Dr. Mike Lappin and I are teaming up with Dr. Carrie Jurney (President of Not One More Vet) and Dr. Steve Weinrauch (Chief Veterinary/Product Officer of Trupanion, founder of MightyVet) for a webinar about canine infectious respiratory disease complex (CIRDC) issues in the US (plus some Canadian content). There may be a lot of “we don’t know yet” comments, but we’ll have some insights, some reasonable guesses and, yes, a bit of new data about the situation.

Disclaimer: This webinar is coordinated by Trupanion, a pet insurance company, but it’s a non-commercial talk, and we’re not being paid to do it. We’re just hoping to get some good information out to a broader audience by making use of Trupanion’s interest and reach.

Here are the details about the webinar and how to join:

Trupanion is inviting pet parents and veterinary professionals to join a free, live webinar – “Separating Fact, Fiction, and Uncertainty: Canine Respiratory Illness Q&A” to be held Thursday, November 30, 2023, at 4:30 PM PT / 7:30 PM ET.

This timely event will include: 

  • REAL-TIME UPDATES: Stay informed with the latest updates on canine respiratory illness, leveraging Trupanion’s database of over 3 million Trupanion-protected pets.
  • PREVENTION STRATEGIES:  Learn effective strategies and practical measures you can take to safeguard your pup’s health.
  • SIGNS TO WATCH FOR: Learn how to recognize early signs, empowering you to take proactive steps to address potential concerns.
  • LIVE ANSWERS TO PARTICIPANT QUESTIONS: Participants can engage directly with the panel of experts to ask questions about canine respiratory health.



  • Panelist | Dr. Scott Weese: Dr. Scott Weese is a veterinary internist, a Diplomate of the American College of Veterinary Internal Medicine, and a Fellow of the Canadian Academy of Health Sciences. He is a Professor at the Ontario Veterinary College, University of Guelph, Director of the University of Guelph Centre for Public Health and Zoonoses, Chief of Infection Control at the Ontario Veterinary College Health Sciences Centre, and is a member of numerous national and international committees dealing with infectious diseases and antimicrobial resistance, including the Quadripartite (WHO, WOAH, FAO, UNEP) Global Leaders Group on AMR. 
  • Panelist | Dr. Michael Lappin: Dr. Michael Lappin is a veterinary internist, a Diplomate of the American College of Veterinary Internal Medicine, holds a PhD in Parasitology, is Director of the Center for Companion Animal Studies at Colorado State University School of Veterinary Medicine and Chair of the World Small Animal Veterinary Association One Health Committee. He is also currently a Professor at the College of Veterinary Medicine and Biomedical Sciences at Colorado State University. 
  • Special Guest | Dr. Carrie Jurney: Dr. Carrie Jurney is a veterinary neurologist and practice owner at Remedy Veterinary Specialists in San Francisco. She is a passionate advocate for mental health and wellbeing, and serves as the president of Not One More Vet 501(c)(3), the world’s largest wellness-focused charity for veterinary professionals. 
  • Host | Dr. Steve Weinrauch: Dr. Steve Weinrauch, BVMS, MRCVS is the Chief Veterinary/Product Officer of Trupanion and founder of MightyVet 501(c)(3). Before joining Trupanion, Steve built and ran three veterinary practices in the Seattle area. He has published his research in numerous peer reviewed journals, and he is licensed to practice in both the U.S.A. and the European Union.

Please note: the webinar recording will be available for on-demand viewing at https://k9illness.trupanion.com/

There’s been a lot of discussion about canine infectious respiratory disease complex (CIRDC) going around in dogs in the US recently. In the last week, I’ve already covered this from a few different angles, including what might really be going on with all the reports of sick dogs, reports of the potential involvement of a potential novel canine respiratory pathogen and when and when not to treat dogs with respiratory disease with antimicrobials. I’ll try to get another post done soon about the data we have (and don’t have). This post will address the most common questions dog owners are asking.

What should dog owners do?

Relax. It seems like there’s more respiratory disease in dogs in some areas, but that’s something we often see. Serious disease is being reported in a small subset of infected dogs, but that’s also something we regularly see. So, being aware is good, being anxious is bad, freaking out is definitely unnecessary.

The vast majority of dogs that get CIRDC recover uneventfully. That’s as true now as it was a year or 10 years ago. However, severe disease can occur so we don’t want to be too dismissive.

My dog is sick. What should I do now?

The default answer is “talk to your veterinarian if you’re concerned.”

However, the answer is not “if your dog coughs, it must be taken to a veterinarian ASAP.” A dog should be taken to a veterinarian if it’s really sick, deteriorating quickly, not getting better over the course of several days (but remember dogs may still cough after they’re feeling better), if there might be complications, or if it’s unclear what’s going on.  If the dog just has mild upper respiratory infection, it rarely needs to be seen by a veterinarian. If it has pneumonia, it definitely needs to see a veterinarian.

Think about it in terms of how we react when we get sick or our kids get sick. If you had a cough and felt a bit run down, you probably wouldn’t go to a doctor unless you had underlying risk factors for severe disease. The same applies to dogs – if they’re pretty bright and alert, are eating and breathing normally, but just have a cough and runny nose or eyes, it’s very unlikely they need to be examined (in part because it’s very unlikely that they need any specific treatment or testing, and because a visit to the veterinary clinic might just cause more stress for the dog and risk exposing other animals.) If you felt like you could barely drag yourself out of bed or you were having a hard time breathing, you’d go to the doctor. That’s also the same for dogs.

While I want to avoid being too prescriptive about who should or shouldn’t see a veterinarian (since there are lots of exceptions and grey areas), if the following signs are present, a prompt visit to the veterinary clinic is indicated:

  • Weakness, severe depression (meaning the dog is really quiet, not engaged and just lies around, doesn’t get up when you’d expect it too (like for food))
  • Loss of appetite
  • Difficultly breathing (breathing faster and harder even when not exercising)
  • Rapid worsening of illness
  • Cough that is causing significant problems such as vomiting or making it hard for the dog to breathe

It’s especially important to see the veterinarian if these signs occur in a high-risk dog, including:

  • Elderly
  • Very young
  • Pregnant
  • Immunocompromised (by disease or treatment)
  • Underlying heart or respiratory tract disease
  • Brachycephalic (i.e. squishy-faced) breeds

What will happen when I take my dog to the veterinary clinic?

That’s depends on a lot of things, so it’s hard to say what you should expect.

