Morbidity and Mortality Weekly Report
Weekly
July 5, 2002 / Vol. 51 / No. 26
Staphylococcus aureus Resistant to Vancomycin — United States, 2002
Staphylococcus aureus is a cause of hospital- and communityacquired infections (1,2). In 1996, the first clinical isolate of
S. aureus with reduced susceptibility to vancomycin was
reported from Japan (3). The vancomycin minimum inhibitory concentration (MIC) result reported for this isolate was
in the intermediate range (vancomycin MIC=8 µg/mL) using
interpretive criteria defined by the National Committee for
Clinical Laboratory Standards (4). As of June 2002, eight
patients with clinical infections caused by vancomycinintermediate S. aureus (VISA) have been confirmed in the
United States (5,6). This report describes the first documented
case of infection caused by vancomycin-resistant S. aureus
(VRSA) (vancomycin MIC >32 µg/mL) in a patient in the
United States. The emergence of VRSA underscores the need
for programs to prevent the spread of antimicrobialresistant microorganisms and control the use of antimicrobial drugs in health-care settings.
In June 2002, VRSA was isolated from a swab obtained
from a catheter exit site from a Michigan resident aged 40
years with diabetes, peripheral vascular disease, and chronic
renal failure. The patient received dialysis at an outpatient
facility (dialysis center A). Since April 2001, the patient had
been treated for chronic foot ulcerations with multiple courses
of antimicrobial therapy, some of which included vancomycin. In April 2002, the patient underwent amputation of a
gangrenous toe and subsequently developed methicillinresistant S. aureus bacteremia caused by an infected arteriovenous hemodialysis graft. The infection was treated with vancomycin, rifampin, and removal of the infected graft. In June,
the patient developed a suspected catheter exit-site infection,
and the temporary dialysis catheter was removed; cultures of
the exit site and catheter tip subsequently grew S. aureus resistant to oxacillin (MIC >16 µg/mL) and vancomycin (MIC
>128 µg/mL). A week after catheter removal, the exit site
appeared healed; however, the patient’s chronic foot ulcer
appeared infected. VRSA, vancomycin-resistant Enterococcus
faecalis (VRE), and Klebsiella oxytoca also were recovered from
a culture of the ulcer. Swab cultures of the patient’s healed
catheter exit site and anterior nares did not grow VRSA. To
date, the patient is clinically stable, and the infection is
responding to outpatient treatment consisting of aggressive
wound care and systemic antimicrobial therapy with
trimethroprim/sulfamethoxazole.
The VRSA isolate recovered from the catheter exit site was
identified initially at a local hospital laboratory using commercial MIC testing and was confirmed by the Michigan
Department of Community Health and CDC. Identification
methods used at CDC included traditional biochemical tests
and DNA sequence analysis of gyrA and the gene encoding
16S ribosomal RNA. Molecular tests for genes unique to
enterococci were negative. The MIC results for vancomycin,
teicoplaninin, and oxacillin were >128 µg/mL, 32 µg/mL, and
>16 µg/mL, respectively, by the broth microdilution method.
The isolate contained the vanA vancomycin resistance gene
from enterococci, which is consistent with the glycopeptide
MIC profiles. It also contained the oxacillin-resistance gene
mecA. The isolate was susceptible to chloramphenicol
INSIDE
567
570
572
574
Heat-Related Deaths — Four States, July–August 2001,
and United States, 1979–1999
Injuries and Deaths Among Children Left Unattended
in or Around Motor Vehicles — United States, July 2000–
June 2001
Certification of Poliomyelitis Eradication — European
Region, June 2002
Food and Drug Administration Approval of a Fifth
Acellular Pertussis Vaccine for Use Among Infants and
Young Children — United States, 2002
Centers for Disease Control and Prevention
TM
SAFER • HEAL
THIER • PEOPLE
HEALTHIER
566
MMWR
The MMWR series of publications is published by the
Epidemiology Program Office, Centers for Disease Control
and Prevention (CDC), U.S. Department of Health and
Human Services, Atlanta, GA 30333.
SUGGESTED CITATION
Centers for Disease Control and Prevention. [Article
Title]. MMWR 2002;51:[inclusive page numbers].
Centers for Disease Control and Prevention
Julie L. Gerberding, M.D.
Director
David W. Fleming, M.D.
