Thank you, appreciate that fine introduction.  I don’t know if I can live up to that.  But I do appreciate being asked to talk today on a topic that is near and dear to my heart and that is hospital acquired infections.  So first do no harm, I think that’s something we need to keep close to our heart and it just saddens me when I see patients that have a pic line in left for convenience and get sepsis, or a Foley catheter left in too long with urinary tract infection and we’re going to talk about a number of different hospital acquired infections today.  And certainly in 40 minutes I cannot do justice to all of them in detail, so I’m going to try to touch on areas of different topics that might be applicable to the generalist out there and try to bring in some new things that have happened over the past year or two and get you up to speed on this stuff.

Just a basic definition of healthcare associated infection is any infection that wasn’t there prior to coming into the hospital or into a long term or any type of institution.  And generally speaking according to the definition if it happens within the first 48 hours it probably was incubating when the patient arrived, any time after that it gets chalked up against the hospital or the surgeon or whoever, and in these days that means financial implications as CMS is now no longer reimbursing any extra and actually penalizing hospitals for having these infections. So not only because of the patient’s pain, suffering and even death it’s also now for financial reasons we get after these, which has actually helped me out a great deal as an infection control practitioner because the administration has swung in behind us over the past 5, 6 years with a greater sense of urgency.

These are a big problem as are pressure ulcers, you can see that probably closer to 1 in 20 but up to 1 in 10 patients admitted to the hospital without infection will develop one after they enter the institution.  One person dies approximately every 6 minutes in the United States from a hospital acquired infection and you can see that they are quite costly.  And they occur in all facilities obviously.

Probably at least half of these infections are preventable, so that’s really one of the things I’m going to try to emphasize today and one of the things that we’ve been working on both at St. Margaret’s and at the system.  I’m very active at the system level and I can tell you at UPMC we have markedly reduced our rate of hospital acquired infections over the past 5 to 10 years.  I mean at least a 50% decrease, and that is gratifying.

Now here are some of the ones I’m going to touch on today.  We’ll talk about C difficile, urinary tract infections, line infections, vascular infections, surgical site infections and pneumonia. So you can see a lot of material to grapple. 

Let’s start with C difficile.   C difficile is a common infection, you probably have all encountered it if you take care of patients.  It’s become more and more problematic over the past decade as the C difficile has mutated, become more virulent, I’m going to point that out.  We’re seeing it in healthier patients and patients who have not even received predisposing antibiotic treatment.  And you can see that C difficile infections cost money. When you see a patient who develops diarrhea in an institution whether it be a nursing home or a hospital one of the most common, far and away the most common thing that you are going to diagnose from an infection standpoint is Clostridium difficile colitis.

One of the new developments with Clostridium difficile is an improvement in diagnosis.  Up until very recently the standard test has been an enzyme assay, you order a C difficile and they send it to the lab. The lab will assess it for a toxin, they don’t culture it, culturing is costly and not as accurate, but they look to see if the toxin is there. The C difficile produces two toxins and both those toxins can cause diarrhea and that’s what is looked at, and up until recently the sensitivity for that test was not that great, it was about 70%.  Now we are in the age of PCR testing. PCR testing has been implemented, I know the Allegheny General system now has it onboard as its primary test, UPMC is about to launch it. It is much more sensitive, you can see 97% sensitivity versus 70%.  This means that there is absolutely no reason to do a repeat test. In the past we might repeat the test once or twice in an effort to improve the sensitivity and it did work a little bit with our old tests. With the new tests it makes no difference, the test is so good that you cannot show any change when you order a second test or a third test.

The stool should always be liquid. If you put a popsicle stick in the stool and it doesn’t fall over it should not be tested. There is no reason to do the test for follow-up, it does not tell you that the patient’s getting better.  In fact many patients who are cured of C difficile will carry that toxin in their stool for days and days and weeks after they clear their symptoms, so you really can’t use that as a measurement to determine if they are cured.  But this new test is important, it’s important to know it costs more than the old test, but the bottom line is it is a much better test and does not need any more than 1 b cent. 

