First detected isolate of glycopeptide-intermediate resistant Staphylococcus aureus in a renal unit at a central academic hospital in KwaZulu-Natal: brief report (original) (raw)
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Staphylococcus aureus with reduced susceptibility to vancomycin
Ceylon Medical Journal, 2011
Staphylococcus aureus with Reduced Susceptibility to Vancomycin-Illinois, 1999 Staphylococcus aureus is one of the most common causes of hospital-and community-acquired infections. Nosocomial methicillin-resistant S. aureus (MRSA) infections have become common, and cases of community-acquired MRSA infections also have occurred (1,2). Since 1996, vancomycin-intermediate S. aureus (VISA; vancomycin minimum inhibitory concentration [MIC]=8-16 µg/mL) has been identified in Europe, Asia, and the United States (3-5). The emergence of reduced vancomycin susceptibility in S. aureus increases the possibility that some strains will become fully resistant and that available antimicrobial agents will become ineffective for treating infections caused by such strains. This report describes the fourth case of confirmed VISA from a patient in the United States. In April 1999, a 63-year-old woman with MRSA bacteremia (MIC <1 µg/mL) was transferred from a long-term-care facility to an Illinois hospital (hospital A). The patient had a history of frequent hospitalizations for complications of hemodialysis-dependent, end-stage renal disease, and intravascular access, including two failed arteriovenous grafts, multiple central venous catheter-associated infections, and intermittent receipt of vancomycin therapy through June 1998. Thirteen days after hospital admission and 25 days after initiating vancomycin therapy (median vancomycin serum con-centration=12.7 µg/mL; range: 12.1 µg/mL-20.9 µg/mL), a culture from her blood grew S. aureus with an MIC of 4 µg/mL; the blood culture was tested using the Vitek ® system (bioMérieux; Hazelwood, Missouri)*. Three subsequent blood specimens drawn within the next 3 days grew S. aureus with MICs of 8 µg/mL on confirmatory testing. The isolates, identical by pulsed-field gel electrophoresis, were resistant to penicillin, oxacillin, clindamycin, erythromycin, ciprofloxacin, and rifampin but susceptible to trimethoprim-sulfamethoxazole, tetracycline, gentamicin, and had intermediate susceptibility to chloramphenicol. No VISA strains were recovered from other body sites. An echocardiogram demonstrated a mitral valve vegetation but the patient declined surgical intervention. Despite treatment with intravenous vancomycin, rifampin, and *Use of trade names and commercial sources is for identification only and does not imply endorsement by CDC or the U.S. Department of Health and Human Services.
Healthcare Infection, 2000
There have been several reported cases to date of Staphylococcus aureus (S. aureus) with decreased susceptibility to the glycopeptide antibiotics, particularly vancomycin. Such isolates have been termed VISA (vancomycin-intermediate S. aureus) or GISA (glycopeptide-intermediate S. aureus). These strains have developed in patients with pre-existing methicillin-resistant S. aureus (MRSA) infections treated with prolonged courses of the drug of choice, vancomycin. Resistance to vancomycin severely limits treatment options for these patients, highlighting the need to preserve the utility of the drug through restricted usage and the need for increased awareness of infection control measures to prevent acquisition of MRSA in the first instance. While vancomycin-resistant Enterococcus (VRE) has received significant attention in the scientific literature and the media, the clinical implications of a vancomycin-resistant strain of S. aureus, a more pathogenic and virulent organism, are far more significant. This review details the clinical features and microbiology of the isolates found so far, the use of vancomycin in staphylococcal infections and some of the measures necessary to prevent the development and spread of vancomycin resistance in Australia.
Vancomycin Resistant Staphylococcus Aureus (Vrsa)
Background: Vancomycin resistant Staphylococcus aureus (VRSA) are serious strains of Staphylococci that are difficult to be treated and have considerable emerging percentage in the world. Objectives: To estimate the percentage of VRSA in Khartoum state. Method:The different specimens were randomly collected from different patients suffering from various clinical manifestations after accepting the informed consents and cultured in number of different culture media according to each sample, then sensitivity testing is done using oxacillin(1 mcg), vancomycin(30 mcg) ,amoxyclav(30 mcg) ,erythromycin(15 mcg), clindamycin(2 mcg) and amikacin (30 mcg)discs and interpreted according to Kirby Bauer reference procedure. Results: According to the outcome of our study, S.aureus that were resistant to vancomycin disc (30 mcg) represents 12% from total 100 S.aureus positive specimens and 3.7% from MRSA group while 15.1% from MSSA group. On the other hand clindamycin resistance represents about 10% ,Inducible clindamycin resistance forming D shape appearance 76.1% while 23.8% showed constitutive resistance. There is a great resistance of S.aureus bacteria to amoxyclav disc(30 mcg (20/10 mcg)) with percentage of 76% while 24% nly were sensitive to the disc. Conclusion: There is a significant percentage of S.aureus bacteria that showed resistance to vancomycin.
