Recommendations for Preventing the Spread
of Vancomycin Resistance
Recommendations of the Hospital Infection Control Practices
Advisory Committee (HICPAC)
Summary
Since 1989, a rapid increase in the incidence of infection and
colonization with vancomycin-resistant enterococci (VRE) has been
reported
by U.S. hospitals. This increase poses important problems,
including a) the
lack of available antimicrobial therapy for VRE infections, because
most
VRE are also resistant to drugs previously used to treat such
infections
(e.g., aminoglycosides and ampicillin), and b) the possibility that
the
vancomycin-resistant genes present in VRE can be transferred to
other
gram-positive microorganisms (e.g., Staphylococcus aureus).
An increased risk for VRE infection and colonization has been
associated with previous vancomycin and/or multiantimicrobial
therapy,
severe underlying disease or immunosuppression, and intraabdominal
surgery.
Because enterococci can be found in the normal gastrointestinal and
female
genital tracts, most enterococcal infections have been attributed
to
endogenous sources within the individual patient. However, recent
reports
of outbreaks and endemic infections caused by enterococci,
including VRE,
have indicated that patient-to-patient transmission of the
microorganisms
can occur either through direct contact or through indirect contact
via a)
the hands of personnel or b) contaminated patient-care equipment or
environmental surfaces.
This report presents recommendations of the Hospital Infection
Control
Practices Advisory Committee for preventing and controlling the
spread of
vancomycin resistance, with a special focus on VRE. Preventing and
controlling the spread of vancomycin resistance will require
coordinated,
concerted efforts from all involved hospital departments and can be
achieved only if each of the following elements is addressed: a)
prudent
vancomycin use by clinicians, b) education of hospital staff
regarding the
problem of vancomycin resistance, c) early detection and prompt
reporting
of vancomycin resistance in enterococci and other gram-positive
microorganisms by the hospital microbiology laboratory, and d)
immediate
implementation of appropriate infection-control measures to prevent
person-to-person transmission of VRE.
INTRODUCTION
From 1989 through 1993, the percentage of nosocomial
enterococcal
infections reported to CDC's National Nosocomial Infections
Surveillance
(NNIS) system that were caused by vancomycin-resistant enterococci
(VRE)
increased from 0.3% to 7.9% (1). This overall increase primarily
reflected
the 34-fold increase in the percentage of VRE infections in
patients in
intensive-care units (ICUs) (i.e., from 0.4% to 13.6%), although a
trend
toward an increased percentage of VRE infections in non-ICU
patients also
was noted (1). The occurrence of VRE in NNIS hospitals was
associated with
larger hospital size (i.e., a hospital with greater than or equal
to 200
beds) and university affiliation (1). Other hospitals also have
reported
increased endemic rates and clusters of VRE infection and
colonization
(2-8). The actual increase in the incidence of VRE in U.S.
hospitals might
be greater than reported because the fully automated methods used
in many
clinical laboratories cannot consistently detect vancomycin
resistance,
especially moderate vancomycin resistance (as manifested in the
VanB
phenotype) (9-11).
Vancomycin resistance in enterococci has coincided with the
increasing
incidence of high-level enterococcal resistance to penicillin and
aminoglycosides, thus presenting a challenge for physicians who
treat
patients who have infections caused by these microorganisms (1,4).
Treatment options are often limited to combining antimicrobials or
experimental compounds that have unproven efficacy (12-14).
The epidemiology of VRE has not been clarified; however,
certain
patient populations are at increased risk for VRE infection or
colonization. These populations include critically ill patients or
those
with severe underlying disease or immunosuppression (e.g., patients
in ICUs
or in oncology or transplant wards); persons who have had an
intraabdominal
or cardio-thoracic surgical procedure or an indwelling urinary or
central
venous catheter; and persons who have had a prolonged hospital stay
or
received multiantimicrobial and/or vancomycin therapy (2-8).
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 (15). However, recent
studies
have indicated that VRE and other enterococci can be transmitted
directly
by patient-to-patient contact or indirectly by transient carriage
on the
hands of personnel (16) or by contaminated environmental surfaces
and
patient-care equipment (3,8,17).
The potential emergence of vancomycin resistance in clinical
isolates
of Staphylococcus aureus and Staphylococcus epidermidis also is a
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
(18,19),
including S. aureus (20). Although vancomycin resistance in
clinical
strains of S. epidermidis or S. aureus has not been reported,
vancomycin-resistant strains of Staphylococcus haemolyticus have
been
isolated (21,22).