  • The first thing the staff should do is assess whether it looks like your dog has infectious respiratory disease, and how stable your dog is (in terms of its lung function). Most dogs with CIRDC don’t need anything but time and TLC; so, if your veterinarian says your dog looks stable and no treatment is needed at this point, take that as a good sign. Don’t ask for unnecessary treatments like antimicrobials “just in case.”
  • If your dog’s cough is disruptive, then a cough suppressant may be warranted (but that depends on a few things).
  • If your dog has signs of pneumonia, radiographs of the chest and bloodwork will likely be needed. If pneumonia is confirmed, antimicrobials are indicated.
  • If your dog is really sick, hospitalization with intensive care, antimicrobials and oxygen therapy may be required. That’s uncommon but it happens, and when there’s more respiratory disease activity in an area at a given time, there will be more cases of severe disease too just based on numbers (e.g. 1% severe disease rate in 1000 infected dogs is more really sick dogs than 1% in 100 infected dogs).

The severity of your dog’s illness, the type of illness, what the clinic can offer and (unfortunately) sometimes budget limitations will influence what’s ultimately done.

Additionally, sick dogs should be kept away from other dogs to help reduce the risk of disease transmission. That includes no going to day care, parks or any other places where non-household dogs would be encountered. For how long? That’s hard to say without a diagnosis but I’d aim for at least 2 weeks.

My dog is healthy. What should I do?

Let’s try to keep your dog healthy by limiting its contact with other dogs, especially large numbers of different dogs with unknown health status. Contact with small, stable groups (e.g. an established walking group, a small day care with the same dogs that don’t see a lot of other dogs) is lower risk. Logically, dogs should be kept away from any obviously sick dogs.

What about vaccines for my dog?

Vaccines are available for some of the causes of CIRDC. For any dogs that have frequent contact with other dogs, vaccination against Bordetella bronchiseptica and canine parainfluenza virus is important. Mucosal vaccination (intranasal is preferred, oral is second best) should be done whenever possible. Critically, it is important to use a vaccine that covers both Bordetella and parainfluenza. I suspect that loss of parainfluenza protection because of increased use of Bordetella-only oral vaccines might be driving some of the issues we’re seeing.

Canine influenza (flu) vaccination can be considered too, but it can be hard to get (there are currently some production and backorder issues) and canine flu is a pretty sporadic disease.

My dog is healthy but higher risk for disease or complications (see high risk list above). What should I do?

Take the same precautions described above for non-high risk dogs, but with more rigour. I’d also be quicker to recommend respiratory disease vaccines for these dogs, irrespective of how much contact they have with other dogs.

My own two dogs probably fall into those two risk categories. Both have fairly cloistered lifestyles from an exposure standpoint. Their dog contacts are largely restricted to a small number of well known and similarly low risk dogs.

The young pest, Ozzie, is a one-year-old, healthy Labrador, and is therefore at low risk of exposure and low risk for serious disease. He got an intranasal Bordetella/parainfluenza vaccine this summer so he could go to day care when we were away at a cottage (to give us some Ozzie-free afternoons to relax). The old guy, Merlin, is an 11-year-old Labrador who’s on chemo for chronic lymphoid leukemia. His exposure risk is low but he’s probably at some degree of greater risk for serious disease if he gets infected. There doesn’t seem to be anything remarkable going on locally compared to normal, so it’s status quo for them, but I’d be quicker to vaccinate Merlin if I decided vaccination might be warranted, especially if influenza hit the area.

As with any emerging issue, the current situation in the US is fluid, and we’re trying to sort out more about what’s happening. At the moment, for your average dog owner, it’s still just a matter of some common sense precautions and good dog care.

As concerns about an outbreak of canine infectious respiratory disease in the US continue, we’re still at a point where media hype massively outweighs any true data. Not much new has been reported recently. If anything, I’d say we’re hearing more about things being stable in different areas, that investigations haven’t turned up anything beyond the usual suspects, and the typical messaging to use common sense but relax.

One thing that is getting some press is a suggestion that a rather bizarre little bacterium might be involved in some of the current canine illnesses. “Might” is the key word though. At the risk of having to eat my words later, I’d guess this bug is probably not going to pan out to be a driver of widespread disease – it’s possible, but there’s a long way to go before we can say that with any confidence. In the meantime, let’s recap what we know:


In the spring of 2023, the New Hampshire Veterinary Diagnostic Lab reported they were investigating a potentially novel organism as a cause of respiratory disease in dogs. I remember reading about it in a taxi on my way to the airport in DC; I thought it was interesting, but in my experience, the vast majority of “new pathogens” end up being commensal organisms (i.e. also present in lots of healthy dogs) or otherwise not panning out to being relevant. But, I never totally discount the possibility, and was glad to see it investigated. The initial (and I think only) report involved a pretty small number of dogs. They found snippets of DNA that were similar to IOLA KY405 in 21/31 samples. Their latest update is here.

What on earth is IOLA KY405?

It’s hard to say. As far as I know, it’s only previously been reported in two papers from the same lab in Japan, where it was found in samples from humans with respiratory disease. It’s reported to be a bacterium with a very small and bizarre genome.

  • The first study (Fukuda et al. 2014) reported finding gene sequences from IOLA KY405 in a lung fluid sample from one person, then followed up by finding those DNA bits in samples from 6/386 samples from other patients with respiratory disease. Some unique aspects of this bacterium are a very small genome, similar to Mycoplasma  (just over 300K base pairs; for reference, staphylococci have about 2.8 million base pairs), and a very high AT content (about 80%).
  • In the second study (Fukuda et al. 2021), they presented the whole genome sequence of the organism. They also used PCR to look for it in samples from more people with respiratory disease, and got positive results in 2.7% of about 500 samples. Eight of the 11 positive patients had significant underlying disease, and five were being treated with corticosteroids or immunosuppressants. So, these individuals had lots of other excuses to have respiratory disease or to be infected with something that’s minimally pathogenic.

Someone with more background in genomics would need to assess the papers to know how confident we can be in the results. If they are real, then the researchers have found a small bacterium that’s similar to Mycoplasma, which maybe isn’t surprising since some Mycoplasma are able to infect lungs (but more often are present as normal respiratory tract inhabitants.)

What we’re still lacking is 1) actually growing the bug to confirm its existence, and most importantly, 2) context. Finding DNA from this bug in a small percentage of people with respiratory disease is interesting, but could it be just as common in healthy individuals and just part of our normal microbiota? I don’t think we can say either way at this point.

