Thursday, June 28, 2012

Awaiting the Supreme Whatever

Will they overturn the Affordable Care Act, or just part of it? How will it affect us as patients and providers? How will it impact public health and prevention efforts (the Prevention Fund is already vulnerable, as we know)? Whatever happens, we have a lot of things to fix, because clearly we’re doing it wrong. Maybe we aren’t screening enough people for MDROs.

Source: OECD

Monday, June 25, 2012

Detecting and preventing carbapenem-resistant Enterobacteriaceae (CRE)

Late last week, the CDC issued new guidance for control of CRE. You can read my 2009 post for thoughts on their initial guidance. This update expands on that guidance, providing tailored recommendations for different settings, ranging from regions where no CRE have been reported to those in which CRE are common. The guidance also emphasizes regional control and the role of long term care (and “long term acute care”) in the epidemiology of CRE.

I think the new guidance is on the mark, and should be helpful as we struggle with how to respond to these bad bugs. As was the case back in 2009, my main concern relates to the screening recommendations. Not all CRE are created equal, and the test methods available to most laboratories are not good at differentiating among the really nasty (e.g. KPC- and NDM-producers) and the moderately nasty (e.g. chromosomal cephalosporinase + porin protein mutation). The former have much greater outbreak and local-regional spread potential, which is why the modified Hodge Test (MHT) has been used to single them out. But the MHT is not always easy to interpret, can have falsely positive and negative results, and seems to perform especially poorly in detecting certain carbapenemases (e.g. NDM). The CLSI has issued lower MIC breakpoints to better detect CRE, but these breakpoints are (appropriately) designed to guide therapy for individual patients, not to provide detailed information about resistance mechanisms for infection prevention or public health purposes. Lower breakpoints means more CRE detected, most of which do not carry mobile resistance elements like KPC and NDM. Do we respond to them in the same way (they are still resistant, after all….)?

I favor making CRE (at least those due to carbapenemases) reportable, as a couple states have done, along with periodic regional prevalence surveys to help facilities and public health departments understand local and regional epidemiology of CRE (and to help detect emerging new resistance mechanisms). These surveys would need to rely on culture, with referral of all isolates that have a CRE phenotype to state or regional labs that can do the molecular work to determine the underlying mechanism(s).

Friday, June 22, 2012

Friday feces blogging (part 5)

A year or so ago, I bought a new external hard drive for my computer (see photo). I marveled at its storage capacity--1 terabyte! That just seemed to be a huge amount of information. So I almost fell off the exercise bike today when I read a statistic in this month's issue of The Atlantic (free full text here) on the data capacity of human feces. According to Larry Smarr, a computer scientist who views the human body as a ginormous database:
"There are about 100 billion bacteria per gram (of stool). Each bacterium has DNA whose length is typically one to 10 megabases--call it 1 million bytes of information. This means human stool has a data capacity of 100,000 terabytes of information stored per gram."
Now to bring all of this home, you should know that I use 30 gm of stool for the fecal transplant procedure. So if my math is correct, I am instilling 3 million terabytes (or 3 exabytes) of information.That is nothing short of amazing!

Bundle fumble?

This week's JAMA has an excellent review (free full text here) on the prevention of ventilator-associated pneumonia (VAP). Specifically, the authors offer a critical assessment of the widely utilized IHI VAP bundle. They offer two important conclusions:
  • "The ability of the bundle to prevent VAP has not been definitively established with high quality studies."
  • "No large randomized study has demonstrated that reducing VAP using any strategy, including the IHI bundle, is associated with improvements in clinical outcomes."
Here's another example where an intervention has been touted as gospel, pushed hard and implemented broadly without the evidence necessary for a hardline approach.

Photo: OregonLive

Thursday, June 21, 2012

NDM-1's knocking at the door, Let 'Em In


This weeks MMWR has a report from Len Mermel's group of a patient initially hospitalized in Viet Nam. Upon readmission earlier this year to a hospital in Rhode Island she had a Klebsiella pneumoniae containing NDM-1 recovered from a urine specimen. The isolate was only susceptible to tigecycline, and the polymyxins.

Extensive surveillance testing was completed and one patient admitted to the same hematology-oncology unit grew an NDM-1 containing K. pneumoniae isolate from a rectal surveillance swab.  This isolate was indistinguishable from the index patient's isolates by PFGE, confirming patient-to-patient transmission.

