The role of weather, season and climate in HAI

The recent attention given to climate change served as a backdrop to this talk (slides posted below) that I just gave at ICPIC in Geneva. ICPIC has been a wonderful conference and it was a nice forum for discussing the larger, international issues hindering HAI control. I look forward to seeing everyone again in two years.

The beginning of the end for...CHG??

Chlorhexidine. We love it, we just can't get enough of it, we are up to our neck in it and we cheer for it. Basically it's the greatest. But some of us have been concerned that the widespread use of CHG would lead to resistance, particularly in Acinetobacter.

There is a new report in PNAS by investigators in Australia and the UK that looked at gene expression in A. baumannii after chlorhexidine exposure. The most highly up-regulated genes were those encoding the RND efflux system AdeAB. Importantly, the investigators also identified a gene encoding a previously uncharacterized membrane protein, AceI, which they determined to be an active CHG efflux protein capable of transporting CHG out of the cell. This novel AceI was said to be a member of the PCE family of efflux systems.

And to give you a sense of the ubiquity and potential importance of these systems in Gram-negative bacteria, I offer this quote from the authors:

"The primary features of the A. baumannii chlorhexidine resistance response, i.e., up-regulation of genes encoding RND and PCE family efflux systems, are conserved in other γ-proteobacteria, as well as β-proteobacteria. Given the phylogenetic distance of these organisms, this similarity of regulatory responses to a compound that has only been synthesized since the early 20th century is intriguing. RND efflux systems are well recognized for their broad protective functions in Gram-negative bacteria and it is not unusual for these systems to constitute part of a general stress response and to mediate resistance to foreign compounds, particularly amphipathic antimicrobials such as chlorhexidine. However, the involvement of the PCE family proteins in seemingly specific resistance to chlorhexidine is unexpected. It is likely that the physiological function(s) of this transporter family were originally unrelated to chlorhexidine resistance and that these proteins provide a fortuitous intrinsic resistance capacity."

h/t Ayush Kumar and Dan Ricciuto

image source: wikipedia

A tale of two outbreaks

Less than two weeks ago, we blogged about the KPC outbreak at the NIH Hospital. This outbreak garnered a lot of media attention, most of which was positive and highlighted how the epidemiologists at NIH worked to control the outbreak, as well as the relatively novel application of whole genome sequencing for outbreak investigation.

Today, the Daytona Beach News Journal reports on a local nosocomial outbreak of Acinetobacter infections. The article as well as the state health department report can be viewed here. Unfortunately, the hospital appears to have had problems with its infection prevention infrastructure that undoubtedly impacted its ability to control this difficult pathogen.

So what are the take home messages from these two outbreaks?

1. The general public is highly interested in hospital infections and the mainstream media finds them to be quite juicy
2. Transparency is paramount
3. Infection Prevention Programs are enormously important patient safety programs that must be funded and staffed to maintain their effectiveness. 

Photo: Acinetobacter. Janice Carr, CDC.

HAI Rates are a Red Herring

"Fictional" Hospital CMO: "Why should I care about hand hygiene or environmental cleaning if I have no CLABSI or CAUTI in my hospital?"

Don't take this the wrong way, since I'd never want a patient to develop a CLABSI or VAP, but I think our focus on device infections is actually harming patients in the long run. If we convince ourselves, like that CMO quoted above or QI and patient safety folks, that we can just prevent device infections (never mind define them away) and everything will be fine, we are missing the bigger picture. The bigger picture is antibiotic resistance and I've yet to see any evidence that our antibiograms are improving.

When did hospital epidemiologists forget we were infectious disease physicians?

In September's ICHE Kerri Thom and colleagues in Maryland published a sobering reminder that resistant pathogens are increasing, particularly Gram-negative pathogens. They (COI alert, I'm a co-author) completed an Acinetobacter baumannii prevalence survey of all mechanically ventilated patients in the state of Maryland. They swabbed intubated patients in 40 of 57 hospitals and collected sputum and/or perianal swabs from  92% of all eligible patients in those hospitals.  What they found was staggering.  Fully 34% of patients were colonized or infected with Acinetobacter baumannii with 16% in acute care settings and an astounding 63% in long-term care settings carrying the pathogen. Even more worryingly, many strains were highly drug resistant with 46% of isolates in long-term care described as "extensively drug resistant," meaning there were no effective therapies - polymixin anyone?

Why does this matter?  Resistant pathogens cause untreatable infections and result in terrible situations like patients being removed from organ transplant waiting lists. These pathogens also carry resistance genes and serve as reservoirs for emerging resistance in other pathogens like E. coli. So, while I'm sure these Maryland hospitals all report zero CLABSI or CAUTI, I guarantee that they all have patients infected and dying of Acinetobacter baumannii and other MDR-Gram negative pathogens. Until we make investments in the science behind hand hygiene improvement, environmental cleaning and other methods for transmission prevention and until we invest in antimicrobial discovery, patients will increasingly die of these untreatable infections.

