group of 4 puppies

We’re getting reports of potential canine parvovirus infection in vaccinated dogs in some parts of northern Ontario. Parvo is a nasty but vaccine-preventable disease, and available vaccines are very effective. True vaccine breakthrough (i.e. infection in a fully vaccinated individual) seems to be rare with canine parvo, but no vaccine is 100% effective, so it is possible.

Whenever I hear reports of canine parvovirus vaccine failure, the first thing that comes to mind is whether the dogs are actually vaccinated, and vaccinated properly. Most of the time, these “breakthrough” infections are not actually due to vaccine failure, but failure to vaccinate the dog properly, or infection that occurs before vaccination has a chance to take effect.

Most young animals some acquire short-term immunity to certain diseases from their mothers. That’s critically important to prevent infections early in life, but it also impacts the effectiveness of early vaccination, because the antibodies that youngsters have from their dam (maternal antibodies) can interfere with vaccine response.

When we vaccinate puppies against parvovirus, we typically start at 8 weeks of age. At that age, vaccination probably won’t work well because of maternal antibodies, but if it does, great. If the pup doesn’t have a lot of maternal antibodies (left) at that stage, we don’t want to risk leaving it unprotected.

We do the same thing at 12 weeks of age, with the same rationale.

By 16 weeks of age, we’re getting confident that maternal antibodies have dropped enough for the pup to respond to a vaccine. A single dose of core vaccines (usually given as a combination vaccine for parvo, distemper and hepatitis) at this age should provide solid immunity. We’ll sometimes give an extra dose at 20 weeks of age if it’s a higher risk area, the dog has a higher risk lifestyle, or we’re not convinced about the dog’s age. That’s a bit of an insurance policy.

We then revaccinate 6-12 months later, and usually go on an every 3 year cycle after that.

Most of the time, when I see parvo “vaccine failures,” it’s when vaccination stopped at 12 weeks of age. That’s not a vaccine failure to me. That’s incomplete vaccination.

True vaccine failure can happen, but it seems to be very rare. We need to watch out for it in case there’s a problem with the vaccine (very unlikely) or a new strain of the virus that current vaccines don’t cover (also very unlikely, but something we’d want to catch as early as possible).

When we hear of large numbers of possible breakthrough parvo cases, it gets more concerning, but it’s still most often from incomplete vaccination. We’ll often start to hear about more cases that were already occurring in the background simply because people start talking about it more. So, an increase in reported cases itself doesn’t necessarily mean something new happening.

For me, the first step in sorting out issues like this is clarifying vaccination status of the affected dogs. If all the dogs were incompletely vaccinated, we have our answer (and an opportunity to better educate owners). On the other end of the spectrum, if we have large numbers of dogs with reliable full vaccination histories (particularly when done by a veterinarian, as we have more confidence in proper administration, as well as vaccine cold chain and handling), I get more concerned, and would want to get samples from cases for virus sequencing.

To start at step 1, we’re trying to collect information about parvo cases occurring in dogs that are reportedly vaccinated (to some extent). People can voluntarily report cases here:

We do this type of on-the-fly surveillance periodically, as needed. Some flop because there’s not much reporting or the problem burns out. Sometimes, we find interesting and actionable information. We’ll see what happens here.


Vaccine hesitancy by pet owners has been in the news a lot recently, largely due to a recent study about the prevalence and consequences of vaccine hesitancy among dog owners in the US (Motta et al. 2023). The survey-based study reported 37% of respondents think vaccines can cause “cognitive issues, like canine/feline autism”, 22% think the risks of vaccination outweigh the benefits, and 30% think most dogs receive vaccines that are not necessary. A colleague and I wrote a commentary for the San Francisco Chronicle about how this kind of vaccine hesitancy among pet owners is a concern for both people and pet, especially if it results in reduced rabies vaccination coverage.

The survey by Motta et al. only scratched the surface of the issues. We need a lot more information about vaccine hesitancy to truly understand the problem, and to be able to properly address it, but it’s definitely a concern.

Vaccine hesitancy, in both people and animals, is a really complex area. I think we’ve tended to over-simplify the issue in the past by lumping people into really broad groups (e.g. “anti-vaxxer,” “cheap”) without properly investigating the reasons behind their actions. People who don’t want to use vaccines aren’t one homogenous group.