Tuesday, June 19, 2012

Europe boosts antibacterial discovery funding from zero to a wee bit more than zero

This week's Lancet has a report on a new European public-private partnership called the Innovative Medicine's Initiative (IMI). The IMI is funded through €1 billion donations from both the EU and European Federation of Pharmaceutical Industries and Associations to stimulate innovation in challenging areas. The goal is to fund antimicrobial drug discovery to the tune of €600 million ($761 million) by 2020, or roughly $100 million/year.

Perhaps this is finally the chance to move beyond the two new classes of antibacterials developed in the past 30 years. Should we be excited? Sure, $100 million/year seems like a lot of money, but this should be seen as a necessary first step.

First, this $100 million has many targets including MRSA or Acinetobacter and if you think about the way NIH defines antimicrobial resistance, most might go to non-bacterial pathogens. Second, when you compare it to the funding spent confronting a single viral pathogen, HIV, it quickly becomes clear that more is needed. For example, NIH spent $3.075 billion on HIV/AIDs research in FY12 and expects to spend the same amount in FY13. Thus, if we assume flat budgets, that would be roughly $23 billion by 2020. $23 billion is 30 times $761 million. Exactly. Well, not exactly, but you get my point.

image source: http://prospect.rsc.org/blogs/cw/2010/02/26/chemistry-worlds-weekly-round-up-of-money-and-molecules-107/

Remember primum non nocere? Ok, then stay home

A new study in the Archives of Internal Medicine reports the results of a survey of 150 Internal Medicine residents from 20 residency programs on presenteeism. 51% reported they had worked at least once in the last year with flulike symptoms, and 16% reported working at least three times. The two top reasons cited for working while ill were not wanting to force colleagues to cover and feeling responsible for patient care.

Tomorrow I give my annual infection prevention talk to all new incoming residents at our medical center. And again I'll make a plea for the young doctors to stay home if they are ill. But when will SHEA and other organizations begin to tackle this issue? It's much easier and cheaper for hospitals to mandate influenza vaccination than reduce presenteeism. While mandating flu vaccine allows hospitals to look tough, reducing presenteeism is likely to be more effective at protecting patients.  

Photo: Zazzle

Monday, June 18, 2012

Blowback

Remember how U.S. intelligence used a physician who was running an immunization campaign as a covert agent, in an attempt to determine if a high value target was living in Pakistan?

Well, this is why aid workers, and others, were so upset about it. There has been great progress toward the goal of polio eradication. Widespread belief that immunization campaigns could be used as a cover for espionage now threatens to stall progress in one of the few countries where polio still has a foothold.

Saturday, June 16, 2012

Whole genome sequencing and infection prevention

While attending a HICPAC meeting this week, I had a chance to chat with David Henderson about the use of whole genome sequencing (WGS) to help investigate an Acinetobacter outbreak at the NIH Clinical Center. I’m sure you’ll hear more about this at IDWeek (yet another reason to attend!). In the meantime you can check out the report in this week’s NEJM describing use of rapid WGS to investigate a NICU MRSA outbreak. My Journal Watch summary is here, if you want an abbreviated version. I’m a little surprised the paper made it into the NEJM, as it isn’t clear how the WGS contributed much to control of this particular outbreak. The work is most useful as an example of how WGS is now rapid and inexpensive enough to contribute to patient care and infection prevention work in real time (rather than only in retrospect, or as a research tool).

However, there are a couple reasons that you won’t see WGS coming to many labs in the near future. First, analysis and interpretation of the enormous amount of resulting data (the entire bacterial genome sequence) is not simple, requiring substantial local expertise. Second, we have a very incomplete understanding of which genetic differences and mutations are clinically important. Until we expand our knowledge base and bring some automation to the analysis and interpretation, bacterial WGS to inform outbreak and transmission investigations will remain limited to a few large centers that have in-house capacity.

Friday, June 15, 2012

Live Stream of Human Microbiome Project Session from asm2012

ASM is providing a live stream of the late-breaker Human Microbiome Project session from asm2012 in San Francisco.  The session starts Tuesday June 19 at 8:15am PDT (11:15 EDT) and runs until 10:45am and includes 8 speakers who will highlight the latest HMP papers published this week in Nature (2 papers - here and here - both open) and PLoS Journals (20+ papers).   There have been dozens of articles covering these findings in places such as the NYT and TheScientist, if you want to take the easy way out. The hard core will want to read all 22+ papers between now and Tuesday, so they can decide what's really important for themselves.