In November 1993 and February 1994, the Subcommittee on the
Prevention
and Control of Antimicrobial-Resistant Microorganisms in Hospitals
of CDC's
Hospital Infection Control Practices Advisory Committee (HICPAC)
responded
to the increase in vancomycin resistance in enterococci by meeting
with
representatives from the American Hospital Association, the
American
Society for Microbiology, the Association for Professionals in
Infection
Control and Epidemiology, the Infectious Diseases Society of
America, the
Society for Healthcare Epidemiology of America, and the Surgical
Infection
Society. Meeting participants agreed with the need for prompt
implementation of control measures; thus, recommendations to
prevent the
spread of VRE were developed. Public comments were solicited and
incorporated into the draft recommendations. In November 1994,
HICPAC
ratified the following recommendations for preventing and
controlling the
spread of vancomycin resistance, with special focus on VRE.
HICPAC recognizes that a) data are limited and additional
research
will be required to clarify the epidemiology of VRE and determine
cost-effective control strategies, and b) many U.S. hospitals have
concurrent problems with other antimicrobial-resistant organisms
(e.g.,
methicillin-resistant S. aureus {MRSA} and beta-lactam and
aminoglycoside-resistant gram-negative bacilli) that might have
different
epidemiologic features and require different control measures.
RECOMMENDATIONS
Each hospital -- through collaboration of its
quality-improvement and
infection-control programs; pharmacy and therapeutics committee;
microbiology laboratory; 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. The following elements should
be
addressed in the plan.
Prudent Vancomycin Use
Vancomycin use has been reported consistently as a risk factor
for
infection and colonization with VRE (2,4,7,8,17) and may increase
the
possibility of the emergence of vancomycin-resistant S. aureus
(VRSA)
and/or vancomycin-resistant S. epidermidis (VRSE). Therefore, all
hospitals
and other health-care delivery services, even those at which VRE
have never
been detected, should a) develop a comprehensive,
antimicrobial-utilization
plan to provide education for their medical staff (including
medical
students who rotate their training in different departments of the
health-care facility), b) oversee surgical prophylaxis, and c)
develop
guidelines for the proper use of vancomycin (as applicable to the
institution).
Guideline development should be part of the hospital's
quality-improvement program and should involve participation from
the
hospital's pharmacy and therapeutics committee; hospital
epidemiologist;
and infection-control, infectious-disease, medical, and surgical
staffs.
The guidelines should include the following considerations:
Situations in which the use of vancomycin is appropriate or
acceptable:
For treatment of serious infections caused by
beta-lactam-
resistant gram-positive microorganisms. Vancomycin may be
less
rapidly bactericidal than are beta-lactam agents for
beta-lactam-
susceptible staphylococci (23,24).
For treatment of infections caused by gram-positive
microorganisms in patients who have serious allergies to
beta-lactam antimicrobials.
When antibiotic-associated colitis fails to respond to
metronidazole therapy or is severe and potentially
life-threatening.
Prophylaxis, as recommended by the American Heart
Association,
for endocarditis following certain procedures in patients
at high
risk for endocarditis (25).
Prophylaxis for major surgical procedures involving
implantation
of prosthetic materials or devices (e.g., cardiac and
vascular
procedures {26} and total hip replacement) at
institutions that
have a high rate of infections caused by MRSA or
methicillin-resistant S. epidermidis. A single dose of
vancomycin
administered immediately before surgery is sufficient
unless the
procedure lasts greater than 6 hours, in which case the
dose
should be repeated. Prophylaxis should be discontinued
after a
maximum of two doses (27-30).
Situations in which the use of vancomycin should be
discouraged:
Routine surgical prophylaxis other than in a patient who
has a
life-threatening allergy to beta-lactam antibiotics (28).
Empiric antimicrobial therapy for a febrile neutropenic
patient,
unless initial evidence indicates that the patient has an
infection caused by gram-positive microorganisms (e.g.,
at an
inflamed exit site of Hickman catheter) and the
prevalence of
infections caused by MRSA in the hospital is substantial
(31-37).
Treatment in response to a single blood culture positive
for
coagulase-negative staphylococcus, if other blood
cultures taken
during 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) could
result in
inappropriate administration of vancomycin, phlebotomists
and
other personnel who obtain blood cultures should be
trained to
minimize microbial contamination of specimens (38-40).
Continued empiric use for presumed infections in patients
whose
cultures are negative for beta-lactam-resistant
gram-positive
microorganisms (41).
Systemic or local (e.g., antibiotic lock) prophylaxis for
infection or colonization of indwelling central or
peripheral
intravascular catheters (42-48).
