Infectious Disease Alert Updates
March 1, 2016 9 minutes read
PUT A LID ON IT
By Carol A. Kemper, MD, FACP
SOURCE: www.nanosafe1.com/blog/uncategorized/hospitals-miss-opportunity-to-help-put-a-lid-on-spread-of-hai/. Jan. 1, 2016.
This blogger suggests that hospitals, by using lidless toilets, have missed an opportunity to help control the spread of enteric organisms within their facilities. Numerous articles through the years have demonstrated the frequency of bacteria and viruses that may colonize toilet bowls, even after flushing. Bacteria literally adsorb to the porcelain surface of the bowl, with gradual reduction in colony counts with each flush. But even repeated flushing does not eliminate all bacteria. Recent data found that sustained spread of Salmonella in a number of households may have been the result of persistence of the organism in the biofilms under the recess of the toilet bowl — an impossible place to clean, if you’ve tried.
Further, aerosolization of bacteria and viruses from flushing is well recognized. Observations made of standard toilets found that 78% of adjacent surfaces and 81% of air samples were contaminated by enteric viruses after flushing.
One investigator simulated fecal samples containing C. difficile, and measured aerosols and splashes following a simple flush from two different types of toilets in hospital. C. difficile organisms were detected in air samples immediately following a flush — and could be found in air samples up to 60 to 90 minutes later.1 These were largely found as the result of aerosolization of large droplets. A mean number of 15-47 large droplets were released when flushing a lidless toilet, depending on the design. C. difficile organisms could be found in air samples up to 25 cm above the toilet seat.
Even toilets with a lid may not solve the problem. How many times have I seen patients too weak to use the toilet, and instead take advantage of the commode, which is then emptied and flushed directly by a staff person without dropping the lid?
REFERENCE
- Best EL, et al. Potential for aerosolization of Clostridium difficile after flushing toilets: The role of toilet lids in reducing environmental contamination risk. J Hosp Infect 2012;80:1-5.
ESBL IS BLASÉ COMPARED WITH THIS SUPERBUG
SOURCES: A ProMED-mail post, Jan. 6, 2016. Antibiotic resistance – Canada: Colistin MCR-1, E coli, grd. beef, human, 2010. www.promedmail.org.
Liu Y-Y, et al. Emergence of plasmid-mediated colistin resistance mechanism MCR-1 in animals and human beings in China: A microbiological and molecular biological study. Lancet Infect Dis 2016;16:161-168.
A plasmid-based colistin resistance gene (mcr-1), described in The Lancet in November 2015, has now also been found in Canada for the first time, in both meat samples and a human.1
Liu and colleagues have been tracking the prevalence of mcr-1 in E. coli and K. pneumoniae strains collected from five different provinces in China between 2011 and 2014.2 They found the mcr-1 plasmid-based colistin resistance gene in 78 of 523 samples of raw meat (15%) and 166 of 804 animals (21%) during this period. In addition, they found evidence of the organism in 16 hospitalized patients. The plasmid could be transferred to another E. coli at a frequency of 10-1 to 10-3 cells per recipient cell by conjugation, and was maintained in both K. pneumoniae and Pseudomonas aeruginosa.
This gene has been spotted elsewhere at much lower levels than described by the Chinese. In Denmark, the mcr-1 gene was found in 5 of 3000 E. coli samples (0.16%) from imported chicken meat, as well as in one Danish patient, who died of sepsis. In the United Kingdom, the mcr-1 gene was observed in 15 of 24,000 E. coli isolates between 2014 and 2015. For the first time, the gene has now been observed on the North American continent. During an investigation conducted in December 2015, using samples collected from earlier research, Canadian health authorities found the gene in E. coli isolates from two samples of ground beef sold in Ontario, as well as from a 62-year-old patient who died in Ottawa. It is believed this patient, who required hospitalization just 3 days after returning to Canada, acquired the organism while living in Egypt.