Link to Live Steam - Tuesday June 19, 2012; 8:15am PDT

Thursday, June 14, 2012

Religion vs infection control: issue #7

The June 15 issue of Clinical Infectious Disease has a letter which attempts to link the Islamic practice of ritual ablution with the development of primary amoebic meningoencephalitis (PAM). In this ritual there is repeated irrigation of the mouth, ears, nostrils, arms and feet; some also irrigate the sinuses. The authors note 20 deaths from Naegleria fowleri infection at a small Pakistani hospital in 2010. All were males who performed the ritual regularly and had no history of swimming. The link between ritual ablution and PAM seem plausible, particularly when the sinuses are irrigated. Last year, there were two fatal cases of PAM in Louisiana which were preceded by the use  of Neti pots for sinus irrigation.

Photo: Laurie Skrivan, St. Louis Post-Dispatch, National Press Photographers Association

Wednesday, June 13, 2012

Worth a thousand words...at least!

Here is one of Eli's papers in graphic format:
Source: CDDEP

Because you all requested another hand-hygiene video


Note the WHO "How to Hand Wash" poster at 1:02.  How can you take something as simple as hand washing and make it so complicated? I think they could get this down to three steps, maybe even two.

The true discoverer of streptomycin is discovered

Dr. Selman Waksman won the 1952 Nobel Prize for the discovery of streptomycin, the first effective TB therapy. However, he might not have actually discovered the drug. Long lost to history, his student at Rutgers, Albert Schatz probably deserved most, if not all of the credit.

Peter Pringle, in a recent NY Times article and his new book, Experiment Eleven, describes the efforts Waksman made to claim the discovery for himself and discredit Schatz.  The mystery is solved when he discovered a small unopened box in the Rutgers University archives that contained the Schatz's lab notebooks...and the truth. It will be interesting to see if the Nobel Assembly awards a medal posthumously to Dr. Schatz, who died in 2005.

image credit: NYTimes

Monday, June 11, 2012

Did Michael Jordan really have the flu?

During an off day between Games 4 and 5 of the 1997 NBA Finals, Michael Jordan got incredibly sick with fever to 103F and vomiting. The series was tied, 2-2, and the whole world wondered how he could possibly play with the flu. When he played, he required IVs at half time and collapsed into Scotty Pippen's arms at the end of the game.

Since we are slowly shifting the blog to cover the NBA and since today is the 15th anniversary of Michael Jordan's famous "flu game," I thought we should reflect back as epidemiologists to see what caused his acute illness. Did he really have "the flu" caused by an influenza virus infection or did he just pick up norovirus from one of his young kids (ages 8, 6 and 4 at the time) or ingest a bad pizza?

Today, DJ Gallo at ESPN.com discussed how selfish it was for Jordan to play since he really could have hurt his team and started a flu outbreak in Utah. Jamal Mashburn, of Kentucky and "Faces of Influenza" campaign fame seems to think Jordan had influenza and wondered if he was vaccinated.

The 1996-1997 Influenza Season was a moderate to severe one in the Northern Hemisphere with H3N2 viruses predominating. Of course June was pretty late for influenza as the MMWR stated that "influenza A(H3N2) viruses were isolated from sporadic cases in the United States during March and April. In addition, two nursing home outbreaks associated with influenza A(H3N2) were reported: one in Delaware during March and one in California during June...influenza B viruses were isolated more frequently than influenza A(H3N2) viruses after mid-February."  So maybe Jordan visited a friend or relative at a California nursing home or had influenza B?

Rick Weinberg's report of the game for ESPN.com's "100 most memorable moments" series sheds the most light on Jordan's condition:

"He remembers waking up in the middle of the night, sweating profusely, shaking, and feeling as if he was going to die... At first, he thought it was a nightmare. Then he realized it was real, that he was seriously ill. "I felt partially paralyzed," he would later say. When he lifted himself up from his bed in his Utah hotel room, his head began spinning. He'd never been so nauseated before. He feared that somehow, some way, someone had slipped some kind of drug in something he ate...  Jordan called the Bulls' medical personnel, which came rushing to his room. They determined that he was suffering from food poisoning or an intestinal stomach virus. "There's no way you'll be able to play Game 5," Jordan was told. Jordan remains in bed for the next 24 hours, missing the Bulls' morning practices the day before and the day of Game 5. He had lost several pounds. He was dehydrated."