Selective decontamination of the digestive tract.
Eradication of MRSA colonization (49,50).
Primary treatment of antibiotic-associated colitis (51).
Routine prophylaxis for very low-birthweight infants
(i.e.,
infants who weigh less than 1,500 g {3 lbs 4 oz}) (52).
Routine prophylaxis for patients on continuous ambulatory
peritoneal dialysis or hemodialysis (48,53).
Treatment (chosen for dosing convenience) of infections
caused by
beta-lactam-sensitive gram-positive microorganisms in
patients
who have renal failure (54-57).
Use of vancomycin solution for topical application or
irrigation.
Enhancing compliance with recommendations:
Although several techniques may be useful, further study
is
required to determine the most effective methods for
influencing
the prescribing practices of physicians (58-61).
Key parameters of vancomycin use can be monitored 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.
Education Programs
Continuing education programs for hospital staff (including
attending
and consulting physicians, medical residents, and students;
pharmacy,
nursing, and laboratory personnel; and other direct patient-care
providers)
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 an aggressive
approach and
high performance standards for hospital personnel, special
awareness and
educational sessions might be indicated.
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 promptly
and
accurately identify enterococci and detect vancomycin resistance is
essential for 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.
Identification of Enterococci
Presumptively identify colonies on primary isolation plates as
enterococci by using colonial morphology, a Gram stain, and a
pyrrolidonyl
arylamidase (PYR) test. Although identifying enterococci to the
species
level can help predict certain resistance patterns (e.g.,
Enterococcus
faecium is more resistant to penicillin than is Enterococcus
faecalis) and
may help determine the epidemiologic relatedness of enterococcal
isolates,
such identification is not routinely necessary if antimicrobial
susceptibility testing is performed. However, under special
circumstances
or as laboratory resources permit, biochemical tests can be used to
differentiate between various enterococcal species. Although most
commercially available identification systems adequately
differentiate E.
faecalis from other species of enterococci, additional tests for
motility
and pigment production are required to distinguish Enterococcus
gallinarum
(motile and nonpigmented) and Enterococcus casseliflavus (motile
and
pigmented) from E. faecium (nonmotile and nonpigmented).
Tests for Antimicrobial Susceptibility
Determine vancomycin resistance and high-level resistance to
penicillin (or ampicillin) and aminoglycosides (62) for enterococci
isolated from blood, sterile body sites (with the possible
exception of
urine), and other sites as clinically indicated. Laboratories
routinely may
test wound and urine isolates for resistance to vancomycin and
penicillin
or ampicillin if resources permit (see Screening Procedures for
Detecting
VRE in Hospitals Where VRE Have Not Been Detected).
Laboratories that use disk diffusion should incubate plates
for 24
hours and read zones of inhibition by using transmitted light
(62,63).
Minimum inhibitory concentrations can be determined by agar
dilution,
agar gradient dilution, broth macrodilution, or manual broth
microdilution (62-64). These test systems should be incubated
for 24
hours.
The fully automated methods of testing enterococci for
resistance to
vancomycin currently are unreliable (9-11).
When VRE Are Isolated From a Clinical Specimen
Confirm vancomycin resistance by repeating antimicrobial
susceptibility testing using any of the recommended methods (see
Tests for
Antimicrobial Susceptibility), particularly if VRE isolates are
unusual in
the hospital, OR streak 1 uL of standard inoculum (0.5 McFarland)
from an
isolated colony of enterococci onto brain heart infusion agar
containing 6
ug/mL of vancomycin, incubate the inoculated plate for 24 hours at
35 C (95
F), and consider any growth indicative of vancomycin resistance
(62,63,65).
Immediately, while performing confirmatory susceptibility
tests,
notify the patient's primary caregiver, patient-care personnel, and
infection-control personnel regarding the presumptive
identification of VRE
so that appropriate isolation precautions can be initiated promptly
(see
Preventing and Controlling VRE Transmission in All Hospitals).
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.
Screening Procedures for Detecting VRE in Hospitals Where VRE Have
Not Been
Detected
In some hospital microbiology laboratories, antimicrobial
susceptibility testing of enterococcal isolates from urine or
nonsterile
body sites (e.g., wounds) is not performed routinely; thus,
identification
of nosocomial VRE colonization and infection in hospitalized
patients may
be delayed. Therefore, in hospitals where VRE have not yet been
detected,
implementing special measures can promote earlier detection of VRE.