When something’s only reported by one group over a long period of time, it raises the question of why. Is one group just way ahead of the curve, or is this something that other people have tried to find but have been unable to replicate the results (or have looked at and dismissed as not being worth investigating)? Publication bias is a big problem in cases like this. If other groups have put in a good effort to investigate this and found nothing, odds are high we wouldn’t find out because there’s a tendency to not publish “negative” results, even though those data are really important. So, we have no idea if there are only two papers because only one group is looking for it, or whether lots of other people have tried and failed to find anything similar.

Genome-based pathogen discovery is an established and effective method. It looks at all the genetic bits we can find in a sample, then tries to assemble them into something interpretable, and then we try to figure out what it actually all means. It’s challenging because we have a vast population of viruses and bacteria that are normal inhabitants in our bodies and those of animals. Most are harmless. Many are beneficial. Some can cause disease. Sorting out into which category a new organism fits takes a lot of work, and is rarely straightforward.

We’ve been lead down the wrong path many times before by reports of a “new” organism found in sick animals (e.g. the panic about canine circovirus). People freak out, start testing more sick animals, find it, and freak out more. However, when the science catches up with the hype, we often realize that we can find the bug in the same percentage of healthy animals, and it’s just a normal inhabitant that we’ve recently discovered, versus something new that is causing disease. With modern molecular techniques, our ability to find something often surpasses our ability to understand it.

While it sounds like I’m downplaying the relevance of this finding, that’s not my intention. I suspect IOLA KY405 is a real organism, I just need a lot more convincing that it’s relevant to disease (in people or animals). In an ideal world, the New Hampshire lab and others would be investigating this robustly, including field studies in dogs, to deterimine what the real story is. Lack of funding for companion animal infectious disease research usually slows these to a crawl. The report from the New Hampshire lab adds good context:

  • It is important to note that this is a preliminary finding, and under normal circumstances of a study we would not release these findings. The technology and methods used by the HCGS include cutting edge metagenomic sequencing, and multiple bioinformatic pipelines that are uncommonly utilized in veterinary medicine. Additionally this is an uncommonly studied group of bacteria. There are multiple experiments that need to be run in order to clarify correlation vs. causation, and this gives reason for pause in releasing the findings. However, the syndrome is ongoing and there may be an opportunity to benefit animal health as we continue to validate these initial findings. There is a chance that this preliminary data is disproven with further study, but at this point it does appear that the bacteria we have identified is a potential causative agent.”

Those disclaimers are key, but unfortunately are usually left out of the media reports.

This is an important but very preliminary finding that needs to be studied. However, we also have to realize that most findings like this don’t turn out to be anything big (or anything at all). We can’t dismiss the potential and it’s great to see the work being done, but we need to make sure that we don’t jump from a preliminary finding of some unusual DNA sequences to “here’s the answer!” which is what human nature wants us to do.

As concerns about canine infectious respiratory disease in the US have taken up most of my time lately, let’s merge that issue with what I had hoped to be the focus of the week: World Antimicrobial Resistance (AMR) Awareness Week.


Despite lots of media attention and associated fear, we’re still not sure what’s going on with all these coughing dogs, or even if there’s really a story at all. This could be something new, but more likely, it’s the usual suspects doing their usual thing (possibly at higher rates in some areas, as fairly commonly occurs periodically).

In the unlikely event this is something new, it’s likely viral. It’s much less likely to be something bacteria.

Either way, we have to think about how that might impact treatment. The short answer is: it probably doesn’t affect our treatment approach.

Viral respiratory illness can’t be treated with antimicrobials. Some affected dogs will develop secondary bacterial pneumonia, and antimicrobials are indicated in those cases. But it doesn’t matter what virus triggered it.

Primary bacterial respiratory infections in dogs are less common. The bacterium Bordetella bronchiseptica is typically the number 2 or number 3 overall cause of canine infectious respiratory disease complex (CIRDC), after canine parainfluenza virus and maybe canine respiratory coronavirus. Streptococcus zooepidemicus is a rare cause of CIRDC and usually causes sporadic but really nasty (often rapidly fatal) disease, most often in shelters or other high stress settings. Secondary infections (i.e. things that move in after a virus has already caused some damage) can be caused by a variety of different bacteria.

When considering antimicrobial therapy, we need to think about the disease we’re targeting. Cough isn’t a disease. It’s a sign of disease. Cough can be triggered by infection, be it bacterial or viral, and often persists even after the infection is over. Too often, we get into a mindset of “the dog is coughing really badly” or “the cough isn’t going away” and we unnecessarily reach for antimicrobials, hoping they will somehow help, when in reality we just need to give the dog more time to fully recover, or we can use other approaches to decrease inflammation and suppress the cough if that’s the part that’s still a problem.

Our 2017 Antimicrobial use Guidelines for Treatment of Respiratory Tract Disease in Dogs and Cats from the International Society for Companion Animal Infectious Disease are a good start for thinking about how to manage these sick dogs. We’re starting a revision, and I think we’ll see a few changes to the guideline, but most of the original content still applies. Some newer approaches to care of these cases are already incorporated into the antimicrobial use guidelines available to veterinarians through the Firstline app (see image below).

Here are some of the basic recommendations:

Basic upper respiratory tract infection: cough, runny eyes and nose, maybe a fever and a bit quiet, but dog is usually pretty bright overall.

  • No antibiotics.
  • This is likely viral, and if it’s bacterial, it’s mild and should resolve on its own. Tincture of time and supportive care are recommended.

More serious upper respiratory tract infection that is probably bacterial: more advanced signs of disease, mucopurulent (yellow, goopy) nasal and ocular discharge, but lungs are clear.

  • Consider antibiotics but most cases probably don’t need them.
  • As these cases are more severe it’s easier to justify antibiotics, but I can often go either way and have a fairly high threshold to say “start antibiotics” (at least right away). However, it’s not unreasonable in many cases.
  • Doxycycline is the drug of choice for treatment. It’s lower tier, effective, safe and works against the main bacterial pathogens of concern.
  • If there’s no response to initial treatment, we need to back up and think about whether that’s because it’s a bacterial infection is not responding, or whether what we’re seeing is more likely viral or non-infectious. That’s often hard to sort out, but we need to consider it carefully rather than just jumping to another drug every time we don’t get the response we expect on the first try.

Mild/moderate pneumonia: Varying upper respiratory signs, but with signs of lung involvement, such as audible crackles and wheezes, and radiographic evidence of pneumonia. These dogs are sicker but are stable. They are breathing reasonably normally, are quiet but alert and do are not crashing.