  • Some are hardcore, true “anti-vaxxers.” This is often driven by mistrust in the system or science, and it’s hard to address this group. You can’t convince someone to trust, and trying to throw more facts at them doesn’t help.
  • Most are “vaccine hesitant,” with concerns that are not unreasonable but may be misplaced, misunderstood or simply not adequately addressed. This is the group on which we should focus, because it’s the group with which we have the most potential to engage, address their concerns and hopefully alleviate those concerns.

A lot of people who are vaccine-hesitant are worried about adverse effects of vaccination. We have to be honest: adverse effects occur. There’s a basic level of risk that we accept when we use vaccines because of the broader benefits. I have no doubt that the core vaccines we currently use in pets do more good than harm. But, I also have no doubt that some harm can occur. I’ve seen it.

That’s tough messaging, because a lot of people don’t really care what happens to 99.9% of the population after vaccination. They care what happens to their individual pet. While we can never tell people that the risk is zero, we can explain what the risks are and try to put them into perspective, so they can make an informed cost-benefit decision.

To do that, we need to understand what the risks really are. What data do we have on vaccine adverse effects in animals?

A landmark study about adverse events in dogs within 3 days of vaccination was published in 2005 in the Journal of the American Veterinary Medical Assocaition (Moore et al, 2005). The authors studied medical records from over 1.2 million vaccinated dogs. Here are a few of the things they found:

  • An adverse event rate of 38.2/10,000 dogs (0.38%).
  • Adverse events were more common in smaller dogs and when more vaccine doses were administered. It’s important to note that this means doses of different vaccines (i.e. number of injections), not the number of antigens. A vaccine that contains 5 different antigens is still just one vaccine dose from the standpoint of adverse event risks.
  • Each additional vaccine increased the risk of an adverse event by 27% in small (<10kg) dogs and by 12% in larger dogs.
  • The highest adverse event rates were in dachshunds, pugs, Boston terriers, miniature pinschers and chihuahuas.
  • 1.7% of the reactions were anaphylaxis (the most serious kind of reaction). That corresponds to about 0.006%.

By vaccine, the adverse event rates were:

  • Injectable Bordetella: 15.4/10,000
  • Rabies: 24.7/10,000
  • DAPP (distemper, adenovirus, parvovirus, parainfluenza): 26.2/10,000
  • Leptospirosis: 28.8/10,000
  • Borrelia (Lyme disease): 43.7/10,000

The highest overall rate was when a combination of rabies and Borrelia vaccines was given (54/10,000). The very common combination of rabies and core vaccines (DAPP) resulted in a rate of 39.3/10,000.

A subset of these records were investigated further to look in more detail at the adverse effects.

  • Facial swelling was the most commonly reported problem (31%), followed by wheals or welts (21%), general itchiness (15%) and vomiting (10%). 
  • Collapse was noted in 1% of dogs with a reaction.

A similar study in cats (Moore et al, JAVMA 2007) looked at adverse reactions in 496,189 cats within 30 days of vaccination. The overall adverse event rate was 51.6/10,000 cats. As for dogs, the risk increased with the number of vaccine doses that were administered. Lethargy was the most commonly reported problem.

The canine study has recently been repeated. I haven’t seen the results published yet, but snippets have been reported, and some data were presented by Dr. George Moore at the 2022 ACVIM Forum.

  • They evaluated the records of 4.9 million dogs that were vaccinated at Banfield Pet Hospitals in the US from 2016-2020.
  • The incidence of adverse events linked to vaccination within 3 days of vaccination was 18.45 per 10,000 dogs (or 0.18% of dogs). That’s less than half the rate of the older study.
  • Dachshunds, Boston terriers, miniature pinschers, French bulldogs and havanese were over-represented, continuing to show the increased risk in small breeds. The higher risk for certain breeds (and consistency between studies over a 20 year timespan) suggests that there are possibly genetic factors that drive the risk.
  • Increased number of vaccine doses given at the same time increased the risk in dogs les than 20kg but not in dogs over 20 kg.
  • There were no significant differences between adverse event rates for DAPP, leptospirosis, rabies or Lyme disease vaccines, with rates ranging between 19.2-21.3/10,000.

With these numbers, we can pretty confidently say that adverse event rates are low in dogs, and the most recent study suggests that they’ve actually dropped. A reason for that is unclear, but it could relate to newer, more refined, vaccines.

