Hand hygiene doesn't prevent healthcare associated infections

Not all transmission leads to infection and not all infections are preceded by transmission. Hand hygiene prevents transmission, not infection.

....some posts are just hard to write.

One of the persistent beliefs in infectious diseases and infection prevention is that hand hygiene compliance prevents healthcare associated infections. Perhaps this harkens back to Semmelweis and the prevention of puerperal fever through hand disinfection. Of course, if puerperal fever was a CDC HAI and clinicians didn't wear gloves, we could still say hand hygiene prevents HAI. However, that's not the current reality.

CDC defines HAI as CLABSI, CAUTI, SSI and VAP. We can even consider hospital-onset BSI and almost any other infection we can track using CMS or EMR data and monthly aggregate hand hygiene compliance is not a significant component in the causal pathway for the development of an HAI.

Sure, hand hygiene/sterile gloves before catheter insertion and hand antisepsis prior to invasive surgical procedures are standard practice. However, when I talk about hand hygiene compliance, I mean monthly hand hygiene on room entry/exit or following the WHO 5 My 5 Moments during care on medical wards and in ICUs. And yes, there are instances where Moment #2 - before clean/aseptic procedure could potentially reduce CLABSI, but the proportion of CLABSI caused by such breaks in moment #2 pale that occur outside of the insertion bundle pale in comparison to those prevented with the highly effective CLABSI bundle. Otherwise, monthly aggregate hand hygiene compliance would have been included in the CLABSI bundle. It wasn't.

Let's discuss SSI prevention. Do we really think that interns and nurses practicing hand hygiene on the wards prevents SSIs to any measurable extent compared to pre-operative CHG bathing or peri-operative antibiotics?  No, I didn't think so.

How about we look at this another way. If you were called by a CT surgeon because of an outbreak of SSI in CABG patients or an outbreak of CLABSI in her ICU, would you first (or second or third) start a hand hygiene campaign? I assume no and thus, you don't think hand hygiene prevents SSI or CLABSI. 

Thus, for all practical purposes, we won't be able to do studies associating improved hand hygiene compliance on the wards or ICUs with reduced infections. Even when such studies are done and do show an association, they have minimal basis in causal reality. Requiring hand hygiene bundles and intervention studies to show reduced HAI is incorrect and counterproductive. Since hand hygiene on wards and ICUs is not in the causal pathway for HAI incidence, we shouldn't expect hand hygiene to prevent them.

But all is not lost. Hand hygiene does prevent MDRO transmission (and indeed transmission of susceptible pathogens) in healthcare settings. Hand hygiene is critical to tackling the MDRO crisis but these benefits aren't currently captured by CMS and most EMR systems. To document the benefits of hand hygiene, we would need to complete surveillance for important pathogens on admission and discharge and document acquisition or transmission. This is expensive and likely not necessary nor feasible.

Keep your heads up and continue to drive hand hygiene compliance. Continue to do hand hygiene surveillance and improvement studies! Hand hygiene is critical to MDRO prevention and likely the future of healthcare. Just stop it with the HAI target.

Addendum: This post was written in response to the question: "Do you care about increases in monthly hand hygiene compliance if you can't document reduced HAI?" I would answer yes. Hand hygiene is an important clinical outcome in itself and requiring HAI reductions is a trap. Don't fall into that trap. I've attempted to explain why here.

Addendum 2: In response to this post, others have mentioned CDI as an HAI that could be targeted with hand hygiene interventions. As Dan mentioned back in 2013, CDI might not be the optimal target since a minority of cases appear to be related to in-hospital transmission. This was shown back in 1994. Stewardship might be a more appropriate intervention for CDI prevention.

A Research Agenda for MDRO Prevention

Of course, I don't need to explain the clinical importance of multi-drug resistant bacterial pathogens to readers of this blog. I probably don't need to remind you that "more research is needed" either - that's why we have controversies! But, I should probably point you to five papers recently published in ICHE that outline the future research agenda for MDRO prevention in the US Veterans Health Administration (the VA).

For our non-US readers, the VHA is the largest integrated healthcare system in the United States with over 130 acute care facilities, 1000 outpatient clinics, numerous long-term care facilities and 9 million enrolled patients. The VA has been a leader in medical and health services research for decades and has been well-ahead of the curve in application of interventions to prevent MDRO including its MRSA prevention bundle and antibiotic stewardship initiative.