  • Antibiotics are definitely indicated.
  • Doxycycline is still the drug of choice. Along with the points listed above, it achieves good drug levels in the lung and is a great first line choice for pneumonia. If it’s a rare, milder or earlier Strep zooepidemicus pneumonia (mainly we’d suspect this because it’s part of an outbreak), amoxicillin would be fine instead, but usually we want a broader spectrum drug than that and one that gets better levels in the lung.
  • Some people are suggesting that enrofloxacin seems to work better in some of the more recently reported cases. That could be a true reflection of better activity against certain bugs, or issues with resistance to other drugs, but could also just be a function of using enrofloxacin as a second line option later in disease (where its use corresponds to natural resolution of disease, versus a true effect of the drug). It’s a good observation and I don’t dismiss anecdotes like that, I want to explore it more to try to tease out the reasons versus making a full switch to regularly using a higher tier drug like that. It could be that enrofloxacin is a better drug (overall or in specific areas), but given the potential issues with use of this higher tier drug, we’re best to be cautious and try to make sure we really have a firm indication that it’s necessary. If we put every dog with pneumonia on a fluoroquinolone like enrofloxacin, we won’t be able to use the drug for long because resistance will quickly become an even bigger problem.
  • Azithromycin is another option for treatment of pneumonia, as it also achieves great levels in the lung.
  • The more convinced I am of a true treatment failure, and the more severe the disease, the more I’d escalate, but sometimes we can be mislead by our observations. If it’s clear that doxycycline isn’t working in one area but another drug is, it’s logical to use that other drug, but we want to make sure we’re limiting changes in approaches and use of higher tier drugs as much as we can, because the more we use them, the quicker we lose them.

Severe/septic pneumonia

  • One of my big considerations when deciding whether to use more broad spectrum treatment in any patient is “What’s likely to happen if my drug choice is wrong?” If the answer is “the animal will probably die,” I can justify using a higher tier drug or combination to help ensure it’s effective on the first try. For the cases above, I wouldn’t typically jump to a broader spectrum combination, but with severe septic pneumonia we are dealing with a subset of dogs that are really sick with significant lung disease. They are not oxygenating well. They have low blood pressure or other signs of severe systemic inflammation. They’re at risk of crashing hard and fast, and I need to get the infection under control pronto. So, I can justify a broad spectrum antimicrobial – nothing crazy (e.g. not meropenem), but a broad spectrum drug/combination that’s higher tier and something I generally avoid, but am comfortable using in a situation like this.
  • Intravenous clindamycin & enrofloxacin, ampicillin & enrofloxacin, or an intravenous 3rd generation cephalosporin (e.g. ceftiofur, cefotaxime) would be reasonable choices in these cases.

How long do we treat a dog with pneumonia?

We have very little duration of treatment data for most infections we deal with in veterinary medicine, especially companion animals. We tend to be quite risk averse and therefore default to really long antimicrobial treatment courses.  Based on the short durations of antimicrobial use in people with similar conditions (where there’s lots of evidence that shorter is better), and even in cattle (where there’s lots of evidence and desire for shorter courses because it’s a hassle treating them), we need to be aim for shorter courses of antimicrobials in pets too.

  • Five days is what I’m recommending now. We don’t have data for that, but we also don’t have data for using any longer duration of treatment, and since we have good comparative data from other species, increasing anecdotal evidence and a duty to consider a “least harm” approach, I’m happy with five days. We can always go longer if needed, based on patient response and complicating factors, but short durations are often effective, come with fewer adverse event risks, and are cheaper and easier for owners (who, realistically, often don’t complete long treatment courses when their pet is doing well anyway).

We have to remember that antibiotics are there to help resolve bacterial infection, but eliminating the infection doesn’t immediately fix everything. Signs like cough and radiographic changes can linger, and more antibiotics don’t help those things resolve any faster.

So, while we’re not sure what’s going on with all the coughing dogs in the US right now, we can be reasonably confident we know how to treat them. Our usual approaches will still work. We need to be conservative with antimicrobials, but also ready to use appropriate drugs (including broad spectrum, higher tier drugs) when indicated. The right drug at the right dose for the right patient still applies.

Next in the World AMR Awareness Week (WAAW) series is a recycled post about our cat Rumple from this past summer. It’s not just because I’m lazy. It’s largely because it’s a great topic and an issue for which there’s a lot of unnecessary antibiotic use (especially in cats).

Rumple’s an indoor-outdoor cat that we adopted years ago through Guelph Humane Society’s working cat program. He was deemed unsuitable for a household, so we got him as a barn cat, but he migrated from the barn to the deck to the garage to being a part time indoor cat afterall (as I write this, he’s stretched out sleeping on my bed). He’s a big suck who spends a lot of time inside, but wouldn’t tolerate being inside 24/7. That creates some risks.

As I was working at my desk, Rumple wandered over the keyboard (typical cat editing that I don’t always realize) and I noticed a little scab on his ear and one on his neck. I figured he’d tangled with something outside (we occasionally see other cats around here, as well as the usual wildlife). No big deal.

However, a few days later, I felt a soft fluctuant swelling on his neck, just past his head. It wasn’t overly painful, there was no inflammation around the site and he seemed perfectly normal otherwise, all of which is consistent with a localized abscess.

Antimicrobials? Nope.

Antimicrobials don’t work well for an abscess. The drugs don’t penetrate the abscess well, and the environment inside the abscess can hinder them from working.

More importantly, we have a much more effective treatment: incision and drainage, as illustrated below.

Clipping around a cat bite abscess in preparation for incision and drainage.
Draining cat bite abscess.

Since he was systemically healthy and there was no evidence of a tissue infection beyond the abscess, incision and drainage was all he needed. There was a soft spot under a scab that I opened up with a hemostat and we got big gush of pus. (Abscesses can be really rewarding to treat when they drain like that!) I flushed it out quickly (he’d had enough of me at that point), and that was it. It stopped draining quickly so he didn’t need any more wound care. A few days later, the site had a bit of a scab but is otherwise normal (see last picture below).

If I’d given Rumple antimicrobials when I drained the abscess, one might have thought “wow, look how well the antibiotics worked – it cleared up right away,” but this shows that they weren’t needed. However, as clinicians, we often feel a need to “do something,” even though that “something” may not be required. We also tend to be quick to ascribe good responses to what we did, vs what was going to happen anyway.

What percentage of cats in Rumple’s situation would have been treated unnecessarily with an antimicrobial?

  • Probably a very high percentage.