Deputy Director for Science and Public Health
Dixie E. Snider, Jr., M.D., M.P.H.
Associate Director for Science
Epidemiology Program Office
Stephen B. Thacker, M.D., M.Sc.
Director
Office of Scientific and Health Communications
John W. Ward, M.D.
Director
Editor, MMWR Series
David C. Johnson
Acting Managing Editor, MMWR (Weekly)
Jude C. Rutledge
Teresa F. Rutledge
Jeffrey D. Sokolow, M.A.
Writers/Editors, MMWR (Weekly)
Lynda G. Cupell
Malbea A. Heilman
Beverly J. Holland
Visual Information Specialists
Quang M. Doan
Erica R. Shaver
Information Technology Specialists
Division of Public Health Surveillance
and Informatics
Notifiable Disease Morbidity and 122 Cities Mortality Data
Robert F. Fagan
Deborah A. Adams
Felicia J. Connor
Lateka Dammond
Patsy A. Hall
Pearl C. Sharp
July 5, 2002
linezolid, minocycline, quinupristin/dalfopristin, tetracycline,
and trimethoprim/sulfamethoxazole.
Epidemiologic and laboratory investigations are under way
to assess the risk for transmission of VRSA to other
patients, health-care workers, and close family and other
contacts. To date, no VRSA transmission has been identified.
Infection-control practices in dialysis center A were assessed;
all health-care workers followed standard precautions consistent with CDC guidelines (7). After the identification of
VRSA, dialysis center A initiated special precautions on the
basis of CDC recommendations (8), including using gloves,
gowns, and masks for all contacts with the patient; performing dialysis with a dedicated dialysis machine during the last
shift of the day in an area separate from other patients; having a dialysis technician dedicated to providing care for the
patient; using dedicated, noncritical patient-care items; and
enhancing education of staff members about appropriate
infection-control practices. Assessment of infection-control
practices in other health-care settings in which the patient
was treated is ongoing.
Reported by: DM Sievert, MS, ML Boulton, MD, G Stoltman, PhD,
D Johnson, MD, MG Stobierski, DVM, FP Downes, DrPH, PA Somsel,
DrPH, JT Rudrik, PhD, Michigan Dept of Community Health;
W Brown, PhD, W Hafeez, MD, T Lundstrom, MD, E Flanagan,
Detroit Medical Center; R Johnson, MD, Detroit; J Mitchell, Oakwood
Health Care System, Dearborn, Michigan. Div of Healthcare Quality
Promotion, Div of Bacterial and Mycotic Diseases, National Center for
Infectious Diseases; S Chang, MD, EIS Officer, CDC.
Editorial Note: This report describes the first clinical isolate
of S. aureus that is fully resistant to vancomycin. S. aureus
causes a wide range of human infections and is an important
cause of health-care associated infections. The introduction
of new classes of antimicrobials usually has been followed by
emergence of resistance in S. aureus. After the initial success
of penicillin in treating S. aureus infection, penicillinresistant S. aureus became a major threat in hospitals and nurseries in the 1950s, requiring the use of methicillin and related
drugs for treatment of S. aureus infections. In the 1980s,
methicillin-resistant S. aureus emerged and became endemic
in many hospitals, leading to increasing use of vancomycin.
In the late 1990s, cases of VISA were reported.
Although the acquired vancomycin-resistance determinants
vanA, vanB, vanD, vanE, vanF, and vanG have been
reported from VRE, these resistance determinants have not
previously been identified in clinical isolates of S. aureus (9).
Conjugative transfer of the vanA gene from enterococci to
S. aureus has been demonstrated in vitro (10). The presence
of vanA in this VRSA suggests that the resistance determinant might have been acquired through exchange of genetic
material from the vancomycin-resistant enterococcus also
Vol. 51 / No. 26
MMWR
isolated from the swab culture. This VRSA isolate is susceptible in vitro to several antimicrobial agents, including antimicrobials recently approved by the Food and Drug
Administration (i.e., linezolid and quinupristin/dalfopristin)
with activity against glycopeptide-resistant Gram-positive
microorganisms.
