<i>Staphylococcus aureus</i> with Reduced Susceptibility to Vancomycin Isolated from a Patient with Fatal Bacteremia

Rotun, Sharon S.; McMath, Virginia; Schoonmaker, D.; Maupin, Peggy S.; Tenover, Fred C.; Hill, Bertha C.; Ackman, David M.

doi:10.3201/eid0501.990118

Cited by 149 publications

(90 citation statements)

References 5 publications

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“…Other investigators have also demonstrated that in-vitroselected VISA retain parental SmaI RFLP patterns (Schaaff et al, 2002). SmaI chromosomal RFLPs are also similar between VISA that arise from vancomycin-susceptible strains during vancomycin therapy in a single patient (Rotun Rotun et al, 1999;Sieradski et al, 1999a;Smith et al, 1999).…”

Section: Resultsmentioning

confidence: 99%

Alterations in phage-typing patterns in vancomycin-intermediate Staphylococcus aureus

Gustafson

O’Brien

Coombs

et al. 2003

Journal of Medical Microbiology

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The ability of phage-typing and SmaI chromosomal RFLPs to conclude appropriate strain relatedness between a collection of 12 well-characterized in vitro-selected vancomycinintermediate Staphylococcus aureus (VISA) strains and their seven vancomycin-susceptible parent strains is reported. Generally, no SmaI RFLP alterations were observed in VISA strains when they were compared with their respective parent strains, and clonal relationships between isogenic strains were clearly evident. Unlike the SmaI RFLP results, parent strains and VISA derivatives generally did not share similar phage-typing profiles. Depending on the phage set investigated, some VISA strains even became untypable by this method. Loss of phage infectivity is probably due to cell wall (phage receptor) alterations that are expressed by the VISA strains investigated. Collectively, these findings indicate that inappropriate relationships between VISA and vancomycinsusceptible parents might be drawn if only phage-typing and antibiotic susceptibility are utilized to determine epidemiological relationships.

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Section: Resultsmentioning

confidence: 99%

Alterations in phage-typing patterns in vancomycin-intermediate Staphylococcus aureus

Gustafson

O’Brien

Coombs

et al. 2003

Journal of Medical Microbiology

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“…The occurrence of colonization with VRE and MRSA appears to be common among patients requiring intensive care [9,19]. Infections caused by strains of Staphylococcus aureus with reduced susceptibility to vancomycin (minimum inhibitory concentration = 8 µg/mL) were described in Japan and United States, each case occurred following a prolonged course of vancomycin therapy [20][21][22]. In the United States clinical infections with vancomycin resistant Staphylococcus aureus (VRSA) were reported, in 2002 [23][24][25][26].…”

mentioning

confidence: 99%

Vancomycin use in a hospital with high prevalence of Methicillin-Resistant Staphylococcus aureus: comparison with Hospital Infection Control Practices Advisory Committe Guidelines (HICPAC)

Melo¹,

Sasaki²,

Grinbaum³

2007

Braz J Infect Dis

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“…La cepa MRSA aislada, denominada Mu50, tenía una CIM para vancomicina de 8 µg/ml determinada por microdilución en caldo. Desde entonces se han reportado cepas VISA en Europa (18,19), Estados Unidos (20)(21)(22)(23), Asia (24) y Brasil (25). El grupo colombiano de resistencia antimicrobiana, RESCOL (26), tras analizar 296 aislamientos nosocomiales de S.aureus en el período 2001-2002 encontró 52% de resistencia a meticilina, pero ninguna cepa VISA mediante la técnica de tamizaje en agar infusión cerebro corazón (BHIA, Brain-Heart infusion Agar) con 6 µg/ml de vancomicina según recomendación del CLSI y de los Centers for Disease Control (CDC) (27).…”

Section: Resistencia Intermedia a Vancomicina: Cepas Visaunclassified

“…Además, los reportes de los Estados Unidos sugieren que las cepas VISA se desarrollaron a partir de cepas de MRSA que infectaron previamente los pacientes, dada la identidad entre sus patrones de electroforesis de campo pulsado (PFGE, pulsedfield gel electrophoresis) (21)(22)(23).…”

Section: Resistencia Intermedia a Vancomicina: Cepas Visaunclassified

Staphylococcus aureus resistente a vancomicina.