Colistin is considered the “last-ditch” antibiotic for many multi-drug-resistant organisms, and is often the only agent with activity against some of these bacteria. Colistin acts by binding to a lipid A moiety in the bacterial cell wall, which then precipitates disintegration of the cell membrane. Gram-negative bacteria employ a number of different strategies to protect themselves from polymixins, including a variety of lipopolysaccharide modifications. The mcr-1 gene is a member of the phosphoethanolamine transferase enzyme family, whose expression allows the organism to add phosphoethanolamine to lipid A, negating the efficacy of colistin. While previous mechanisms of colistin resistance were considered intrinsic and not directly transferable, it’s the presence of the mcr-1 gene on a plasmid that makes this finding so hair-raising.
This finding should prompt some kind of global response to the use of colistin in animal feed and therapeutics. While countries in Europe restrict the use of colistin to veterinarians, other countries (e.g., China) use colistin as a growth promotor, and at dosages lower than that used for therapeutic purposes. No wonder colistin resistance in gram-negative isolates from China is so unexpectedly common.
REFERENCES
- A ProMED-mail post, Jan. 6, 2016. Antibiotic resistance – Canada: Colistin MCR-1, E coli, grd. beef, human, 2010. www.promedmail.org.
- Liu Y-Y, et al. Emergence of plasmid-mediated colistin resistance mechanism MCR-1 in animals and human beings in China: A microbiological and molecular biological study. Lancet Infect Dis 2016;16;161-168.
CLEANER DATA ON CLEANING NEEDED
SOURCE: Han JH, et al. Cleaning hospital room surfaces to prevent health care-associated infections. A technical brief. Ann Intern Med 2015;163:598-607.
I often find articles describing disinfectants and cleaning procedures not only dry but hard to compare with other similar literature. And for good reason, apparently. These authors provide a systematic review of clinical studies examining environmental cleaning procedures, disinfectants, as well as the methods for monitoring such cleaning procedures to prevent health-care-associated infections in hospital. They identified 80 clinical publications in English, 76 of which were primary studies and four of which were other systematic reviews. Only five were randomized, controlled clinical trials. Of the 80 clinical studies, 49 (61%) focused on cleaning and disinfecting, while a smaller number focused on methods for monitoring or implementation of cleaning or monitoring strategies. Various outcomes were reported, most of which focused on surface contamination (measured in a variety of ways), but few used patient-centered outcomes, such as the reduction in colonization or infection. Even when studies examining the efficacy of a certain product reported favorable results, the results often were provided for only one pathogen.
The authors identified some important gaps in this literature that they believe hinder the development of better cleaning techniques and products, as well as our ability to monitor cleanliness. They suggest that future studies provide more comparative data. They also suggest developing a standardized definition of “cleanliness,” defining a standardized check-list for what are considered high-touch items in a hospital room, proposing a list of specific equipment requiring testing and monitoring, and deciding how that testing should be done.
For example, while the use of fluorescent UV surface markers and adenosine triphosphate (ATP) bioluminescence were the most commonly reported monitoring methods — and gave useful and direct feedback to staff (as opposed to direct visualization, which was poor) — these methods are not properly standardized, nor do they have good clinical correlates. We’ve been using an ATP device to monitor our environmental staff’s performance, and have found it exceedingly useful in both monitoring cleanliness and providing ongoing education to the staff. But we still don’t have any idea what those cut-off values mean in terms of viable bacteria. For example, for a patient infected with an NDM-containing organism, what ATP cut-off for their tray table or toilet is acceptable? If we use ATP to monitor our ERCP/duodenal scopes, is the recent recommendation for a cut-off value of 200 RLU (recently proposed by our 3M Company representative) significantly safer than a cut-off of 250 RLU? I wish we had better data.
ALL THOSE FAKE KNEES AND HIPS
SOURCE: Tande AJ, et al. Clinical presentation, risk factors, and outcomes of hematogenous prosthetic joint infection in patients with Staphylococcus aureus bacteremia. Am J Med. 2016;129:221.e11-20.