Antimicrobial susceptibility survey. Perform periodic
susceptibility
testing on an epidemiologic sample of enterococcal isolates
recovered from
all types of clinical specimens, especially from high-risk patients
(e.g.,
those in an ICU or in an oncology or transplant ward). The optimal
frequency of testing and number of isolates to be tested will vary
among
hospitals, depending on the patient population and number of
cultures
performed at the hospital. Hospitals that process large numbers of
culture
specimens need to test only a fraction (e.g., 10%) of enterococcal
isolates
every 1-2 months, whereas hospitals processing fewer specimens
might need
to test all enterococcal isolates during the survey period. The
hospital
epidemiologist can help design a suitable sampling strategy.
Culture survey of stools or rectal swabs. In tertiary medical
centers
and other hospitals that have many critically ill patients (e.g.,
ICU,
oncology, and transplant patients) at high risk for VRE infection
or
colonization, periodic culture surveys of stools or rectal swabs of
such
patients can detect the presence of VRE. Because most patients
colonized
with VRE have intestinal colonization with this organism, fecal
screening
of patients is recommended even though VRE infections have not been
identified clinically (2,4,16).
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 health-care facilities in a
hospital's
area and/or if a hospital's staff decides to determine whether VRE
are
present in the hospital despite the absence of recognized clinical
cases,
stool or rectal-swab culture surveys are useful. The cost of
screening can
be reduced by inoculating specimens onto selective media containing
vancomycin (2,17,66) and restricting screening to those patients
who have
been in the hospital long enough to have a substantial risk for
colonization (e.g., 5-7 days) or who have been admitted from a
facility
(e.g., a tertiary-care hospital or a chronic-care facility) where
VRE have
been identified.
After colonization with VRE has been detected, all the
enterococcal
isolates (including those from urine and wounds) from patients in
the
hospital should be screened routinely for vancomycin resistance,
and
efforts to contain the spread of VRE should be intensified (i.e.,
by strict
adherence to handwashing and compliance with isolation precautions)
(see
Preventing and Controlling VRE Transmission in All Hospitals).
Intensified
fecal screening for VRE might facilitate earlier identification of
colonized patients, leading to more efficient containment of the
microorganism.
Preventing and Controlling Nosocomial Transmission of VRE
Eradicating VRE from hospitals is most likely to succeed when
VRE
infection or colonization is confined to a few patients on a single
ward.
After VRE have become endemic on a ward or have spread to multiple
wards or
to the community, eradication becomes 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, the hospital's
quality-assurance/improvement department should be involved at the
outset
to identify specific problems in hospital operations and
patient-care
systems and to design, implement, and evaluate appropriate changes
in these
systems.
Preventing and Controlling VRE Transmission in All Hospitals
The following measures should be implemented by all hospitals,
including those in which VRE have been isolated infrequently or not
at all,
to prevent and control transmission of VRE.
Notify appropriate hospital staff promptly when VRE are
detected (see
When VRE Are Isolated From a Clinical Specimen).
Inform clinical staff of the hospital's policies regarding
VRE-infected or colonized patients. Because the slightest
delay can
lead to further spread of VRE and complicate control efforts,
implement the required procedures as soon as VRE are detected.
Clinical staff are essential to limiting the spread of VRE in
patient-care areas; thus, continuing education regarding the
appropriate response to the detection of VRE is critical (see
Education Programs).
Establish system(s) for monitoring appropriate process and
outcome
measures (e.g., 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 identified promptly and placed on isolation precautions).
Relay
these data to the clinical, administrative, laboratory, and
support
staff to reinforce ongoing education and control efforts (67).
Initiate the following isolation precautions to prevent
patient-to-patient transmission of VRE:
Place VRE-infected or colonized patients in private rooms
or in
the same room as other patients who have VRE (8).
Wear gloves (clean, nonsterile gloves are adequate) when
entering
the room of a VRE-infected or colonized patient because
VRE can
extensively contaminate such an environment (3,8,16,17).
When
caring for a patient, a change of gloves might be
necessary after
contact with material that could contain high
concentrations of
VRE (e.g., stool).
Wear a gown (a clean, nonsterile gown is adequate) when
entering
the room of a VRE-infected or colonized patient a) if
substantial
contact with the patient or with environmental surfaces
in the
patient's room is anticipated, b) if the patient is
incontinent,
or c) if the patient has had an ileostomy or colostomy,
has
diarrhea, or has a wound drainage not contained by a
dressing
(8).
Remove gloves and gown before leaving the patient's room
and
immediately wash hands with an antiseptic soap or a
waterless
antiseptic agent (68-71). Hands can be contaminated via
glove
leaks (72-76) or during glove removal, and bland soap
does not
always completely remove VRE from the hands (77).
