Showing posts with label VRSA. Show all posts
Showing posts with label VRSA. Show all posts

Thursday, April 30, 2015

ECCMID 2015 - "Best Of" Infection Control Literature (Part 1)

Every year it seems that one of us at the University of Iowa is roped into giving one of these "Best of Infection Control" talks at an annual conference. This year it seems that almost all of us have been asked and for some inexplicable reason, we all said yes! I was the lucky one to kick off the 2015 season with this talk I gave last week at ECCMID in Copenhagen. I covered S. aureus, MRSA, VRE, VRSA, surgical site infections and hand hygiene. I look forward to Mike's talk at SHEA. Loren Herwaldt's talk at ICPIC and Dan's talk at IDWeek. On Iowa.

Sunday, April 27, 2014

Vancomycin-resistant S. aureus (VRSA) update

The time intervals between introduction of penicillin and the emergence of penicillin-resistant S. aureus, and between the introduction of methicillin and the emergence of MRSA, were very short (3-5 years), and were followed by rapid emergence and spread of the resistant strains. For unclear reasons, the same hasn’t been true for VRSA. Vancomycin was introduced in the 1950s, and use of the drug increased almost exponentially during the advance of MRSA as a hospital pathogen in the 1980s. Yet it wasn’t until 2002 that the first VRSA infection was reported. As soon as it was recognized that plasmid-mediated transfer of the vanA gene to MRSA was responsible, many considered the rapid spread of VRSA to be inevitable. 

Interestingly, this spread hasn’t yet happened—appearance of VRSA strains has remained rare and sporadic, with only 13 confirmed cases in the US since the first report, barely one per year. Furthermore, person-to-person spread hasn’t been demonstrated to be a problem. The first 12 cases were all in the similar genetic background (clonal complex 5, most of which were t002, the most common healthcare-associated MRSA spa type). Furthermore, vancomycin pressure seemed a prerequisite, suggesting that a high fitness cost is associated with maintaining vanA in S. aureus.

In this context, two recent publications should raise new concern about the potential for further emergence of VRSA. As documented in a CDC report of the 13th VRSA case in the US, and in last week’s NEJM report of a VRSA case from Brazil, VRSA has now emerged in the genetic background of community-associated MRSA strains (USA1100 and USA300). USA300 (clonal complex 8) has been particularly successful at rapidly spreading and replacing other MRSA lineages, so stable carriage of vanA in a USA300 background would be a major public health problem.


The above image of the pBRZ01 plasmid harboring vancomycin resistance genes and found in the Brazilian bloodstream infection case is from the NEJM report.

Sunday, June 30, 2013

More VRSA

Earlier this week, Eli posted on the first case of VRSA in Europe. Today, a posting on ProMed reports on the first VRSA case in Latin America. This is also the first time VRSA has been isolated from the blood; all previous strains were isolated from wounds. The patient was a 35 year old man from Sao Paulo, Brazil with diabetes and Sezary Syndrome. His bloodstream infection was controlled with daptomycin but he died 3 weeks after VRSA was isolated. The vanA gene was detected in the VRSA strain as well as from an Enterococcus faecalis strain isolated from the same patient.

Graphic:  Wikipedia

Tuesday, June 25, 2013

VRSA - First Case in Europe

Lost among the attention given to MERS in the recent NEJM and the H7N9 papers published in the Lancet today is a report of the first vancomycin-resistant S. aureus case in Europe. 

The case was in a 74yo in Portugal with diabetes on dialysis. She had prior pseudomonal and MRSA diabetic foot infections treated with vancomycin. This May she had VRSA detected in pus from a toe amputation wound with MIC for vancomycin of >256 μg/mL and MIC of 24μg/mL for teicoplanin. VRE and P. aeruginosa were also cultured. The VRSA strain was sequence type ST105, SCCmec type II, and had both the mecA and vanA genes (from her VRE). This VRSA was resistant to erythromycin, clindamycin, gentamicin, and ciprofloxacin, and susceptible to co-trimoxazole, tetracycline, tygecycline, linezolid, daptomycin, quinupristin/dalfopristin, fusidic acid, cloramphenicol, rifampicin, and mupirocin.

Wednesday, April 7, 2010

VRSA's back

There is a new report of a patient in a Philadelphia hospital that is infected with vancomycin-resistant Staph. aureus (VRSA). Fortunately, VRSA has remained very rare. Like previous patients, this patient is a dialysis patient, but few other details about the patient were available in the article.

OSHA! OSHA! OSHA!

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