So, while I’d never guarantee that someone’s dog or cat won’t have a vaccine reaction, we know the rates are low and we have ways to reduce the risk even further. If we had lower vaccination rates we’d have fewer animals with vaccine reactions (that are almost always transient) but a lot more animals with severe and potentially fatal disease (which can have permanent long-term consequences, even if the animal survives.

The cost:benefit calculation is clear to me.

Avian flu caused an uptick in discussion about health risks associated with feeding dogs and cats raw meat, based on the possible (and still pretty tenuous) link between raw poultry and a large number of H5N1 infections in cats in Poland.


The link between raw diets and flu infections is new, and something we need to look at more, but since common things occur commonly, we need to also pay attention to the traditional concerns with raw diets. A recent report from Quebec about multidrug-resistant Salmonella infections in people highlights one of the major human health risks of raw pet foods. Salmonella contamination of raw diets is common, and this bacterium can cause disease in both people and animals.

The report was based on an investigation of 15 human infections with a multidrug-resistant Salmonella enterica serotype 4,[5],12:i:- (not all Salmonella serotypes have specific – or pronouncible – names).

  • The 15 infections were identified by 10 different health regions in Quebec between July 2020 and December 2022. They then found 2 more cases in Dec 2022.
  • As is typical, kids bore the brunt of the problem. Nine of cases were in kids less than two years of age.
  • The bacterium was resistant to a variety of antibiotics, including ampicillin, cefotaxime, ceftriaxone and trimethoprim sulfa, and resistant or of intermediate susceptibility to fluoroquinolones and azithromycin. That’s pretty concerning, because if you end up in hospital with salmonellosis, those are all the typical go-to drugs for initial treatment. If someone is seriously ill with Salmonella and is started on one of those drugs pending culture results, the treatment won’t work and they’ll get sicker or potentially develop more complications before an effective treatment is identified.

As is typical, when the investigation started, they asked questions about the common sources of Salmonella. Initial results indicated some patients had contact with cattle farms and some with raw pet foods. This led to a more detailed investigation, and then they found that 14 of 17 people had contact with raw pet foods.  The same bacterium was also found in 2 dogs that were fed these raw diets, further supporting the link to pet food.

The report also briefly mentions 10 cases in Ontario with the same strain, at least 2 of which had contact with raw diets.

This doesn’t really change anything, since we already know that animal and human infections occur from exposure to raw animal-based pet diets. It’s important information to get out, though, because there is a still a general lack of awareness of these risks and lots of misinformation. Some manufacturers take steps to reduce (not eliminate) the risk of bacterial contamination in their raw diets (mainly high pressure pasteurization). Some try to explain the risks and how to reduce them (if you’re going to feed a raw diet, use those companies). Some do nothing, and worst of all some downplay the risks and even provide false information.

My typical take home messages for people thinking about feeding raw diets are:

  • There is risk to people and animals.
  • The risk can be reduced a lot with common sense, but not eliminated.
  • The risk is probably low with common sense and in a low risk household.
  • The risk is unacceptably high in households with high risk people (e.g. young kids, elderly, pregnant, immunocompromised individuals) and high risk dogs (similar groups).
  • If you want to feed a raw diet, use some basic precautions to reduce the risks. We have more on that in our Raw Meat Infosheet available on the Worms & Germs Resources – Pets page.

I’ve held off writing about this unusual outbreak of cat deaths on the island of Cyprus for a few reasons, a big one being a lack of clear information, but the situation has drawn a lot of attention.

In general, when we have reports of strange disease events, there are a few scenarios to consider:

  1. It’s a completely new disease
  2. Something has change regarding an known disease
  3. It’s a known disease doing what it normally does, but circumstances have led to a unique local, short term situation
  4. It’s a known disease doing what it normally does, but with more attention being paid to it

All of these happen. I’d say that numbers 3 and 4 are most common, with number 4 being particularly common due to amplification of routine disease situations by social media.

What’s going on in Cyprus?

Clear details have been pretty sparse, so I think it could still be any of these scenarios.

How many cats have been affected?

The story started around January 2023, with subsequent reports of “thousands” of cats dying in Cyprus. There appears to be some debate about the scope of the problem. One claim is that 200,000-300,000 cats, or roughly 20-30% of the cat population on the island, have died.

However, that claim has not been substantiated, and it has been suggested that the actual number of deaths is less than 10,000. That’s still a lot of cats, so clearly significant, but some context is needed.

