"Nightmare" on Hospital Street

Not sure how we missed last week's JAMA medical news piece featuring our very own co-blogger Dan, but I suspect we might have been distracted by something pretty terrible. The article highlights the rise of carbepenem (CRE) and 3rd-generation cephalosporin-resistant Klebsiella pneumonia strains originally described in ICHE by Braykov et al. The CDC's Arjun Srinivasan emphasized that these strains are almost exclusively hospital-associated and now is the time for hospitals to implement the latest CRE recommendations from the CDC 2012 toolkit.

Dan "emphasized the importance of infection control basics such as ensuring a high rate of hand hygiene adherence among staff and making sure that surfaces and equipment are properly disinfected."  And said "If you don't shore up those things, screening [for CRE] isn't going to help."

I'll just paste in my favorite section: "An additional problem is the piecemeal approach to tracking these infections. Only 6 states require facilities to report CRE cases. “We need a more coordinated response,” Diekema said. He explained that the CDC is doing as much as it can with the resources it has, but underfunding of public health at the national and state levels makes it difficult to mount a more coordinated national effort to contain the spread of these infections. More research is also needed on the best strategies for environmental disinfection, ensuring adherence to hand hygiene and other measures that would prevent the spread of health care–acquired infections."

CRE isn't just a nightmare, it's a recurring nightmare. And just like the nine Nightmare on Elm Street films, it'll get worse over time. Especially if we continue with the current "piecemeal approach" prevention plan.

Source: Bridget Kuehn, JAMA 4/27/2013
Image source: wikipedia

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The Environment and HAI – Where does Biological Plausibility Come In?

This May's Infection Control and Hospital Epidemiology (ICHE) contained a randomized trial of copper-coated surfaces in ICU settings which reported a 50-70% reduction in several aggregate outcomes that included hospital-acquired infections and colonization with MRSA and VRE.  In this guest blog post, physician-scientists Dr. Matthias Maiwald from the KK Women’s and Children’s Hospital in Singapore and Dr. Stephan Harbarth from University of Geneva Hospitals in Geneva, Switzerland question the plausibility of these findings and put them in the larger context of what actually causes HAIs.

In 1965, Sir Austin Bradford Hill published a landmark paper, entitled “The Environment and Disease: Association or Causation?” in which he outlined what would become known as the “Bradford Hill Criteria.” The “Hill Criteria” help distinguish association from causation in epidemiological research. One of nine criteria was biological plausibility. Quoting: “It will be helpful if the causation we suspect is biologically plausible. But this is a feature I am convinced we cannot demand. What is biologically plausible depends upon the biological knowledge of the day.” As commented elsewhere, the spirit of this criterion is to check whether the proposed causation violates any of the known laws and facts of science of biology, and as Hill outlines, this depends on currently available knowledge. It is said that Hill did not intend the criteria to be applied rigidly in the sense of a checklist approach; instead, he regarded them as “viewpoints” that would merely help in the assessment.

Fast-forward to the May 2013 Special Topic Issue of ICHE concerning the role of the environment in infection prevention. In the issue’s introduction, Weber and Rutala quote figures from a 1991 article by Weinstein concerning the biologically plausible sources of healthcare-acquired infections (HAIs): “patients’ endogenous flora, 40-60%; cross infection via the hands of personnel, 20-40%; antibiotic-driven changes in flora, 20-25%; and other (including contamination of the environment), 20%.”

In the same issue, an article by Salgado and colleagues caught our attention. This clinical trial compares 614 patients randomly placed into standard ICU rooms or into rooms where 6 frequently-touched items (e.g. bed rails, overbed tables, intravenous poles, etc.) had been replaced with copper alloy surfaces. The measured primary outcomes, according to the paper’s methods, were:
   (a) any HAIs and
   (b) colonization with methicillin-resistant Staphylococcus aureus (MRSA) or vancomycin-resistant enterococci (VRE). Besides HAI and colonization, outcomes presented in the results section included the numbers of patients who had
   (c) both HAI and colonization,
   (d) HAI and/or colonization,
   (e) HAI only but no colonization (i.e. number of patients who had HAI minus the ones who had both HAI and colonization), and
   (f) colonization only but no HAI.