In 1997, the Healthcare Infection Control Practices Advisory Committee published guidelines for the prevention and
control of staphylococcal infection associated with reduced
susceptibility to vancomycin (8); plans to contain VISA/VRSA
on the basis of CDC recommendations have been established
in some state health departments. In the health-care setting, a
patient with VISA/VRSA should be placed in a private room
and have dedicated patient-care items. Health-care workers
providing care to such patients should follow contact precautions (i.e., wearing gowns, masks, and gloves and using antibacterial soap for hand washing). These control measures were
adopted by dialysis center A immediately following confirmation of the VRSA isolate. To date, there has been no documented spread of this microorganism to other patients or
health-care workers.
Strategies to improve adherence to current guidelines
to prevent transmission of antimicrobial resistant microorganisms in health-care settings should be a priority for all
health-care facilities in the United States. S. aureus should be
tested for resistance to vancomycin using a MIC method. The
isolation of S. aureus with confirmed or presumptive vancomycin resistance should be reported immediately through state
and local health departments to the Division of Healthcare
Quality Promotion, National Center for Infectious Diseases,
CDC, telephone 800-893-0485.
References
1. CDC. National Nosocomial Infections Surveillance report, data summary from October 1986–April 1996, issued May 1996. Am J Infect
Control 1996;24:380–8.
2. Waldvogel FA. Staphylococcus aureus (including toxic shock syndrome).
In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and
Benett’s Principles and Practice of Infectious Diseases, 4th ed. New
York, New York: Churchill Livingstone, 1995:1754–77.
3. Hiramatsu K, Hanaki H, Ino T, Yabuta K, Oguri T, Tenover FC.
Methicillin-resistant Staphylococcus aureus clinical strain with reduced
vancomycin susceptibility. J Antimicrob Chemother 1997;40:135–6.
4. National Committee for Clinical Laboratory Standards. Methods for
dilution antimicrobial susceptibility tests for bacteria that grow aerobically. 5th ed. Approved standard, M7-A5. Wayne, Pennsylvania:
National Committee for Clinical Laboratory Standards, 2000.
5. Smith TL, Pearson ML, Wilcox KR, et al. Emergence of vancomycin
resistance in Staphylococcus aureus. N Engl J Med 1999;340:493–501.
6. Fridkin SK. Vancomycin-intermediate and -resistant Staphylococcus
aureus: what the infectious disease specialist needs to know. Clin
Infect Dis. 2001;32:108–15.
7. CDC. Recommendations for preventing transmission of infections
among chronic hemodialysis patients. MMWR 2001;50(RR-5).
8. CDC. Interim guidelines for prevention and control of staphylococcal
infections associated with reduced susceptibility to vancomycin.
MMWR 1997;46:626–8,635.
567
9. Woodford N. Epidemiology of the genetic elements responsible for
acquired glycopeptide resistance in enterococci. Microb Drug Resist
2001;7:229–36.
10. Noble WC, Virani Z, Cree RG. Co-transfer of vancomycin and other
resistance genes from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus. FEMS Microbiol Lett 1992;93:195–8.
Heat-Related Deaths — Four States,
July–August 2001,
and United States, 1979–1999
Each year in the United States, approximately 400 deaths
are attributed to excessive natural heat; these deaths are
preventable (1). This report describes heat-related deaths in
Missouri, New Mexico, Oklahoma, and Texas when elevated
temperatures were recorded for several consecutive days during July–August 2001; summarizes heat-related deaths in the
United States during 1979–1999; and presents risk factors
and preventive measures associated with heat-related illness
and death, especially in susceptible populations.
In late July 2001, the National Oceanographic and Atmospheric Association (NOAA) reported temperatures averaging 5º F (-15º C)–10º F (-12º C) above normal in the southern
plains states (2). The intense heat and humidity prompted
NOAA’s National Weather Service to issue heat advisories* in
Missouri, New Mexico, Oklahoma, and Texas (2; Missouri
Department of Health and Senior Services, personal communication 2002). During July–August 2001, a total of 95
deaths was attributed to excessive natural heat in the affected
states. Provisional mortality statistics were obtained from the
vital statistics section of each state, and information about
underlying cause of death, age, sex, date of death, and contributing causes were provided. Peak mortality occurred during the reported 8-day heat advisory period (Figure 1). Six
(6%) deaths occurred among children aged 75 years; 69 (73%) deaths
occurred among males.