To continue the VA's success in MDRO prevention and link future research questions to the greatest clinical need, we invited a multidisciplinary group with 37 participants to Iowa City in September 2016. The aim of the panel was to outline the VHA's research agenda for MDRO prevention. Dan Livorsi describes the process we used to identify the domains and research questions in an introductory editorial. The outlined research agenda was broad in scope and included efficacy, effectiveness and implementation questions. In addition, many of these questions are broadly applicable to study in non-VA and non-US hospitals. We are all more alike than different.

Research questions fell into four domains:

1. Transmission dynamics: Resistant pathogens are spread via human hands and environmental surfaces. Disrupting this transmission is essential to controlling MDROs.

2. Antimicrobial stewardship: Strategies to reduce and improve the use of antimicrobials will slow the emergence of resistant pathogens.

3. Microbiome: There may be ways to manipulate or augment the human microbiome to eradicate or prevent colonization with resistant pathogens.

4. Special populations: Strategies need to be tailored to patient populations with distinct underlying conditions and in nontraditional care settings.

All 5 papers are open access. Thanks ICHE!  And thank you to the brilliant group of VA investigators, clinicians and operational partners who traveled to Iowa City and contributed to this effort. We all hope it's helpful.

Time, Power and Infection Prevention

With the increased attention to infection prevention and antimicrobial resistance globally, we now have more seats at the table. In fact, many of us are or will soon be at the table in positions of leadership (power) in our hospitals or organizations. We can include our colleagues at CDC, who are being asked to do more and manage larger research portfolios. The time we imagined 10-20 years ago, where our clinical and research roles would be appreciated is now, but with the now comes an overwhelming urgency - we are overworked.

With that in mind, I read a very interesting post by Maria Popova on UC Berkeley psychologist Dacher Keltner's book, The Power Paradox: How We Gain and Lose Influence. Two quotes in particular struck me as they applied to our current situation as hospital epidemiologists and infection preventionists:

"The power paradox is this: we rise in power and make a difference in the world due to what is best about human nature, but we fall from power due to what is worst. We gain a capacity to make a difference in the world by enhancing the lives of others, but the very experience of having power and privilege leads us to behave, in our worst moments, like impulsive, out-of-control sociopaths"

"But in reading these alarmingly consistent studies, I had to wonder about one crucial confound(er) that remains unaddressed: People in positions of power also tend to be busier — that is, they tend to have greater demands on their time. We know from the now-iconic 1970s Good Samaritan study that the single greatest predictor of uncaring, unkind, and uncompassionate behavior, even among people who have devoted their lives to the welfare of others, is a perceived lack of time — a feeling of being rushed. The sense of urgency seems to consume all of our other concerns — it is the razor’s blade that severs our connection to anything outside ourselves, anything beyond the task at hand, and turns our laser-sharp focus of concern onto the the immediacy of the self alone."

I encourage you to read her full post and ponder how the Power Paradox might (or might not) apply to our new and larger roles in infection prevention. For example, I've noticed during discussions at national meetings and in peer-reviewed publications that we're blaming healthcare workers if they don't wash their hands or criticizing physicians if they overprescribe antibiotics. Keltner suggests that the Paradox can be handled by putting our focus on other people including empathizing, giving, expressing gratitude, and telling stories. It might seem that our focus on others (patients) might protect hospital epi folks, but what about the people we need to work with if we're to be successful - other healthcare workers?

Excess Mortality in CRKp: A Non-Randomized (Fortunately) Trial

Understanding the burden of antimicrobial resistance is critically important if we are to appropriately target research and clinical resources. For years, lack of proper estimates of the morbidity, mortality and costs associated with multidrug-resistant bacteria greatly limited the attention paid to these pathogens. This changed with the 2013 CDC Antibiotic Resistance Threats Report which provided the public with the number 23,000.  In the report, carbapenem-resistant Klebsiella pneumoniae (CRKp) was estimated to cause 7,900 infections and 520 deaths per year. But questions remain: Is the 6.5% (520/7900) mortality estimate high or low and how can we estimate the burden of resistance since we can't (fortunately) perform randomized trials where we randomly infect patients?