Ensure that after glove and gown removal and handwashing,
clothing and hands do not contact environmental surfaces
in the
patient's room that are potentially contaminated with VRE
(e.g.,
a door knob or curtain) (3,8).
Dedicate the use of noncritical items (e.g., a stethoscope,
sphygmomanometer, or rectal thermometer) to a single patient
or cohort
of patients infected or colonized with VRE (17). If such
devices are
to be used on other patients, adequately clean and disinfect
these
devices first (78).
Obtain a stool culture or rectal swab from 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.
Adopt a policy for deciding when patients infected or
colonized with
VRE can be removed from isolation precautions. The optimal
requirements remain unknown; however, because VRE colonization
can
persist indefinitely (4), stringent criteria might be
appropriate,
such as VRE-negative results on at least three consecutive
occasions
(greater than or equal to 1 week 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).
Because patients with VRE can remain colonized for long
periods after
discharge from the hospital, establish a system for
highlighting the
records of infected or colonized patients so they can be
promptly
identified and placed on isolation precautions upon
readmission to the
hospital. This information should be computerized so that
placement of
colonized patients on isolation precautions will not be
delayed
because the patients' medical records are unavailable.
Local and state health departments should be consulted when
developing
a plan regarding the discharge of VRE-infected or colonized
patients
to nursing homes, other hospitals, or home-health care. This
plan
should be part of a larger strategy for handling patients who
have
resolving infections and patients colonized with
antimicrobial-resistant microorganisms.
Hospitals With Endemic VRE or Continued VRE Transmission
The following measures should be taken to prevent and control
transmission of VRE in hospitals that have endemic VRE or continued
VRE
transmission despite implementation of measures described in the
preceding
section (see Preventing and Controlling VRE Transmission in All
Hospitals).
Focus control efforts initially on ICUs and other areas where
the VRE
transmission rate is highest (4). Such areas can serve as
reservoirs
for VRE, allowing VRE to spread to other wards when patients
are well
enough to be transferred.
Where feasible, cohort the staff who provide regular, ongoing
care to
patients to minimize the movement/contact of health-care
providers
between VRE-positive and VRE-negative patients (4,8).
Hospital staff who are carriers of enterococci have been
implicated
rarely in the transmission of this organism (8). However, in
conjunction with careful epidemiologic 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 of
these
workers. Remove from the care of VRE-negative patients those
VRE-positive personnel linked epidemiologically to VRE
transmission
until their carrier state has been eradicated.
Because the results of several enterococcal outbreak
investigations
suggest a potential role for the environment in the
transmission of
enterococci (3,8,16,17,79,80), institutions experiencing
ongoing VRE
transmission should verify that the hospital has adequate
procedures
for the routine care, cleaning, and disinfection of
environmental
surfaces (e.g., bed rails, bedside commodes, carts, charts,
doorknobs,
and faucet handles) and that these procedures are being
followed by
housekeeping personnel. To verify the efficacy of hospital
policies
and procedures, some hospitals might elect to perform focused
environmental cultures before and after cleaning rooms that
house
patients who have VRE. All environmental culturing should be
approved
and supervised by the infection-control program in
collaboration with
the clinical laboratory (3,8,16,17,79,80).
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.
Detecting and Reporting VRSA and VRSE
The microbiology laboratory has the primary responsibility for
detecting and reporting the occurrence of VRSA or VRSE in the
hospital. All
clinical isolates of S. aureus and S. epidermidis should be tested
routinely, using standard methods, for susceptibility to vancomycin
(62).
If VRSA or VRSE is identified in a clinical specimen, confirm
vancomycin
resistance by repeating antimicrobial susceptibility testing using
standard
methods (62). Restreak the colony to ensure that the culture is
pure. The
most common causes of false-positive VRSA reports are
susceptibility
testing on mixed cultures and misidentifying VRE, Leuconostoc, S.
haemolyticus, or Pediococcus as VRSA (81,82).
Immediately (i.e., 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
(depending on the site{s} of infection or colonization) adapted
from
previous CDC guidelines (83) and those recommended for VRE
infection or
colonization in this report (see Preventing and Controlling
Nosocomial
Transmission of VRE). Furthermore, immediately notify the state
health
department and CDC, and send the isolate through the state health
department to CDC (telephone {404} 639-6413) for confirmation of
vancomycin
resistance.
