Staphylococcus aureus FREE

MMWR. 2002;51:565-567

Staphylococcus aureus is a cause of hospital- and community-acquired 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 vancomycin-intermediate 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 antimicrobial-resistant microorganisms and control the use of anti-microbial 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 methicillin-resistant 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 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.

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.

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, penicillin-resistant 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 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 vancomycin⁸; 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 micro-organisms 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: 10 available

MMWR. 2002;51:589-592.

2 tables omitted

Despite substantial reductions in U.S. infant mortality during the past several decades, black-white disparities in infant mortality rates persist. One of the Healthy People 2010 national objectives for maternal and infant health is to reduce deaths among infants aged <1 year to ≤4.5 per 1,000 live births among all racial/ethnic groups (objective 16-1c).¹ Important determinants of racial/ethnic differences in infant mortality are low birth weight (LBW), defined as <2500 grams, and very low birth weight (VLBW), defined as <1500 grams. High birth weight–specific mortality rates (BWSMRs) occur at these low birth weights. Healthy People 2010 goals include reducing LBW to 5% and VLBW to 0.9% of live births (objectives 16-10a and 16-10b, respectively). To assess progress toward meeting these national objectives, CDC analyzed birth and death certificate data from the National Center for Health Statistics. This report describes trends in mortality and birth weight among black and white infants, which indicate persistent black-white disparities and underscore the need for prevention strategies that reduce preterm delivery and specific medical conditions that lead to infant death.

CDC analyzed race-specific infant mortality data for 1980-1999² and preliminary mortality data for 2000. Trends in LBW and VLBW were calculated by using birth certificate data for 1980-2000, with 2000 being the most recent year for which data were available.³ BWSMRs were calculated from linked birth and infant death files for 1983-1991 and 1995-1999; LBW infants were divided into VLBW and moderate LBW (MLBW), defined as 1500-2499 grams. Both race-specific LBW/VLBW data and BWSMRs were calculated by using the race of the mother.

In 1980, a total of 3,612,258 live births occurred among all races (2,936,351 to white women and 568,080 to black women). In 2000, a total of 4,064,948 live births occurred among all races (3,202,932 to white women and 619,970 to black women). Although infant mortality declined 45.2% for all races during 1980-2000 (from 12.6 to 6.9 deaths per 1,000 live births), the decline was greater for whites than for blacks. During the same period, infant mortality among whites declined 47.7% (from 10.9 to 5.7), and infant mortality among blacks declined 36.9% (from 22.2 to 14.0). During 1980-2000, the black-white ratio of infant mortality increased 25.0% (from 2.0 to 2.5). However, the ratio remained unchanged during 1990-1998 (2.4 for all years).

During 1980-2000, the percentage of LBW infants increased 11.8% and that of VLBW infants increased 24.3%. Although the black-white ratio of LBW births decreased 10.0% (from 2.2 to 2.0), the LBW rate increased 2.4% for blacks (from 12.7% to 13.0%) and increased 14.0% for whites (from 5.7% to 6.5%). Black LBW rates increased 6.3% during the 1980s and decreased 2.3% during 1990-2000. LBW rates remained stable for whites during the 1980s but increased 14.0% during 1990-2000. VLBW rates increased 23.8% for blacks (from 2.48% to 3.07%) and 26.7% for whites (from 0.90% to 1.14%). The VLBW black-white ratio decreased 2.5% (from 2.76 to 2.69) during the entire period but increased 12.7% during the 1980s and decreased 12.4% during 1990-2000. This was due to a reversal in VLBW trends during each decade; during the 1980s VLBW increased 19.0% for blacks and 5.6% for whites, but during 1990-2000, VLBW increased 5.1 % for blacks and 20.0% for whites.

Over time, BWSMRs varied by race of mother. During 1983-1999, BWSMRs for LBW declined 36.9% for all races (46.7% for MLBW and 38.3% for VLBW). Both whites and blacks had similar percentage declines in BWSMRs among infants whose birth weights were ≥2,500 grams, and the black-white gap for this birth weight group increased slightly. However, for both MLBW and VLBW categories, whites had greater declines. White BWSMRs decreased 49.4% for MLBW infants and 41.6% for VLBW infants, and black BWSMRs decreased 38.0% for MLBW infants and 28.4% for VLBW infants. The black-white ratio of BWSMRs increased 39.0% (from 1.03 to 1.43) for all LBW infants, increasing 22.4% (from 0.85 to 1.04) for MLBW infants and 22.3% (from 0.94 to 1.15) for VLBW infants. Accordingly, the historically lower BWSMRs among black MLBW and VLBW infants have disappeared; during the 1980s, BWSMRs were lower among VLBW black infants than among white infants, and during the 1990s, BWSMRs were lower among VLBW white infants than among black infants. Similar reversals in BWSMRs are shown for MLBW infants in 1999.

