Tuesday, August 31, 2010

10 years of the Interagency Task Force on Antimicrobial Resistance (ITFAR)

In 1999 the ITFAR was created to bring together the 10 US federal agencies (CDC, FDA, NIH and AHRQ, CMS, DOA, DOD, DVA, EPA, HRSA and USAID) working on areas of antimicrobial resistance.  With the 10 year anniversery of the ITFAR, Resources for the Future's Abigail Colson has put together a nice 4-page policy brief that describes the outcomes of this joint effort.

The summary is that "the task force has successfully documented progress on federal antimicrobial resistance-related projects and increased communication both within the agencies and between the agencies and external partners," yet "has failed to live up to its potential as a priority-setting and decisionmaking body." Given the important and even central position of ITFAR, one hopes there is more left in the tank.

link to pdf from CDDEP (RFF's Center for Disease Dynamics, Economics & Policy)

Today's Science Times

Every Tuesday brings the Science Times section of the New York Times. This morning, there are two articles of interest for our readers:

  • There's an article on bedbugs which explains the reasons why they have become so common in recent years.
  • There's an essay on isolation by Abigail Zuger, an infectious diseases physician, which focuses on the human dimensions of a practice that can be rather cruel to patients. She writes of an elderly woman placed in isolation for C. difficile who sobbed continuously: "Increasingly, modern medicine forces us to specialize in the invisible. Here we had invisible germs with an inviolable mandate, and an all too visible patient pleading with us to ignore it. It was quite a struggle to try to see the one, to try not to see the other."

Monday, August 30, 2010

Presenteeism: It plagues us

The August edition of the Journal of General Internal Medicine has a paper and editorial on presenteeism that are important for the infection prevention community. Presenteeism is the situation that occurs when workers report to work ill. In the case of communicable diseases in the healthcare setting, presenteeism has the potential to spark outbreaks of illness such as norovirus gastroenteritis, influenza, and other respiratory infections.

As I mentioned in a previous posting, our influenza control plan for the upcoming season is to encourage (but not mandate) vaccination of healthcare workers, coupled with a greater emphasis on avoiding presenteeism. Unlike vaccination, reducing presenteeism is a multipotent intervention, and a great example of the horizontal approach to infection control.

Barbara Kowalcyk Awarded LennonOno Grant For Peace

My friend Barb Kowalcyk will receive the LennonOno Grant for Peace this October in Iceland for her work in food safety.  You might remember Barb from her appearance in Food, Inc., where she described her efforts to pass Kevin's Law.  Food safety is closely linked to antibiotic resistance and hospital infections.  We live in an interconnected world in more ways than we think. Her tireless efforts are very important and it's nice to see her receive this recognition.

CFI award announcement

Sunday, August 29, 2010

A new epidemic?

I'm sure most hospital epidemiologists would agree that the issues that cause some of the biggest headaches in day-to-day practice are not the invisible viruses and bacteria that cause all sorts of horrible diseases, but rather the bigger bugs like lice and scabies. Now we have a new one to contend with--bed bugs. My IPs have begun to receive calls about them, and the recent spotting of the bugs in a Newark clinic forced a shutdown of an exam and waiting room, and prompted a newspaper article. Fortunately no diseases are transmitted by these pests. Click here for CDC's guidance and links to other resources.

Photo:  Dr. Harold Harlan, Armed Forces Pest Management Board Image Library

Saturday, August 28, 2010

Another reason to like frogs

As if us toads needed another reason to like frogs, there is a new report out of the American Chemical Society meeting that suggests frog skin may be an excellent source for new antimicrobials including ones active against MRSA and acinetobacter. More than 100 potential compounds have been identified.  Now if we could just convince frog to let us sleep in more. That bit where he rips the calendar pages off until he gets to May is not that cool...

Article from BBC News

Weekend Wash Your Hands Video by Chromeo

My kids reminded me to wash my hands before playing the piano.  I asked them why and they said it was because we share pianos and if we share something, we should wash our hands.  I was a proud dad but then asked them how they knew this. They responded "Yo Gabba Gabba."  Oh well.