References
CDC. Nosocomial enterococci resistant to vancomycin -- United
States,
1989-1993. MMWR 1993;42:597-9.
Rubin LG, Tucci V, Cercenado E, Eliopoulos G, Isenberg HD.
Vancomycin-resistant Enterococcus faecium in hospitalized
children.
Infect Control Hosp Epidemiol 1992;13:700-5.
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.
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;16:750-5.
Frieden TR, Munsiff SS, Low DE, et al. Emergence of
vancomycin-resistant enterococci in New York City. Lancet
1993;342:
76-9.
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:
1280-5.
Montecalvo MA, Horowitz H, Gedris C, et al. Outbreak of
vancomycin-,
ampicillin-, and aminoglycoside-resistant Enterococcus faecium
bacteremia in an adult oncology unit. Antimicrob Agents
Chemother
1994;38:1363-7.
Boyce JM, Opal SM, Chow JW, et al. Outbreak of multi-drug
resistant
Enterococcus faecium with transferable vanB class vancomycin
resistance. J Clin Microbiol 1994;32:1148-53.
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;31:1695-9.
Sahm DF, Olsen L. In vitro detection of enterococcal
vancomycin
resistance. Antimicrob Agents Chemother 1990;34:1846-8.
Zabransky RJ, Dinuzzo AR, Huber MB, Woods GL. Detection of
vancomycin
resistance in enterococci by the Vitek AMS System. Diagn
Microbiol
Infect Dis 1994;20:113-6.
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.
Hayden MK, Koenig GI, Trenholme GM. Bactericidal activities of
antibiotics against vancomycin-resistant Enterococcus faecium
blood
isolates and synergistic activities of combinations.
Antimicrob Agents
Chemother 1994;38:1225-9.
Mobarakai N, Landman D, Quale JM. In-vitro activity of
trospectomycin,
a new aminocyclitol antibiotic against multidrug-resistant
Enterococcus faecium. J Antimicrob Chemother 1994;33:319-21.
Murray BE. The life and times of the enterococcus. Clin
Microbiol Rev
1990;3:46-65.
Rhinehart E, Smith N, Wennersten C, et al. Rapid dissemination
of
beta-lactamase-producing aminoglycoside-resistant Enterococcus
faecalis among patients and staff on an infant and toddler
surgical
ward. N Engl J Med 1990;323:1814-8.
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;117:112-6.
Uttley AH, George RC, Naidoo J, et al. High-level
vancomycin-resistant
enterococci causing hospital infections. Epidemiol Infect
1989;103:
173-81.
Leclercq R, Derlot E, Weber M, Duval J, Courvalin P.
Transferable
vancomycin and teicoplanin resistance in Enterococcus faecium.
Antimicrob Agents Chemother 1989;33:10-5.
Noble WC, Virani Z, Cree R. Co-transfer of vancomycin and
other
resistance genes from Enterococcus faecalis NCTC12201 to
Staphylococcus aureus. FEMS Microbiol Lett 1992;72:195-8.
Veach LA, Pfaller MA, Barrett M, Koontz FP, Wenzel RP.
Vancomycin
resistance in Staphylococcus haemolyticus causing colonization
and
bloodstream infection. J Clin Microbiol 1990;28:2064-8.
Degener JE, Heck MEOC, Vanleeuwen WJ, et al. Nosocomial
infection by
Staphylococcus haemolyticus and typing methods for
epidemiological
study. J Clin Microbiol 1994;32:2260-5.
Small PM, Chambers HF. Vancomycin for Staphylococcus aureus
endocarditis in intravenous drug users. Antimicrob Agents
Chemother
1990;34:1227-31.
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;34:2348-53.
American Heart Association Committee on Rheumatic Fever and
Infective
Endocarditis. Prevention of bacterial endocarditis.
Circulation
1984;70:1123-4.
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: a
double-blind randomized trial. J Thorac Cardiovasc Surg
1992;104:
1423-34.
Classen DC, Evans RS, Pestotnik SL, Horn SD, Menlove RL, Burke
JP. The
timing of prophylactic administration of antibiotics and the
risk of
surgical-wound infection. N Engl J Med 1992; 326:281-6.
Conte JE Jr, Cohen SN, Roe BB, Elashoff RM. Antibiotic
prophylaxis and
cardiac surgery: a prospective double-blind comparison of
single-dose
versus multiple-dose regimens. Ann Intern Med 1972;76:943-9.
DiPiro JT, Cheung RP, Bowden TA Jr, Mansberger JA. Single-dose
systemic antibiotic prophylaxis of surgical wound infections.