Why is that? There are lots of potential reasons:

  • Risk aversion
  • Habit
  • Lack of education on abscess management
  • Lack of confidence treating without antimicrobials.
  • Veterinarians thinking the client expects it.
  • Owners asking for antimicrobials.
  • More fear of someone complaining that the veterinarian didn’t use antimicrobials if things don’t go well, than concern about adverse effects of antimicrobials (in the individual or the population).
  • It’s easier and quicker to give an antibiotic than to explain to an owner why it’s not being given.

Sometimes, animals do need antimicrobials if they have an abscess, such as when they have concurrent active tissue infection or systemic disease. (Rumple had a soft tissue infection a few years ago, likely also from a bite, but that time he needed antimicrobials.) In most cases, though, cat bite abscesses are discrete abscesses that just need incision and drainage.

Not using antimicrobials is easier on the cat (no need for pilling or injections), easier on the owner (no need to pill the cat, cheaper), and means there are no risks of adverse drug reactions or promoting antimicrobial resistance.

Another question that will come up about this case: Did I culture Rumple’s abscess?

No. There are a few reasons I chose not to do a bacterial culture, but the biggest one is that it doesn’t really matter what bug is present – I’m going to treat it the same regardless with incision and drainage. A culture is more useful if I am going to use a systemic antimicrobial, but since I wasn’t going to, it wouldn’t add any value (apart from satisfying my curiosity). Culture is a really valuable tool that’s underused overall, but it’s also overused in some situations, providing information that’s not needed or that can even be misleading. For your typical abscess that’s easily managed with incision and drainage, it’s pretty low yield.

After the initial post, a reader commented “why weren’t you wearing gloves”? Fair question. In the clinic, I would have. At home, it wouldn’t have been a bad idea either but to be honest, it was a quick procedure and I really didn’t think about it given the atypical circumstances. Gloves would have been to protect me and I washed my hands well. He was low risk for having a significant zoonotic risk or multidrug resistant bug. It still would have been a reasonable idea and in a clinic with a patient, I definitely would have. I think we tend to be a little lax doing things to our own pets at times.


I’ve held off writing about this but since I’ve been answering many emails about it every day, here we go.

The questions I keep getting (as usual) are “What’s going on with this reported outbreak of respiratory disease in dogs in the US? What new disease is this?”

I’m not sure there’s a new disease here. I’m not even sure there’s a major outbreak (or any outbreak).

Various groups in different areas of the US are reporting cases of respiratory disease in dogs (which we refer to as canine infectious respiratory disease complex, or CIRDC) in dogs in various parts of the US. There’s always limited info about true numbers, and the disease description is vague and quite familiar (coughing dogs, some that get pneumonia, a few that die).

The issue is, that largely describes the every day status quo when it comes to CIRDC. This syndrome is endemic in dogs and has a variety of known causes (e.g. canine parainfluenza virus, Bordetella bronchiseptica, canine respiratory coronavirus, canine pneumovirus, canine influenza virus, Streptococcus zooepidemicus… roughly in that order of occurrence, and maybe the enigmatic Mycoplasma as well). There are also presumably a range of other viruses involved that have been present for a long time but that we don’t diagnose.

We see CIRDC all the time, anywhere there are dogs. There’s a background level of disease that usually flies under the radar, alongside periodic clusters of cases. I get lots of emails every week asking whether there’s more or more severe CIRDC activity at the moment, but I’ve been getting those reports for years, from across North America. To me, that reflects the fact that CIRDC is always circulating, but we notice it more at certain times than others, either because of local clusters or, increasingly, local increases in awareness, often due to media coverage. Media and social media can drive outbreak concerns. They can be great to get the word out and help sort out issues, but often, they lead to false alarms.

  • For example, we might have 100 dogs with CIRDC every week in Guelph (a complete guess since we have no way to track this). Usually, only a few people hear about it. The dogs typically get better and life goes on. However, if someone starts talking about it on social media, we might hear about 50 of those 100 cases. All of a sudden, we have an “outbreak of a disease affecting dozens of dogs” when in reality, we might just have our normal background level of disease that people are actually noticing.

The same thing can happen on a larger scale. There are thousands of coughing dogs in the US every day, since there are millions of dogs. Once people start talking about it, some of these go from “Oh, my dog is coughing. I guess he picked up something at the park. Whatever.” to “OMG, my dog has this new disease that’s sweeping the nation, I need to tell someone!” With the first approach, no one but the owner usually knows or cares. Once we hit the panic button, many owners start to tell everyone about it.

We don’t have any idea if the current stories reflect:

  • A multistate outbreak caused by some new bacterium/virus
  • A multistate outbreak caused by our usual suspects, for some reason
  • Unconnected sporadic local outbreaks caused by usual suspects
  • A slight increase in baseline disease
  • Our normal disease activity with an outbreak of media attention.

I suspect it’s one of the last two. My perception is that we have been seeing a bit more CIRDC activity over the past couple of years, and that we are now seeing a somewhat greater incidence of severe cases. However, with more cases, we see more severe disease, so those are linked. Also, with the explosion of breeds like French bulldogs that are much more likely to have severe outcomes from any respiratory disease (since a large percentage of them have been bred to have completely dysfunction respiratory tracts), increases in deaths could be linked to dog factors, not disease factors.

I never outright discount reports of something potentially new, and we continue to try (futilely so far) to get a better handle on what’s happening with regard to CIRDC activity in different areas. It’s tough, since there’s no effective surveillance system, the voluntary reporting that we’ve tried tends not to get much buy-in (understandably knowing veterinary clinics are swamped by other priorities), testing of sick dogs is expensive and rarely impacts how we care for an individual animal (great for surveillance but harder to justify the cost to an individual owner), and we have little to no funding to do much with companion animal infectious diseases at all.

My guess is this is simply an outbreak of media attention piggybacked on a somewhat increased rate of CIRDC cases that we’ve seen over the past year.

I might be wrong, which is why we’re still trying to collect more data, but I don’t currently see a reason for extra concern.

If you’re worried about canine respiratory disease:

  • Limit your dog’s contacts, especially transient contacts with dogs of unknown health status
  • Keep your dog away from sick dogs
  • If your dog is sick, keep it away from other dogs
  • Talk to your veterinarian about vaccination against canine parainfluenza virus (CPIV) and Bordetella bronchiseptica (plus canine influenza, but influenza is much more sporadic (especially in Canada) and vaccine availability is still an issue).

And, at risk of a flurry of emails, I’ll add… consider health when choosing a dog. That doesn’t mean no Frenchies, but get one that looks like they used to – one with a nose, not the current popular version of the breed.