Are you confused? Separate data for outcomes in each trial arm were only reported for (d-f) but not (a-c).

For HAI and/or colonization (d), the article reported what amounted to a 49% reduction in the copper rooms vs. non-copper rooms (21 vs. 41 patients; p=.02), for HAI only (e) a 62% reduction in the copper rooms (10 vs. 26; p=.013), and for colonization only (f), a 67% reduction (4 vs. 12; p=.063, NS). What was was not reported were the numbers of patients with (a) HAI and (b) colonization, listed separately for each trial arm, but the article concluded – in the discussion – that copper surfaces in rooms reduced the risk of HAIs by more than half. Conventional wisdom, however, would suggest that (a) any HAIs and (b) any colonization events, would be the most biologically relevant outcomes, and that it may not be so informative to combine these two events (under d) in the same statistical calculation, because they are biologically very different from each other. So, we extracted the missing numbers from the other numbers presented and arrived at (a) HAIs 17 vs. 29, and (b) colonization, 11 vs. 15 events. Putting these into our statistics calculator, they were – non-significant.

Now, let us revisit possible transmission routes in hospitals. We have: (i) endogenous transmission, from within the patient’s own flora, (ii) exogenous transmission via direct transfer, (e.g. as in handborne without surfaces), and (iii) exogenous transmission via surfaces and secondary transmission from surfaces onto the patients. If we look at (a) HAIs and (b) colonization with MRSA or VRE, then all three pathways can lead to HAIs, while only the two exogenous pathways can lead to colonization. If there is a >50% reduction of HAIs through copper surfaces (pathway iii), this would mean that the overall proportion of transmission from pathways (i) and (ii) plus the proportion of transmission from the remaining non-copper surfaces in the copper-treated rooms among pathway (iii) among all HAIs together would contribute less than 50% to overall HAIs.

The obvious question comes to mind: is that consistent with the known proportions of the different pathways leading to HAIs? The preliminary answer, given the Weinstein data (see above), would be, “given the biological knowledge of the day, apparently not.” It is also noted that the overall numbers of HAI and colonization events in the present article are relatively small.

Finally, anyone of us engaging in research can accidentally have outcomes that are surprising or do not quite add up with existing knowledge in the field. That is, in our opinion, where the intended purpose and scope of a discussion section of an article comes in, and where the Hill Criteria provide important food for thought. As one of us has put forward (Teleclass Feb. 7, 2013) on a different occasion and concerning a different topic, we would welcome the broad application of a check for biological plausibility when findings from clinical trials – and even systematic reviews – are reported. But we are not confident that our voices will be heard.

Image of Sir Austin Bradford Hill, source: toxipedia

Surveillance under pressure

There’s a great success story now published online in ICHE. The CDC, using National Nosocomial Infection Surveillance (NNIS) and National Healthcare Safety Network (NHSN) data, estimates that 100-200K central line associated bloodstream infections (CLABSIs) have been prevented since 1990 through implementation of evidence-based prevention practices. This accomplishment should be celebrated as a demonstration of the real progress that has been made in hospital infection prevention. As Mary Dixon-Woods and our fellow blogger Eli point out in an accompanying editorial, however, these results are also a time to reflect on how much surveillance has changed since 1990.

The CLABSI surveillance that we once performed exclusively to guide local prevention efforts is now used for much different purposes, with rates reported publicly and soon to have a real impact on each hospital’s bottom line. The pressure to bring CLABSI rates to “zero”, by any means necessary, gets passed along from hospital administrators to unit directors and infection prevention programs, turning CLABSI rates into what Mary and Eli correctly describe as a “reactive measure.” To quote their editorial,

“the more that organizations are incentivized by the prospect of shaming or financial penalties to decrease sensitivity—and thus not to find cases—the less certain it is that they are reporting a valid assessment of their infection rate”

It is instructive to examine what happens in other professions when intense pressure is brought to bear on a metric. Five minutes on The Google is enough to inform about what happens when law enforcement is under pressure to lower crime rates, or when teachers are under pressure to improve student test scores. Are police officers and teachers more inclined to “cheat” than are those tasked with counting infections in hospitals? Do officers who misclassify a burglary as a theft after receiving a call from a commander really have nothing in common with the IP program that misclassifies a primary CLABSI as secondary after a call from a unit director or hospital administrator?