To answer these important questions, a group of investigators formed The Consortium on Resistance against Carbapenems in K. pneumoniae (CRACKLE) and just published a cohort study in Clinical Microbiology and Infection. This group, of what appears to be 18 Great Lakes hospitals, prospectively collected CRKp BSI (N=90), pneumonia (N=49), and UTI (N=121) isolates along with a control group (N=223) of patients with CRKp urinary tract colonization. The use of patients colonized but not infected with the pathogen as controls is interesting. The authors explain that they chose these controls since "non-infection-associated contribution to overall mortality is relatively larger in patients colonized with CRKp compared with patients colonized with more susceptible organisms, since risk factors for mortality such as chronic and acute illness, overlap with risk factors for CRKp colonization. An estimate of this non-infection-related mortality may be approximated in patients who are colonized, but not infected with CRKp." This is another way of saying that they wanted to isolate the attributable mortality risk of infection, not underlying disease.

The primary outcome was time-to-hospital-mortality from the time of the first positive CRKp culture as calculated by an adjusted hazard ratio using Cox proportional hazard models. I've included the unadjusted outcomes below. The full paper includes separate models and Kaplan-Meier curves for each infection, which don't differ greatly from the unadjusted outcomes.

As you can see, 39% of both BSI and pneumonia patients died or were transferred to hospice care compared to 12% of controls giving an attributable mortality of 27% for CRKp infection. In the Cox models, the adjusted hazard ratio was 2.59 (1.52-4.50) for BSI and 3.44 (1.80-6.48) for pneumonia. In contrast CRKp UTI was protective in both the unadjusted (3% lower mortality) and adjusted (aHR=0.68, p=0.33) analyses. This is further evidence that we need to rethink our definitions and focus on UTI.

Overall, a very nice study that utilized a novel control group of patients colonized but not infected with the organism of interest. It is likely that this approach when coupled with multivariable analysis reduced the effects of measured and unmeasured confounders. And it looks like CDC should increase the attributable mortality from 6.5% in their 2013 report to something a bit higher - say 27%.

Public Reporting - Do we need big brother?

I was fortunate to be an invited speaker at the 2016 ECCMID meeting in Amsterdam last week. My topic was "Monitoring Process of Care: Do We Need Big Brother?" I used the opportunity to take a big picture view of public reporting of HAI and MDRO data in the US and Europe and a closer look at the selection of process versus outcomes measures for reporting. I've posted my slides below and you can also listen to my talk on ECCMID's website. As I believe Dan stated earlier, I hope that all meetings evolve to allow free/open access to presentations like ECCMID has.

Coordination of what?

I’m glad that the new CDC Vitals Signs report, based upon a modeling study of the impact of regionally-coordinated interventions to reduce healthcare associated infections (HAIs) due to selected multiple drug resistant organisms (MDROs) and C. difficile, is gaining some media attention. The investigators modeled three different scenarios for control: (1) status quo, (2) “augmented” efforts at selected individual facilities, and (3) augmented activities coordinated across a health care network. Using data from various sources to inform the model (Emerging Infections Program and National Healthcare Safety Network for disease burden; Orange County, California and the VA system for patient movement across healthcare facilities; and experience from the UK and Israel for reductions in MRSA, C. difficile, and carbapenem-resistant Enterobacteriaceae (CRE) after national interventions), the model suggests that prevention approaches coordinated by public health authorities could reduce HAIs due to CRE by 55-74%.

This analysis has several limitations, most of which are pointed out by the authors in their discussion—models are models. And I don’t think anyone disagrees that coordinating infection prevention activities across healthcare systems is a desirable goal. The sad fact, though, is that we are very far from achieving this goal. I think Judy Stone has a good take on this, here. Furthermore, even if public health funding were increased enough to provide resources for state and regional coordination of MDRO control, the impact would depend upon each facility’s capacity to implement basic infection control practices (as the authors point out, “Optimizing implementation of basic infection control practice within individual facilities will be of fundamental importance to this effort”).

So while we wait for the inevitable boost in public health funding that is sure to come from our current Congress, we should remain focused on improving the basic “horizontal” infection control practices of individual facilities. It is not possible to know in advance which patient harbors a life-threatening bacterial pathogen (resistant or not), so it is best to assume that everyone does.

The limitations of patient-centered infection control

"You can't just ask customers what they want and then try to give that to them. By the time you get it built, they'll want something new." - Steve Jobs

I woke up to Vineet Chopra and Sanjay Saint's editorial advocating for a patient-centered approach to selecting clinician attire. In the editorial they point out that in the 21 of 30 papers they reviewed "patients had strong preferences about what physicians wore. And it looks like patients more often prefer for their doctors to wear formal clothing and white lab coats than not." They also reference the SHEA guidance document on healthcare attire and state there is little evidence "that germs on male doctors’ neckties, long sleeves, or white coats actually spread infections in a nonsurgical setting. So bans on such garments, such as those in place in some countries, may go too far."

