growth indicative of vancomycin 
resistance.\17\,\18\
    2. Determine the minimum inhibitory concentration by agar dilution, 
broth macrodilution, or manual broth microdilution.\17\,\18\
    C. When VRE is isolated from a clinical specimen: 1. Confirm 
vancomycin resistance by repeating antimicrobial susceptibility testing 
using any of the recommended methods above, particularly if VRE 
isolates are unusual in the hospital.
    2. Immediately, while performing confirmatory susceptibility tests, 
notify the patient's primary caregiver, patient-care personnel on the 
ward on which the patient is hospitalized, and infection control 
personnel regarding the presumptive identification of VRE, so that the 
patient can be placed on appropriate isolation precautions promptly 
(See Section III-A-4). Follow this preliminary report with the (final) 
result of the confirmatory test. Additionally, highlight the report 
regarding the isolate to alert staff that isolation precautions are 
indicated.
    D. Screening procedures for detecting VRE in hospitals where VRE 
has not been detected: In many hospital microbiology laboratories, 
antimicrobial susceptibility testing of enterococcal isolates from 
urine or nonsterile body sites such as wounds is not performed 
routinely; thus, recognition of nosocomial VRE colonization and 
infection in hospitalized patients may be delayed. Therefore, in 
hospitals where VRE has not yet been detected, special measures can 
allow earlier detection of VRE.
    1. Antimicrobial susceptibility survey. Perform periodic 
susceptibility testing on enterococcal isolates recovered from all 
types of clinical specimens, especially from high-risk patients, such 
as those in an ICU or oncology or transplant ward. The optimal 
frequency of testing and number of isolates to test are unknown and may 
vary from hospital to hospital, depending on the hospital's patient 
population and number of cultures performed. Hospitals processing large 
numbers of culture specimens will need to test only a small fraction 
(e.g., 10%) of enterococcal isolates every 1-2 months, whereas 
hospitals processing fewer specimens may need to test all enterococcal 
isolates during the survey period. The hospital epidemiologist can be 
consulted to help design a suitable sampling strategy.
    2. Culture survey of stools or rectal swabs. In tertiary medical 
centers and other hospitals with many critically ill (e.g., ICU, 
oncology, transplant) patients at high risk for VRE infection or 
colonization, periodic culture surveys of stools or rectal-swabs of 
such patients can detect the appearance of VRE. Fecal screening is 
recommended before VRE infections have been identified clinically 
because most patients colonized with VRE will have intestinal 
colonization with this organism.\2\,\4\,\11\ The frequency and 
intensity of surveillance should be based on the size of the population 
at risk and the specific hospital unit(s) involved. If VRE have been 
detected in other institutions in a hospital's area and/or if a 
hospital wishes to determine whether VRE is present in the hospital 
despite the absence of recognized clinical cases, stool or rectal-swab 
culture surveys are very useful. The cost of screening can be reduced 
greatly by inoculating specimens onto vancomycin-containing selective 
media\2\,\12\ and restricting screening to those patients who have been 
in the hospital long enough (e.g., 5-7 days) to have a substantial risk 
of colonization, or who have been admitted from a facility, such as a 
tertiary-care hospital or a chronic-care facility, where VRE is known 
to be present. Once colonization with VRE has been detected, it would 
be appropriate to begin to screen routinely all of the enterococcal 
isolates from patients in the hospital (including those from urine and 
wounds) for vancomycin resistance and to intensify efforts to contain 
VRE spread, i.e., by strict adherence to handwashing and compliance 
with isolation precautions (See Section III-A-4 below). Intensified 
fecal screening for VRE may facilitate earlier identification of 
colonized patients, leading to more efficient containment of the 
microorganism.