I mentioned that the C dif has mutated and that indeed is the case.  Starting around the beginning of the millennium we had a new strain, and here you can see some very severe cases of C dif, this is a colon with a lot of pseudomembranes, you do not have to have pseudomembranes, you can still have colitis from C difficile without, but this patient obviously had a lot of them.  This is the CT scan. When you get a positive CT scan this is what they are looking at, this is the colon and you can see how thick the wall is. This mucosal thickening, the edema, the wall gets very edematous and this is what the radiologist is reading out.

This is the new strain that goes under a number of different names as microbiologists like to do.  But the bottom line is that it produces a lot more toxin.  So that it may produce up to 40 times as much toxin as the old strains, and it seems to cause illness in patients that are less predisposed. 

One thing that’s important to know is which antibiotics are more prone to cause it, because there really is a tier of antibiotics from high risk to low or no risk and you can see on this chart that extended spectrum Cephalosporins and Penicillins like Socin and Timentin, Quinolones, Quinolones now the leading cause, Ciprofloxacin, Moxifloxacin, Ibafloxacin, these drugs are high on the list as causes, Clindamycin we know causes it a fair amount when it’s used. But the lower risks, things like Bactrim, Tetracyclines, they don’t cause it nearly as often and there are some drugs that seem to cause it extremely infrequently and those that I have in yellow actually have been used to treat C difficile and have activity in vitro.  The Tigecycline I put on there, it’s not, I don’t think it’s on your – there is a few subtle changes from these slides to what you have.  So there is some literature now to show that Tigecycline may be effective in treating it, you might want to pencil that one in.

There are some recent data to show that acid suppressive drugs will increase the incidence of C difficile and the morbidity of C difficile. This is a very recent article from late last year showing pretty clearly that patients receiving PPIs and histamine blockers have 3 times the risk for complicated courses of C difficile. 

These are some guidelines for treatment, just run through these quickly.  There haven’t been a lot of changes.  Obviously if at all possible you’d like to stop the drug that causes it, which is usually an antibiotic and stopping that antibiotic will help, and often times that alone will allow the patient to become cured.  Certainly though when we diagnose it by the time they have mild to moderate disease we are going to treat them and the treatment for mild disease according to the IDSA which is Infectious Disease Society of America Guidelines and the reference is on the bottom, and I don’t think it’s on your slide because I noticed that last night. So I put it there if you want to write it down.

Nonetheless Metronidazole versus Vancomycin, when the disease gets more severe we have been feeling that Vancomycin is better than Metronidazole.  And the optimal way to administer both of these drugs is orally.  Vancomycin will not work when given intravenously, and we know this from the animal models. It does not get good intraluminal levels.  It’s not absorbed from the gut so you get sky high intraluminal levels after a few doses when you give it orally.  That’s the way to go.  Metronidazole is absorbed into the system but Metronidazole can be used intravenously and in patients that cannot take an oral medication we do give intravenous Metronidazole.  In patients that have severe disease we frequently add intravenous Metronidazole or Flagyl to the oral Vancomycin, but I can tell you that there is little to no evidence based data that support what we do there. We do that, we feel better, sleep better, not so sure that that IV Flagyl is helping out though. 

Now with fulminant disease we generally most of these recommendations including IDSA recommend oral Vancomycin and the literature is mixed though. There is some recent literature to show that maybe Flagyl isn’t any worse than Vancomycin but I can tell you that most experts still trend toward Vancomycin and I’ll show you some data on that.  If they can’t take it orally we will give it to them rectally by enema and generally speaking 500 mg 4 times a day rectally and it says 100 mm in the guidelines but a lot of experts think you need 250 or 500 to really get it to get up in there. So I generally go with a larger volume of diluent when we are giving enemas.  Again we’ll add the Metronidazole. 