So how can we decide what the safest attire is for our patients? I would recommend epidemiological studies that track bacteria spreading in hospitals and attempt to determine if those same strains are contaminating clinician attire using whole genome sequencing.  In fact, CDC released a SHEPheRD Task Order 2015-006 last month that seeks to do just that and more. I very much look forward to the results.

Drs. Chopra and Saint recommend a different patient-centered approach as they "plan to survey thousands of patients from the US, Italy, Switzerland and Japan" and "will specifically assess how factors such as age or how often a person interacts with the health system shape patient opinions." Is this a rigorous or unbiased method? Will the surveyed patients know that a quarter of white coats are coated with invisible S. aureus or MRSA and that they are rarely washed? Will they understand that a lack of data supporting transmission from white coat or long sleeve or neck tie is because no one has ever funded such studies? Will they understand that the circumstantial evidence supporting bare below the elbows is as strong as that supporting a clean environment in hospitals? Will their next editorial say that bleach is stinky and irritating to patients, so we shouldn't use it in hospitals unless supported by a patient-centered survey?

Thus, there are several potential limitations to patient-centered infection control and the planned physician attire survey, which I hope they will consider before collecting data and selling the findings. I'm all for patient-centered healthcare where applicable and data are fairly presented to patients and I support evidence-based medicine when we fairly rate the science based on what studies have been funded or will ever be funded. I'm not sure any patients "feelings" about the dirty white coat are worth the increased risk of MRSA or Acinetobacter infection, but we can disagree. All I would ask is that if we do patient-centered research, it's with properly informed patients.

***
Oh, and if we're going to require evidence before making physician attire recommendations, how can the authors write that "scrubs do not belong outside the hospital environment. Especially not in the grocery store." Where is the study that scrubs spread bacteria outside of hospitals and that there is any risk to population health in grocery stores? Clearly the bacteria on cantaloupes are riskier than those on scrubs! And surely the immobile ICU patient with central venous and urinary catheters is at greater infection risk when you wipe your MRSA-contaminated white coat on their catheter than when you brush up against a healthy grocery store patron with your scrubs? Scrubs are at least washed daily - white coat laundering occurs somewhere between every two weeks and... never.

*****
Additional thought, I am not aware that the US, Italy, Switzerland and Japan have mandatory bare-below elbows policies. It might be important to add Scotland or England to the survey since they have had BBE policies for some time and patients may have adjusted their preferences for physician attire.

Numbers Matter: Why counting only resistant bacteria ultimately harms our patients

You've seen the numbers. The CDC estimates that 23,000 deaths are caused by antibiotic resistant pathogens annually and as many as 14,000 of these deaths are linked to C. difficile. Every time I look at those numbers, they make me incredibly sad. First, they include all C. difficile deaths and not just those attributed to fluoroquinolone-resistant C. difficile, for example. This tends to incorrectly overweight the importance of C. difficile relative to other pathogens. Second, and you've heard me rant about this before, they only count deaths caused by the small proportion of bacterial pathogens that happen to be resistant, as narrowly-defined. This would tend to diminish the importance of bacterial pathogens compared to other causes of death (e.g. accidents). But I'm getting ahead of myself.

The numbers I'm about to throw at you are very rough estimates. I'm using these estimates to illustrate a point and hope that others will eventually provide more accurate estimates. If you think I need to correct a specific number, let me know in the comments, and I'll do my best to make the change - but I'm not promising. 

Let's take S. aureus as an example. The CDC estimates that 80,000 infections and 11,000 deaths are attributed to MRSA each year. In 2005, they also estimated that MRSA was associated with 18,650 deaths, but I'll be conservative and stick with 11,000. Per this 2013 NHSN report, the proportion of S. aureus that were MRSA ranged from 43.8% (SSI) to 58.7% for CAUTI. I'll use the lower proportion (44%) since this allows for some mortality secondary to more community (less MRSA) infections. However, I suspect most patients that die from S. aureus infection will ultimately be hospitalized. For simplicity, I will also assume that MRSA is twice as lethal as MSSA (AKA penicillin-resistant S. aureus).