S Iyasu, MBBS, K Tomashek, MD, Div of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion; W Barfield, MD, EIS Officer, CDC.

The findings of this report indicate that although infant mortality has decreased among all races during the past two decades, the overall black-white gap for infant mortality has widened. The lack of progress in closing this gap is a consequence of (1) the persistence of a two- to threefold risk for LBW and VLBW among black infants compared with white infants, and (2) smaller reductions in BWSMRs over time among black VLBW births compared with white VLBW births. Although small reductions occurred in black-white disparities in LBW births and VLBW births during the 1990s, these were attributed partly to greater increases in percentages of LBW and VLBW births among whites, rather than to large reductions in LBW and VLBW among blacks. If these trends persist, the national health objectives to eliminate racial disparities in LBW and VLBW births will not be met. In addition, increases in LBW and VLBW births will slow reductions in infant mortality.

Recent increases in LBW and VLBW births among whites probably are a result of increases in preterm delivery, changes in obstetrical practices, and induction of labor. During 1989-1996, the crude singleton preterm birth rate increased 8% among non-Hispanic whites but decreased 10% among non-Hispanic blacks.⁴ In addition, increases in white LBW and VLBW births might be attributed partly to increases in multiple births from assisted reproductive therapies. During 1980-1997, the rate of twin births among white mothers increased at a rate nearly twice that of black mothers.⁵ Although multiple gestations increase the risk for LBW and VLBW births, LBW rates are higher among singleton infants conceived with assisted reproductive technology.⁶ Nevertheless, blacks continue to have a two- to threefold higher risk than whites for LBW and VLBW. In 1991, >66% of the black-white racial disparity in infant mortality occurred among VLBW infants.⁷ The specific causes for increased low birth weight and preterm delivery might differ for blacks and whites. The etiology of black-white disparities in low birth weight is complex and is not explained entirely by demographic risk factors such as maternal age, education, or income.⁸ Factors that might contribute to the disparity include racial differences in maternal medical conditions, stress, lack of social support, bacterial vaginosis, previous preterm delivery, and maternal health experiences that might be unique to black women.⁹

Of additional concern are disparate improvements in BWSMRs for blacks and whites over time. During the 1980s, BWSMRs for black VLBW infants were lower than for white VLBW infants. Although these differences are poorly understood, the relative advantage of lower BWSMRs among VLBW blacks has disappeared. Because BWSMRs are influenced by access to quality obstetric and neonatal care, particularly among VLBW births, differential access might exist for blacks compared with whites. Declines in neonatal mortality because of improvements in treatment for specific medical disorders (e.g., respiratory distress syndrome) have been greater for whites than for blacks.¹⁰

The findings of this report are subject to at least three limitations. First, infant mortality was calculated by using the race of the infant as the numerator and the race of the mother as the denominator, and might differ slightly from total BWSMRs. This number might affect calculations of infant mortality in which the race of the mother and that of the infant are reported as different. Second, linked data from 1983 are the earliest linked birth infant death data by race of mother and were not available for 1980-1982 and 1992-1994. Finally, vital records data contain mostly demographic information and do not explain specific reasons for racial disparities in outcomes. Studies that examine quality of health-care delivery, specific maternal and neonatal interventions, and social and environmental determinants might identify the reasons for these differences.

Prevention strategies must focus on reducing LBW and VLBW births to eliminate racial disparities in infant mortality. During the last decade, these disparities have decreased, not because of reductions in LBW births among blacks but because of increases in LBW births among whites. Research should be aimed at preventing preterm delivery and associated factors (e.g., infection, medical complications of pregnancy, or poor prenatal care), and the promotion of effective and culturally sensitive intervention programs.⁹ Strategies to reduce black-white disparities also should address disparate reductions in specific medical conditions that lead to infant death.

References: 10 available