One of the big issues in severely ill patients and we see a few of these every year is when do you get the surgeons involved to do colectomy?  We’re talking fulminant disease. And there is no question that patients with toxic megacolon and peritonitis and severe C difficile will survive, have a better surviving, less mortality with early colectomy.  And I actually, on your slides again there is a change where the yellow is here, the white blood cell count I think on your handouts is 20,000, it’s actually gone up to 50. I think 50,000 is more reliable, the new guidelines move it up because we see leukocytosis so common. If you see diarrhea and leukocytosis, elevated white count, C difficile is always near the top of the list and a probable issue.  I also moved the lactate up to 5 mmo. 

Now one of the things that’s being done here in Pittsburgh preliminarily is looking at taking out – instead of doing a colectomy right off the bat they do a laparoscope and see, and if there is not a lot of gross peritonitis and the colon looks somewhat viable they pull out the right side of the colon, do big time lavage in the OR and then start putting Vancomycin through the colon from the right side through to the left.  And the preliminary literature in the patients that they select out compared to colectomy actually looks quite good.  And the big value there is if you save it, eventually they reverse that and the colon is preserved.  So there may be some changes down the road soon where a lot of our colectomies can be not colectomies but what we do with colonic lavage and temporary ostomies, what have you.   So that’s kind of exciting.

Intravenous immunoglobulin when there is a lot of C difficile antibody in there may be beneficial in fulminantly ill patients.  Now when you have pooled IV IG which is what we use, if you order IV IG that’s what you get and there are antibodies in there against C difficile. That really hasn’t been looked at too well, we sometimes use it in patients that are very ill with fulminant disease. I have kind of anecdotally seen some patients get better but certainly that’s not evidence based data.  But in the animal model now it looks pretty favorable when you give hyperimmune C difficile immunoglobulin. There is also literature, small series looking at patients that get recurrent disease, relapsing disease, that seems to be fairly effective, but it’s not available commercially at this point in time.

I want to put my Fidaxomicin up here, which is Xifaxan.  This drug is out there and it’s strongly being pushed, recently released a year ago or so, approved for C difficile. They got an article in the New England Journal of Medicine, in the Bible, so what it shows, it does work and it looks like it works as well as Vancomycin.  The one advantage they found in this one study was lower relapse rate. One out of four, up to one out of three patients may relapse after they get treatment.  Here they went down to 10%, but that was only in the subsection that did not have the hypo virulent strain.  Now we have that hypo virulent strain here in Pittsburgh, exactly what it is isn’t clear.  At Presbyterian Hospital they’ve done studies years ago to try to get what the prevalence is. It could be 30%, 40%, it can be pretty high, and no benefit there. But the one thing you need to know about Fidaxomicin is it costs significant dollars. If you send the patient home with a prescription you will get a phone call, and that phone call will either come from the patient or the patient’s insurance company, or the pharmacist because it’s $3,000 per course and one of the reasons we don’t use much of it, I’ve used it a couple of times but I – you hardly ever have started it. 

This slide just shows that with severe disease in this study from Clinical Infectious Diseases they seem to have a better outcome with Vancomycin, in the mild disease they couldn’t show a significant difference.  But there have been other studies to kind of say well we can’t really make that significant difference.  There have been no studies I know of to show that where Flagyl came out the better, better actor. 

And finally with recurrent disease what to do, these again are some guidelines, straight from the guidelines. They can occur in 10 to 30% of cases, it’s – I’m sure that probably most of you have seen patients with relapsing C difficile.  It usually happens within a couple of months, generally within a month or a few weeks.  It may be the same or different strains, it’s not due to the fact that it was resistant to whatever you treated with.  It’s probably due to the spore forming resistance, crips, we don’t really know for sure. We make up some good stories why it comes back but we don’t really know. 

