Reasonable Rascal
07-07-02, 23:58
STAPH. AUREUS, VRSA - USA (MICHIGAN)
************************************
A ProMED-mail post
ProMED-mail, a program of the
International Society for Infectious Diseases
<http://www.isid.org>
Date: 3 Jul 2002
Source: MMWR 5 July 2002 (edited)
<http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5126a1.htm>
_Staphylococcus aureus_ resistant to vancomycin - USA, 2002
--------------------------------------------------
_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 USA. The emergence of VRSA underscores the need for programs to prevent the spread of antimicrobial resistant 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 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 the Centers for Disease Control and Prevention (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.
Epidemiological 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, et al, at Michigan Dept of Community Health; W Brown, et al, at Detroit Medical Center; R Johnson, 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, CDC.
[MMWR} 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, 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 [first identified in about 1960. - Mod.SH] 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 (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 (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 USA. _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.
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 Bennett's principles and practice of infectious diseases, 4th ed. New York: Churchill Livingstone, 1995: 1754-77.
3. Hiramatsu K, Hanaki H, Ino T, et al. 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 Morb Mortal Wkly Rep 2001; 50(RR-5).
8. CDC. Interim guidelines for prevention and control of staphylococcal infections associated with reduced susceptibility to vancomycin. MMWR Morb Mortal Wkly Rep 1997; 46: 626-8,635.
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.
--
ProMED-mail
[The discovery of a clinical isolate of _S. aureus_ fully resistant to vancomycin is unsurprising, given the progression of antimicrobial resistance in this significant community and hospital acquired pathogen.
Since the recognition of VISA strains in 1996, attempts to modify vancomycin use have confounded by the continued high prevalence of MRSA in hospitals for which vancomycin has remained the treatment of choice. The recognition of MRSA in community settings has begun to occur as well and is likely, as the spread of beta-lactamase producing _S. aureus_ did in the middle of the last century, to become much more entrenched in the ensuing years. This will further contribute to the problem.
As in this VRSA case, a number of the VISA isolates occurred in chronic renal failure patients with previous vancomycin treatment for MRSA. However, acute and chronic care health care facilities are awash with chronically ill, often morbidly debilitated, individuals with known or suspected infection or colonization with MRSA. This cohort continues to receive vancomycin as well as other broad spectrum antimicrobials and represent a huge potential melting pot for the development of this and other polyresistant pathogens.
It is unknown just how long it will take for VRSA to develop a beach head in the pathogen wars or whether more controls on glycopeptide antimicrobial use could forgo it. If VRSA proves to be a worthy pathogen, the next cycle in antistaphylococcal wars will begin. We hope this battle will be more of a 40 year war than a one or two year downhill struggle. The conflict will be fought with troops that still need to be proven to be effective warriors. The efficacy of the tetracyclines, linezolid, quinupristin/dalfopristin and trimethoprim/sulfamethoxazole in deep seated, life-threatening, invasive staphylococcal infections remain to be demonstrated in large scale studies involving the 21th century health care recipient. -Mod.LL]
--------------------------------------------------
Provided under Fair Use for Education doctrine. Original copyright remains with quoted journal.
************************************
A ProMED-mail post
ProMED-mail, a program of the
International Society for Infectious Diseases
<http://www.isid.org>
Date: 3 Jul 2002
Source: MMWR 5 July 2002 (edited)
<http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5126a1.htm>
_Staphylococcus aureus_ resistant to vancomycin - USA, 2002
--------------------------------------------------
_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 USA. The emergence of VRSA underscores the need for programs to prevent the spread of antimicrobial resistant 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 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 the Centers for Disease Control and Prevention (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.
Epidemiological 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, et al, at Michigan Dept of Community Health; W Brown, et al, at Detroit Medical Center; R Johnson, 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, CDC.
[MMWR} 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, 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 [first identified in about 1960. - Mod.SH] 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 (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 (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 USA. _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.
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 Bennett's principles and practice of infectious diseases, 4th ed. New York: Churchill Livingstone, 1995: 1754-77.
3. Hiramatsu K, Hanaki H, Ino T, et al. 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 Morb Mortal Wkly Rep 2001; 50(RR-5).
8. CDC. Interim guidelines for prevention and control of staphylococcal infections associated with reduced susceptibility to vancomycin. MMWR Morb Mortal Wkly Rep 1997; 46: 626-8,635.
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.
--
ProMED-mail
[The discovery of a clinical isolate of _S. aureus_ fully resistant to vancomycin is unsurprising, given the progression of antimicrobial resistance in this significant community and hospital acquired pathogen.
Since the recognition of VISA strains in 1996, attempts to modify vancomycin use have confounded by the continued high prevalence of MRSA in hospitals for which vancomycin has remained the treatment of choice. The recognition of MRSA in community settings has begun to occur as well and is likely, as the spread of beta-lactamase producing _S. aureus_ did in the middle of the last century, to become much more entrenched in the ensuing years. This will further contribute to the problem.
As in this VRSA case, a number of the VISA isolates occurred in chronic renal failure patients with previous vancomycin treatment for MRSA. However, acute and chronic care health care facilities are awash with chronically ill, often morbidly debilitated, individuals with known or suspected infection or colonization with MRSA. This cohort continues to receive vancomycin as well as other broad spectrum antimicrobials and represent a huge potential melting pot for the development of this and other polyresistant pathogens.
It is unknown just how long it will take for VRSA to develop a beach head in the pathogen wars or whether more controls on glycopeptide antimicrobial use could forgo it. If VRSA proves to be a worthy pathogen, the next cycle in antistaphylococcal wars will begin. We hope this battle will be more of a 40 year war than a one or two year downhill struggle. The conflict will be fought with troops that still need to be proven to be effective warriors. The efficacy of the tetracyclines, linezolid, quinupristin/dalfopristin and trimethoprim/sulfamethoxazole in deep seated, life-threatening, invasive staphylococcal infections remain to be demonstrated in large scale studies involving the 21th century health care recipient. -Mod.LL]
--------------------------------------------------
Provided under Fair Use for Education doctrine. Original copyright remains with quoted journal.