This increased pressure is also felt at the CDC and NHSN, as a metric that was initially designed for one purpose is now appropriated for very different purposes. We recently performed an email survey of over 50 prominent hospital epidemiologists to gather their opinions about the direction of surveillance over the next decade. The results can be found here. Some of the highlights:

• Over 75% of those surveyed thought it likely or extremely likely that their local surveillance efforts will erode to focus only on those linked to payment policies or state/federal requirements.
• All thought that HAI surveillance metrics linked to payment policies and state/federal mandates would continue to grow to include more outcome and process measures.
• Respondents felt that pay-for-performance metrics were most likely to drive practice change (moreso than public disclosure of data, use of data by practitioners, or release of national summary statistics).
• Fewer than half thought it was likely that fully automated metrics from existing data elements would replace manual review of records for HAI determination.
• About half of respondents thought that the increased attention to HAI prevention from payment policies, mandates and public reporting has made patients safer (13% thought it hadn’t, and 40% thought the jury was still out).
• Almost 80% of respondents thought that infection prevention experts and clinical providers should have a much larger role in developing and modifying state/federal reporting requirements.

In other words, there is real concern in the HAI prevention community that the increased attention to HAIs, the drive to “zero”, the link to payment policies and public reporting requirements, is a double-edged sword. It has resulted in some tangible successes (CLABSI reductions being a prime example), but threatens to undermine our ability to respond nimbly to emerging local priorities by consuming all of our time and energy, and by producing data that no longer accurately reflect the true rate of adverse outcomes. To quote again from Mary and Eli:

"Undermining our surveillance system to serve ill-designed demands for accountability means that it may no longer be useful for monitoring and driving patient-safety improvements. That would truly be a shame."

Prevention Fund love (finally!)

At long last, someone is showing a little backbone in trying to protect the Prevention and Public Health Fund.  The fact that it's the Senator from Iowa makes it all the sweeter.  Go Tom!  The money quote from Senator Harkin:

"I am greatly disappointed that the administration chose to help pay for the Affordable Care Act in fiscal year 2013 by raiding the Public Health and Prevention Fund. The Prevention Fund works. Thanks to this funding, more children are being immunized. More people are quitting smoking. More communities are fighting chronic disease. More people are being screened for hepatitis C. Robbing prevention when we know these efforts can improve people's health and lower healthcare costs goes against the very mission of healthcare reform."

h/t to Mike for e-mailing me the link.

Give Gloves a Chance: Benefits of Mandatory Gloving Policy in Pediatrics

We spend a lot of time discussing the importance of clean hands in preventing hospital-acquired infections (HAIs). Most of the time we equate clean hands with hand-hygiene compliance and complicated and fleeting surveillance and educational programs. It would be one thing if these efforts led to compliance levels above 90%, but even the Joint Commission could barely get compliance above 80% after massive efforts.

Which leads me to one question - are we asking the wrong question?

Instead of focusing solely on driving hand hygiene compliance above 90%, perhaps we should focus on clean hands. If we ask a new question: "What do we need to do at our hospital to get healthcare worker hands to be 90% clean?", we get very different answers than if we focus solely on increasing hand rub use. For example, we could begin studying long-acting hand disinfection products that work all day or environmental cleaning products that keep hands clean in the first place. And another thing we could consider looking at is the benefits of the humble examination glove. We just published a study in Pediatrics, led by Jun Yin a PhD student in statistics, that aimed to do just that.