Now how to treat these, with the first recurrence we usually give them – I usually give them Vancomycin the second time around.  The official guidelines say you can go either way with Vanco or Flagyl. I might treat them for 3 weeks instead of 2 weeks. But if they recur once then they are likely to recur a second, third, fourth time.  And I have found that the best treatment is when they come the third time is a prolonged course of taper pulse regimen, and the reason for the pulsing is because the C difficile forms spores that are resistant to treatment.  And they can hang out.  So what you do is you get it down to a low dose, then you start to pulse so the antibiotic goes away, allows these spores to sporulate, become more sensitive to the drug and you keep hitting them. And this is really a regimen that I’ve been having a lot of success with, I’ve treated tons of patients. You can find different taper pulse regimens in the literature.  But this one has worked for me.  I have some patients that fail this, those patients I just throw my hands and I put them on one dose of Vancomycin a day, some for the rest of their life.  Often times you can get with one dose every other day. I try to get them to one dose every other day. I have some patients that can do that, some go one a day.  And I had one lady on it for 4 years, no diarrhea, no nothing.  We had tried her a couple of times, every time we stopped, we stopped at 4 years straight, whomp, came right back. 

All right, I put this in there but nobody really thinks this works anymore.  But if you see it, it’s using Rifaximin as kind of a salvage therapy in relapsing disease.  I tried it when this article first came out, this article only had 8 patients, so far I don’t know if anybody has been able to replicate this type of improvement. So I generally go with the taper pulse Vancomycin. 

How do we prevent C difficile?  Obviously that’s better than treating it.  And certainly restricting antibiotic use, antibiotic stewardship is key. Giving only the amount of antibiotics needed is the right job, and I tell the students and residents when they round with me that our primary job is to stop antibiotics. Everybody starts antibiotics, they wait for the IV people to come by and we stop them. Now generally we are on the antibiotic stoppage team.  And I want you guys to all join the team and start stopping antibiotics whenever possible because treating people with all these antibiotics has shown more and more with a lot of diseases not to be that beneficial, and with C difficile as such a problem back there in the background it can be problematic. I mean even the Heart Association has come and greatly restricted who we prophylax for endocarditis.  The prophylaxis for joint replacement is pretty controversial but is probably going to go all the way to no drug. So there’s just, we are trying to get – and one of the things driving this and looking at this is c difficile. 

We do things in the hospital, bleach, identification, gowns, gloves, the thing at the bottom which should be in the biggest print is wash hands.  I mean when we say do no harm, how you can harm your patient greatly is by not washing your hands, going into the room and out of the room.  I can bet all of you who were in the hospital today have had MRSA on your skin, you have it on your I Phone, you’ve got it on your stethoscope, it’s on all those computer terminals and telephones at the nursing station because we culture them. I know it’s there.  And when you touched those you got it back on your hands and you can go into somebody with an open wound or a fresh surgical wound, you examine that patient, bam, you did some harm.  So please wash those hands in and out.

Urinary tract infection, it is often times listed as the most common cause of infection although we have gotten so aggressive with urinary tract infections and Foley catheter management at St. Margaret’s that it’s way down the list now. And we’re real proud of that, and we are doing that system-wide.  And the way we do that primarily is getting those catheters out or not putting those Foley catheters in.  You can see that the vast majority of these infections are due to – are related to the Foley catheter, the longer that catheter is in the more likely you are to give your patient a symptomatic significant UTI.  At least 15% of patients in the hospital will have some type of catheter. 

And these catheters, they are like restraints, I mean people trip over them, they fall, it’s – there is more to it than just infection, so whenever I see a catheter – I mean I’m looking for those catheters and that’s one of the first things I’m going after.  Just to put here that Providencia, what organisms when you get an infection then you have to treat it, you have to worry about everything. If it’s acquired in the hospital. This is true with most all hospital acquired infections, all the bad bugs live there, that’s why you want your patients home as soon as possible, you don’t want little babies in there, they are rolling around on the bed, they’ve got MRSA on them and Pseudomonas and Acinetobacter, but nonetheless Providencia is the Board exam answer when they ask you to match Foley catheter UTI and Providencia, that’s the only reason it’s in yellow. But you can get anything, E. coli, MRSA, whatever. 