Journal of Clinical Microbiology, 2010
Strain D958, a methicillin-resistant Staphylococcus aureus strain with reduced susceptibility to vancomycin, was isolated from a 69-year-old Saudi male patient presenting with severe sepsis immediately after admission. Despite high serum levels of vancomycin, the same S. aureus strain was isolated from five blood culture sets during 1 week. Treatment failure under therapeutic levels of vancomycin prompted us to investigate the resistance profile of this strain in further detail. The MIC values for vancomycin as determined by Etest and microdilution were 3.0 and 2.0 mg/liter, respectively, and remained unchanged during the treatment course. The macro-Etest method showed a MIC of 4 mg/liter. The strain showed liquid vancomycin and lysostaphin MBCs of 2.0 and 5.0 mg/liter, respectively. The isolates were confirmed as heterogeneously vancomycinintermediate S. aureus (hVISA) by vancomycin population analysis profile. The areas under these curves were similar for Mu3 and D958 for vancomycin and teicoplanin (ratio values were 1 and 1.1 for vancomycin and teicoplanin, respectively). Extensive genotyping and molecular characterization demonstrated that the strain harbored a staphylococcal cassette chromosome mec element (SCCmec) type III cassette and was of sequence type ST241, a single-locus variant of the successful multiresistant clone ST239. Microarray results demonstrated that D958 contained numerous resistance determinants (generally plasmid or phage encoded). These results suggest that this strain is constitutively expressing an altered susceptibility to vancomycin. Further studies are warranted to assess the clonal distribution of such strains displaying reduced susceptibility to vancomycin prior to any antimicrobial therapy. Staphylococcus aureus is a major cause of serious hospitaland community-acquired infections associated with morbidity and mortality (42). In recent years, prevalence rates of methicillin-resistant S. aureus (MRSA) strains have varied between (and within) countries, but they have increased significantly since the early 1990s. In the first decade of the new millennium, MRSA rates have reached worrisome levels in numerous countries, such as the United Kingdom (40%), France and Greece (35%), and Italy (45%) (53). Simultaneously, the United Kingdom, Ireland, and Greece have reported some of the highest rates of MRSA from bloodstream isolates (44, 41, and 44%, respectively, in 2004) (15). In 1996, the first clinical strain of S. aureus with reduced susceptibility to vancomycin (MIC of 8.0 mg/liter) was reported in Japan (25). In 2002, the first two clinical infections caused by vancomycin-resistant S. aureus strains (VRSA) were confirmed in the United States (10, 38). The latter report describes the first documented case of an infection caused by VRSA (vancomycin MIC, Ն32 mg/ liter) resulting from the transfer of a vanA gene from Enterococcus faecalis to S. aureus. Although the emergence of vancomycin-intermediate S. aureus (VISA, or GISA for glycopeptide-intermediate S. aureus) (21, 23
Vancomycin‐ResistantStaphylococcus aureusin the Absence of Vancomycin Exposure
Clinical Infectious Diseases, 2004
We report findings from our investigation of the world's second clinical isolate of vancomycin-resistant Staphylococcus aureus (VRSA). An elderly man was hospitalized with an infected chronic heel ulcer and osteomyelitis. Before hospital admission, he received multiple courses of antibiotic therapy but, notably, no vancomycin. Numerous cultures of ulcer specimens (performed on an outpatient basis) grew methicillinresistant, vancomycin-susceptible S. aureus and vancomycin-resistant Enterococcus species. At admission, an additional culture of a specimen from the heel ulcer grew S. aureus that was identified as VRSA (minimal inhibitory concentration for vancomycin [by broth-microdilution], 32 mg/mL). Further evaluation confirmed the presence of the vanA gene mediating vancomycin resistance. To assess VRSA transmission, we performed a carriage study of 283 identified contacts and an environmental survey of the patient's home; no VRSA isolates were recovered. This case illustrates that recent exposure by patients to vancomycin is not necessary for development of vanA-containing VRSA. For clinical and public health reasons, it is essential that microbiology laboratories adequately test for vancomycin-resistance in S. aureus. Staphylococcus aureus is one of the most common causes of serious infection in community and hospital settings [1, 2]. Methicillin-resistant S. aureus (MRSA) is now endemic in health care facilities, with rates of 150% in some health care settings [3]. Also, recent reports describe MRSA carriage in persons in the community who do not have health care-associated risks [4]. The increased incidence of MRSA has led to more frequent use of vancomycin, the drug commonly relied on for treating MRSA infections.
Methicillin and vancomycin resistant S. aureus in hospitalized patients
Journal of Global Infectious Diseases, 2010
S. aureus is the major bacterial cause of skin, soft tissue and bone infections, and one of the commonest causes of healthcareassociated bacteremia. Hospital-associated methicillin-resistant S. aureus (MRSA) carriage is associated with an increased risk of infection, morbidity and mortality. Screening of high-risk patients at the time of hospital admission and decolonization has proved to be an important factor in an effort to reduce nosocomial transmission. The electronic database Pub Med was searched for all the articles on "Establishment of MRSA and the emergence of vancomycin-resistant S. aureus (VRSA)." The search included case reports, case series and reviews. All the articles were cross-referenced to search for any more available articles. A total of 88 references were obtained. The studies showed a steady increase in the number of vancomycin-intermediate and vancomycinresistant S. aureus. Extensive use of vancomycin creates a selective pressure that favors the outgrowth of rare, vancomycin-resistant clones leading to heterogenous vancomycin intermediate S. aureus hVISA clones, and eventually, with continued exposure, to a uniform population of vancomycin-intermediate S. aureus (VISA) clones. However, the criteria for identifying hVISA strains have not been standardized, complicating any determination of their clinical significance and role in treatment failures. The spread of MRSA from the hospital to the community, coupled with the emergence of VISA and VRSA, has become major concern among healthcare providers. Infection-control measures, reliable laboratory screening for resistance, appropriate antibiotic prescribing practices and avoidance of blanket treatment can prevent long-term emergence of resistance.