III. Prevention and Control of Nosocomial Transmission of VRE

    Eradication of VRE from the hospital is most likely to succeed when 
VRE infection or colonization is confined to a few patients on a single 
ward. Once VRE has become endemic on a ward or has spread to multiple 
wards or to the community, eradication becomes extremely difficult and 
costly. Aggressive infection control measures and strict compliance by 
hospital personnel are required to limit nosocomial spread of VRE.
    Control of VRE requires a collaborative institution-wide 
multidisciplinary effort. Therefore, involve the hospital's quality 
assurance/improvement department at the outset in order to identify 
specific problems in hospital operations and patient-care systems and 
to design, implement, and evaluate appropriate changes in these 
systems.
    A. For all hospitals, including those where VRE have been isolated 
infrequently or not at all:
    1. Notify appropriate hospital staff promptly when VRE is detected. 
(See Section II-C-2 above).
    2. Make clinical staff aware of the hospital's policies regarding 
VRE-infected or colonized patients. Implement the required procedures 
as soon as VRE is detected because the slightest delay can lead to 
further spread of VRE and complicate control efforts. Clinical staff 
play a pivotal role in limiting the spread of VRE in patient-care 
areas. Accordingly, continuing education is critical regarding the 
appropriate response to the detection of VRE (See Section I above).
    3. Establish system(s) for monitoring appropriate process and 
outcome measures, such as cumulative incidence or incidence density of 
VRE colonization, rate of compliance with VRE isolation precautions and 
handwashing, interval between VRE identification in the laboratory and 
implementation of isolation precautions on the wards, and the 
percentage of previously colonized patients admitted to the ward who 
are promptly recognized and placed on isolation precautions. Relay 
these data to the clinical, administrative, laboratory, and support 
staff as reinforcement to ongoing education and control efforts.\19\
    4. Isolation precautions to prevent patient-to-patient transmission 
of VRE:
    a. Place VRE-infected or colonized patients in single rooms or in 
the same room as other patients with VRE.
    b. Wear gloves (clean nonsterile gloves are adequate) when entering 
the room of a VRE-infected or colonized patient; extensive 
environmental contamination with VRE has been noted in some 
studies.3,11,20 During the course of caring for a patient, a 
change of gloves may be necessary after contact with material that may 
contain high concentrations of VRE (e.g., stool).
    c. Wear a gown (a clean nonsterile gown is adequate) when entering 
the room of a VRE-infected or colonized patient if substantial contact 
with the patient or environmental surfaces in the patient's room is 
anticipated, or if the patient is incontinent, or has diarrhea, an 
ileostomy, a colostomy, or a wound drainage not contained by a 
dressing.
    d. i. Remove gloves and gown before leaving the patient's room, and 
wash hands immediately with an antiseptic soap.4 Hands can be 
contaminated via glove leaks21 or during glove removal and bland 
soap has been shown to be relatively ineffective in removing VRE from 
the hands.\22\
    ii. Ensure that after glove and gown removal and handwashing, 
clothing and hands do not contact environmental surfaces potentially 
contaminated with VRE (e.g., door knob or curtain) in the patient's 
room.
    5. Dedicate the use of noncritical items, such as stethoscope, 
sphygmomanometer, or electronic rectal thermometer, to a single patient 
or cohort of patients infected or colonized with VRE.\12\ If such 
devices are to be used on other patient(s), adequately clean and 
disinfect them first.\23\
    6. Culture stools or rectal swabs of roommates of patients newly 
found to be infected or colonized with VRE to determine their 
colonization status, and apply isolation precautions as necessary. 
Perform additional screening of patients on the ward at the discretion 
of the infection control staff.
    7. Adopt a policy for deciding when patients infected and/or 
colonized with VRE can be removed from isolation precautions. The 
optimal requirements remain unknown; however, since VRE colonization 
may persist indefinitely,\4\ stringent criteria may be appropriate, 
e.g., VRE-negative results on at least three consecutive occasions, one 
or more weeks apart, for all cultures from multiple body sites 
(including stool or rectal swab, perineal area, axilla or umbilicus, 
and wound, Foley catheter, and/or colostomy sites if present).