Thursday, August 26, 2010

Alcohol hand rubs in the workplace: A Randomized Trial

Just a quick post because I've got to get the kids to bed.  Researchers in Germany randomized 134 administrative employees at the Ernst-Moritz-Arndt University Greifswald to alcohol hand rub or nothing (n=67 in each group).  Subjects were to use >3ml of hand rub at least 5x/day especially after using the bathroom, blowing their nose, before eating and after contact with an ill person. The study lasted from March 2005 to April 2006.  People who used hand disinfects prior to the study were excluded.  They found significant reductions in common cold symptoms, fever, cough, and fewer days of illness with each symptom. A thing to note is that 111 of the 134 subjects were female, although it is hard to figure how this would hurt the generalizability. Alright, story time...

BMC Infectious Disease article by Hubner et al.

Daily chlorhexidine in SICU for CLABSI prevention? Not so much.

A nice report is out in Intensive Care Medicine by Kyle Popovich and collegues from Rush University Medical Center in Chicago. In the RUMC SICU the clinicians decided to start using 2% CHG-impregnated clothes in Fall 2005.  The investigators analyzed CLABSI rates using the time-series data in the before period (Sept 2004-October 2005) and after period (November 2005 - October 2006). 

They found no significant difference in the CLABSI rate after the introduction of CHG clothes (3.81/ 1,000 central line days vs. 4.6/1,000 central line days; p = 0.57). A couple things to note.  The first is that they did a great job identifying their study as a quasi-experimental study and using Poisson regression and segmented regression analyses. They reported the Poisson-regression results after segmented regression did not identify changes in slope or intercept around the time of the CHG cloth introduction.  Nice job!  They also used C. diff, BSI, VAP and UTI rates as "control" variables, as they are thought not to be reduced with CHG bathing.  These 'control' variables are called 'non-equivalent dependent variables' and inclusion of these types of "outcomes" improves the internal validity of quasi-experimental studies since they typically would be reduced by other infection prevention interventions but not the intervention under study. Thus, they help rule out the impact of concurrent interventions that could have biased the study findings.

Previous studies, which were also mostly quasi-experimental studies but in MICUs, have found reduced CLABSIs with CHG.  It's great that the authors spent the time writing up and publishing these results and the journal should also be commended.  There's nothing worse than publication bias; negative studies are just as important as positive ones, even if they make decision making more difficult.  The authors concluded that they would not recommend routine use of CHG baths in SICUs; I would recommend further study.

Popovich, et al. Intensive Care Medicine

Wednesday, August 25, 2010

Random thought of the day: Impossible Possibility

The dog days of summer are here, but almost over.  I suspect we will post infrequently these next couple of weeks as we survive/enjoy our transition to the 2010-11 academic year.  The thing that most excites me about fall is the start of the English Premier League Football (soccer) season, so I've been reading more about player transfers and transfer rumors than infection prevention studies.  I came across an entertaining Brian Phillips article in Slate that sums up the player transfer period quite well.  I especially enjoyed this quote:

"A really good transfer rumor doesn't have to be untrue. It just has to make claims that it can't support, allowing us to fill the gaps with a fizzy sense of impossible possibility."

I thought this quote could be rephrased or recycled for use in infection prevention articles/editorials or in any other important area of life.  For instance, if you substitute "infection prevention intervention study" in for "transfer rumor", you get:

"A really good infection prevention intervention study doesn't have to be untrue. It just has to make claims that it can't support, allowing us to fill the gaps with a fizzy sense of impossible possibility."

You could also substitute phrases like "research grant hypothesis" or "economic analysis" in the same place.  For some reason, this just makes me happy, which these days can sometimes be an impossible possibility.

Slate Article

Tuesday, August 24, 2010

Antibiotics in food production: September 16th Webinar

We've often covered the topic of routine antimicrobial use in food production and their potential association with development of MDR-bacteria.  IDSA is co-sponsoring an upcoming webinar called "Superbugs, Super Problems: Agricultural Antibiotics and Emerging Infections"  The Webinar will be held on September 16 from 11 am-12noon PDT/12noon-1pm MDT/1-2 pm CDT/2-3 pm EDT.  Speakers include James Johnson from the Minnesota VA, Gail Hansen from PEW Charitable Trusts and Superbug author Maryn McKenna.  A great group. I look forward to listening in.