Luckily, when a kidney transplant patient dies of MDR-Acinetobacter sepsis, the hospital CMO can still sleep at night. At least the patient didn't die of a CLABSI.  I'm sure the patient's family will find comfort in that.


red herring image source: misocrazy

The Changing Face of Transmission Prevention

Yesterday I gave a talk at a 3-day VA-sponsored conference titled: "Infection Prevention and Control in the 21st Century - It's Everybody's Business."  It was a well-attended conference in Dallas. Most of the talks were titled: "The changing face of..."  I focused my talk on how novel MRSA strains, mupirocin resistance and the increasing importance of Gram-negative bacteria will result in a shift toward horizontal infection-control interventions. Please note that the VA MRSA Initiative actually included 3 horizontal interventions (hand hygiene, culture change and support for an MRSA coordinator) and only one vertical intervention (surveillance swabs and isolation), so VA has made great strides in implementing horizontal infection-control interventions.

Just a reminder that Dan, Mike and I have posted many of our recent talks in a section called "Presentations" down a bit on the right-side column of our blog.

Can you tell a hospital is safe by its "broken windows"?

This past weekend there were many discussions of James Q. Wilson's "broken windows" theory. Dr. Wilson, unfortunately, passed away this past week. The theory and research suggest that perception of a safe neighborhood prevents crime. If people feel they're in a safe place, they are less likely to commit a crime. If, however, they feel the neighborhood is unsafe or crime-ridden, they're more likely to commit crime. Thus, under this theory, police forces should arrest and prosecute even the smallest crimes, such as graffiti, and cities should quickly repair broken windows.

I lived in Rudy Giuliani's New York City during the implementation of this strategy, but I'm not here to defend his law enforcement policies one way or another, since I'm not an expert. Crime did fall, but it might have been for other reasons.  What I'm more interested in is if there could be an analogous theory in hospitals?  Is there a safe hospital theory?  It made me wonder if clinicians in safer or cleaner hospitals are more apt to practice hand hygiene or have higher compliance with CLABSI checklists.

I'm not aware of much data in this regard.  Two of the better analyses were done by Pat Stone's group at Columbia (I was a co-author). Looking at data from 415 ICUs in 250 hospitals they found that there was no convincing evidence of a cross-over effect between CLABSI and VAP; that is compliance with the CALBSI Bundle elements was never associated with a decrease in VAP rates.  In a separate paper, they found that compliance with the VAP bundle did not lower CLABSI rates. So for at least two device infections, there appears to be no such thing as a safe hospital. Lankford et al. in EID (2003) hypothesized that hand hygiene would increase after construction of a shiny new hospital. It actually decreased from 53% to 23%.  Hopefully Mike and Dan can add to this list of studies.

There has been a lot more research on what makes a quality hospital outside of infection prevention.  Twenty years ago, there was an important study in Medical Care that looked at disease-specific mortality in acute myocardial infarction, congestive heart failure, pneumonia, stroke, obstructive lung disease, or gastrointestinal hemorrhage in 30 hospitals. They found little correlation between disease-specific mortality rates within each hospital. So, MI mortality was not correlated with CHF mortality, even if they were likely to be treated by the same physicians and nurses. If mortality isn't a quality indicator, one wonders if other quality indicators have any relevance.

And what is a post without a non-scientific anecdote? Several years ago, when I was the hospital epidemiologist at a large hospital in Baltimore, we had high rates of MDR-Acinetobacter infections. This led our group to conduct a pilot study looking at the impact of universal gown and gloves in ICU-settings. At the time a new Chief Medical Officer, who happened to be a pulmonary-critical care specialist, started attending in our ICUs. He was struck at the level of gown/glove compliance that he saw and declared that he had never seen such a safe hospital. This actually meant something, since he had just moved from Barnes Jewish Hospital in St. Louis; home to one of my heroes, Vicki Fraser.  Were we really safer than BJH? I don't know, but the sight of all of those gowns and gloves did make it appear that we were really trying our best to be safe. Soon after, our CLABSI rates fell drastically, after a lot of effort sure, but the culture was changing. Maybe there is something in this theory that applies to hospitals after all? Too bad there appears to be no such thing as a "safe" hospital.

Weekend Update: Almost Thanksgiving Edition

Batterio killer al II Policlinico: due bambini fuori pericolo
„Il Secondo Policlinico: Source NapoliToday“

Leggi tutto: http://www.napolitoday.it/cronaca/batterio-II-policlinico-neonati-fuori-pericolo.html
Diventa fan: http://www.facebook.com/NapoliToday

Just some random stuff for your enjoyment while you're running around trying to get everything ready before you (a) are invaded by family/friends or (b) invade family/friends or (c) both.