At the University of Iowa, we have a policy that mandates that healthcare workers wear gloves for all patient contacts during RSV season. We wanted to see if we could take advantage of this natural experiment to see what happened to HAI infection rates during the mandatory gloving periods compared to non-gloving periods.  To do that we completed a quasi-experimental study using time series analysis (Poisson regression models) on data from 2002-2010. We studied the effect in 5 units including a 20-bed PICU, a 62-bed NICU, a 5-bed Pediatric Bone Marrow Transplant Unit, a 26-bed Pediatric Hematology-Oncology Special Care Unit, and a 35-bed Pediatric Medical/Surgical Mixed Acuity Unit.

What did we find? Universal gloving periods were associated with a 25% reduction in HAI rates after adjusting for long term trends and seasonal effects. There was a 37% reduction in bloodstream infections (BSIs), a 39% reductions in central line-association BSIs and an 80% reduction in hospital-acquired pneumonias. The reductions were statistically significant in the PICU, NICU and Bone-Marrow Transplant Unit.

Yes, this unfunded study has limitations. It's a non-randomized, single center study. There could have been other factors that started just when RSV season started every year along with the gloving policy (although we couldn't think of any). Since this intervention was turned on and off every year for 9 years (with an exemption in 2009 for the novel H1N1 pandemic), it's unlikely there were other interventions that biased these results every year at the exact same time. 

Perhaps we need further study and cluster-randomized trails. We won't have to wait long. There is an important AHRQ-funded study that Anthony Harris's group is just completing at the University of Maryland that looks at the benefits of mandatory glove+gown policies in ICUs. However, this study won't tell us if it's the gowns or gloves or if they work in Pediatrics. So what do we do in the interim while waiting for future trials and magical interventions that get hand hygiene compliance above 90%?  All we are saying is "Give Gloves a Chance."

Reference: Yin J et al. Pediatrics April 22, 2013

Image: wikipedia

Media coverage: Reuters Health and Wired (Superbug)

Good riddance?

This week we suspended our tuberculin skin test program for healthcare workers due to the nationwide shortage of tuberculin. I say, Glory Hallelujah! I can't think of a more poorly performing test. Really, it's junk. And we've reached a point at our hospital that no healthcare worker will take isoniazid after a positive skin test until an interferon-gamma release assay has been done and is positive. However, there doesn't appear to be a good correlation between the skin test and the IGRA, so when the two tests are discordant, it's a coin toss as to which is the true result. To complicate matters even more, there's also a nationwide shortage of isoniazid. And don't even get me started on the use of isoniazid to treat latent TB (see here).

Photo:  Mayo Clinic

Nosocomial listeriosis

The Sydney Morning Herald is reporting that 3 patients in 2 Sydney hospitals have developed listeriosis after consuming profiteroles served to patients at the hospitals. The infecting strain in all patients was identical. One of the patients has died from an apparently unrelated cause.

Nosocomial foodborne illnesses, particularly those of bacterial origin, are seemingly uncommon. I suspect this is likely due to a lack of appetite in many hospitalized patients, and the highly processed nature of hospital foods (sometimes I'm not sure it's actually food).

A few weeks ago, while making morning rounds on the inpatient infectious diseases consult service, I went to see an immunosuppressed patient with pneumonia. As I was about to leave his room, I noted a clear plastic container of macaroni salad on his overbed table that had been served the evening before. My paranoia of foodborne infections must have been palpable. He thought it was quite funny that I alarmingly said, "Don't eat that!" While laughing at me, he said, "that's old Doc, I'm not gonna eat that." Just to be sure, I threw it in the garbage, which made him laugh all the more.

Photo: Culinary Catastrophy

Prevention: Who needs it?

We’ve been blogging for some time about threats to the Prevention and Public Health Fund, a fund that supports many critical prevention efforts, including funding state health departments to coordinate healthcare-associated infection (HAI) prevention and enhancing laboratory capacity to detect infectious diseases threats.

As Sarah Kliff points out in the WaPo wonkblog, congressional gridlock has led to a “good news, bad news” situation with this fund. The good news is that Republicans haven’t been able to eliminate the fund entirely, as is their wont. The bad news is that funding for implementation of the Affordable Care Act is also being held up, so the fund is now being raided to pay for those activities (in 2013, nearly half of the funds will be used to set up the federal health exchanges).

