A recent presentation at ECCMID (European Congress of Clinical Microbiology and Infectious Diseases) in Amsterdam described a series of linezolid-resistant enterococci in dogs and cats in the UK. I’m only able to get information from media reports, so details are limited (and potentially lost in translation); however, it’s an interesting story. It’s unsurprising in many ways, but highlights some important issues.
Linezolid is an antibiotic that’s typically used in human medicine for infections caused by multidrug-resistant Gram-positive bacteria such as staphylococci (including MRSA) and enterococci. It’s rarely used in veterinary medicine, but has been used in dogs and cats for the same types of infections. Because it’s one of few options for treatment of MRSA in people, it’s an important drug, and resistance is a significant concern.
The UK story involves a cluster of infections at one veterinary clinic. Enterococci that were resistant to linezolid were found in two cats and one dog. They were found to carry a gene, optrA, that confers linezolid resistance. This is the first time this gene has been found in a bacterium from a companion animal in the UK. optrA is found on a plasmid, a small piece of DNA that can be move relatively easily between bacteria, meaning it can potentially spread to other bacteria of the same species, or even to those of other bacterial species. There are no details in the reports I’ve seen about timing of the infections, and whether the cluster in the clinic was likely due to direct contact between animals, contact with a contaminated environment or contact with people who were either contaminated (e.g. carrying the bug on their hands from touching an infected animal or contaminated surface in the clinic) or colonized (i.e. people who harbour the bacterium in their intestines and can be a source of contamination themselves).
Where did the linezolid-resistant enterococci originate?
It’s hard to say from the limited information I’ve seen. It could have come from a person, as there are lots of instances of humans infecting their pets with a variety of bacteria. That’s largely how MRSA originates in dogs and cats, and other resistant bacteria that are common in humans have entered the pet population in this way.
Use of linezolid in animals should not have played a role. Articles have stated that linezolid is not used in dogs and cats in the UK, and while I question whether that’s actually true, linezolid use is so rare to non-existent in pets that there’s probably no realistic risk of emergence of resistance from use of that drug in these species. However, optrA doesn’t just confer resistance to linezolid. It also confers resistance to chloramphenicol and florfenicol, drugs that are (uncommonly) used in dogs and cats. This highlights the “co-selection” issue, when the use of one drug can select for resistance in other drugs. I suspect a human source is more likely here but it’s hard to say.
According to one article, the authors indicated “Our findings further the ‘One-Health’ view that antibiotic-resistant bacteria can be shared by animals and humans, although the direction of transfer is often difficult to prove. We currently do not know the prevalence of linezolid-resistant enterococci in companion animals and therefore a joint approach to monitoring emergence and dissemination of resistance mechanisms of public health importance is needed”, says Dr. Hopkins. “In this instance, further transmission was stopped by cleaning and decontamination and we have no evidence that any people acquired an infection from these animals.”
What this means in the big picture is hard to say, but it shows how resistant bacteria and resistance genes can move between and within species, sometimes in unexpected ways. It also shows how the common bug-drug-species focus (i.e. looking at one type of resistant bacterium in just one (human or animal) species) can miss the big picture. Antimicrobial resistance is a complex ecological problem that requires a complex and comprehensive approach, which is currently still lacking.