Continuing my World Antimicrobial Resistance (AMR) Awareness Week series, let’s talk about antimicrobial prophylaxis in animals.

If you asked random people on the street “Should antibiotics be given to healthy animals?” I’d expect the answer to be a resounding no. But, as with most things related to AMR, the answer is not as simple as it seems.

Prophylaxis (or “preventive treatment”) is a very broad categorization of antimicrobial use (AMU) that lacks a consistent definition, but a  a consistent component of most definitions is administration of antimicrobials to healthy animals that are deemed (rightly or wrongly) to be at increased risk of bacterial infection, where prophylaxis is assumed (rightly or wrongly) to be able to reduce the risk of disease.

Prophylaxis encompasses a large percentage of the antibiotic use in animals, particularly in food animals. Prophylactic antimicrobials are massively overused, often (for various reasons) when they’re not needed, and not uncommonly as a crutch to compensate for poor management or husbandry practices that increase the risk of disease.


Is there any role for antimicrobial prophylaxis in animals?

When we talk about prophylaxis at international interdisciplinary tables, there’s very often an attitude of “Just stop using antimicrobials prophylactically in healthy animals. Next topic.” I understand that, because at face value, it makes no sense to use antimicrobials in healthy animals.

But… there are some buts. Not all prophylactic use of antimicrobials is the same. Most of it can likely be stopped or reduced, but some is necessary. Appropriate prophylaxis applied in a targeted manner in high-risk situations for bacterial infections (that can’t necessarily be prevented through other means) can reduce animal illness, death and welfare concerns. It can also potentially decrease overall AMU if it prevents the need for therapeutic courses of antimicrobials later on (which may require more use of higher tier drugs for a longer time).

However, with large scale use, use that is poorly targeted, use that is not based on proper risk assessment, and when antimicrobials are used in lieu of improvements in animal management and preventive medicine, prophylaxis is harder to justify.

Accordingly, efforts to assess, reduce and optimize prophylaxis are warranted, but complete cessation of it isn’t going to be practical or necessarily beneficial overall.

When someone thinks about antimicrobial prophylaxis in animals, they probably think about a large barn with thousands of animals that are getting treated en masse. That’s just one example though. There are different types of prophylaxis, with different risks and benefits, including scenarios such as:

  1. Administration of antimicrobials to a group of animals in a routine manner because of a high endemic rate of a specific disease in the group.
  2. Administration of antimicrobials to a group of animals in response to a specific, defined disease threat that is known to be mitigated through a targeted prophylactic course of antimicrobials.
  3. Administration of antimicrobials to a group of animals as a routine practice for most or all animals at a high-risk stage of life or production (e.g. tetracycline treatment of pigs at the time of weaning to prevent post-weaning diarrhea, intramammary antibiotic treatment of dairy cattle at the end of lactation).
  4. Administration of antimicrobials to a specific individual animal at a specific and well defined high risk time.

#1 can be addressed through other means or may not be useful at all. It’s often done because that’s the way it’s been done, not because there’s any evidence it’s needed. This type of prophylaxis would be the top priority to phase out.

#2 might be addressed reasonably through prophylaxis, but it also might be better addressed through management changes, vaccination and other approaches. Prophylaxis might be needed in the short term as other measure are implemented.

#3 would need more investigation since it’s such a wide area, but there could be substantial decreases, if not total replacement of antimicrobial use. It might require non-antimicrobial treatments, vaccination, changes in management and (most of all) behavioural change (the human brain being the biggest barrier to better antimicrobial stewardship in most situations).

#4 is necessary in many situations. We overuse antimicrobials in this scenario, but there are some situations where the benefits of a short course (or single dose) of antimicrobials greatly outweighs the risks, particularly for high risk surgical procedures.

Prophylaxis absolutely needs to be a focus for antimicrobial stewardship strategies in animals (and humans). However, we can’t just say “stop it” – we should be aiming to massively reduce but not completely eliminate it.

We also can’t say “change it all now.” We could have a massive impact on prophylaxis immediately with no disruption to animal health or production, since much prophylactic use is unnecessary. However, to achieve further decreases without adverse animal health and welfare impacts, we need to improve animal management, infection control, access to veterinary care, access to vaccines and alternatives, and support (logistical, technical, financial) to make these necessary changes. That’s particularly true when we look at the issue internationally. A farmer in a low/middle income country can’t make massive changes without support, or we’re going to run into serious food security and economic issues. This is why we have to step up and do more than say “just stop it.” Yes, we need to provide motivation and pressure, and we need to have some degree of regulation. But, we need to provide support so we can massively reduce the misuse and overuse of prophylactic antimicrobials. It’s feasible, but it’s not as simple as the sound-bite approach to AMR might have people think.

This is a question I get a lot. My typical answer is “yes, but…”


The “but” can lead to a long discussion. I have a bit of a complex relationship with antimicrobial use (AMU) targets.

  • Targets can be useful for driving change, to ultimately help us combat antimicrobial resistance (AMR).
  • Targets can also be misleading, ineffective, impractical, unrealistically aspirational and disconnected from what we really need to do.

We need targets that lead to action, but more specifically to effective action.

We don’t need targets that are just used for sound bites, to make it look like we’re doing something but that don’t have a real impact. We have too much of that already.

The concept behind AMU targets is simple. We set a threshold for amount of antimicrobials we use that we want to stay under. Targets can be at the national level, species (human, cattle, pigs, etc.), sector (human hospital, veterinary clinic), prescriber (veterinarian, physician, dentist) or another level.

Targets can be useful if they provide encouragement to act and reduce AMU.

  • However, they can also be a smokescreen or sound bite with inadequate underpinning to stand a chance of having any effect.

Targets can be good if they improve AMU.

  • Combating AMR is not just about reducing AMU. How we use antibiotics, how long we use them and what drugs we use are as, or more, important than the total amount.

Targets can be bad if they compromise animal health and welfare, disrupt animal care, or result in shifts in drug use that reduce the total amount used but worsen how we use antimicrobials.

Most often, the focus is on the mass of antibiotics used (kgs, tonnes). That’s particularly true at national or international levels, such as the 2022 Muscat Manifesto’s call for a 30-50% reduction in AMU in animals (see excerpt below):

Overall mass is usually the easiest number to calculate, and it’s often a big, scary number that gets lots of attention. However, there are a lot of limitations to using this metric for AMU. We can get more information by looking at use in specific populations or animals, for example, people in hospitals, or cattle in feedlots.