Taking the above numbers, if there were 80,000 MRSA infections, we would expect 102,648 MSSA infections. If the mortality rate for MRSA was 13.75% (11,000/80,000) then MSSA's mortality rate would be half of that or 6.875%. So there would be 7057 deaths from MSSA. If you add that to the 11,000 you get 18,057 deaths due to S. aureus. We can quibble about numbers, but I suspect that 7,000 deaths caused by MSSA, passes the so-called giggle test.

Thus, if we used the CDC rankings to fund research and prevention activities, we would rank C. difficile at the top of the report. However, if we used my ranking system, S. aureus (MSSA+MRSA) ranks ahead of CDI. Since most interventions to prevent MRSA deaths would also work against MSSA (vaccines, new antibiotics) shouldn't both types be included in burden of disease estimates? The imbalance gets worse when you look at Gram-negative infections. Do we really only care if grandma dies of the 2-12% of E. coli or Klebsiella that are resistant to carbapenems? Do we really only count the 610 deaths from CRE and 1700 from ESBL? Clearly it would be better if we counted all deaths from E. coli and Klebsiella and projected a future where almost all strains would be ESBL or CRE.  This would allow us to make better decisions regarding current and future research priorities and prevention efforts.

I suspect if the S. aureus mortality estimate jumps from 11,000 to 18,000 when counting MSSA, it's not a stretch to imagine that deaths from bacterial infections would approach 100,000 in the US. If we count attributable mortality appropriately, deaths from bacterial infections would be a top 10 cause of death in the US. Top 10 means more money for research and prevention. Let's get these numbers right - grandma is counting on us.

What we talk about when we talk about MDR-GNR

I’m supposed to give a talk at SHEA 2014 on “Lab Identification and Surveillance for Multidrug-Resistant Organisms” (that title is a real barn-burner, right?). I dashed off material on MRSA and VRE pretty quickly, but got bogged down fast when I hit the category of “multidrug-resistant gram negative rods (MDR-GNR)”. Why? Two major reasons: (1) MDR-GNRs encompass a vast array of different species, each with its own bag of tricks, and (2) most labs are underprepared to accurately detect and characterize the most fearsome of the MDR-GNRs (e.g. carbapenemase-producing Enterobacteriaceae (CRE)). Therefore, it is a major challenge to even define what we are talking about when we talk about MDR-GNRs.

One of the articles in the current special issue of Infection Control and Hospital Epidemiology drives this point home nicely. In a survey of hospitals in the SHEA Research Network, Marci Drees and colleagues tallied 14 unique definitions for MDR-Acinetobacter, 18 for MDR-Pseudomonas, and 22 for MDR-Enterobacteriaceae (that’s a lot of definitions for just 66 responding hospitals!). There was similar variation in what these hospitals did when MDR-GNRs were identified (isolation practices, cohorting, etc.), and in how equipped laboratories were to find the organisms of greatest interest (e.g. CRE). This isn’t an indictment of the hospitals or their labs, it simply reflects the fact that drug-resistance among gram-negative organisms is extraordinarily complex, and the molecular methods needed to rapidly characterize the most troublesome organisms are beyond the reach of most clinical labs.

In the absence of affordable commercial methods for detection of common MDR-GNR resistance mechanisms, we desperately need to develop a network of specialized regional referral labs that can quickly characterize pathogens submitted from clinical laboratories. Whole-genome sequencing could be introduced in such labs as a first step to wider adoption and development of automated data interpretation software. Let’s hope that the $30 million CDC budget allocation for responding to antibiotic resistance will move us in that direction.

Image from Wikipedia Commons

Resistance versus Virulence

The conventional wisdom is that bacteria pay a “fitness cost” as they accumulate antibiotic resistances, a phenomenon I discussed in a short post last year. More resistant, but less fit, and (one hopes) less virulent. Thus some of the most problematic multi-drug resistant organisms (MDROs), such as Acinetobacter, cause disease almost exclusively in the most vulnerable patients—those bugs simply aren’t virulent enough to wreak their havoc in the healthy. When an MDRO does emerge as a major community scourge, as was the case with community-associated MRSA, it’s big news.

