[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
_______________________________________________________________________
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.
10. Murray BE. The life and times of the enterococcus. Clin
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:
National Committee for Clinical Laboratory Standards, 1993.
18. Swenson JM, Ferraro MJ, Sahm DF, Charache P, The National
Committee for Clinical Laboratory Standards Working Group on
Enterococci, Tenover FC. New vancomycin disk diffusion breakpoints
for enterococci. J Clin Microbiol 1992; 30:2525-2528.
19. Nettleman MD, Trilla A, Fredrickson M, Pfaller M. Assigning
responsibility: using feedback to achieve sustained control of
methicillin-resistant Staphylococcus aureus. Am J Med 1991; 91 suppl
3B:228S-232S.
20. Zervos MJ, Kauffman CA, Therasse PM, Bergman AG, Mikesell
TS, Schaberg DR. Nosocomial infection by gentamicin-resistant
Streptococcus faecalis: an epidemiologic study. Ann Intern Med 1987;
106:687-691.
21. Olsen RJ, Lynch P, Coyle MB, Cummings J, Bokete T, Stamm WE.
Examination gloves as barriers to hand contamination in clinical
practice. JAMA 1993; 270:350-353.
22. Wade JJ, Desai N, Casewell MW. Hygienic hand disinfection
for the removal of epidemic vancomycin-resistant Enterococcus
faecium and gentamicin-resistant Enterobacter cloacae. J Hosp Infect
1991; 18:211-218.
23. Favero MS, Bond WW. Sterilization, disinfection, and
antisepsis in the hospital. In: Manual of Clinical Microbiology.
Washington, D.C.: American Society for Microbiology, 1991:183-200.
24. Wells VD, Wong ES, Murray BE, Coudron PE, Williams DS,
Markowitz SM. Infections due to beta-lactamase-producing, high-level
gentamicin-resistant Enterococcus faecalis. Ann Intern Med 1992;
116:285-292.
25. Weinstein RA. Epidemiology and control of nosocomial
infections in adult intensive care units. Am J Med 1991; 30:2525-
2528.
26. Small PM, Chambers HF. Vancomycin for Staphylococcus aureus
endocarditis in intravenous drug users. Antimicrob Agents Chemother
1990; 34:1227-1231.
27. Cantoni L, Glauser MP, Bille J. Comparative efficacy of
daptomycin, vancomycin, and cloxacillin for the treatment of
Staphylococcus aureus endocarditis in rats and role of test
conditions in this determination. Antimicrob Agents Chemother 1990;
34:2348-2353.
28. American Heart Association Committee on Rheumatic Fever and
Infective Endocarditis. Prevention of bacterial endocarditis.
Circulation 1984; 70:1123-1124.
29. Maki DG, Bohn MJ, Stolz SM, Kroncke GM, Acher CW, Myerowitz
PD. Comparative study of cefazolin, cefamandole, and vancomycin for
surgical prophylaxis in cardiac and vascular operations. J Thorac
Cardiovasc Surg 1992; 104:1432-1434.
30. Conte JE, Jr., Cohen SN, Roe BB, et al. Antibiotic
prophylaxis and cardiac surgery: A prospective double-blind
comparison of single-dose versus multiple-dose regimens. Ann Intern
Med 1972; 76:943.
31. DiPiro JT, Cheung RPF, Bowden TA, et al. Single-dose
systemic antibiotic prophylaxis of surgical wound infections. Am J
Surg 1986; 152:552.
32. Nelson CL, Green TG, Porter RA, et al. One day versus seven
days of preventive antibiotic therapy in orthopedic surgery. Clin
Orthop 1983; 176:258-263.
33. Rubin M, Hathorn JW, Marshall D, Gress J, Steinberg S, Pizzo
PA. Gram-positive infections and the use of vancomycin in 550
episodes of fever and neutropenia. Ann Intern Med 1988; 108:30-35.
34. Shenep JL, Hughes WT, Roberson PK, et al. Vancomycin,
ticarcillin, and amikacin compared with ticarcillin-clavulanate and
amikacin in the empirical treatment of febrile neutropenic children
with cancer. N Engl J Med 1988; 319:1053-1058.
35. Pizzo PA, Hathorn JW, Hemenz J, et al. A randomized trial
comparing ceftazidime alone with combination antibiotic therapy in
cancer patients with fever and neutropenia. N Engl J Med 1986;
315:552-558.
36. Karp JE, Dick JD, Angelopulos C, et al. Empiric use of
vancomycin during prolonged treatment-induced granulocytopenia. Am J
Med 1986; 81:237-242.
37. Pestotnik SL, Evans RS, Burke JP, et al. Therapeutic
antibiotic monitoring: surveillance using a computerized expert
system. Am J Med 1990; 88:43.