#1: Recently, there was a serious outbreak of Acinetobacter infections in the neonatal care unit of Batterio killer al II Policlinico: due bambini fuori pericolo
„Secondo Policlinico di Napoli, which resulted in the closure of the unit/department/hospital depending on the report you read. English or Italiano

h/t Maryn McKenna

#2: November 14-20, 2011 is Get Smart About Antibiotics Week. SHEA, APIC and IDSA all support this effort and so do we. See also the CDC Get Smart website.

#3: CDDEP has a new ResistanceMap showing US antibiotic prescriptions per capita at the state level. Each state's use is listed.  The worst offender: West Virginia which uses approximately 1.2 antibiotic prescriptions/person. Alaska has the lowest use with about 0.5 prescriptions/person. Where does your state rank? Check out CDDEPs map!

#4: Scientific America has an interesting post by Katherine Harmon reviewing two recent Science papers.  There is new evidence as to how S. aureus, E. coli and P. aeruginosa respond to stress and how this new knowledge might be exploited to enhance existing antibiotics. Shatalin et al. Science 18 November 2011: Vol. 334 no. 6058 pp. 986-990 and Nguyen et al. Science pp. 982-986

 “

Climate change and hospital pathogens

Do hospital pathogens like living in a Greenhouse?

Nothing should dare threaten your coffee.  So when Starbucks announced today that global climate change is threatening coffee supplies, you knew it would get media attention. What's a journalist without their coffee and cigarettes? (aaaack) What about hospital pathogens? Could climate change impact hospital infection rates. We thought it might. (Note: by we, I mean my colleague from Maryland Judy Johnson - She's now in Gainesville).

Back in 2006, Judy and I were sitting on a park bench (it was a nice day) discussing the upcoming ICAAC abstract deadline and pondering what we should submit, when she suggested we look for seasonal variation in Gram-negative pathogens.  Judy mentioned some data suggesting Gram-negative infections were more common in tropical countries and we also discussed the high incidence of Acinetobacter infections in troops returning from Iraq. Sure, we also knew that others had noticed summer peaks in certain pathogens, but the prior research didn't control for meteorologic factors and also combined summer data from across the entire US (hint: Maine ≠ Texas). Thus, we felt there was room for further exploration.

In our initial analysis, published in ICHE (2008), we reported that summer season (vs. winter) was associated with 28% more P. aeruginosa, 46% more E. cloacae, 12% more E. coli and 21% more A. baumannii clinical cultures over 8 years. Importantly, we found that for each 10°F increase in temp, there was a 17% increase in the monthly rates of infection caused by P. aeruginosa and also A. baumanii. Of course, this was a single center study, so we needed more proof.

Mike Eber and our group have just published a follow-up study in PLoS One looking at BSI data from 132 hospitals over 8 years. Using 211,697 inpatient blood isolates, we again found that Gram-negative organisms were more frequent in summer months ranging from 12.2% higher rates for E. coli to 51.8% higher for Acinetobacter spp. And more interestingly, we reported that independent of season, monthly humidity, monthly precipitation, and long-term trends, each 10°F rise in mean monthly temperature was associated with higher Gram-negative bacterial BSI frequencies ranging between 3.5% for E. coli to 10.8% for Acinetobacter spp.  Thus, warm temps = more Gram-negative bacteremias; that is, even a warm winter is a bad thing.  Lots more work to do to figure out why this might be, but I think it's an interesting first (or second) step. Cheers.

Note: Special thanks to Ramanan Laxminarayan and Extending the Cure for supporting this project.

Your dirty laundry

Photo:  Mary Ann's Cupboards

There's a new paper in Infection Control and Hospital Epidemiology that includes a series of experiments designed to evaluate the effectiveness of laundering scrubs in your home washing machine. This is important since most healthcare workers who do not work in the operating room launder their own scrubs at home, and some hospitals even have OR staff wash their scrubs at home as a cost-savings measure. The major difference between home and hospital laundering is water temperature--hospital laundries typically use water temperatures of 160°F, whereas home washing machines are generally set to deliver water temperatures at 60-80°F (cold), 90-110°F (warm), or >130°F (hot).

Key findings were:

• Hot water (140°F) with or without detergent was highly effective in killing MRSA and Acinetobacter.
• Warm water (104°) with detergent was highly effective in killing MRSA and Acinetobacter. Without detergent, warm water was still highly effective against MRSA, but only moderately so against Acinetobacter.
• When clothes are washed with warm water but no detergent, they become contaminated with gram-negative organisms (Klebsiella, Enterobacter, Serratia) from the washing machine's biofilm, though washed clothes are largely free of gram-positive skin flora.
• When fabric swatches that were inoculated with Acinetobacter were ironed (on the iron's highest setting) with a contact time of at least 7 seconds, the organisms were killed.