So I was surprised (not pleasantly) to read this report in PNAS about Pseudomonas aeruginosa strains that refused to adhere to convention. Using a mouse model and well-characterized P. aeruginosa mutants, the investigators found that strains with mutations in a gene encoding a particular outer membrane protein (one that provides an entry channel for carbapenem antibiotics) were more virulent—more likely to disseminate from the mouse GI tract, and more resistant to in vitro killing by acidic conditions or human serum. Now mice are not men, and a murine gut colonization model isn’t necessarily predictive of an organism’s ability to cause infection at various human body sites. Still, it is nerve-wracking to know that our carbapenem use might produce P. aeruginosa strains that are not only more resistant, but also more virulent! As the title of the accompanying editorial points out, it is indeed a “worst case scenario”.

Scanning EM of P. aeruginosa from the Public Health Image Library

Search and destroy is so last century...

A few weeks ago, Dick Wenzel and I responded to a letter in the New England Journal of Medicine regarding our editorial on Susan Huang's paper on targeted vs universal MRSA decolonization. We have long argued that active detection and isolation (AKA search-and-destroy, a vertical strategy) wasn't a necessary or particularly wise approach. A letter refuted this. In our response, we stated:

The key question remains: given an optimally functioning horizontal program (i.e., near perfect compliance with hand hygiene and chlorhexidine bathing), what is the incremental benefit of a superimposed vertical strategy?

Voila! A new study in Lancet Infectious Diseases by Marc Bonten et al addresses our question. In this 3-year study in 13 European ICUs, involving over 8,500 patients, there was a baseline data collection phase (6 months), followed by a hygiene improvement phase (hand hygiene campaign + universal chlorhexidine bathing for 6 months), followed by cluster randomization to a rapid screening group + contact precautions for carriers or a conventional screening group + contact precautions for carriers. Both screening groups used chromogenic agar to detect MRSA, VRE and ESBL; the rapid screening group also used PCR testing for MRSA and VRE. Primary endpoints were the acquisition of MRSA, VRE or MDR-GNR.

The study showed:

• Hand hygiene increased from 52% in phase 1, to 69% in phase 2, and 77% in phase 3.
• Chlorhexidine bathing was 0% in phase 1, and 100% in phases 2 and 3.
• Improved hand hygiene + chlorhexidine bathing (phase 2) resulted in a significant decrease in MRSA acquisition, with no change for VRE or MDR-GNR.
• Neither search-and-destroy strategy resulted in any further reduction for any of the targeted pathogens.
• There was no change in the prevalence of chlorhexidine resistance genes in MRSA isolates in phase 1 vs. phase 3 (13% vs 14%).

So we now have another study demonstrating the lack of need for active detection and isolation to control multidrug resistant pathogens. Will the search-and-destroyers finally pack it up and go home?

Photo:  Jeff Swensen, New York Times

The ghosts of the "prior room occupant"

"Well, you know, Doc, when something happens, [it] can leave a trace of itself behind. Say like, if someone burns toast. Well, maybe things that happen leave other kinds of traces behind. Not things that anyone can notice, but things that people who "shine" can see….I think a lot of things happened right here in this particular hotel over the years. And not all of 'em was good."

-From the movie The Shining, 1980 

I’m reviewing papers for a talk I’m preparing on “control of multiple drug resistant gram negative rods (MDR-GNRs)”. So I’m looking again at a set of studies that always scare me (even more than a Stephen King novel)—those that demonstrate that a variety of bad bugs (C. difficile, MRSA, VRE, and MDR-GNRs) can be “left behind” after a patient is discharged, poised to colonize or infect the next occupant of that hospital room. It is a scandalous indictment of current hospital disinfection practices that patients must be haunted by the pathogens of the previous occupant of their hospital bed! 

There are still some practical (and financial) hurdles that must be overcome before new disinfection technologies (UV light, H2O2 vapor, antimicrobial surfaces, etc.) become standard of care. In the long run, though, I think that’s where the future lies—excellence in cleaning will remain important (organic debris will always require removal), but for microbial eradication in the environment, these technologies are going to replace our existing, more rudimentary approaches.

Montgomery County is now in the loop!

The next time a contagion sweeps through the NIH Clinical Center, Montgomery County officials will be on it, thanks to a new agreement between NIH, Maryland and Montgomery County. The back-story is that Montgomery County officials were unhappy that they weren’t informed promptly about the deadly KPC outbreak at NIH.

This raises the question of when a hospital should communicate with public health officials (and the public generally) about fairly common SNAFUs. At any given time, 5-10% of hospitals are dealing with clusters or outbreaks of multiple-drug resistant gram negative bacteria (KPCs, ESBLs, MDR-Acinetobacter, etc.), and even more are in the midst of MRSA, VRE, fungal or other outbreaks. The population at risk during these outbreaks is pretty clearly defined, and doesn’t include the general public. General notification can generate media frenzy, free-floating panic and anxiety, and waste precious time and resources for the personnel trying to contain the outbreak (responding to media, doing damage control of various types, etc.). Furthermore, most states don’t include common healthcare associated bacterial pathogens among their legally reportable diseases.