My personal opinion is that mass-based metrics for AMU, which are the main focus for AMU targets, largely suck. I use them, but that’s because it’s typically all we have, but I know they have major limitations. Here’s why:

  • Mass just tells us how much weight of antimicrobials went into the overall population (be it animals or people). It doesn’t tell us why, when, how, or what type. Overall mass data (all antimicrobials combined) is particularly useless since we use different doses for different antimicrobials, treat different species differently and there are major differences in sizes of different animals, from grams (chicks) to hundreds of kilograms (cattle).
  • Differences in drug potency are also a big problem. For example, if I change from a drug that is dosed at 20 mg/kg twice a day to one that is used as 2 mg/kg once a day, I’ve dropped overall antimicrobial mass used by about 95% (40 mg/kg/day to 2 mg/kg/day). That’s an impressive reduction and it sounds great. However, it could also be the last thing we want, since higher potency (lower dosed) drugs are usually newer, broad spectrum, higher tier drugs that are very important in human medicine. So, if you said we have to reduce antimicrobial use in livestock in Canada by 50%, we could do that quickly by switching to higher potency drugs, but risk making AMR issues much worse (which is the complete opposite of our goal).     
  • Overall mass data can be useful if we’re comparing apples to apples, such as looking at total kgs of antimicrobials used in beef cattle when the cattle population hasn’t changed and when relative use of different drugs hasn’t changed. That approach has been used successfully to reduce antimicrobial use in livestock in Denmark, through their Yellow Card system. So, I don’t discount the use of refined mass-based approaches, but we can do better, as overall mass used can be misleading in different situations and doesn’t guide optimal antimicrobial stewardship (AMS) activities. Ultimately, it’s a very crude measure that can be hard to use outside of situations where there’s a very narrow and well defined scope of use.

Ok, so I’ve whined enough about how mass-based metrics suck (or at least aren’t good enough). What can we do instead?

I’m pragmatic enough to know that we’re likely going to focus on pretty crude, high level metrics for international declarations, like a 30% reduction in tonnage of AMU in animals. That can be okay if we use more actionable and relevant metrics to underpin that high level goal.

I think we need to move more to appropriate use metrics for AMU targets. From an animal AMU standpoint, we could target things like:

  • no use of medically important antimicrobials for growth promotion in any country by 2030
  • no use of highest-priority critically important antimicrobials (HPCIAs) for group prophylaxis in animals
  • 100% of AMU is done under the guidance of a veterinary professional
  • species and life-stage specific targets (e.g. prophylaxis of less than 40% of groups of post-weaning piglets, prophylactic treatment of less than 20% or dry cows)
  • percentage of AMU that is consistent with national or international AMU guidelines

We also need to think about targets that don’t directly relate to AMU but which drive AMU indirectly, such as targets that involve access to antimicrobials, healthcare and preventive medicine:

  • access to at least one first line antimicrobial for common diseases in all countries
  • access of all animal producers to a veterinarian or trained allied animal health professional
  • free availability of guidelines that are relevant for the species, region and language of veterinarians and other prescribers
  • access to preventive health tools such as vaccination

Can we reach these targets today (or in the very near future)?

  • We can achieve some of them, in some countries.

Using effective AMU targets isn’t an immediate fix for improving AMU and reducing AMR. We need to be aware of the many other things that also need to be done:

  • We need to be able to accurately measure AMU at an adequately granular level to be able to understand AMU in any given population
  • We need to facilitate access to resources and guidelines to improve AMU decision making
  • We need to provide support (logistical, expertise, financial) to food animal producers, particularly in developing regions, to improve animal management and preventive medicine as food animal production ramps up
  • We need to work with animal owners/producers to overcome barriers to stewardship, which are often psychological (e.g. resistance to change, fear of change)
  • We need to streamline access to preventive health tools such as vaccines, as well as access to quality antimicrobials everywhere.
  • We need adequate private and public funding to implement the measures needed to reduce the need for AMU and to better monitor AMU

Additionally, we need to monitor to see what works, including impacts on both AMU and AMR. “Doing something” shouldn’t be the end goal. “Doing something that works” should be the target.

As we start World Antimicrobial Resistance (AMR) Awareness Week (WAAW) 2023, I’ll cover a variety of areas about this important topic.

Why do we even care about AMR?

AMR is an urgent international problem. It threatens the healthcare (human and animal) gains that we’ve made over the past century. It’s estimated that AMR was associated with almost 5 million deaths globally in 2019 (Murray at al. 2022). The World Bank has estimated that, by 2050, AMR could reduce the global gross domestic product (GDP) by 3.8% and push 28 million people into poverty.

Those are pretty striking numbers, but despite that, AMR is also an overlooked problem… a silent pandemic.” For something that kills millions, harms more, will almost inevitably get worse, and which has major social and economic impacts, the “give a crap” factor by the general public is really low. People will march in the streets about climate change (another serious and complex problem) but they don’t seem to give a thought to AMR, unless they or someone close to them is directly affected by it.

Why doesn’t the public seem to care about AMR?

AMR is insidious. It’s not seen by most people. It’s hard to understand. It’s poorly communicated. It’s oversimplified. It’s not well understood.

It’s a “wicked problem.”

Wicked problems, like AMR and climate change, are tough to define, tough to address and tough to fix. There are lots of definitions of a “wicked problem” but they share some similar characteristics (see diagram below):

  • The problem is hard to clearly define.
  • Data are weak, lacking or contradictory.
  • There’s no clear pathway to solving the problem, with a start and end.
  • There are lots of stakeholders, often with different agendas, needs, perspectives and motivations.
  • True solutions are hard to identify, difficult or costly to implement and often can’t be tested without implementation.
  • There are lots of interconnections between disparate issues and groups, leading to massive social complexity.
  • Possible solutions might cause new problems, or solutions that work for one component (e.g. humans) may harm another (e.g. animals).

There is no magic bullet to fix the AMR problem. And backing up another step, I’d argue about the use of the “AMR problem” term I used above.

AMR isn’t really the problem.

Yes, it’s what we’re worried about. However, AMR is largely the end result of antimicrobial use (AMU).

AMU is the problem.

Realistically, AMU isn’t even the root problem. Why we use antimicrobials (so many and so often) is the issue. That’s because of health, or more specifically, sub-optimal human and animal health (real or perceived)(see diagram below).

To address AMR, we need to address AMU.

To address AMU, we need to address healthcare (human and animal) access, equity, food security, innovation, preventive medicine, how we raise animals, how people live and myriad related issues that go beyond the bug-drug-disease triad.