38. European Organization for Research and Treatment of Cancer
(EORTC) International Antimicrobial Therapy Cooperative Group,
National Cancer Institute of Canada Clinical Trials Group.
Vancomycin added to empirical combination antibiotic therapy for
fever in granulocytopenic cancer patients. J Infect Dis 1991;
163:951-958.
39. Riikonen P. Imipenem compared with ceftazidime plus
vancomycin as initial therapy for fever in neutropenic children with
cancer. Pediatr Infect Dis 1991; 10:918-923.
40. Maki DG, Schuma AA. A study of antimicrobial misuse in a
university hospital. Am J Med Sci 1978; 275:271-282.
41. Ranson MR, Oppenheim BA, Jackson A, Kamthan AG, Scarffe JH.
Double-blind placebo controlled study of vancomycin prophylaxis for
central venous catheter insertion in cancer patients. J Hosp Infect
1990; 15:95-102.
42. Hendrickson KJ, Posell KR, Schwartz CL. A dilute solution of
vancomycin and heparin retains antibacterial and anticoagulant
activities. J Infect Dis 1989; 157:600-601.
43. Schwartz CL, Hendrickson KJ, Roghmann K, Posell K.
Prevention of bacteremia attributed to luminal colonization of
tunneled central venous catheters with vancomycin-susceptible
organism. J Clin Oncol 1990; 8:1591-1597.
44. Hendrickson KJ, Dunne WM. Modification of central venous
catheter flush solution improves in vitro antimicrobial activity. J
Infect Dis 1992; 166:944-946.
45. Gaillard I, Merlino R, Pajot N, et al. Conventional and
nonconventional modes of vancomycin administration to decontaminate
the internal surface of catheters colonized with coagulase-negative
staphylococci. J Paren Enter Nutr 1990; 14:593-597.
46. Kaplan AH, Gilligan PH, Facklam RR. Recovery of resistant
enterococci during vancomycin prophylaxis. J Clin Microbiol 1988;
26:1216-1218.
47. Gradon JD, Wu EH, Lutwick LI. Aerosolized vancomycin therapy
facilitating nursing home placement. Acta Pharmacother 1992; 26:209-
210.
48. Weathers J, Riggs D, Santeiro M, Weibley RE. Aerosolized
vancomycin for treatment of airway colonization by methicillin-
resistant Staphylococcus aureus. Pediatr Infect Dis 1990; 9:220-221.
49. Johnson S, Homann SR, Bettin KM, et al. Treatment of
asymptomatic Clostridium difficile carriers (fecal excretors) with
vancomycin or metronidazole. Ann Intern Med 1992; 117:297-302.
50. Moller JC, Nachtrodt G, Richter A, Tegtmeyer FK.
Prophylactic vancomycin to prevent staphylococcal septicemia in
very-low-birth-weight infants. Lancet 1992; 340:424.(abstract)
51. Lam TY, Vas SI, Oreopoulos DG. Long-term intraperitoneal
vancomycin in the prevention of recurrent peritonitis during
continuous ambulatory peritoneal dialysis: Preliminary results.
Perit Dial Inter 1991; 11:281-282.
52. Bestani B, Freer K, Read D, et al. Treatment of gram-
positive peritonitis with two intraperitoneal doses of vancomycin in
continuous ambulatory peritoneal dialysis patients. Nephron 1987;
45:283-285.
53. Soumerai SB, McLaughlin TJ, Avorn J. Quality assurance for
drug prescribing. Quality Assurance in Health Care 1990; 2:37-58.
54. Everitt DE, Soumerai SB, Avorn J, Klapholz H, Wessels M.
Changing surgical antimicrobial prophylaxis practices through
education targeted at senior department leaders. Infect Control Hosp
Epidemiol 1990; 11:578-583.
55. Soumerai SB, Avorn J, Taylor WC, Wessels M, Maher D, Hawley
SL. Improving choice of prescribed antibiotics through concurrent
reminders in an educational order form. Medical Care 1993; 31:552-
558.
56. Soumerai SB, McLaughlin TJ, Avorn J. Improving drug
prescribing in primary care: a critical analysis of the experimental
literature. Milbank Quarterly 1989; 67:268-317.
57. Orgberg PK, Sandine WE. Common occurrence of plasmid DNA and
vancomycin resistance in Leuconostoc spp. Appl Environ Microbiol
1984; 48:1129-1133.
58. Schwalbe RS, Ritz WJ, Verma PR, Barranco EA, Gilligan PH.
Selection for vancomycin resistance in clinical isolates of
Staphylococcus haemolyticus. J Infect Dis 1990; 161:45-51.
59. Garner JS, Simmons BP. Guideline for isolation precautions
in hospitals. Infect Control Hosp Epidemiol 1983; 4(Suppl):245-325.
[FR Doc. 94-11913 Filed 5-16-94; 8:45 am]
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