Am J
Surg 1986;152:552-9.
Heydemann JS, Nelson CL. Short-term preventive antibiotics.
Clin
Orthop 1986;205:184-7.
Rubin M, Hathorn JW, Marshall D, Gress J, Steinberg SM, Pizzo
PA.
Gram-positive infections and the use of vancomycin in 550
episodes of
fever and neutropenia. Ann Intern Med 1988; 108:30-5.
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;319:1053-8.
Pizzo PA, Hathorn JW, Hiemenz 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;315:552-8.
Karp JE, Dick JD, Angelopulos C, et al. Empiric use of
vancomycin
during prolonged treatment-induced granulocytopenia:
randomized,
double-blind, placebo-controlled clinical trial in patients
with acute
leukemia. Am J Med 1986;81:237-42.
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;163:951-8.
Riikonen P. Imipenem compared with ceftazidime plus vancomycin
as
initial therapy for fever in neutropenic children with cancer.
Pediatr
Infect Dis 1991;10:918-23.
Lamy T, Michelet C, Dauriac C, Grulois I, Donio PY, Le Prise
PY.
Benefit of prophylaxis by intravenous systemic vancomycin in
granulocytopenic patients: a prospective, randomized trial
among 59
patients. Acta Haematol 1993;90:109-13.
Isaacman DJ, Karasic RB. Lack of effect of changing needles on
contamination of blood cultures. Pediatr Infect Dis J
1990;9:274-8.
Krumholz HM, Cummings S, York M. Blood culture phlebotomy:
switching
needles does not prevent contamination. Ann Intern Med
1990;113:290-2.
Strand CL, Wajsbort RR, Sturmann K. Effect of iodophor vs
iodine
tincture skin preparation on blood culture contamination rate.
JAMA
1993;269:1004-6.
Maki DG, Schuna AA. A study of antimicrobial misuse in a
university
hospital. Am J Med Sci 1978;275:271-82.
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.
Henrickson KJ, Powell KR, Schwartz CL. A dilute solution of
vancomycin
and heparin retains antibacterial and anticoagulant
activities. J
Infect Dis 1988;157:600-1.
Schwartz C, Henrickson KJ, Roghmann K, Powell K. Prevention of
bacteremia attributed to luminal colonization of tunneled
central
venous catheters with vancomycin-susceptible organism. J Clin
Oncol
1990;8:1591-7.
Henrickson KJ, Dunne WM Jr. Modification of central venous
catheter
flush solution improves in vitro antimicrobial activity. J
Infect Dis
1992;166:944-6.
Gaillard JL, 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;14:593-7.
Spafford PS, Sinkin RA, Cox C, Reubens L, Powell KR.
Prevention of
central venous catheter-related coagulase-negative
staphylococcal
sepsis in neonates. J Pediatr 1994;125:259-63.
Kaplan AH, Gilligan PH, Facklam RR. Recovery of resistant
enterococci
during vancomycin prophylaxis. J Clin Microbiol
1988;26:1216-8.
Gradon JD, Wu EH, Lutwick LI. Aerosolized vancomycin therapy
facilitating nursing home placement. Ann Pharmacother
1992;26:209-10.
Weathers L, Riggs D, Santeiro M, Weibley RE. Aerosolized
vancomycin
for treatment of airway colonization by methicillin-resistant
Staphylococcus aureus. Pediatr Infect Dis 1990;9:220-1.
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.
Kacica MS, Horgan MJ, Ochoa L, Sandler R, Lepow ML, Venezia
RA.
Prevention of gram-positive sepsis in neonates weighing less
than 1500
grams. J Pediatr 1994;125:253-8.
Lam TY, Vas SI, Oreopoulos DG. Long-term intraperitoneal
vancomycin in
the prevention of recurrent peritonitis during CAPD:
preliminary
results. Perit Dial Int 1991;11:281-2.
Bastani 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;45:283-5.
Newman LN, Tessman M, Hanslik T, Schulak J, Mayes J,
Friedlander M. A
retrospective view of factors that affect catheter healing:
four years
of experience. Adv Perit Dial 1993;9:217-22.
Capdevila JA, Segarra A, Planes AM, et al. Successful
treatment of
haemodialysis catheter-related sepsis without catheter
removal.
Nephrol Dial Transplant 1993;8:231-4.
Edell LS, Westby GR, Gould SR. An improved method of
vancomycin
administration to dialysis patients. Clin Nephrol
1988;29:86-7.
Soumerai SB, McLaughlin TJ, Avorn J. Quality assurance for
drug
prescribing. Qual Assur Health Care 1990;2:37-58.
