World Running Out of Weapons to Fight Superbugs

Add this the, “Well duh!” file.  I guess it is “news to those outside of the medical field, but to those of us on the frontlines, it’s nothing new.  A colleague of mine was telling me about a patient who had a MDR Acinetobacter bacteremia that ws resistant to everything we had in the formulary.  Nothing could touch it.  The patient suprisingly survived and went home, but scary nonetheless.

Besides the “guided” evolution of bacteria (due in part to an overabundance of antibitoics in the environemnt), one thing that seems to be causing the development of new antibiotics is that they aren’t “sexy”.  More money can be made off of the latest ED drug, anti-lipid med or novel combination antihypertensive/statin, than new antibiotics.  Just the truth.

Sensational MRSA Headline

How our hospitals unleashed a MRSA epidemic | Seattle Times Newspaper

It says it right there:  MRSA is the fault of hospitals.  If it wasn’t for hospitals, MRSA wouldn’t be so prevalent, wouldn’t be so deadly or such a large issue.  Right.  What a crock of shit.

It mentions nothing abot the over-prescribing of antibiotics.  Nothing of the emergence of the USA300 clone of MRSA in community-acquired infections.  Nothing of the reality that this is based on environmental pressure on the bugs that cause them to acquire resistance in the first place.  No, it’s the hospitals’ fault.

Now I will give due.  We suck when it comes to handling these issues.  And we can do better.  Unfortunately this is a multi-factorial issue and difficult to address whitout pointing fingers.  Wahing hands?  We don’t do it nearly enough.  And nurses aren’t the only culprits.

Physicians can be the most lackadaisical about infection control.

In April 2006, doctors at the UW Medical Center carried personal items from home into sterile operating rooms and dropped them on the floor. These items included backpacks and satchels, made of porous materials friendly to germs. Hospital administrators told inspectors this was “common practice.”

In November 2006, a physician at St. Joseph Medical Center in Tacoma removed his surgical mask during an operation. He had complained it was uncomfortable. Hospital officials told inspectors the physician was a “repeat” violator and had been warned before to keep his mouth and nose covered.

In hospitals, the most common violation is the failure to wash hands upon entering or leaving a patient’s room.

In the worst cases, as few as 40 percent of staff members comply with hand-washing standards. Doctors are the worst offenders, according to confidential hospital records reviewed by The Times.

I’ve lost track of times I’ve seen docs walk into isolation rooms and not don any PPE.  VRE?  MRSA?  C.DIff?  Not a problem, it seems their white coats magically protect them from the all but the worst offenders.  Not to mention becoming a vector in their own right.

While measures like presumptive isolation, isolating anyone who has ever had MRSA, screening everyone on admit my help to slow the rise of the germ in hospitals, it does nothing to prevent it coming from the outside.  All of the MRSA patients I have taken care of, have had it on admit.   It’s why they were there.  In a perfect world, we would have private rooms or all patients.  There would be a fast bedside screening tool for MRSA and other community-acquired resistant germs.  Rooms would be cleaned appropriately and thoroughly.  We would all wash our hands or use foams/gels every single time.  But it’s not a perfect world.  Even in our new unit we have double rooms.  Even though our housekeepers do a pretty good job, there is still the risk of acquiring MRSA from a previous occupant just on odds alone.  It is going to happen.

One problem the article doesn’t address is the rise of the USA300 clone that is present in nearly 97% of community-acquired MRSA infections, most notably in skin and soft tissue infections.  This virulent and nasty strain, with its included Panton-Valentin Leukocidin exotoxin can cause necrotizing fascitis, sepsis and pneumonia.  It’s nasty. But again, like any MRSA, good hand hygeine and terminal room cleaning can help to prevent its transmission inside hospital walls.

While hospitals may have covered up cases and mortality due to MRSA, as shown pretty damningly in the Times article, this not just a focused problem.  It is a multi-systemic issue that reaches across disciplines.  Therefore its going to take a multi-system effort to combat it.

Staph and the NFL

A little Monday morning football related shenanigans for y’all:  A Slew of Staph Infections Tackles the NFL.

As health-care providers we all see this.  We know staph.  We’re almost all colonized by some variety, many of us probably with MRSA thanks to our unique patient populations.  It never ceases to amaze me though how this little bugger pops up in all sorts of odd places.

There were several telling quotes though from the article that I found both hilarious and frightening.  Now remember folks, the is Time (not Ma’ n’ Paws’ Newsie Magazine).  When talking about the the frequency of staph they drop this gem on us, “were either treated for staph or symptoms caused by the virus.”

Wait a sec’.  Did they say virus?  Uh…, yep.  Gee, I guess that’s why all the anitbiotics we’re throwing at it aren’t working: it’s a virus.  Wrong.  Big time wrong.  We all know staph is a bacteria, a gram-positiive cocci usually found in clusters.  It seems Time never got the message.

I also liked little gem:

In 2003, a team of researchers tracked the St. Louis Rams and found five players who caught eight MRSA infections. “We observed a lack of regular access to hand hygiene (i.e., soap and water or alcohol-based hand gels) for trainers who provided wound care,” they wrote in The New England Journal of Medicine. Other offenses included “skipping of showers by players before the use of communal whirlpools; and sharing or towels — all factors that might facilitate the transmission of infection in this setting.”

Like our infection control folks have been saying for a long time: wash your f*cking hands!  Yes, even big, bad, strong football players need to do simple things like hand-hygeine.  Simple ain’t it?

Plus with the recent news that Tom Brady has to go under the knife again, which sounds like a washout procedure of an infected knee, it shows that anyone can contract this, not just skin-popping junkies.

Expanding Multidrug-Resistant MRSA

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.

Panton-Valentine leukocidin

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.

Multi-Drug Resistance

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.

Cross-species evolution

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.

S.F Researcher follow strain of drug-resistant bacteria

Multi-Drug-Resistant MRSA Hitting Gay Men

Skin and Soft Tissue Infections Caused by MRSA USA300