Webinar registration and information

Links to our previous food safety articles

Monday, August 23, 2010

C. difficile in the news

Tomorrow's Washington Post has an article on C. difficile, which unfortunately depicts the organism as a purely nosocomial pathogen. I recently blogged about contamination of the food supply with the organism and just last week cared for a patient with C. diff who had no exposure to hospitals or healthcare settings and had not taken antibiotics in the last year. I suspect we'll continue to see an increase of community-acquired cases. We still need to work on prevention in the hospital, but as for MRSA, VRE and many other bugs, hand hygiene should do the trick.

Why do we blog? - Please comment!

I can't speak for Mike and Dan, but I suspect that we all enjoy blogging for many of the same reasons.  It's a great way for the three of us to share ideas with each other and our readers/friends/colleagues without spamming them with emails. Unfortunately, I still do that occasionally.  Sorry guys! However, it would add to the fun if we received more comments.  I'm sure you all have insights, additional links, etc. that you want to share, and we want you to share them.  Do you have some ideas as to how we could improve the blog? Are there topics you want to see covered? Comment away!

Apparently, I'm not the only blogger to feel this way.

Sunday, August 22, 2010

More on NDM-1s

A few weeks ago, Eli blogged on the emergence of NDM-1 producing Enterobacteriaceae in Asia. Now, 3 patients with the organisms have been detected in Canada. You can read about it here.

Saturday, August 21, 2010

The bean counters are missing some beans

There is a recently released report from the Society of Actuaries entitled the Economic Measurement of Medical Errors. It's nearly 300 pages long and includes data on catheter-associated UTI, central line associated bloodstream infection, and surgical site infections. It is based entirely on administrative claims data, which are notoriously inaccurate for healthcare-associated infections. See Kurt Stevenson's paper on this topic here.

As I looked through the report, I noted that the numbers looked quite odd based on my familiarity with the literature. So I compared the SOA report data to CDC's estimates on the burden of HAIs in the US (Klevens et al) and Eli's review of the literature on attributable cost in the table below.

Estimated annual number of cases
Attributable cost/case

SOA Report
SOA Report

Now there a number of caveats to point out:

  • The SOA reports the estimated number of cases due to error; to convert from number of cases to cases due to error they multiplied the number of cases by 0.95. Therefore, I divided the "error" cases by 0.95 to convert back to number of cases (Does anyone believe that 95% of CA-UTI cases are due to error, that is, preventable???)
  • Eli used 2005 dollars for cost data, and SOA used 2008
  • SOA used 2008 claims data, and CDC (Klevens et al) used 1990-2002 NNIS data and National Hospital Discharge Survey 2002 data
  • CDC data appear to included non-device associated infections, though we know that the vast majority of UTIs and BSIs are device related
However, despite the differences I note, the SOA data seem hugely flawed. They appear to vastly underestimate the frequency of HAIs, while substantially overestimating the attributable costs. I suspect the SOA report will be widely quoted, so take a look at it and be prepared!

Friday, August 20, 2010

Don't wait in a doctor's waiting room

I should have said don't wait too long in the "waiting area of healthcare premises" especially if another occupant/patient has measles, as the authors of a new study in BMC Infectious Diseases report.  The authors analyzed the likelihood of acquiring TB, influenza or measles during stays of 30 or 60 minutes in a standard waiting room using a mathematical model simulation.  One caveat is that they assumed one person in the waiting room was infectious with one of the organisms. Thus, while the results provide nice theoretical estimates of airborne transmission for these highly (measles), moderately (influenza) and minimally (TB) infectious organisms, they don't adjust for the probability of an occupant having the infection in the first place (influenza>TB>measles).   