So we see higher incidence of resistant pathogens, because of that if we have a patient and we are worried that they developed their infection in the hospital and they are significantly ill we are going to probably load them up with 2 or 3 antibiotics.  It’s time to pull out the Howitzers here and blast away until you get your culture results back. And that’s because we see so many resistant bugs there.  So what we are typically worried about is gram negative rods with urinary tract infection. One thing is the hospital acquired and particularly the nursing home acquired bugs are usually resistant to Cipro, and what I see so often is the patient comes from the nursing home into the ER, they have fever, they have UTI they get Cipro. And it’s resistant more often than not anymore so be concerned about that and put the patient at least on a second drug or avoid Cipro altogether until you get their results back and I usually am going to go with a broad spectrum beta lactam like Ceftazidime, Cefepime, Socin, something that’s going to get pseudomonas and gram negatives and if they are really sick I may give them a bolus of Aminoglycoside like Tobramycin or I may add a Quinolone depending on the situation, but not a Quinolone by itself. 

Again how do we prevent these infections?  Really the big way is to minimize the duration. At UPMC now we have instituted nurse driven Foley removal policies, they no longer need orders to remove the Foleys.  They have – if the Foley is in for more than a couple of days and they are not meeting certain criteria, it comes out.  Obviously you know the doctors can override that if they want and certainly should when they need to, but we have that policy in place within the past year.  And now we are looking at do they really need a Foley to begin with?  Some of these patients in for short term surgery and stuff may not need Foley catheters. 

What about coated catheters with antibiotics or silver?  This is controversial.  I’ve looked at this literature in-depth and at UPMC when we use these things we are using the silver. The reason for that is we are concerned with any antibiotic coated thing that the organism can become resistant.  But we have seen, we have implemented those with some of our higher risk units with silver coated catheters, they cost more and once you do all these other things it’s getting harder and harder to show a difference because they are already – our waits have come so low.  One thing to know is if you have a patient with a long term catheter, whether it be a suprapubic or a Foley, giving antibiotics prophylactically does not help at all to prevent infection, it just makes things worse. It gives them C-Diff or it gives them a resistant bug to whatever you are giving them, so and there is a lot of evidence based data to show that that doesn’t work. 

How about IV catheter infections?  These are not that common but they are deadly. These are infections that originate right inside the blood stream, cause high grade bacteremia. This is an actual patient that I cared for, he had this infection here, this was actually not a central line, this was a cephalic vein infection full of pus.  He was septic, he had a chest x-ray with multiple septic emboli and went on to die from his peripheral IV.  So these IVs you’ve got to take them seriously or don’t do it.

I just put this here because this is from the CDC.  And looking at central line blood stream infections, I’m real proud of this slide, this, this, they came here, the CDC has this slide on their website to show how they figured it out. Well it was in Pittsburgh where they figured it out and they came to St. Margaret’s. We actually way back in the day when I had a lot more hair, we put together a team and we said well people just aren’t using the drapes and the gloves and I said well and our team said let’s put the gloves and the gowns and the needles and everything all – drapes all in one package so it’s you know bundled.  And we didn’t think much of this, but the CDC was around here doing some stuff, they heard about it, they sent a team up from Atlanta and this is where the Pittsburgh Regional Healthcare came out of St. Margaret’s, we were the – one of the first users of the bundles for central lines.  So I thought that was kind of – I’m just showing off here.  I’ve got to live up to my introduction, huh?

All right, catheter infections, whenever you have a patient that gets febrile and they have an IV catheter or an IV port that is – you’ve got to be thinking that could be the case. Why these patients have Foley catheters in, so they are going to have an abnormal urine, don’t go after that, look at the catheter because and then if the blood cultures are positive that’s a high correlation obviously. Usually they get high grade bacteremia, we pull the catheter tip, catheter tip cultures are frequently a bone of contention for many people, they can’t figure these things out.  If you pull out catheter tips and culture them at least about 2/3 are going to grow something.  And we don’t really care about the majority of those, the only way they help is if you get the same bug on that catheter tip culture that’s grown in the blood. And if they match up and there is a significant number on there, then that’s probably the source.  But lots of times the patient will get an antibiotic through that catheter and that may not grow at all, but it’s still if you have another source for your high grade bacteremia likely the source. 