    8. Establish a system of highlighting the records of infected or 
colonized patients so that they can be recognized and isolated promptly 
upon readmission to the hospital because patients with VRE may remain 
colonized for long periods following discharge from the hospital.
    9. Discharging VRE-infected or colonized patients:
    Consult local and state health departments in developing a plan 
regarding the discharge of VRE-infected or colonized patients to 
nursing homes, other hospitals or home health-care, as part of a larger 
strategy for handling patients with resolving infections and patients 
colonized with antimicrobial-resistant microorganisms. This plan should 
emphasize handwashing and the appropriate use of gloves and gowns when 
having direct contact with the above-mentioned patients who are 
transferred from hospitals.
    B. In hospitals with endemic VRE or continued VRE transmission 
despite implementation of measures described in III-A-1 through III-A-
9:
    1. Focus control efforts initially on ICUs and other areas where 
VRE transmission rate is highest.\4\ Such units may serve as a 
reservoir of VRE, from where VRE spreads to other wards when patients 
are well enough to be transferred.
    2. Cohort staff so that nurses and others providing care to 
patients with VRE do not provide care to noncolonized patients during 
the same work shift.\4\ Healthcare workers who must provide care to 
both groups of patients during the same shift should make every effort 
to limit their movement between the two patient groups.
    3. Carriers of enterococci on the hospital staff have rarely been 
implicated in the transmission of this organism.\11\ Nonetheless, in 
conjunction with careful epidemiological studies and upon the direction 
of the infection control staff, examine personnel for chronic skin and 
nail problems and perform hand and rectal-swab cultures on them as well 
as on other personnel providing care to VRE-infected or colonized 
patients. Remove VRE-positive personnel epidemiologically linked to VRE 
transmission from the care of VRE-negative patients.
    4. The results of several enterococcal outbreak investigations 
suggest a potential role for the environment in the transmission of 
enterococci. In one study, nonoutbreak-related strains of vancomycin-
susceptible enterococci were isolated from cultures of environmental 
surfaces in patient rooms before and after terminal room cleaning and 
disinfection.CDC unpublished data In institutions experiencing 
ongoing VRE transmission, verify that the hospital has adequate 
procedures for the routine care, cleaning, and disinfection of 
environmental surfaces (e.g., bedrails, charts, carts, doorknobs, 
faucet handles, bedside commodes) and that these procedures are being 
followed by housekeeping personnel. Some hospitals may elect to perform 
focused environmental cultures before and after cleaning of rooms 
housing patients with VRE to verify the efficacy of hospital policies 
and procedures. All environmental culturing should be approved and 
supervised by the infection control program in collaboration with the 
clinical laboratory.11,12,20,24
    5. Consider sending representative VRE isolates to reference 
laboratories for strain typing by pulsed field gel electrophoresis or 
other suitable techniques to aid in defining reservoirs and patterns of 
transmission.

IV. Prudent Vancomycin Use

    Vancomycin use has been reported consistently as a risk factor for 
colonization and infection with VRE2,4,12,25 and may increase the 
possibility of the emergence of vancomycin-resistant S. aureus (VRSA) 
and/or vancomycin-resistant S. epidermidis. Therefore, all hospitals, 
even those where VRE has never been detected, should develop a 
comprehensive antimicrobial-utilization plan to provide education for 
medical staff, oversee surgical prophylaxis, and develop guidelines for 
the proper use of vancomycin. Guideline development should be part of 
the hospital's quality improvement program and involve participation 
from the hospital's pharmacy and therapeutics committee, hospital 
epidemiologist, and infection control, infectious diseases, medical, 
and surgical staffs. The guidelines should include the following 
considerations:
    A. Situations in which the use of vancomycin is appropriate or 
acceptable:
    1. For treatment of serious infections due to beta-lactam resistant 
gram-positive microorganisms. Clinicians should be aware that 
vancomycin may be less rapidly bactericidal than beta-lactam agents for 
beta-lactam susceptible staphylococci.26,27
    2. For treatment of infections due to gram-positive microorganisms 
in patients with serious allergy to beta-lactam antimicrobials.