Case Reports
Case 1. In Oklahoma in mid-July 2001, a man aged 29
years was found disoriented and wandering in a commercial
parking lot. He apparently had fallen and had abrasions on
his knees and a broken tooth. In the emergency department,
* The National Weather Service issues a heat advisory when the maximum
daytime heat index is expected to be >105º F (40.6º C) and the minimum
nighttime heat index is expected to be 80º F (26.7º C) for 2 or more consecutive
days. The heat index takes into account air temperature and relative humidity
and indicates the actual feel of the temperature to the body.
568
MMWR
July 5, 2002
FIGURE 1. Reported cases of heat-related deaths*, by date and site — Missouri, New Mexico,
Oklahoma, and Texas, August 2001
10
New Mexico
Oklahoma
Missouri
Texas
Heat Advisory Issued
9
8
Number
7
6
5
4
3
2
1
0
1
6
11
16
21
26
31
5
Jul
10
15
20
25
Aug
Day
30
incoherent on the street. A witness reported that he had complained about abdominal pain
and vomiting. He arrived at an
emergency department in New
Mexico 3 hours after he was
found. His rectal temperature
was 105.7º F (40.9º C). The
patient had laboratory evidence of rhabdomyolysis,
severe dehydration, and renal
failure. Blood alcohol level and
a screen for drugs were negative. He died 3 hours after
arrival at the hospital. Cause
of death was attributed to
hyperthermia due to environmental heat exposure. High
temperature at the border that
day was 90º F (32º C).
* n=95.
he was semiconscious but combative. His rectal temperature
increased from 105.4º F (40.7º C) to 107.8º F (42.1º C) in
39.4º C] or a rectal temperature of 106º F [41.1º C]); red, hot, dry skin and no sweating;
rapid pulse; throbbing headache; dizziness; nausea; confusion;
disorientation; delirium; and coma. Heatstroke can occur in
the absence of physical exertion. Infants, elderly persons,
socially isolated persons, bedridden persons, and persons with
certain mental and chronic illnesses are at highest risk (6,7).
The elderly, especially those aged >80 years, are susceptible to
heat-related illness because they are less able to adjust to physiologic changes (e.g., vasodilation) that occur with exposure
to excessive heat and are more likely to be taking medication
for chronic illness (e.g., tranquilizers and anticholinergics) that
increase the risk for heat-related illness (5). Infants also are
sensitive to heat. Conditions such as mild fever can progress
quickly to heatstroke if heat stress occurs. Parents and other
caregivers should provide adequate hydration during summer months and refrain from dressing children too warmly
(5). Adults also should keep well hydrated during summer
months.
Heatstroke also can occur in young, healthy persons who
are exercising (6), because physical exertion during hot weather
increases the likelihood of fainting and cramps caused by
increased blood flow to the extremities (5). Onset of heatstroke can be rapid and is considered a medical emergency.
569
The findings in this report are subject to at least three limitations. First, information on decedents is provided by surrogates, who might not accurately describe characteristics or
behavior of the decedents. Second, heat-related deaths due to
weather conditions or exposure to excessive natural heat might
represent only a portion of actual heat-related deaths. These
deaths often are a diagnosis of exclusion and can be
misclassified as a stroke or heart attack. Deaths attributed to
cardiovascular and respiratory disease increase following heat
waves (8). In addition, jurisdictions might use different definitions of heat-related death. Finally, ICD-10 coding was
introduced in 1999 and might not be comparable with previous data for 1979–1998.
To reduce morbidity and mortality from heat-related illness, many cities have developed emergency response plans.
Local officials use meteorologic information and assess population characteristics to implement prevention strategies (7).
Spending time in an air-conditioned area is the strongest factor in preventing heat-related deaths (1,9). The use of fans
does not appear to be protective during periods of high heat
and humidity (1). If exposure to heat cannot be avoided, prevention measures should include reducing or eliminating
strenuous activities or rescheduling them for cooler parts of
the day; drinking water or nonalcoholic fluids frequently;
taking cool showers frequently; wearing lightweight, lightcolored, loose-fitting clothing; and avoiding direct sunshine
(9).
Public health messages disseminated to all age groups can
make the public aware of the signs and symptoms of heatrelated illness. Prevention messages delivered as early as possible in the media can prevent heat-related illness, injury, and
death (1).
Because many heat-related illnesses and deaths occur among
the elderly population, older persons should be encouraged
to take advantage of air-conditioned environments (e.g., shopping malls, senior centers, and public libraries) for part of the
day. Parents and other caregivers should be educated about
the heat sensitivity of children aged