I think most of us would agree that Michael Jordan probably had a virus other than influenza virus.  Yet we don't know if he was tested for influenza or other viruses and since HIPAA was enacted in 1996, we may never know.

Sunday, June 10, 2012

Working the refs

As the Miami Heat and Oklahoma City Thunder prepare to do battle in the NBA finals, we should recognize the importance of home court advantage and the pressure placed on referees by coaches and players. There are data that home teams benefit from fewer fouls, and everyone knows coaches and players who are good at “working the refs” to influence their calls. There are also data that as the pressure mounts (game 7 in a 7 game series), referee influence is even greater.

Now, as a mental exercise, picture your infection preventionists (IPs) in referee outfits. It shouldn’t be surprising that as the pressure mounts for hospitals to eliminate reportable HAIs, the refs (those who “make the calls” as to whether an event meets the NHSN criteria for an HAI) are under increasing pressure. We’ll soon publish survey data revealing how commonly hospitals use “consensus methods” (e.g. adjudication panels that include clinical leaders and/or hospital administrators) or even allow clinicians to “veto” HAI calls. These approaches all drive HAI rates lower, as I know of no hospitals where clinicians or hospital administrators bring cases to the IPs to ask why they failed to report them as HAIs. They are also corrosive of the prevention culture, and contribute to IP burnout.

However, even if all hospitals stopped these practices immediately, the increasing pressure to demonstrate HAI elimination would remain a problem. The celebrations units have when they reach “zero” for a period of time, and the massive disappointment when a single VAP or CLABSI ruins the celebration, are akin to the crowds and coaches during game 7, cheering a call for the home team and booing a call for the opposition. And in those centers where financial rewards and penalties accrue to unit directors based upon HAI rates, the pressure is even greater. 


The answer? Eliminate subjectivity in HAI definitions, and move to objective definitions that are amenable to electronic reporting. These HAI events may no longer correlate well with the infectious disease syndromes we diagnose and treat at the bedside, but as long as they are associated with important adverse outcomes (length of stay, mortality) and are preventable, they should suffice (see VAC vs. VAP).

Friday, June 8, 2012

Baltimore Hooters' waitress contracts...TB?

The Baltimore Sun Paper reports that a 19-year old worker at the Inner Harbor Hooters contracted TB from a co-worker. Since that time she has been under quarantine and subject to directly observed therapy. Per the article: "multiple other members of the Hooters staff were confirmed to have latent or nonactive tuberculosis after the restaurant and the Health Department scheduled two separate testings for staff at downtown hotels last October and in March."

Still, I think you should plan your trip to Baltimore.  The Inner Harbor is beautiful in June and the Orioles are in first place. And on the plus side in this case, the woman was awarded workers' compensation from Hooters to cover lost wages and mounting medical expenses and Baltimore TB cases continue to decline with about 32 cases/year down from 60 in 2001. Back those bags and head to Charm City.

h/t Dan Morgan

Thursday, June 7, 2012

The flu season that wasn't

It's official: CDC has proclaimed that the flu season that just ended was one of the mildest on record. See all the details here.

Photo: Eastern Connecticut State University

Hand hygiene compliance at your hospital is not 90% and it's probably not even 80%

A few weeks ago, we got a review back on a manuscript (fortunately accepted with minor revision) but one of the reviewer's comments was an example of truthiness invading infection prevention.  The comment was one we hear often and since you can't typically communicate with a blinded-reviewer, I thought I'd mention the comment and what my response would be here.

Reviewer: "...only 63% of HCWs performed hand hygiene on exiting the room...in the year 2012, compliance rates of 50-63% is just plain depressing..." This comment and the other comments by the same reviewer seem to suggest that the four hospitals in our study were outside the norm and that we should clearly have hand hygiene compliance above 90%.

My (theoretical) reply: Hand hygiene compliance rates are not as high as reported.  Many things can explain this from the Hawthorne effect to only collecting data during 9-5 business hours. Fortunately, we have data from The Joint Commission Center for Transforming Healthcare.  In 2009 they began a hand-hygiene project.  Dr. Mark Chassin, President of The Joint Commission, described the project in a 2010 interview:

"We are collecting data from all Center hospitals. We are continuing to do so even for the eight hospitals that participated in the hand hygiene project, past its formal closure. In April 2009, at the beginning of the project, performance was collectively at 48% and has now stabilized at around 82%. It’s interesting that a number of the hospitals were misled by faulty data to believe that they were doing as well as, say, 85%, at baseline rather than 48%. So getting reliable measures was understandably a big issue at the start of the project."