And ideally we like to get those, anything that’s infected hardware we like to get it out, it makes life a lot easier for us but sometimes with certain, and I’m not going to get into that, there are a few times when we try to save ports and things like that if they get better quick and it’s a benign bug like a coag negative staph, but the vast majority of the times whenever possible we like to pull it out.  What are the bugs?  You are worried about MRSA, staph aureus, enterococcus, the big mistake that’s commonly made is well we worried about a line infection, we’ll put them on Vancomycin, we’ll wait for the cultures.  The problem is 15% of these people will have gram negative rods, and you are not going to cover it with vancomycin. And these patients have high grade bacteremia with their gram negative rods, so again I would advise in patients that have sepsis syndrome with an IV catheter in place and you are worried about that, make sure you give some broad spectrum gram negative treatment in addition to the Vancomycin. So again we are talking things like Ceftazidime, Cefepime, Socin, those kind of drugs.  Or aminoglycosides, Aztreonam is a nice drug is they are Penicillin allergic.

It’s helpful when we do blood cultures to get one from the existing line if they have a pic line in for instance and one from a peripheral stick. That’s because the line cultures are frequently contaminated it kind of helps us figure out if just we are going one or two bottles from the line and nothing peripherally we’re less apt to think about or attribute the sepsis syndrome to the line. 

Okay, again, getting catheters out, we actually electronically monitor catheters. We know if any medication is going in through those IV, if there is no intravenous medication going through those catheters a flag comes out at many of our hospitals and tells the nurse see if we can get that line out, because if they are not putting anything through it we would like it out if at all possible.  Again, the same deal with Foley catheters.

Dedicated IV teams have been shown to be useful in decreasing infection rates and you can try to convince your administration if they are hesitant to pay for that, that just one or two of these line infections particularly in this day of CMS penalties financially will pay for that.  

Finally here I’m going to talk about surgical site infections, this is an area that we are working hard, this is like one of the hardest ones for us. We’ve really made great strides with line infections, with urinary tract infections, actually C difficile has fallen off and we don’t  know if that’s due just to what we are doing or just kind of God is making it fall off. It’s across the country the incidence has gone down. We like to think that we are pushing it along but I never know for sure. 

Surgical site infections though have been more of a problem.  And we really put a lot of focus on that now.  Two to five percent of patients depending on what surgery they have, where they are, who the surgeon is will get an infection.  Certainly significant mortality, again these are costly, you know billions and billions, whatever.  When it happens it’s usually a staph aureus, but again it can be different things, and it kind of depends is your patient a diabetic, it is a sternal wound infection, there are some areas that are more compromised than others. Generally you want to cover staph including MRSA and if they are really sick again I would cover gram negatives. 

Now what do we do to prevent surgical wound infections?  Now these skipped measures, the surgical care improvement program nationwide probably are useful, although again it’s hard to show from evidence based data, but I think they are.  We’ve shortened, or we give the correct antibiotic at the time or surgery at the right time, you want to give it shortly before the wound because you get better concentration there, you want to stop it. The only good that antibiotic does is while the surgery is ongoing, as soon as that wound is closed the antibiotics do no more good. So you want to stop them shortly after the surgery. 

We look at other things, we look at skin preps, we are trying all kinds of skin preps. Certainly I’m going to – you can see here at the bottom of the slide big, big news again from the Bible, the New England Journal in January of 2010 looking at chlorhexidine alcohol versus beta dynes or standard povidone, and 60% reduction with that.  And we have gone all out to convince our surgeons to switch over. 

How about screening?  We are screening a lot of patients, particularly patients that come in for joint, back, high risk surgeries, we screen them for MRSA prior to coming in because then we give them Vancomycin perioperatively instead of Cephalone as well as giving them Mupirocin ahead of time whether they have what kind of staph you can see this is another article from the same issue of the New England Journal pretreating patients with intranasal Mupirocin ointment for 5 days twice a day and they cut the infection rate in half.   And we do that and these are good policies, lots of patients to get in the New England Journal you’ve got to have a lot of patients and it looks you know most people are believers of this stuff.