    3. When antibiotic-associated colitis (AAC) fails to respond to 
metronidazole therapy or if AAC is severe and potentially life-
threatening.
    4. Prophylaxis, as recommended by the American Heart Association, 
for endocarditis following certain procedures in patients at high risk 
for endocarditis.28
    5. Prophylaxis for surgical procedures involving implantation of 
prosthetic materials or devices at institutions with a high rate of 
infections due to MRSA or methicillin-resistant S. epidermidis.29 
A single dose administered immediately before surgery is sufficient 
unless the procedure lasts more than 6 hours, in which case the dose 
should be repeated. Prophylaxis should be discontinued after a maximum 
of 2 doses.30-32
    B. Situations in which the use of vancomycin should be discouraged:
    1. Routine surgical prophylaxis.30
    2. Empiric antimicrobial therapy for a febrile neutropenic patient, 
unless there is strong evidence at the outset that the patient has an 
infection due to gram-positive microorganisms (e.g., inflamed exit site 
of Hickman catheter), and the prevalence of infections due to beta-
lactam-resistant gram-positive microorganisms (e.g., MRSA) in the 
hospital is substantial.2,33-39
    3. Treatment in response to a single blood culture positive for 
coagulase-negative staphylococcus, if other blood cultures drawn in the 
same time frame are negative, i.e., if contamination of the blood 
culture is likely. Because contamination of blood cultures with skin 
flora, e.g., S. epidermidis, may cause vancomycin to be inappropriately 
administered to patients, phlebotomists and other personnel who obtain 
blood cultures should be properly trained to minimize microbial 
contamination of specimens.
    4. Continued empiric use for presumed infections in patients whose 
cultures are negative for beta-lactam-resistant gram-positive 
microorganisms.37,40
    5. Systemic or local (e.g., antibiotic lock) prophylaxis for 
infection or colonization of indwelling central or peripheral 
intravascular catheters or vascular grafts.41-46
    6. Selective decontamination of the digestive tract.
    7. Eradication of MRSA colonization.47,48
    8. Primary treatment of AAC.49
    9. Routine prophylaxis for very low-birth-weight infants.50
    10. Routine prophylaxis for patients on continuous ambulatory 
peritoneal dialysis.51,52
    Further study is required to determine the most effective methods 
for influencing the prescribing practices of physicians, although a 
variety of techniques may be useful.53-56 In addition, key 
parameters of vancomycin use can be tracked through the hospital's 
quality assurance/improvement process or as part of the drug-
utilization review of the pharmacy and therapeutics committee and the 
medical staff.

V. Detection and Reporting of VRSA

    The microbiology laboratory has the primary responsibility for 
detecting and reporting the occurrence of VRSA in the hospital.
    A. Antimicrobial susceptibility testing: Routinely test all 
clinical isolates of S. aureus for susceptibility to vancomycin by 
using standard methods.17
    B. When VRSA is identified in a clinical specimen:
    1. Confirm vancomycin resistance in S. aureus by repeating 
antimicrobial susceptibility testing using standard methods.17 It 
is advisable to restreak the colony to ensure that the S. aureus 
culture is pure. The most common causes of false-positive VRSA report 
are susceptibility testing on mixed cultures and misidentification of 
VRE, Leukonostoc, S. haemolyticus or Pediococcus as VRSA.57,58
    2. Immediately, while performing confirmatory testing, notify the 
hospital's infection control personnel, the patient's primary 
caregiver, and patient-care personnel on the ward on which the patient 
is hospitalized so that the patient can be placed promptly on isolation 
precautions adapted from, depending on the site(s) of infection or 
colonization,59 those recommended for VRE infection or 
colonization. (See Section III-A-4 through III-B-5 above.)