A friend’s 85-year-old father recently was hospitalized with community-acquired methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia. He had developed sudden onset of left groin pain and progressive weakness 5 days earlier. He had multiple medical problems, including a prior CVA with residual left-sided weakness, as well as bilateral hip prostheses. Blood cultures quickly cleared with treatment, but he continued to complain of left groin and left hip pain. Studies of the hip were unrevealing, including plain films, a CT scan, and nuclear medicine white blood cell scan. An initial arthrogram failed to aspirate fluid, but a sample of sterile saline injected into the joint yielded six colonies of MSSA, with a somewhat similar antibiogram to the blood isolate (but the aspirate contained only 561 WBC cells/mm3). A second attempted aspiration was dry. The patient was clinically improving, and his fever resolved.
What is the likelihood the hip is infected? Certainly everyone was reluctant to take this fragile elderly man to the operating room for a wash-out or a hip explantation. It wasn’t until a PET-CT scan, ordered for the purposes of evaluating a lung nodule, lit up the left hip like a pinball machine was the decision made to proceed with surgery (the operative cultures were positive for scant MSSA).
These authors at the Mayo Clinic provide good answers to this question. They conducted a chart review of all cases of S. aureus bacteremia in adults admitted to their facility between 2006-2011, who also had at least one prosthetic joint (knee, hip, shoulder, or elbow) existing at the time of bacteremia. Patients with post-surgical prosthetic joint infection were excluded. Clinical features and outcomes were examined.
A total of 678 patients with S. aureus bacteremia were admitted during the study period, 97 (14.3%) of whom had 166 existing joint arthroplasties. Of these, 50 (51.6%) had no prosthetic joint infection, 35 (36.1%) had hematogenous seeding of at least one joint prosthesis, and 12 (12.4%) were either primary post-surgical infections or indeterminate and were excluded. Of the 85 remaining patients, their prosthetic joints included 73 knees, 59 hips, 10 shoulders, and one elbow.
Thirty-four (97%) of the joint infections presented with at least one clinical sign or symptom. The most common symptoms of joint infection were pain (97%), peri-articular swelling or effusion (61%), and peri-articular warmth (46%). The exception was a patient with a septic prosthetic knee joint, and aspiration of the asymptomatic contra-lateral prosthetic knee joint also demonstrated infection.
All 35 of the prosthetic joint infections were associated with community-onset S. aureus bacteremia. None of the cases of nosocomial bacteremia were associated with prosthetic joint infection. Seven patients had catheter-associated line infections — none of whom developed prosthetic joint infection.
Community-acquired S. aureus bacteremia was associated with an 18-fold increased odds of prosthetic joint infection compared with those patients with nosocomial S. aureus bacteremia (odds ratio, 18.07, P = 0.001). In multivariate analysis, the presence of three or more prosthetic joints also significantly increased the risk of hematogenous seeding of at least one joint by at least nine-fold compared with those patients with two or fewer prosthetic joints. In patients with hematogenous seeding of a joint, infection occurred in about one-third of the knees and shoulders, and nearly one-fifth of the hips.
Surgical I&D or explantation was performed in 32 patients. Three patients were managed with comfort care measures and, in total, four patients died (11.4%). Overall, treatment was considered successful in 26 patients (74%) and in 29 of 43 (67%) prosthetic joints. Subsequent orally suppressive antibacterial therapy was administered to 17 of 31 survivors. Among the nine patients who failed therapy, seven required explantation of the device despite earlier attempted wash-out, one required repeated debridement, and four patients died. Furthermore, 14 of the 35 patients (40%) died within a median of 11 months of their joint infection. Four of the 50 patients (8%) without prosthetic joint infection subsequently developed joint infection over the next 3.4 years.
At least 1 million total hips and knees are replaced annually in the United States. An estimated 4.2% of Americans older than the age of 50 have at least one prosthetic hip or knee joint. While the risk of surgically related prosthetic joint infection is estimated to be < 1.2%, these joints remain at risk for hematogenous seeding throughout the life of the patient.
Put a Lid on It; ESBL Is Blasé Compared with this Superbug; Cleaner Data on Cleaning Needed; All Those Fake Knees and Hips
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