I blogged on mcr-1 (colistin resistance) in China last week, to share the latest reassuring data. Well, the paper on which todays’ blog is printed will be used to wrap tomorrows’ market fish (typical Dutch expression). Nicolle Stoesser (Oxford) send me the latest news, coming from a Nature Microbiology study providing evidence for the potential of spread of carbapenamases by flies and birds. Not reassuring at all, and potentially with major consequences.
The authors collected material in a specific region (mainly faeces) from poultry, dogs, sewage, wild birds and flies and took samples in commercial farms, a slaughterhouse and supermarkets and determined the presence of mcr-1 and blaNDM with targeted PCRs. In all 245 CRE were recovered (from 739 samples), most harboring NDM, and 37 CREC (= E. coli) were also positive for mcr-1. Direct sampling yielded mcr-1 positivity in >85% of material from hatcheries, poultry and meat, but the harboring species could not be specified. So, the prevalence of colistin and carbapenem resistance in cultured Enterobacteriaceae is an underestimation of the true amount of species harboring these genes. However, Willem van Schaik told me that there were no clear controls to prevent contamination of PCRs, which could potentially lead to false positives and an overestimation of the rate of mcr-1 and blaNDM positivity. Be warned, if you plan to read the paper: you must be a professional sudoku player to put all the numbers together….
The take home message, though, is that both mcr-1 and NDM were highly prevalent in animals, farms and slaughterhouse, and were even detected simultaneously in some E. coli isolates, and these bacteria, plasmids and genes were also detected in dogs, flies and birds, fit to fly away.
This would make AMR a “vector-borne disease”. This was already recognized in healthcare settings where staff acts as the mosquito. Yet, there is a potential to train human vectors to adhere to infection control measures. That will be more difficult with flies and birds. For global policy makers: you can’t protect your country against AMR by building a wall, you will need a cave.
The other novelty from this paper is the introduction of the “phantom resistome”, defined as the phenomenon that you will detect – in a single sample – more resistance gene positivity by PCR than isolated bacteria with the same resistance phenotype. Ergo, there are uncultured bacteria harboring these genes (if not false positives). Now I am lost: I thought that the resistome was all bacterial DNA conferring resistance to an antibiotic, present in culturable and non-culturable species, and including even genes that we don’t know yet. The trick here is that gene detection by PCR is pimped as “targeted resistome characterization”. But now you can only detect what you look for. You can phrase this as the “phantom resistome”, but sooner or later someone will call this the “phantasome”.