So warm or hot water with detergent is your best bet (though I have to wonder who washes their clothes without detergent?). I do iron my scrubs, though many people don't, but I'm sure that my ironing contact time is less than 7 seconds, and some scrub fabrics can't tolerate the iron's highest setting.

Funding for antibacterial resistance research. Not so much.

At least no funding for ESCKAPE pathogen research

I just got back from attending the World HAI Forum in Annecy and the 1st ICPIC meeting in Geneva.  Both great meetings.  I will share my thoughts on the implications of ICPIC in a later post.

Last year at IDSA, Roy (Trip) Gulick stated that there are now 10,000 possible ART combinations for HIV treatment.  When he said that, I instantly got a sinking feeling in my gut.  Right now, there are many people colonized and infected with resistant bacteria for which we have NO EFFECTIVE THERAPY.  Sorry for shouting.  Think about the MDR-Acinetobacter or NDM-1 strains that are circulating.  Pretty soon we won't even have effective therapy for community UTIs.

As I thought about why this might be, I looked for the federal funding picture for antibacterial resistance research, but there were no published data.  So, we found the numbers ourselves.  I presented the data last week and Marin McKenna kindly described our findings at the World HAI Forum on her Wired Superbug blog.  She did a much better job describing our research findings than I could have.  If you're interested in reading about how much NIH/NIAID spends on antibacterial resistance research, head on over to her blog...

UPDATE:  We published these findings in the first batch of articles in the ARIC journal, see: Kwon et al. 2012 ARIC

Gloves and gowns are not enough...

Back at Maryland, we had a surgeon who always asked for evidence that hand hygiene was necessary if he wears gloves. We gave him some evidence, but like many clinicians, he wanted data from his own institution. I guess everyone is the exception. Like good soldiers, we proceeded to collect that data. We gathered a great team over the years - Graham Snyder, Stephen Liang, Catherine Smith, Hannah Day and others to approach healthcare workers (HCW) before they entered patient rooms and collect cultures on their hands before entry and gowns/gloves after exiting the room.

The initial study from this work was published by Graham Snyder et al in ICHE 2008. He reported that MRSA was detectable on 19% of gowns/gloves of HCW after exiting an MRSA+ patients room, while that result for VRE was 9%.

The latest report from this group published in this month's ICHE by Dan Morgan et al, provides somewhat more humbling data. HCW had MDR-acinetobacter on their gloves 36% of the time after entering a colonized/infected patient's room. Wow. But the truly humbling finding was that after removing their gloves, 4.5% of the HCW still had it on their hands. Thus, while gloves reduce contamination of hands by around 85% per contact, to achieve true infection prevention, HCW must wash their hands after they remove there gloves.

I have posted Table 2 from the paper, which shows the likelihood of HCW contamination that would occur at various levels of compliance with contact precautions and hand hygiene. Even with 90% compliance with both wearing gloves and hand hygiene, almost 1% (0.8%) of contacts would be expected to contaminate the HCW hand and place them at risk for contaminating other patients and the environment. Multiply that 1% (or higher if lower compliance exists) by the number of HCW that enter the patients room in a day and you have an estimate of the daily transmission of MDR-AB. This sort of data highlights the Achilles heal of active detection and isolation strategies. No matter how much effort and money go into rapid detection of MDR organisms, without 100% compliance to gowns and hand hygiene, the effort is wasted. We have shared this data with our favorite surgeon. The description of how that went must wait for another study, or at least another day.

Graham Snyder 2008 ICHE paper (here)
Dan Morgan July 2010 ICHE paper (here)

Move over, MRSA!

This morning's New York Times has a piece by Andrew Pollack on healthcare associated infections. That in itself is not a surprise anymore since the general public is quite interested in the topic. What is surprising is that the article isn't about MRSA--it's about Acinetobacter and the lack of effective drugs to treat multidrug resistant gram-negative organisms. Could this be a harbinger that the fixation on MRSA is starting to wane? Pollack remains, to my knowledge, the only journalist that has linked the frenzy to culture inpatients for MRSA with big profits by the companies who manufacture the MRSA testing kits.

A new MEGA SUPERBUG

As if on cue, the media is abuzz with a new dire threat. This time there is a mega superbug called MDR-acinetobacter. The good news is that David Paterson of the University of Queensland, has a new Australian government grant to assist in the development of new antimicrobials. He has received $2 million over 5 years to study this Mega Superbug. That's a new term for me. Perhaps if we have antibiotics to treat the infection they are just superbugs but if there are no effective antibiotics it becomes a mega superbug. I think someone should write a guideline to clarify this - but that would also take a $2 million grant, I suspect. There is a nice picture of David here for those of you, like me, who miss seeing him since he left Pittsburgh. I hope there is funding at NIH that can assist in drug discovery for MDR-Gram negative rods, since we don't have many options currently.