When we do hand hygiene studies we use a uniform extraction sheet and collect data from all hours. We also collect 1000's of hours of data. From our experience, it is likely that hand hygiene in most hospitals is closer to the 50% reported in the 2009 Joint Commission study and not near the claimed 90% that everyone likes to see.

Final note:  If we think compliance is 90% we will do nothing, but if we accept the fact that it is 50% or 63%, we can address that with further interventions or initiatives. Acknowledging this is a necessary first step in making our hospitals safer.

Source: An Interview with Mark Chassin, The Joint Commission on Quality and Patient Safety, October 2010.

Wednesday, June 6, 2012

Hospital shifts focus from Contact to Standard Precautions for MRSA and VRE: Costs decline and infections decrease

Since local factors can be dominant in infection prevention (e.g. size of hospital, number of ICUs or prevalence of MRSA on admission) it is important to acknowledge that one size doesn't always fit all, as far as use of Contact Precautions for MDRO control. At the 2012 APIC meeting in San Antonio Maureen Hodson, RN CIC, at HealthAlliance Hospital in Massachusetts presented her hospital's experience with shifting towards a stronger emphasis on Standard Precautions and away from Contact Precautions. Contact Precautions were limited to MRSA and VRE patients who present with uncontained secretions and ESBL, MDR-GNR and active C. difficile patients.

When comparing the 4-month intervention period to prior periods, costs for gowns and gloves declined by $20,000 and VRE infections declined while MRSA infections were unchanged (see table below).  It will be nice to see if this can be sustained and what the impact is on ESBL or C. difficile, but this approach makes a lot of sense.


Reference: Hodson et al, oral presentation #117, APIC 2012

Tuesday, June 5, 2012

Schadenfreude

Poor APIC! No sooner than they rolled out their new grand vision, healthcare without infection, the keynote speaker at their national meeting tells them it ain't gonna happen. Allan Morrison, a member of the reality based community an infectious diseases doctor, delivered the bad news to APIC. It's not the first time APIC's been rebuked in a plenary session of a national meeting, but this time it happened at their own meeting. Next time, they better make sure all speakers sign the zero pledge card before they let them on the stage.

Thanks, CDC laboratories!

I am on call this month for our clinical microbiology laboratory, so I spent part of yesterday afternoon squinting through a microscope and scratching my head (yes, at the same time). Another Iowa lab had sent us a slide and was asking our opinion regarding the identity of a parasitic form in section. After conferring briefly with a couple colleagues and our state lab, we sent several images to the CDC DPDx team. They responded less than four hours later (about 9 pm CDC time). In cases like this (which occur all day, every day, at hospitals around the country), patients may never know that CDC laboratorians were directly involved in establishing a diagnosis. And presumably, some of those patients will receive appropriate care based upon a correct diagnosis, and recover enough strength to vote for a candidate who wants to gut the CDC budget.

Read this report, recently submitted to a Senate committee, about the work of the CDC laboratories. Then consider contacting your own legislators to ask them to boost, not cut, essential public health and prevention funding.

Saturday, June 2, 2012

Influenza for dummies

Here's a really cool video on influenza:

Friday, June 1, 2012

Daptomycin non-susceptible enterococcus

There was a time, way back in the 1990's, back before quinupristin/dalfopristin (1999), linezolid (2000) or daptomycin (2003), that we had to treat VRE with an antibiotic called chloramphenicol. You remember chloramphenicol and its association with reversible bone marrow suppression and fatal aplastic anemia. Even then, VRE developed resistance to chloramphenicol, but we didn't have many other options.

So, it was an exciting time a decade ago when we suddenly had three new treatment options for the always resistant enterococcus.  Those good times have passed us by quickly.  In a new study published in ARIC, Jeremy Storm (COI alert: an ID fellow in Dan's ID division) analyzed a case-series of daptomycin non-susceptible enterococci from a 6-year period (2005-2011) at the University of Iowa.  This is a case-series, so risk factors can't specifically be measured; however, 60% of the 25 patients had prior daptomycin exposure. I've pasted Table 3 below, so you can look at the resistance profile of the isolates. Hopefully, we won't have to dig out chloramphenicol anytime soon, but I'm brushing up on its dosing just in case.

If you need more depressing enterococcal news, you can also read about a high-prevalence (61 patients) of vanB containing E. faecium in a southwest Germany neonatal ICU.