We were talking at work the other night about a news report about a new fiercer clone of MRSA. It seems to be adding to it repertoire of resistance. This is of particular interest on my floor as we see a fair share of MRSA infections, they range anywhere from skin-popper with abscesses to post-CABG patients with sternal wound infections. Like Sun Tzu noted, knowledge about your enemy is vital. Here’s some stuff I found.
This is what makes the USA300 strain of CA-MRSA so nasty. From the CDC:
Most CA-MRSA strains carry the intracellular toxin Panton-Valentine leukocidin (PVL), which is known for pore formation on polymorphonuclear cells of the host (10,11). In addition, the USA300 clone contains the arginine catabolic mobile element (ACME), which inhibits polymorphonuclear cell production (10)
So in essence it goes after the very cells intended to take it out. The USA300 variant has been most common in skin and soft tissue infections, but now has spread into pneumonia and necrotizing fasciitis. In some places, the USA300 variant is the most predominant form of MRSA, with extremely high mortality rates in pneumonias, especially in the immuno-compromised. In a case study presented at a conference I went to in November, they illustrated a case of PVL positive USA300 MRSA pneumonia. From time of presentation to death in this particular case study was approximately 72 hours. Granted, this was a immuno-compromised individual who had delayed treatment, but the rapid onset, even with supportive therapies was astounding. At the same conference they showed pathology specimens of rat lungs infected with non-USA300 and USA300 MRSA. The non-USA300 lungs looked worse for wear, but the USA300 lungs looked nearly liquid due to the effects of the PVL.
The frightening development in the USA300 variant is the expansion of drug resistance. From a SF Gate.com article:
Further along the gene map are sections that produce resistance to the antibiotics tetracycline, erythromycin, clindamycin, Cipro and mupirocin, a topical ointment often used to kill MRSA colonies living in people’s noses.
And from a MedpageToday.com article:
Thanks to its acquisition of multiple resistance genes, the multi-drug-resistant USA300 strain is also able to battle fluoroquinolones, tetracycline, macrolide, clindamycin, and mupirocin.
This extra level of drug resistance will only increase the use of vancmycin to treat MRSA infections. For many of our MRSA patients, this is all they are on. Increasingly though, we’ve been seeing Levaquin, Cubicin and Zyvox being used to combat the infection, especially in re-offenders (we had one guy come back 3 times with recurrent MRSA sternal infections, even with Wound V.A.C. and I&D therapy the 2nd and 3rd times, he still kept coming back). It’s only a matter of time before we start seeing increased resistance to those drugs. All that we really need s someone with VRE to have a MRSA infection. While there are a few (inter)national cases of vancomycin intermediate resistance Staph and only 1 documented case of resistant Staph, odds are it will only be a matter of time. So instead of MRSA, we’ll be talking bout VRSA. Unfortunately, the hospital becomes a hotbed of evolution due to the co-mingling of conditions and infection. While infection-control tries, they aren’t always able to keep up.
One final reason that USA300 is so nasty is that it appears to have picked up genes from another Staph species. In the SF Gate.com article:
The gene map, published in the British medical journal the Lancet in February 2006, has yielded clues to why this strain spreads so quickly. The bug appears to have swapped genes from Staphylococcus epidermidis, a usually harmless staph species that is commonly found on human skin. Researchers theorize that, by stealing a trick from the milder staph bug, the malevolent USA300 may colonize on human skin more easily than other varieties of MRSA.
This evolution does make it more virulent and a bigger to threat to health-care workers. Think about it. We’re in contact with the patient, doing our nursing duties. Yes, we’re applying the principles of universal precautions and good hand-washing, but still there is a decent chance of us acquiring it. With resistance to mupirocin, knocking out the colonies that may develop on health-care workers becomes infinitely more difficult.
The fascinating element to all of this is the ability of this little bacteria to do this. I didn’t do so great in microbiology and have a basic understanding of resistance, transference and mechanisms of evolution with bacteria and it piques my interest.
Hope you found the information useful . Here’s links to the articles above, it’s good reading.