To quote Rick Mayes and Thomas Oliver again on the “prevention paradox”:

“If public health measures are effective, the problems they are aimed at are often solved or never even materialize, thereby making them virtually invisible.”

If we continue to starve prevention efforts, those problems won’t remain invisible for long…

Why surgical complications may actually hurt profits despite what you've just read.

If there is no financial incentive to reduce excess length of stay, why has every hospital spent the past 20 years trying to reduce it?

There's a high-profile and important paper in JAMA this week by Sunil Eappen and colleagues. The study looked at surgical discharges during 2010 from a single 12-hospital system and determined that admissions that included a surgical complication were associated with a higher profit (defined as the contribution margin) than admissions without complications. The authors concluded that this creates a disincentive for hospitals to prevent surgical complications since they might see reduced profits as a result.  This is a very provocative finding and it's getting a lot of well-placed media attention, as you might expect. However, there is an important caveat with the study that I would like to highlight.

In the study the authors report that admissions with surgical complications result in $39,000 higher "profits" if the care is reimbursed via a private payer and $1800 if Medicare is the payer. However, as Dr. Reinhardt correctly noted in the editorial, "Allocating profit and loss is exquisitely sensitive to the many assumptions made in economic modeling and must be performed carefully to provide useful evidence about the financial ramifications of surgical complications and other services." His concern dealt mostly with how the authors allocated fixed costs in their calculations. My concern has to do with what the authors assumed happens to an empty bed once a patient is discharged in a US hospital.

This is what the authors assumed (and mentioned as a limitation): "We did not estimate the effect of 3 potential factors that could affect the hospital economics of surgical complications. First, the shorter lengths of stay of procedures without complications could benefit the small percentage of hospitals operating at full capacity because they might be able to admit additional patients with favorable insurance who were “crowded out.”" What this means is that they didn't include any profits that might be generated by an empty bed filled with a second (or third or fourth) patient. In the study, around 5% of patients developed a complication and stayed an excess of 11 days (at the median) - the mean would be higher.

Note: Based on recommendations of Johns Hopkins professor and retired CFO, Bill Ward, we focused on estimating the costs of HAI using return-on-investment calculations from filling empty beds that manifest through HAIs avoided in the Business-Case SHEA Guideline. In discussions he suggested that excess bed capacity is quickly taken off line and therefore doesn't impact economic evaluation to a large degree. If there is no financial incentive to reduce excess length of stay, why has every hospital spent the past 20 years trying to reduce length of stay?

The big question: Do you believe that 5% of beds in hospitals with high surgical volumes sit completely empty for almost two weeks? Of course, there is excess capacity in the US system, but the amount of excess capacity is most important here, not that it exists. You can't completely ignore profits from increased admissions. For example, if only one patient was admitted into a bed vacated by a "healthy" patient discharged at day three that would would have otherwise been occupied by a patient with a surgical complication discharged at day 14, the results of the study would be have been negated - i.e., it would have been a negative study. If more than one patient was admitted into an empty bed over 11 days, which seems likely at most high-volume hospitals, admissions with surgical patients with complications would result in reduced profits compared with admissions without complications. It would have been nice to see estimates of the excess capacity at the 12 hospitals under study.

A provocative study and wonderful analysis. However, as Dr. Reinhardt states, the study "provides important data on a pressing clinical and financial problem affecting hospitals" yet "much of this represents a shell game of how costs are allocated." I would add, and which profits are included or excluded.

Image source: wikipedia

H7N9 Mortality

A week ago, in response to some scary reports, I tweeted this:

I wanted to see how my public prediction held up in the H7N9 outbreak after an admittedly short 7 days and approximately 2 weeks after the outbreak gained widespread attention. To do this, I simply plotted the reported mortality rate using the daily case and mortality counts available through the @WHO twitter feed between April 1st and April 16th.