With that important caveat, the likelihood of acquiring TB during a 30 minute stay in a waiting room was 0.3% and was 0.8% for a 60 minute stay.  For influenza, the numbers were 2.6% and 6.6% at 30 and 60 minutes and were 13% and 31% for measles.  With those numbers, if there is measles in the community at all, it's probably best to avoid any waiting area (unless you've been vaccinated). Nothing surprising in the results, really, but still worth quantifying and thinking about.  During the H1N1 season last year, I was always worried about transmission in the various hospital waiting areas.  In those situations, it was likely that >1 person had infectious influenza in the waiting room.  I hope future studies analyze the impact of # of infectious occupants and likelihood of those infectious occupants being present during various seasons (RSV, Influenza etc).

Once last thought.  Next time a clinician keeps you waiting, you might mention that he/she has put you at increased risk for getting sick.

Beggs et al. BMC ID article

Thursday, August 19, 2010

Killer Flu!!!! - the video game

Do we need another distraction in our lives? I thought blogs were the last straw, but to the list of distractions we can add an educational influenza game.  Killer Flu is an Adobe Flash-based game (sorry no i-device version yet) which "allows you to learn more about how the influenza virus is transmitted and how it changes every year - which explains why you can get more than one dose of the flu over your lifetime and why vaccines need changing every year." The game gives you 180 days to infect as many people as possible using one of three scenarios: seasonal flu, re-assortment and H5N1 avian influenza.  I guess you can waste time and learn at the same time. What could be better?

Link to UK Clinical Virology Site
Lancet ID review

Tuesday, August 17, 2010

Gentamicin-collagen what?

Am I the only hospital epidemiologist who had absolutely no idea these things existed? Now I’m glad I ignored them for so long, because they don’t seem to work worth a damn, according to studies recently published in JAMA and NEJM. They might even be harmful!

The Show Me State?

Here is a new twist on public reporting: how long should a state be required to keep hospital-specific data easily accessible to the public? Missouri’s Department of Public Health is taking heat for removing older data from their website (essentially, they just “write over” the old data with new data, so the older data gets purged).

The data still exists at the department...as the state’s data manager says, “it just isn’t handy”. To get it you have to formally request it, a programmer must be available, and you have to pay the cost of retrieval.

An interesting side note—the 2004 Missouri statute mandating public reporting came with no appropriation, even though the state’s health department spends over 240K each year to implement it. It’s true that you get what you pay for—if public reporting is important, it needs to be appropriately funded. And doing it correctly (including independent validation) is expensive!
Addendum: Never mind, the older data will be restored. By the time Iowa starts public reporting of HAI data, we'll have all these lessons to draw on!

Saturday, August 14, 2010

Influenza and HIV vaccine update: Seth Berkley

Something to enjoy this weekend if it's too hot, too rainy etc.

Link for iPhone/iPad

Friday, August 13, 2010

C. difficile in the hospital: Time to quit counting?

One of my IPs is assigned the task of looking at each inpatient with C. difficile and trying to determine whether the case should be classified as nosocomial. She says it drives her crazy. There's a new review in Clinical Infectious Diseases that looks at contamination of retail foods, primarily ground meat products, with C. difficile. The authors seem cautious in claiming that contamination of food leads to disease in humans, but given that we are increasingly seeing patients with C. difficile infection who have not had contact with healthcare facilities, it seems highly plausible. The editorial points out that new strains of C. difficile are constantly being imported into the hospital from the community. So when an inpatient who has never before been hospitalized develops C. difficile diarrhea on hospital day 12 is this from nosocomial acquisition or from the hamburger he ate a week before admission? Maybe I should quit driving my IP crazy.

Thursday, August 12, 2010

Why are we colonized with Staphylococcus aureus?

A truly successful parasite is commensal, living in amity with its host, or even giving it positive advantages...A parasite that regularly and inevitably kills its host cannot survive long, in the evolutionary sense, unless it multiplies with tremendous rapidity....It is not pro-survival.

Who said that? I will post the answer tomorrow. You can guess by posting a comment or since you're all busy stamping out hospital infections, you can just google it.