Rodríguez¹,

Vesga

2005

biomedica

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Objetivo. Revisar la evolución y mecanismos moleculares de la resistencia de Staphylococcus aureus a vancomicina. Fuente de los datos. Se consultó la base de datos MEDLINE y se seleccionaron artículos tipo reportes de caso, estudios bioquímicos, de microscopía electrónica y biología molecular pertinentes. Síntesis. Después de casi 40 años de eficacia ininterrumpida de la vancomicina, en 1997 se reportaron los primeros casos de fracaso terapéutico debido a cepas de Staphylococcus aureus con resistencia intermedia, denominadas VISA (concentración inhibitoria mínima, CIM, 8 a 16 µg/ml), así como a cepas con resistencia heterogénea hVISA (CIM global = 4 µg/ml, pero con subpoblaciones VISA), en las cuales la resistencia está mediada por engrosamiento de la pared celular y disminución de su entrecruzamiento, lo que afecta la llegada del antibiótico al blanco principal, los monómeros del peptidoglicano en la membrana plasmática. En 2002 se aisló la primera de las 3 cepas reportadas hasta la fecha con resistencia total al antibiótico, denominadas VRSA (CIM>32 µg/ml), en las que se encontró el transposón Tn1546 proveniente de Enterococcus spp, responsable del reemplazo de la terminación D-Ala-D-Ala por D-Ala-Dlactato en los precursores de la pared celular con pérdida de la afinidad por el glicopéptido. Conclusiones. La resistencia a vancomicina es una realidad en S. aureus, mediada en el caso de VISA por alteraciones en la pared celular que atrapan el antibiótico antes de llegar al sitio de acción, y en el caso de VRSA, por transferencia desde Enterococcus spp. de genes que llevan a la modificación del blanco molecular.Palabras clave: Staphylococcus aureus, peptidoglicano, biosíntesis, antibióticos glicopéptidos, vancomicina, resistencia microbiana a drogas, resistencia a vancomicina. Vancomycin-resistant Staphylococcus aureusThe evolution and molecular mechanisms of vancomycin resistance in Staphylococcus aureus were reviewed. Case reports and research studies on biochemestry, electron microscopy and molecular biology of Staphylococcus aureus were selected from Medline database and summarized in the following review. After almost 40 years of successful treatment of S. aureus with vancomycin, several cases of clinical failures have been reported (since 1997). S. aureus strains have appeared with intermediate susceptibility (MIC 8-16 µg/ml), as well as strains with heterogeneous resistance (global MIC ≤ 4 µg/ml), but with subpopulations of intermediate susceptibility. In these cases, resistance is mediated by cell wall thickening with reduced cross linking. This traps the antibiotic before it reaches its major target, the murein monomers in the cell membrane. In 2002, a total vancomycin resistant strain (MIC ≥ 32 µg/ml) was reported with vanA genes from Enterococcus spp. These genes induce the change of D-Ala-D-Ala terminus for D-Ala-D-lactate in the cell wall precursors, leading to loss of affinity for glycopeptides. Vancomycin resistance in S. aureus has appeared; it is mediated by cell wall modifications that trap the ...

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Staphylococcus aureus with Reduced Susceptibility to Vancomycin Isolated from a Patient with Fatal Bacteremia

Cited by 149 publications

References 5 publications

Alterations in phage-typing patterns in vancomycin-intermediate Staphylococcus aureus

Alterations in phage-typing patterns in vancomycin-intermediate Staphylococcus aureus

Vancomycin use in a hospital with high prevalence of Methicillin-Resistant Staphylococcus aureus: comparison with Hospital Infection Control Practices Advisory Committe Guidelines (HICPAC)

Staphylococcus aureus resistente a vancomicina.

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