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;11:578-83.
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. Med Care
1993;31:552-8.
Soumerai SB, McLaughlin TJ, Avorn J. Improving drug
prescribing in
primary care: a critical analysis of the experimental
literature.
Milbank Q 1989;67:268-317.
National Committee for Clinical Laboratory Standards. Methods
for
dilution antimicrobial susceptibility tests for bacteria that
grow
aerobically. 3rd ed. Villanova, PA: National Committee for
Clinical
Laboratory Standards, 1993; publication M7-A3.
Swenson JM, Ferraro MJ, Sahm DF, Charache P, Tenover FC,
National
Committee for Clinical Laboratory Standards Working Group on
Enterococci. New vancomycin disk diffusion breakpoints for
enterococci. J Clin Microbiol 1992;30:2525-8.
CDC. Recommendations for prevention of HIV transmission in
health-care
settings. MMWR 1987;36(No. 2S).
Swenson JM, Clark NC, Ferraro MJ, et al. Development of a
standardized
screening method for detection of vancomycin-resistant
Enterococci. J
Clin Microbiol 1994;32:1700-4.
Edberg SC, Hardalo CJ, Kontnick C, Campbell S. Rapid detection
of
vancomycin-resistant enterococci. J Clin Microbiol
1994;32:2182-4.
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.
Doebbeling BN, Stanley GL, Sheetz CT, et al. Comparative
efficacy of
alternative hand-washing agents in reducing nosocomial
infections in
intensive care units. N Engl J Med 1992;327:88-93.
Jones MV, Rowe GB, Jackson B, Pritchard NJ. The use of alcohol
paper
wipes for routine hand cleansing: results of trials in two
hospitals.
J Hosp Infect 1986;8:268-74.
Nicoletti G, Boghossian V, Borland R. Hygienic hand
disinfection: a
comparative study with chlorhexidine detergents and soap. J
Hosp
Infect 1990;15:323-37.
Butz AM, Laughon BE, Gullette DL, Larson EL.
Alcohol-impregnated wipes
as an alternative in hand hygiene. Am J Infect Control
1990;18:70-6.
Korniewicz DM, Laughon BE, Butz A, Larson E. Integrity of
vinyl and
latex procedure gloves. Nurs Res 1989;38:144-6.
Korniewicz DM, Kirwin M, Cresci K, Markut C, Larson E. In-use
comparison of latex gloves in two high-risk units: surgical
intensive
care and acquired immunodeficiency syndrome. Heart Lung
1992;21:81-4.
DeGroot-Kosolcharoen J, Jones JM. Permeability of latex and
vinyl
gloves to water and blood. Am J Infect Control
1989;17:196-201.
Paulssen J, Eidem T, Kristiansen R. Perforations in surgeons'
gloves.
J Hosp Infect 1988; 11:82-5.
Korniewicz DM, Laughon BE, Cyr WH, Lytle CD, Larson E. Leakage
of
virus through used vinyl and latex examination gloves. J Clin
Microbiol 1990;28:787-8.
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:
211-8.
Favero MS, Bond WW. Sterilization, disinfection, and
antisepsis in the
hospital. Chapter 24. In: Balows A, Hausler WJ Jr, Herrman KL,
Isenberg HD, Shadomy HJ, eds. Manual of clinical microbiology.
5th ed.
Washington, DC: American Society for Microbiology,
1991:183-200.
Zervos MJ, Kauffman CA, Therasse PM, Bregman AG, Mikesell TS,
Schaberg
DR. Nosocomial infection by gentamicin-resistant Streptococcus
faecalis: an epidemiologic study. Ann Intern Med
1987;106:687-91.
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:
285-92.
Orberg PK, Sandine WE. Common occurrence of plasmid DNA and
vancomycin
resistance in Leuconostoc spp. Appl Environ Microbiol
1984;48:1129-33.
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.
Garner JS, Simmons BP. Guideline for isolation precautions in
hospitals. Infect Control 1983;4(suppl):245-325.
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|
|
| Erratum: Vol. 44, No. RR-12
|
|
|
| SOURCE: MMWR 44(41);782 DATE: Oct 20, 1995
|
|
|
| In the MMWR Recommendations and Reports "Recommendations for
|
| Preventing the Spread of Vancomycin Resistance: Recommendations
of the |
| Hospital Infection Control Practices Advisory Committee
(HICPAC)," the |
| publication date printed at the top of even-numbered pages ii-12
should |
| have been September 22, 1995.
|
|
|
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