While the case counts have gone from 3 to 63 over this period, reported deaths have risen more slowly from 2 to 14 and the mortality rate has fallen from 67% to 22%. When I made the prediction it was 30%. If I had included data from April 17th, the mortality rate would have fallen further to 20.7%, 17 deaths and 82 cases. I've plotted the daily mortality rate below. Good news, but still a ridiculously virulent virus. Hopefully, as more surveillance specimens return, the mortality rate will continue to fall. Hopefully.

Addendum: Immediately after posting this, several twitter discussions began. To clarify, I know many of the sick patients are still hospitalized in the ICU. Even cases that appear to initially recover could succumb to secondary bacterial infections. Helen Branswell made the important observation that two of the three cases in the recent NEJM report were infected with Carbapenem-resistant Acinetobacter baumannii and at least one of them didn't appear to receive appropriate antibiotic therapy. Hopefully, as recognition increases, so will early diagnosis and early antiviral therapy along with effective antibiotic therapy (if available).

Four-legged hospital visitors

A recent piece in the New York Times discusses pet visitation in hospitals. This is different than pet therapy programs in which trained animals visit multiple patients. In this case, pets visit their hospitalized owners. Some hospitals allow this, believing that the benefit to the patient outweighs the infection control concerns. I have heard many wonderful and powerful stories from my wife, a palliative care physician, on the impact of pet visitation for her patients who are at the end of life.  Two of the hospitals noted in the article are near and dear to us--the University of Iowa Hospitals and Virginia Commonwealth University Medical Center.

Painting: A Strong Warm Hug by Diana Roberts

Influ-Venn-Za

Having trouble keeping those H's and N's straight? Here's a great graphic from Information is Beautiful.

Preventing Norovirus Transmission in Your Home

Several weeks ago, my son came down with norovirus. There has been a lot of norovirus this year in Iowa, the US and the world. One of the reasons is that there's a new variant of genotype II.4, named Sydney 2012, that was reported through CDCs CaliciNet to be causing 58% of outbreaks in December 2012. So it's likely that none of us are immune to this variant, meaning that the three others in my family were now at high risk of becoming ill with norovirus. To make matters worse, we were about to celebrate my daughter's birthday and I didn't want her to become ill on such an important day. So my wife and I, educated by previous norovirus outbreaks in the family (2005 and 2010), hatched a plan to beat the virus this time. Let me foreshadow a bit, none of us got sick. Let me tell you how we did it.

The enemy
Noroviruses has a very low infectious dose (≥18 viral particles) and infected patients shed 5 billion infectious doses in each gram of feces. The virus is environmentally stable, can survive up to two weeks on surfaces and is resistant to many common disinfectants. Alcohol hand rub, is thought to be a suboptimal form of hand disinfection with soap and water being preferred. The virus is transmitted fecal-orally and is aerosolized, meaning it spreads widely in the environment. Recent evidence even suggests that commercial dishwashers are ineffective in cleaning norovirus off of dishes and silverware. Finally, since 51% of cases caused by Sydney 2012 were caused by human to human transmission, household transmission is a big mechanisms of spread.

Caveats, Limitations and Yes I Know, but Humor Me
Now, as many of you know, I'm an ID physician and epidemiologist and I like to identify limitations in almost anything I read. So, I'll save you some of the trouble and point out the weaknesses in this case report. First, it's a case report. Second, we never tested for norovirus in clinical or environmental specimens. Third, we don't know if we were susceptible to this strain, however unlikely that would be.

Case Report
Our kindergarten-aged son, first expressed norovirus symptoms when strapped into his booster seat in the back seat of our car. The other three of us were in the car at the time. We drove home and he was sick 3-4 more times in the bathroom. We quickly changed his clothes and quarantined him to a bathroom with a TV to watch for the next 24 hours. We then cleaned up the car and hatched a plan to beat back in-house transmission.

The plan
1) We began practicing strict hand hygiene with soap and water. We rarely used alcohol hand rub, if at all.

2) We realized that all dishes in the dishwasher from the morning he became ill were potentially contaminated and double washed them in the dishwasher. We also removed those dishes from circulation for ~7 days.