    3. Immediately notify the state health department and CDC, and send 
the isolate through the state health department to CDC (telephone 
number 404-639-1550) for confirmation of vancomycin resistance.

References

    1. Centers for Disease Control and Prevention. Nosocomial 
enterococci resistant to vancomycin--United States, 1989-1993. MMWR 
1993; 42:597-599.
    2. Rubin LG, Tucci V, Cercenado E, Eliopoulos G, Isenberg HD. 
Vancomycin-resistant Enterococcus faecium in hospitalized children. 
Infect Control Hosp Epidemiol 1992; 13:700-705.
    3. Karanfil LV, Murphy M, Josephson A, et al. A cluster of 
vancomycin-resistant Enterococcus faecium in an intensive care unit. 
Infect Control Hosp Epidemiol 1992; 13:195-200.
    4. Handwerger S, Raucher B, Altarac D, et al. Nosocomial 
outbreak due to Enterococcus faecium highly resistant to vancomycin, 
penicillin, and gentamicin. Clin Infect Dis 1993; 16:750-755.
    5. Frieden TR, Munsiff SS, Low DE, et al. Emergence of 
vancomycin-resistant enterococci in New York City. Lancet 1993; 
342:76-79.
    6. Boyle JF, Soumakis SA, Rendo A, et al. Epidemiologic analysis 
and genotypic characterization of a nosocomial outbreak of 
vancomycin-resistant enterococci. J Clin Microbiol 1993; 31:1280-
1285.
    7. Tenover FC, Tokars J, Swenson J, Paul S, Spitalny K, Jarvis 
W. Ability of clinical laboratories to detect antimicrobial agent-
resistant enterococci. J Clin Microbiol 1993; 31:1695-1699.
    8. Sahm DF, Olsen L. In vitro detection of enterococcal 
vancomycin resistance. Antimicrob Agents Chemother 1990; 34:1846-
1848.
    9. Moellering RC, Jr. The Garrod lecture. The enterococcus: a 
classic example of the impact of antimicrobial resistance on 
therapeutic options. J Antimicrob Chemother 1991; 28:1-12.
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Microbiol Rev 1990; 3:46-65.
    11. Rhinehart E, Smith N, Wennestern C, et al. Rapid 
dissemination of beta-lactamase-producing aminoglycoside-resistant 
Enterococcus faecium. N Engl J Med 1990; 323:1814-1818.
    12. Livornese LL, Jr., Dias S, Samel C, et al. Hospital-acquired 
infection with vancomycin-resistant Enterococcus faecium transmitted 
by electronic thermometers. Ann Intern Med 1992; 117:112-116.
    13. Uttley AH, George RC, Naidoo J, et al. High-level 
vancomycin-resistant enterococci causing hospital infections. 
Epidemiol Infect 1989; 103:173-181.
    14. Leclercq R, Derlot E, Weber M, Duval J, Courvalin P. 
Transferable vancomycin and teicoplanin resistance in Enterococcus 
faecium. Antimicrob Agents Chemother 1989; 33:10-15.
    15. Noble WC, Virani Z, Cree R. Cotransfer of vancomycin and 
other resistance genes from Enterococcus faecalis NCTC12201 to 
Staphylococcus aureus. FEMS Microbiology Letters 1992; 93:195-198.
    16. Veach LA, Pfaller MA, Barrett M, Koontz FP, Wenzel RP. 
Vancomycin resistance in Staphylococcus haemolyticus causing 
colonization and bloodstream infection. J Clin Microbiol 1990; 
28:2064-2068.
    17. National Committee for Clinical Laboratory Standards. 
Methods for dilution antimicrobial susceptibility tests for bacteria 
that grow aerobically. Publication M7-A3. 3rd ed. Villanova, PA: 
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