What an excellent start of 2017. A great study from the USA today in Lancet: In a pragmatic cluster-randomized crossover study they tested 4 patient room cleaning strategies on the effectiveness to reduce acquisition with relevant bacteria for the incoming patients. The conclusion states that “enhanced terminal room disinfection decreases the risk of pathogen acquisition.” Yet, this paper is so “data-dense” that you must read the methods (and supplements) to get the picture. In one shot: Not for C. diff, may be for MRSA and yes for VRE. Continue reading
Another of my favourite guitarists succumbed to sepsis following surgery just before Xmas, with the sad passing of Rick Parfitt following shoulder surgery, spookily the day after his band Status quo performed their final electric gig (which I was at). The other was Rory Gallagher, who died a few years ago now of MRSA. Surgical procedures are normally carried out under what should be the most controllable of conditions, yet there are variations in practice, a paucity of quality studies on even the most basic of interventions (such as pre-op bathing) and even when there is good evidence, it is ignored. However I do also wonder if we have been missing something. A paper that suggests no difference between Chlorhexidine (CHG) and Povidone Iodine (PI) for pre-surgical skin prep (both aqueous) recently piqued my interest. It was an RCT (non-blinded) undertaken in clean-contaminated upper gastrointestinal or hepatobiliary–pancreatic open surgery, however that wasn’t the aspect that I became interested in. Continue reading
Community-associated MRSA (CA-MRSA) are characterised by the ability to cause infections – and sometimes serious invasive infections – in previously healthy individuals without healthcare contact. We don’t see this clinical manifestation in healthcare-associated MRSA (HA-MRSA), so it’s is logical to conclude that CA-MRSA are somehow more virulent than HA-MRSA. However, a recent study published in the Journal of Medical Microbiology shows that CA-MRSA strains were no more virulent than HA-MRSA strains in a battery of laboratory tests. This suggests that CA-MRSA’s ability to cause infections in healthy individuals without healthcare contact has more to do with transmissibility than virulence. And this explains the curious phenomenon that CA-MRSA seem to cause the same spectrum of disease as HA-MRSA when they infiltrate a healthcare setting.
Over the last years, we have been getting used to the fact, that commercial pig, veal, and chicken farms, as well as horse breeding, is associated with a risk of animal to human transmission of livestock-associated Methicillin-resistant Staphylococcus aureus (LA-MRSA). In the line of suspects, chicken were the last to be conformed as true source of LA-MRSA. Van Duijkeren et al (J Antimicrob Chemother 2016;71:58-62) investigated addition feathered suspects, namely dugs and turkeys.
First of all lets get Donald & friends of the list of suspects. In only one of 10 duck farms that were investigated, MRSA was found in the samples from the animals and duck houses. None of the humans living or working on duck farms, nor any part of their residence, was MRSA-positive. It therefore seems save to conclude that ducks pose no danger for transmission of LA-MRSA.
Unfortunately, the story about turkeys seems to be different. Overall, 3 of the 10 turkey farms harbored MRSA. In addition, MRSA was found in 16% of the humans and 31% of the farmhouse samples. The highest risk was seen among the turkey farmers themselves (45.5% MRSA-positive), but employees and family members (6.3%) weren’t free of risk, either. Significant risk factors found by the investigators were: having physical contact with the animals and visiting poultry houses.
In 2 out of 3 frams in which MRSA was found among the animals and the humans, whole genome mapping showed >95% homology, corroborating the strong evidence for animal-to-human transmission of MRSA on turkey farms.
As you can probably tell from the title, this post comes with a warning: it presents some rather “un-PC” data, but I’ll do my best to deliver it calmly and dispassionately! My old research team from KCL have just published a paper in PLOS Medicine on the association between social and material deprivation, and MRSA.
I’ve been interested in the dynamic between hospital-associated (HA) and community-associated (CA) MRSA for years (not least because it was the subject of my PhD thesis). I wrote a review several years ago on how community MRSA should be seen as a genotypic phenomenon with epidemiological implications. Using this framework, it is possible to get your head around CA strains of MRSA beginning to cause hospital-acquired infections. The aim of this study was to use a large collection of MRSA from across several regions of London to explore the transmission dynamics and epidemiological associations of HA and CA types of MRSA.
Jon posted a blog last week on mupirocin resistance in MRSA. This week, guest blogger Dr Gwen Knight (bio below) writes about a companion paper also published in the Journal of Antimicrobial Chemotherapy, which models mupirocin resistance…
It is a truth universally acknowledged, that acquiring most mechanisms of drug resistance incurs a fitness cost to the host bacterium. Determining the size of this cost and the impact that this cost will have on the spread of drug resistance is difficult. Is a 10% reduction in growth rate in the laboratory enough to stop resistance spreading in a hospital?
I’ve blogged before that mupirocin resistance is an inevitable consequence of mupirocin use. Whilst I still think that this is true, my old colleagues from GSTT / KCL have just published an article suggesting that mupirocin resistance in MRSA has more to do with clonal variation than with mupirocin use.
The study is part of an ambitious project to sequence the genome of around 1000 MRSA isolates from across Central and South-East London (Guy’s and St. Thomas’, King’s, and Lewisham). Each isolate was then tested for phenotypic high (HMR) and low (LMR) mupirocin resistance, the genome was scoured for the genetic determinants known to be associated with mupirocin resistance, and clone was derived from the genome sequence. Risk factors for both HMR and LMR were then explored.