3) We each began using a unique set of dishes. We each had our own glass, bowl, dish and utensils. We each rinsed and washed those individually so that we couldn't transmit virus to each other. At the time, we didn't know if others were contagious or not.

4) We didn't wash the booster seat, clothes, towels etc that were overtly or potentially contaminated for ~2 weeks; we just kept them in a bag in the corner of the basement.

5) Finally, we were lucky that we have two bathrooms in the house. One was our son's bathroom for one week and the other was for the three "uninfected" family members.

That's it. Most of these steps are easily reproducible in any household. I completely understand that the availability of a second toilet could have made a big difference and not everyone has one available. Although in 2010, we also had a second toilet available and it didn't make a difference since all got sick. Finally, the big change to our infection control in 2013 versus 2010 or 2005 was that we all had our own utensils, glasses and dishes. I suspect that made the difference this time and is probably worth future study.  It would be hard to do a randomized trial of such an intervention (which is why I wrote up this case report), but it could be done.

So good luck out there. Be safe. You never know when norovirus will strike, but don't think you can't beat back this virus. You just gotta use your head, soap and water and your own spoon. Oh, and I know I've now totally jinxed myself. I'll be OK. I'm keeping a bucket next the bed.

reference: Hall AJ, J Infect Dis 2012

Influenza at the “human-animal interface”

The first three novel avian influenza A (H7N9) viruses have been sequenced, and the sequences uploaded to the Global Initiative on Sharing All Influenza Data (GISAID). Not surprisingly, there were genetic changes found that have been associated with increased transmissibility of other avian flu strains to mammals.

I have no deep thoughts on this--it is what influenza does, after all, with avian and other non-human strains occasionally making the leap to humans. The few things we know about this particular strain, as of late yesterday, can be found at the CDC and WHO websites, and include the following:

• a total of 21 cases have been laboratory confirmed in China, including six deaths, 12 severe cases and three mild cases
• more than 530 close contacts of the confirmed cases are being closely monitored
• the viruses isolated to this point appear to be susceptible to neuraminidase inhibitors (e.g. oseltamivir) but resistant to adamantanes (e.g. amantidine, rimantadine)
• there is no current evidence of “ongoing human-to-human transmission"
• the virus should be detectable with existing PCR methods as an “unsubtypeable” influenza A virus (the CDC is working on adding this strain to their testing approach so that it can be more quickly subtyped if it spreads outside of China)

The most recent interim guidance for case investigation, testing, infection control and treatment are here.

Finally, for those interested in a regular update on the threat of non-human flu strains, the WHO publishes monthly updates on “influenza at the human-animal interface” (wait, aren’t Homo sapiens also animals? Maybe it should be, “influenza at the human-nonhuman interface”…).

Shouldn't evidence guide our selection of hand-hygiene surveillance systems?

It's amazing how little evidence is required before infection prevention interventions are adopted. A current example of this is the installation of automated hand-hygiene surveillance systems that track healthcare worker room entry and hand hygiene compliance. Hospitals are committing significant resources, both financial and person-time, to implement these systems with minimal evidence that they sustainably improve compliance or are accurate and cost-effective. To channel Jerry Maguire, before hospitals "show them the money", shouldn't they ask companies to "show me the meta-analysis"?

With that in mind, I really enjoyed reading the study in February's ICHE by Luke Chen and colleagues at Duke describing the implementation of an electronically-assisted, directly-observed hand hygiene surveillance system. The investigators recognized that directly observed compliance remains the gold standard, but also realized that economic and time costs, along with potential biases such as the Hawthorne effect, limit its utility. Thus, they set out to improve on the gold standard by modifying it to address potential biases and reduce costs.

Beginning in 2009, non-secret (they wore ID badges) auditors began monitoring compliance in 40 wards/clinics. They observed two moments of compliance, before/after room entry. All data was entered into wireless-PDAs that were linked to a centralized server allowing instantly updated 30-day tracking reports.