I've been thinking a lot about S. aureus recently for some reason. By recently, I mean spring 2009 when I attended a S. aureus conference in St. Augustine and had the chance to speak with Chip Chambers and Heiman Wertheim, among others. The question was and is, why are 30% of us colonized with S. aureus and what possible survival advantage could there be for this colonization status. Sure there are downsides - carriers are more likely to be infected with S. aureus, but are the costs outweighed by the benefits? Does S. aureus colonization prevent colonization and infection with other pathogens? Perhaps even S. aureus colonization prevents the morbidity and mortality associated with S. aureus infection. What? Did I just say that?

A few years ago (2004), before this blog was started so it's fair game, Prof. Wertheim and colleagues published an interesting study in the Lancet. I will just post the findings from the paper's abstract:

Nosocomial S aureus bacteraemia was three times more frequent in S aureus carriers (40/3420, 1.2%) than in non-carriers (41/10588, 0.4%; relative risk 3.0, 95% CI 2.0-4.7). However, in bacteraemic patients, all-cause mortality was significantly higher in non-carriers (19/41, 46%) than in carriers (seven/40, 18%, p=0.005). Additionally, S aureus bacteraemia-related death was significantly higher in non-carriers than in carriers (13/41 [32%] vs three/40 [8%], p=0.006).

Pretty cool. S. aureus carriers were 3 times more likely to have a nosocomial S. aureus bacteremia as non-carriers, but had one-quarter the risk of death from S. aureus bacteremia. So, if you are a S. aureus carrier you have a 3/3420 or 0.000877 chance of death from S. aureus. If you're a non-carrier you have a 13/10588 or 0.001228 chance of death. Yes, I know, sig figs. Amazingly, being colonized, while increasing the risk of infection, drastically cuts the risk of death such that colonized patients are 30% LESS likely to die. Is this enough to explain why 30% of us are colonized? Obviously not, it's just one paper. Their work and other's since has studied factors associated with colonization, but there is more work to do.

I guess, my question is, what if all of the efforts at decolonization actually increased the mortality in the patients we are trying to benefit? Surely, that would be measured in the intervention trials or at least the meta-analyses, or would it? If you don't think of the question, you might not find the answer.

Wertheim 2004 Lancet Paper

Update:  Answer to the question above:  Mr. Spock, Star Trek II.
I found this quote at the beginning of Janice Moore's excellent book "Parasites and the Behavior of Animals"  Thanks to Dave Smith for recommending the book to me many years ago and also for inviting me to the St. Augustine S. aureus conference.

Wednesday, August 11, 2010

NDM-1 containing Enterobacteriaceae

With yesterday's report suggesting a decline in MRSA, it is now time to switch gears and panic about other organisms. As Dan said so well yesterday, "MRSA isn't the only bug out there, it's just the most famous." Today's report is from Lancet ID by researchers in UK, Pakistan and India on a novel resistance mechanism in Gram-negative bacteria called the NDM-1. NDM-1 stands for New Dehli metallo-B-lactamase 1. I guess when you name it "1" you are expecting a "2" and maybe a "3". Even the Great War wasn't called WWI until World War II started or at least ended.

The report is very nice and includes background information discussing the rise of various resistance mechanisms in GNR including ESBLs (CTX-M-15) and KPCs. The group initially discovered the NDM-1 containing resistance gene in a patient in Sweden after the patient returned from a hospital admission in New Dehli. This new report includes descriptions of isolates collected in Chennai (south India), Haryana (north India), UK and other areas in India, Bangladesh and Pakistan. Little information is given as to how the samples were obtained. After initial screening, all isolates were tested for presence of the bla(ndm-1) by PCR.

As an example of the results, from Chennai there were 3521 isolates of Enterobacteriaceae screened with 141 (4%) resistant to carbapenems. 44 of the 141 were NDM-1 positive, which is about 1% of all of the isolates. Most were E coli (19), K pneumoniae (14) and E cloacae (7). By 2009, NDM-1 strains were the dominant carbapenemase-producers in the UK. In most isolates NDM-1 was carried on plasmids although 3 UK isolates carries the NDM-1 on their chromosome.