However, as state and local public health officials become increasingly involved in HAI issues, it would be wise to establish explicit criteria for when healthcare facilities should report clusters and outbreaks. Provided they have sufficient funding (which they currently do not!), public health departments should play a critical role in coordinating responses to HAI outbreaks, which often involve multiple healthcare facilities in a region (across the spectrum of acute, long-term, and long-term acute care).

So when do you think a hospital should notify their state and/or local public health department? Two cases of MRSA infection in the NICU? A single serious post-operative Group A strep infection? New introduction of a carbapenemase into the ICU?

Oh, and Happy Thanksgiving!

The boiling frog and antibacterial resistance

I just returned from IDWeek in San Diego (as many of you have). I will say that it wasn't the same as having a standalone SHEA meeting - fewer impromptu hotel lobby discussions and few Europeans - but it had its moments. For one, the sessions were better attended - I think many ID physicians who would normally not travel to a spring SHEA meeting, wandered into infection prevention sessions. Perhaps they direct the infection control committee at their hospital and wanted an update. It was also interesting to see the community protesters out in force; we don't get that kind of attention in infection prevention...but perhaps we should.

The Lyme disease guideline protesters did get me thinking about community action and infection control and why we don't get that kind of attention.  The early nineties saw plenty of HIV/AIDS protests and now that MRSA alone is associated with similar mortality (imagine if you add MSSA, VRE, KPC, NDM-1, ESBL, MDR-acinetobacter), I wondered if and when the public and clinicians would wake up to a world without antibiotics and get angry.  I know there are differences between the HIV and MDRO epidemics. Yes, HIV is a single virus that struck young people down in the prime of their lives, but with MDROs we're facing a world with unsafe surgery (or no surgery), death during neutropenic fever and perhaps fewer transplants. So why is there such a huge difference in our responses?

I think a major reason that MDROs attract little attention is that the emergence of resistance occurs too gradually. A useful metaphor in this case is the boiling frog.  The story goes that if you place a frog in boiling water, it will immediately jump out, but if you place it in cool water and slowly turn up the heat, it will be boiled alive. Since carbapenem-resistance Gram-negatives didn't just appear one day like HIV, we see less response to the problem. We had penicillins to protect us and when they failed we had cephalosporins and then when they failed we had the carbapenems. The problem is, we stopped investing in antibiotic discovery 30 years ago, and there is nothing after carbapenems. So now, we must wait 10-20 years for new antibiotics and we MUST invest in infection prevention research and implementation. I think MDROs are due for a protest movement, but it probably won't appear. We all love a good warm bath, now don't we.

Call me when your disease kills more than HIV….

HIV has become the standard against which all infectious public health threats are now measured. First with MRSA, now with hepatitis C virus (HCV), the media are abuzz with the news that another infection kills more people than HIV does. There are many reasons for this meme, perhaps the most instructive is that the resources put into research and prevention efforts for HIV are astronomical compared with those for many other infectious disease threats (a point Eli has made clearly). This investment has paid off, too, in the form of steadily falling HIV-associated mortality rates in developed nations. I look forward to the day when shark attacks, or “events of undetermined intent”, kill more people than HIV. Check out Table 2 in this document to see if your disease-of-interest kills more than HIV.

Maybe if we invested as much in research and prevention of multiple-drug resistant bacterial infections and other healthcare-associated infections, we’d see similar success.

The dirty curtain story

We recently began a study of microbial contamination of hospital privacy curtains (a study funded by one of several manufacturers of an antimicrobial fabric). The comparative study is ongoing, but the “baseline” sampling confirmed what Curtis Donskey’s group has already described: hospital privacy curtains are often contaminated with bacterial pathogens (the main additional findings from our study have to do with how quickly the curtains become contaminated (spoiler alert: very quickly), and how some organisms persist on curtains over time). Figuring the results might generate some interest among a few attendees, and perhaps spark some useful discussion of this and other environmental infection control issues, we decided to submit the baseline data to ICAAC. We had yet to learn this valuable lesson:

Never underestimate the media’s fascination with the presence of bacteria on inanimate objects.

