A new paper by Hopman and colleagues (Andreas is also another author but is being modest) has evaluated the effect of removing sinks from the ICU. The trigger for this intervention was an outbreak caused by an ESBL-Enterobacter that could be related to contaminated sinks. The study looked at what happens if you remove all water sources from the ICU, and all water-related activities were migrated to a tap water-free solution. Continue reading
I posted a blog a couple of years ago (was it really that long!) on a fascinating study suggesting that only 1/5 of S. aureus in hospital patients is hospital-acquired. My key conclusion from that study was that the number of potential sources for S. aureus that the team investigated was inadequate to draw any firm conclusions (they didn’t include staff, surfaces, or visitors). I concluded that ‘the next frontier of transmission mapping must be a more comprehensive evaluation of other potential sources…’. The authors must have been reading, because this study from the same group was published recently in Lancet ID, which is a more comprehensive evaluation of other potential sources.
Tabloids have repeatedly warned the people for superbugs on chicken meat, after researchers had convincingly shown that the chicken filets that we buy are contaminated with ESBL-producing bacteria, mainly E. coli. Widely considered a public health threat, it was a decisive argument to insist on reductions in antibiotic use in the agricultural industry in the Netherlands. Yet, whether meat contamination constitutes a risk for human health is unknown. This was now quantified, with surprising results. Continue reading
Last Friday Jarne van Hattem presented findings on ESBL carriage in Dutch travelers returning from ESBL-rich countries at our NCOH meeting and the next day the results appeared in Lancet ID. A great study; quantifying things we already thought, extending our knowledge on risk factors and providing new information on the public health aspects of these imported bacteria. They concluded that acquistion and spread are “substantial and worrisome”. Too bad: all the quantified knowledge lost in 2 meaningless words.
In short, they studied 2001 travelers (ESBL carriage before travel 6.1%) and 34.3% of the non-carriers acquired ESBL during travel; especially in southern Asia (75.1%). Risk fators for acquisition: persisting diarrhea, ciprofloxacin use and eating street food. The median duration of carriage after return was 30 days and 11.3% was still colonized ater 1 year. This implies that returning travelers (depending on region) must be considered at risk for ESBL-carriage (no matter whether they have additonal risk factors) during a certain period of time. Yet, median duration of carriage is short and after 1 year that risk is fairly close to the ESBL-prevalence in the Dutch population.
Is this carriage a health risk for travelers? With >500,000 Dutch travelers to ESBL high-endemicity regions per year, many will acquire (according to what we can detect) ESBL, but how many will develop infections caused by these ESBL-producing bugs? That now is a burning question.
Is this import of ESBL a risk for the Dutch public, that we intend to protect against infections caused by AMR? They also investigated the occurrence of within-household transmission of these bacteria in 215 non-travelling household members and quantified rates with a Markov model. The figure that got most attention was the “12% probability of transmitting ESBL-E to another household member”. Yet, much more informative is the actual transmission rate from which one can derive the effective R0. This rate was 0,0013/carriage day and the calculated effective R0 was around 0.2 (Martin Bootsma personal communication), which might include some overestimation due to false-positive transmission events (no molecular typing). An R0 of 0.2 seems not enough to cause continued transmission – leading to endemicity – coming from these sources, especially since transmission to the next ring (to non-household members) will be less effective. Simply said: returning travelers their household members seem to be – in the Netherlands – dead-end roads for ESBL-producing bacteria. That could be expressed as reassuring.
*Title stolen from Gary Brooker
A new paper in Clinical Infectious Diseases suggests that aerosols and the airborne/inhalation route could transmit Norovirus, demonstrating that Norovirus genomes could be detected in air samples inside and outside of rooms during outbreaks. The authors suggest that a healthcare worker could inhale up to 60 copies of virus during a 5-minute stay in a ‘symptomatic’ patient’s room. These particles, it is suggested, are available then to be swallowed.
So, given the fact that I still have some staff left in the hospital when Norovirus comes to call I’m thinking either this virus has a larger infectious dose than we think or the assumptions are not quite right. There was no linkage with the time lapse from the symptomatic ‘event’ apart from this was within 24 hr. of the sampling or with the type of event, or putting it bluntly, which end of the body the virus was ejected from the body from. Presumably the top end is a more effective disperser of viral particles than the lower end (depending on how sharply the sheets are pulled back..) and it would be interesting to see the effect of frequency of symptoms. Continue reading
Interesting publication being highlighted as part of the WHO hand hygiene day in Leeds, UK suggests through modelling that the type of care, number of surface contacts and the distribution of surface pathogens are most likely to affect the relative quantity of pathogens accried on hands. The paper is published in ‘Indoor Air’, (not a journal that inhabits my bedside table) and we do have to remember that, as G.E.P Box stated, “Essentially, all models are wrong. But some are useful”.