All of this is quite concerning. It is not this specific gene/mechanism that's troubling, it's the constant introduction and spread of many different types of resistant GNRs in our inter-connected world. Look at the figure. The chickenpox spread of NDM-1 that now covers India and the UK will soon spread to Germany, the US and beyond. While we have new classes of antibiotics recently introduced that are active against MDR-Gram positive bacteria, we have very few new classes in the pipeline that are active against GNR. When the US Surgeon General, Dr. William H Stewart said in the 1960's that it was "time to close the book on infectious disease" and/or "the war against infectious diseases has been won", he probably wasn't thinking about Gram negative bacteria.

Lancet ID article

link to newer NDM-1 post

Tuesday, August 10, 2010

MRSA in decline

Today’s news is the JAMA publication of CDC surveillance data showing a steady decrease in healthcare-associated MRSA infections from 2005-2008. Eli and I wrote the accompanying editorial, so I refer you to that for our commentary on this. We may have more on this later.

JAMA article
Our editorial
NPR story (click link to listen)
Reuter’s Health story

Monday, August 9, 2010

What happens in Vegas...

...stays in Vegas? Always a good catchphrase, although not necessarily a good movie. I do often wonder if we should adopt a slogan in infection prevention such as "What happens in the ICU, stays in the ICU," where the happens part is MRSA or MDR-Acinetobacter acquisition.

It looks like there is a move afoot in Nevada to mandate universal MRSA screening. Sheila Leslie, D-Reno, whose otherwise healthy cousin recently died from MRSA infection at a California hospital, is considering drafting a bill on the subject. A recently posted Las Vegas Sun piece focused on the MRSA surveillance mandate in the VA system and quoted from the usual and also unusual subjects in the never ending debate around MRSA control.

Some of the more interesting quotes from the article:

“You get paid and paid and paid for doing the wrong thing in medicine. You don’t get paid for keeping people well,” said Phillip Longman, author of “Best Care Anywhere: Why VA Health Care Is Better Than Yours.”

“I know the bundled approach works, but I don’t know which component of the bundle is the most essential component of success.” Dr. Rajiv Jain, who leads the VA’s MRSA prevention program.

It appears that Nevada will look to the VA's data and experience in MRSA control. What isn't clear is if states or hospitals or even local health systems should try to apply data from a federal system with >150 acute-care hospitals. I do welcome the VA publishing their results and hope we see some nice VA-based interrupted time series data analyzed soon. When it comes to the results of the VA's MRSA mandate, what happens in the VA shouldn't stay in the VA.

Thursday, August 5, 2010

Thomas Peebles (1921-2010)

Dr. Peebles, who was known for discovering and culturing the measles virus and also shifting the tetanus booster schedule from annual injections to every ten years, died July 8th but he death was just announced in a NY Times obituary. In the non-ID world, he was known for his work on flouride vitamins for children.

There were several interesting things about him that I didn't know, but the most amazing was the fact that when he discovered how to grow the measles virus, no one in the lab believed him including John Enders. Dr. Enders even took him off of the measles project and Dr. Peebles had to complete the work on the side on his own time. When he finally was able to infect monkeys using the cultured virus, they knew he had done it. This discovery led directly to the development of the measles vaccine and numerous lives saved.

In 1967, when discussing the measles discovery, Dr Peebles wrote “I am sure, as is often the case in scientific endeavor, that much of the successful recognition and isolation of this virus lay in perseverance, newness to the field, and failure to be bound by preconceived ideas that caused others in the laboratory to miss this new effect."

There is much truth in his words. Successful scientists are often immune to the dogma that surrounds them. If only the scientific community could find better ways to identify and support such free thinking individuals.

Wednesday, August 4, 2010

FDA releases a "Dear ICP" letter for positive displacement needleless connectors

Similar to a "Dear Doctor" letter, the FDA just sent out a "Letter to Infection Control Practitioners Regarding Positive Displacement Needleless Connectors" and addressed it to "Dear Infection Control Professional." My first thought was that there are no more ICPs, so someone should alert the FDA.