Overall, the compliance rate reported was 88% after 100,000 observations. That's pretty good. What's more, they reported compliance by the order of observation. For example, they calculated the average compliance for the first opportunity observed, the second opportunity and so on. The reason they did this, is they hypothesized that the Hawthorne effect wouldn't kick-in until the observer was seen by the healthcare worker and that this would become more likely the longer the direct observer remained on the ward. What did they find? Look for yourself:

What do you see? They found compliance for the first five observations was less than 86% while the average over the 35th to 43rd observations was 95%. We see an actual Hawthorne effect. Excellent. After seeing this, and for other reasons as well, they created standard operating procedures that observers used. The most important change to their procedures was they limited observations to 10 minutes or 10 total opportunities before moving to the next ward. Following these changes, compliance was reported to be 86%.

Of course there are limitations to this study in that it was a single-center study and lacked economic data to help guide its broader adoption. The authors acknowledged these and are addressing them already in a future study. My sense is that this method will be more effective and cost-effective than fully-automated systems and also keep infection preventionists visible on the wards to identify and address other important issues, which they can't do from behind their computer screens. But unlike many pushing for a new hand hygiene monitoring system, I'm going to start collecting the data and let the evidence guide my decision making.

Image: Luke Chen, MBBS MPH

Another Staph aureus vaccine failure

The April 3rd JAMA contains the results of a wonderfully designed and executed study by Fowler and colleagues assessing the benefits of a novel (V710) vaccine targeting S. aureus infection in cardiothoracic surgery. The study was negative (i.e. the vaccine didn't work) and highlights how little we know in 2013 about how humoral immunity works for this important human commensal. But first the study and results...

Among 8031 patients entered into the study, the vaccine was given between 14 and 60 days pre-op to 3981 randomly-selected patients prior to surgery while 3982 received saline placebo. The study was powered to detect a 20% reduction in S. aureus bacteremia or deep surgical site infection through 90-days post-op. Secondary outcomes were any invasive S. aureus infection. Three interim analyses were planned but the data monitoring committee terminated the study after the second interim analysis. Thus, only around ~5100 patients completed the full study with 90-day endpoints. Of note, 67% were male, 24% had diabetes, 18% were S. aureus colonized and 2% were MRSA colonized. Randomization appears excellent.

As I suggested, the results are sobering. The primary outcome (deep SSI or bacteremia) occurred in 2.6% of vaccinated patients and 3.2% of controls, p=0.58. There were more adverse events at 14 days in the vaccinated group (31% vs 22% ) and a greater incidence of multiorgan failure. Depressingly, there was far higher mortality secondary to S. aureus infection in the vaccinated group, 23 vs 4.2 per 100 person-years. The overall comparison between vaccinated and unvaccinated for S. aureus related outcomes is striking and humbling. I've pasted Table 4 from the study below, for your review (click on it to enlarge).

The authors of the study point out that their study isn't the first to find worse outcomes in a vaccinated group and also that MRSA infections were more common in the vaccinated arm of the trial. But I don't buy their suggestion that MRSA was a significant contributor to the poorer S. aureus related outcomes in the vaccinated group. There just wasn't enough MRSA disparity between the vaccinated and control groups. I wonder if part of the answer to higher mortality in the vaccinated group could be explained by this old paper by Heiman Wertheim and colleagues that I discussed several years ago. Wertheim report significantly lower mortality among S. aureus carriers vs. non-carriers. Could the vaccine be upsetting the delicate protective effect of pre-existing S. aureus colonization?

There is an excellent accompanying editorial by Preeti Malani and I urge you to read it. She does a wonderful job putting this study in historical context and pointing a path forward for HAI prevention research. The money quote from her editorial is: "Ultimately, the results of the study by Fowler et al say more about the need to rigorously study infection prevention in general than about S aureus per se." I couldn't agree more.

Image source: Vance Fowler, MD MHS from Duke

Partnership in Prevention Award

Have you assembled an effective team and achieved exceptional success in some aspect of infection prevention in your hospital or healthcare system? Then please consider submitting an application for the Partnership in Prevention award, an award jointly sponsored by SHEA, APIC and HHS to recognize such achievements. Read about the award, and instructions for applying, here. The application period is from today through July 1, 2013.