The science is challenging, but in some ways it’s the easy part.

The biggest barrier to addressing AMR is the human brain. That’s in part because antibiotics are often used for their profound psychoactive properties: they make the prescriber feel better because they are doing something, even when that something may be harmful.

Is it hopeless? No.

Do we have the tools to address the problem? Yes.

Do we have the expertise to address the problem? Yes, but we need more.

Do we have the political will to do what’s needed?

  • Not usually. It varies, but in most places it’s not really on the radar and politicians are often reluctant to take the steps we really need to take without drive from the people who elect and support them.

Do we have the necessary financial support? Not a chance.

Pretty pessimistic overview? Yes, but there are encouraging signs:

  • AMR is getting more attention. There’s still a lot of room for improvement but it’s coming along and some countries are taking a lead.
  • Lots of good research continues to be done, with increasing involvement of social scientists, a key aspect to addressing behaviour (of both patients and prescribers).
  • There’s a UN General Assembly High Level Meeting on AMR in 2024 – a big deal, and one that can help drive action.
  • Numerous national, international and sector initiatives are underway.
  • Ground level support for antimicrobial prescribers is increasing. For veterinarians, that includes our Firstline: OVC/CPHAZ prescribing app for companion animals.

So, as we embark on WAAW 2023, I’ll cover some interesting (to me, at least) topics in the AMR field.

We’re not going to fix this problem with one tool, one discovery, one action or one group. We’re going to do it through myriad small, incremental gains by a massive number of individuals. Like climate change, the impact of a single person seems inconsequential, but fixing AMR will rely on small actions by everyone involved in researching, making, distributing, prescribing and using antimicrobials.


Back in August, I wrote about a high-profile but poorly described “outbreak” of feline infectious peritonitis (FIP) in cats in Cyprus. Now, a preprint publication (Attipa et al. 2023) has come out with some interesting information, but lots of questions still remain. That’s the nature of emerging diseases – a single report gets us farther down the path but rarely answers all of the important questions.

Here’s a quick refresher about FIP: Feline infectious peritonitis is a nasty disease caused by feline coronavirus (FCoV), a very common virus in cats that circulates widely in the cat population. Whenever you have a large group of cats, you can be pretty sure there’s FCoV circulating somewhere in the group. It’s usually not a problem because the virus doesn’t typically make most cats sick. However, FIP develops in a small percentage of infected cats when there’s a random mutation in the spike protein of the virus that occurs after the cat is infected. So FIP is not spread cat-to-cat, it’s FCoV that spreads between cats, with an unpredictable change to the virulent version of the virus causing FIP in some cats.

In the past, FIP has been considered an almost invariably fatal disease. There are some new treatment options, but those are mainly black market-sourced in North America. I’ll get back to that topic later as there are some new developments.

Back to the cat deaths in Cyprus…

Reports came out of Cyprus earlier this year of thousands of cats dying from what they suspected was FIP. The numbers varied a lot and tended to decrease when people started asking questions, but still, there were lots of cats dying. It’s tough to assess the significance of reports like that when we have little data about what’s going on now and little historical data for comparison. There are lots of cats on Cyprus and most are feral. If you have a million feral cats, I’d expect a hundred thousand (or more) deaths per year in that population under normal circumstances, many due to FIP among other things, but we almost never hear about those deaths in the population because people don’t look, count or test. However, I also don’t dismiss boots-on-the-ground observations, so when people start talking about remarkable increases in deaths, I pay attention.

The preprint (Attipa et al. 2023) provides some more epidemiological and clinical information:

  • They only had 165 confirmed FIP cases, which is a very small number for a country with so many feral cats, but since diagnosis requires lab testing which costs money, only a subset of cats ever get tested.
  • This rate is considerably higher than the 3-4 cats per year in Cyprus that are normally diagnosed with FIP, but we don’t know if that’s because of a marked increase in disease, a marked increase in testing, or a combination of both.
  • Disease in the confirmed cases was pretty typical for FIP (i.e. no unusual clinical findings).

So was this a huge outbreak or not?

When there’s more discussion and awareness of a disease, you get more diagnoses of endemic disease that may have been there all along. Often these “outbreaks” are combination of a small overall increase or a small local cluster of disease and increased testing and reporting, leading to over-estimation of the true increase in the disease rate. Only a few cats a year were diagnosed with FIP in Cyprus before this, but how many did they test? If you start to look, you find things that have always been there.

However, the genomics data included in the paper support concerns that this could be a true, new, large FIP outbreak. The virus they found appears to be a recombination of a feline coronavirus with a pantropic canine coronavirus strain (see diagram below). Those are both alphacoronaviruses, which are different from SARS-CoV-2, which is a betacoronavirus. This kind of recombination event can happen, so it’s not a shocker. What it means and whether it will play a role in changes in disease or disease patterns is unclear, but it will need to be studied.

The big question is whether this new strain might be transmissible between animals as an FIP virus, versus the typical situation where a random mutation needs to occur in the FeCoV in a previously infected cat in order to cause FIP.

  • Based on some genomic characteristic and the very close similarity of different virus isolates, the authors suggest that this could be a virus that is transmissible in a FIP-causing form. If so, that would be a big concern, and could plausibly cause a true, large outbreak of FIP.

It’s also unclear if this is a new issue or whether it’s a newly discovered issue that’s already been there for some time. If it’s driving an outbreak, we’d expect that it’s a new emergence. However, due to lack of surveillance before the outbreak, we can’t be sure it wasn’t there before. I’d guess it’s fairly new based on the similarity between the strains they tested, as viruses tend to develop more population diversity over time (e.g. you find a wider variety of strains the longer the virus has been circulating, but all the strains they found were very similar).

This virus strain was also found in a couple of cats imported from Cyprus to the UK. That’s not surprising since lots of cats get moved around and they bring pathogens like this with them. It raises concern about whether this could result in seeding of a new, more virulent, strain in other countries around the world.

It’s still too early to make a definitive call on whether this is a transmissible FIP virus, whether it’s likely to cause other outbreaks or whether it’s spread beyond Cyprus. Unfortunately, as is often the case with infectious diseases, it’s a “time will tell” scenario, but we need to keep investigating to figure out what’s going on, what the risks are and, if this is an issue, what we can do to reduce there risk and impacts.

They also used molnupiravir in lots of cats during this outbreak, as they were using up stockpiled and expiring COVID-19 drugs for people. That scares the hell out of me given that drug’s crap-tastic performance as a COVID-19 drug and its tendency to cause more viral mutations. But, that’s a separate story…