On a serious note, the FDA is requiring nine companies to conduct postmarketing surveillance of positive displacement needleless connectors as they have been associated with higher CLABSI rates. However, while the FDA is not recommending changing the use of these devices, they refer people to the SHEA/IDSA HAI Prevention Compendium. Since the Compendium states to "not routinely use positive‐pressure needleless connectors with mechanical valves before a thorough assessment of risks, benefits, and education regarding proper use," it appears that FDA has taken a risk-averse stance. The studies, which are expected to take up to 3 years, have to answer the following two questions:

1) What is the rate of bloodstream infections for subjects receiving your positive displacement connector for central line access and is it statistically non-inferior to the rates seen in subjects receiving other needleless connectors (e.g. negative, neutral, or split-septum connectors) for central line access, given comparable patient populations?

2) Are there patient demographics, comorbidities/severity of illness, or device cleaning practices for which placement of your positive displacement connector for central line access increases subjects’ risk of bloodstream infections compared with other needleless connectors?

Full FDA letter is here.
SHEA/IDSA HAI Prevention Compendium
Image from Edgar K. Infect Control Hosp Epidemiol, April 2009

Robert Chanock (1924-2010)

There are few that have contributed as much to our understanding of infectious diseases as Dr. Chanock. His career was most tightly linked to his discovery of RSV and subsequent vaccines including the one in trials today. However, when he was chief of NIAID's Laboratory of Infectious Diseases from 1968-2001, his work involved other important viruses including norovirus, Hep A, rotavirus, West Nile, etc etc. Oh, and the first intranasal influenza vaccine. The picture is from a 1999 story in the NIH Record. There are several nice obituaries:

Tuesday, August 3, 2010

Laziest possible post about the new CMS rule

I am on vacation. Last week I biked across Iowa with 9,999 other people (see photo below), and I’m now in Michigan, recovering from my bike ride across Iowa. So I haven’t done much deep thinking about the new CMS rule related to healthcare associated infections. From what I understand, participation in the Medicare program (at least receipt of full payment) will soon require surveillance and reporting (through NHSN) of CLABSI (beginning in 2011; ICU only) and SSI (beginning in 2012). The rates will eventually be reported via the hospital compare website. This doesn’t mean a lot to hospitals that already perform CLABSI and SSI surveillance, unless they don’t currently report through NHSN, in which case they’ll have to get enrolled.

We’ve already blogged about pitfalls in public reporting, and about problems with the NHSN definitions, validation, etc. So I really don’t have anything new to say about this rule. I refer all interested readers to a six-part series at Safe Healthcare (only 2 posts so far, 4 to come) on the new rule.

Monday, August 2, 2010

Vancomycin: even worse than you thought?

This month’s issue of Antimicrobial Agents and Chemotherapy has a disturbing report comparing three generic versions of vancomycin with the brand name version (referred to as “the innovator” in pharma parlance). All three vancomycin generics had similar in vitro activity to the innovator (i.e. same antibacterial effect by MIC testing and time-kill curves), and had similar pharmacokinetics and protein binding. However, none of the generics could kill S. aureus in vivo (in a neutropenic mouse thigh infection model), while the innovator exhibited the expected bactericidal activity. In the authors’ words, “pharmaceutical equivalence does not imply therapeutic equivalence for vancomycin”. But the WHO and other agencies consider therapeutic equivalence to be “self-evident” for compounds that exhibit pharmaceutical equivalence.

How can two versions of vancomycin exhibit similar in vitro activity but different in vivo activity? It turns out that the manufacturing process for vancomycin is tricky, and results in the formation of fermentation impurities known as “crystalline degradation products” (CDPs). CDPs bind to the vancomycin target (D-Ala-D-Ala) just like the active drug, but with much less efficacy, exhibiting an “agonistic-antagonistic” pharmacodynamic pattern. Eli Lilly developed a purification method that effectively reduced the concentration of CDPs, but generic preparations have been shown to have 2-3 times the CDP concentration. Interestingly, one of the generic manufacturers was quickly able to produce effective vancomycin immediately after Eli Lilly sold them their brand name rights and manufacturing secrets in 2005.

Avoiding SSIs

It's not often that a major newspaper prints an editorial on healthcare associated infections, but here's one from this morning's Boston Globe.