Stethoscopes, ties, white coats, rings, cell phones, you name it. If you want media attention, grab some swabs, head up to your nearest patient care unit, and find some new object to culture! By Friday after ICAAC, the story had been picked up by CBS News, Reuters Health, Fox News, etc., etc. (I can’t bother with all the links, just type “privacy curtain” into Google News). It has turned into a minor annoyance, as we seek to put these findings into perspective in our own hospital, and navigate the obvious conflict-of-interest inherent in managing the findings of a study sponsored by an industry that has a vested interest in the outcome.

So, what are the implications of this study? Most importantly, consider privacy curtains to be like any other high-touch surface in the patient environment, and perform hand hygiene after contact with the curtain. This can be a real challenge in an ICU environment that doesn’t have private rooms, so other approaches seem wise as well: more frequent cleaning/changing of curtains (in most hospitals they are changed only when visibly soiled), use of a “pull rod” or other plastic object to allow one to pull the curtain around without touching the fabric (the plastic surface can be more easily disinfected), or use of other barriers (e.g. glass doors that turn opaque). There’s a burgeoning interest in antimicrobial fabrics (not just for this purpose, but for healthcare worker clothing, etc.), and these may also play a role. Finally, Mike’s prior posts on single patient rooms are pertinent—well-designed private rooms can obviate the need for frequent use of privacy curtains.

Things that make you go "hmmm"...

I’ve been in an undisclosed location for the past week or so. Hint—if I were to hop on the above watercraft and drive directly across the above body of water, I’d be in the city that in the Potawatomi language translates (roughly) as “fine land”.

In among my beach reading I ran across this article, about a recent biowarfare exercise:

“AVI BioPharma, Inc., and the Naval Research Center recently announced the successful completion of a rapid-response exercise conducted by the Joint Project Manager Transformational Medical Technologies…..In a total of 18 days, AVI conceived, designed and manufactured two novel RNA-based drug candidates, one against a Gram negative bacterial target and one against a viral target.”

Eighteen days to conceive, design and manufacture a drug active against a Gram negative pathogen! Meanwhile, the only option for treatment of many multiple-drug resistant Gram negative infections is a drug that’s over 50 years old.

Changing the equation?

Remember Eli’s post from last month, about a tipping point at which the risk for a multiply-drug resistant infection begins to outweigh the benefit of a “discretionary” surgical procedure? I thought about that when I read this report about MDR-GNR sepsis after prostate biopsy, which may lead to a re-evaluation of PSA screening guidance. Hat tip to Jason Barker for sending me the link. The two money quotes:

“We’re all beginning to see more and more sepsis as a result of resistant bacteria after prostate biopsies,” said Peter T. Scardino, chief of surgery at the Memorial Sloan- Kettering Cancer Center in New York, which does about 2,000 of the tests annually. “This is an extremely worrisome problem”

........

“There has been this huge enthusiasm for everyone getting their PSA checked, which has led to a lot of prostate biopsies that have not benefited anyone,” said James R. Johnson, an infectious diseases physician at the Veterans Affairs Medical Center in Minneapolis. “The more dangerous the biopsy becomes because of infection risk, the more likely it is that the balance is shifting toward harm, rather than benefit.”

David Livermore fights NDM-1, the 'super' superbug

David Livermore and NDM-1

There is a new story at MSNBC.com highlighting David Livermore, NDM-1, and the myriad of reasons for the expansion of MDR-bacteria and hospital infections: little investment in antibiotic discovery and infection prevention.  I like this quote from the article in regards to infection prevention: "If it is done properly, it can ease the demand for drugs in the first place."  Dr. Livermore is the Director of the Antibiotic Resistance Monitoring & Reference Laboratory (ARMRL) at the HPA Centre for Infections in London. The story is surprisingly well-written, includes the usual human-interest angle and quite long but worth a read.

h/t Mark Vander Weg

Sensitivity of perianal swabs for MDR-GNR

Quick last abstract from ICAAC.  Graham Snyder et al. from Beth Israel Deaconess Medical Center in Boston enrolled 35 patients with known multidrug-resistant Gram-negative bacteria in clinical cultures (Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Enterobacter cloacae, Proteus mirabilis, and Morganella morganii). Each patient received a perianal swab. The sensitivity was 79%. It was a small study with the usual caveats.

Conflict of Interest: Graham was a medical resident that I worked and published with at Maryland.

link to medpage article