I have pneumonia here, coming down the home stretch.  Pneumonias don’t occur that often, but again like vascular infections and even more so they are the most deadly hospital acquired infections, 20% mortality and can be higher depending on what type of patients you have.  Intubated patients are certainly at high risk, but you have to be careful, most of these are aspiration pneumonias, over sedation, whatever can do this. Again, like these other infections you are looking at a broad range of potentially resistant organisms, pseudomonas, MRSA, all these things cause pneumonia. 

And I just want to talk finally about Linezolid and Vancomycin because Linezolid has been pushed now for treating MRSA pneumonia, and we see MRSA pneumonia, sometimes it’s hard to know for sure what’s causing it, but we know it’s MRSA is Linezolid a better agent? And this has been the only data up until this month so I have another slide that’s not on – the next slide is not there because it wasn’t there when I had to put this in.  But Linezolid has much better penetration to the lung, they looked at the data that they used to get Linezolid approved. This was not looking specifically at pneumonias, they kind of went back and picked it out and said well let’s say all the patients that ended up with pneumonia not the perfect way to compare, but when they did that they found that Linezolid worked better than Vancomycin.  So we have used Linezolid particularly in patients that are very ill with MRSA pneumonia, or failing Vancomycin.  And you may not know this for a couple of days, if they are getting better on Vancomycin by the time you get the cultures back we may just continue it.

But this is a brand new study from this month in the clinical infectious diseases by the same gentleman from Chicago and a crew of him who looked at a large number of patients, 448 patients, exactly split in half. These were the measureable group, Linezolid versus Vancomycin, and you can see that the Linezolid works somewhat better, not quite as dramatic as the previous study.  One of the interesting things though is renal failure, much higher with the Vancomycin group.  And that’s significant, can impact things.  We are now using Vancomycin at much higher doses than we used to use and at those higher doses there is no question that we are seeing more renal adverse effect. 

So how do we treat these?  Again, multiple agents, get gram negatives, get MRSA, you really don’t need to worry about Legionella in most hospitals, they are treating their water for it. But if you have a problem in your hospital for Legionella you better cover for that too. 

And these are ways to prevent this.  We do all these things, elevate the head of the bed, the Chlorhexidine mouthwashes definitely make a difference in those patients that are intubated.  And over sedation and I’m going to stop there, I’m kind of running out of time, and I don’t know am I supposed to take questions? 

We have some time for questions.

Okay, he says we have a few time, we are coming up against the break.  And if there is questions after this that we run into come and talk to me afterwards, during the break, I’ll be glad to speak with you.

Thank you.  Yes, sir?

Before this we were looking at pressure ulcers and my question is, is there a special relationship between pressure ulcers and death from resistant bacteria?

Well the question is, is there resistant bacteria caused problems in pressure ulcers?  The answer is certainly yes. When pressure ulcers get infected, because a lot of pressure ulcers occur in nursing homes and in hospitals and they are just, that’s where we can see the acquisition of these multidrug resistant organisms like MRSA and resistant gram negatives.  Does that answer your question? 

Well yes, except for the question of a specially approved death, because it’s hard to work with the pressure ulcers themselves.  In other words is there an influx in bacteremia that continues on in the resistant, in the resistant –

Are resistant bugs more virulent?

Yeah, do they kill patients?

 Okay, maybe yeah, that’s a question, are they more virulent and you know some are and some aren’t. Some multidrug resistant organisms like Acinetobacter, when they cause infection are really bad, but aren’t – but a regular staph aureus is more virulent. So some, MRSA is virulent but you know isn’t more virulent than staph aureus.  I think Dr. Luder who spoke earlier would say that probably they are to a degree.  He knows more about that than I do.  But the answer is it depends.   Okay, looks like my time is up.  Thank you very much.