  • How many feral cats normally die every week in Cyprus?
  • Is this mortality rate higher than normal, or are people just paying more attention to it?
    • If the true number of cats that have died is around 10,000, that would be approximately 1% mortality, and a 1% mortality rate over a few months is actually on the low side for what would normally be expected in such a population.

Those are key initial questions that need to be answered to help us determine if we actually have something different happening on the island.

What’s the cause?

The outbreak was quickly attributed to feline infectious peritonitis (FIP). This didn’t make a lot of sense based on what we know about FIP, which is caused by feline coronavirus (FCoV). The disease develops in a small minority of infected cats, when the FCoV mutates to become more virulent. FCoV is very common, especially in large cat populations. If you have more than 10 or so cats in a group (e.g. shelter, colony, feral cats), it’s almost certain that one or more of them are infected. So, finding FCoV in dead cats is not surprising. We’d find lots of it in live cats, too.

FIP outbreaks are uncommon, though. When they occur, they are usually small outbreaks associated with some local factors in the cat population (e.g. age, genetics, health status) that make a small group of cats more likely to develop FIP. A country-wide outbreak, even in a small country, would be pretty surprising.

Diagnosis of FIP involves more than just finding the virus. We have to figure out if it’s actually causing disease. I haven’t seen details about how the diagnosis of FIP has been made in these cases. It could be that a large number of cats have been solidly diagnosed with FIP, a small number of cats amongst a large number of untested dead cats had FIP, or that there wasn’t actually any solid diagnosis of FIP (and someone was just guessing).

The question is whether FCoV is causing disease or it’s just there, and whether any cats with FIP were representative of the outbreak or there were just some cats with FIP alongside something else. That’s what’s unclear to me. I’ve heard that FCoV from some infected cats is being sequenced, which is a great start. This will help determine if there’s something unique about the virus in these cats and if it’s one strain that’s present in the majority of affected cats.

A good epidemiological investigation to define what’s happening is key to sorting out situations like this, but often, that gets neglected (or at least done superficially). With a better understanding of the situation and context regarding how it compares to normal, we’re better able to target the laboratory investigation and figure out what we need to do to contain the outbreak. Hopefully that’s underway.

There was also a recent report that extra COVID-19 drugs are being used in some cats on the island. Details are sparse and it’s hard to see how that will help much in the context of an outbreak. Some COVID-19 drugs (mainly remdesivir) have great promise for treatment of FIP, which is usually a fatal disease in cats. However, while it will help the small number of sick cats that get access to the drug, it won’t help stop the outbreak since it will have no impact on transmission within the population. It’s circulation of the wild-type FCoV that’s the problem, and treatment of a handful of cats with FIP won’t do anything for that. Presumably they’re not treating healthy cats preventatively, since that probably wouldn’t help anyway, would require a massive amount of drug, would be impractical for feral cats (that would be the main reservoir) and, depending on the drug, might just be setting the scene for harmful mutations (especially if molnupiravir is used).

If this is something new, what do we have to do?

The first step is make a diagnosis. We need to know whether this is a new version of FCoV, a new disease or whether it’s just normal viruses doing their normal things. Until we know that, it would make sense to ban importation of cats from Cyprus.  

Here’s a question I get surprisingly often.

I found a dead raccoon (or raccoon poop) in my pool and I’m freaking out about raccoon roundworms. What should I do?

The raccoon roundworm, Baylisascaris procyonis, is certainly a parasite of concern, but it’s also one that often leads to over-reaction and panic. While it can cause severe disease in people, infectious are really rare, and almost always associated with ingestion of a pretty reasonable amount of raccoon poop. A large percentage of raccoons carry the parasite in their intestinal tracts so there’s really widespread opportunity for exposure, but the rarity of disease shows how low level and casual contact with the parasite’s eggs likely pose little to no risk to most people.

The concern with a dead raccoon or raccoon poop in a pool is that there will likely be roundworm eggs (the infectious form of the parasite) in the water. The eggs survive very well in the environment, so they persist for a long time outside the host, and they aren’t destroyed by either chlorine or salt water.

However, in a pool we have two important protective mechanisms: dilution and filtration.

Although we have no hard data, I’d say the odds of getting infected with Baylisascaris from pool exposure are pretty much zero (as long as you don’t ingest floating piles of feces…). That said, it’s still reasonable to take some precautions to remove as much contamination from the pool as possible.

The US CDC has quite a detailed guidance specifically for cleaning pools potentially contaminated with raccoon feces. The guidance says to test the raccoon/raccoon feces for Baylisascaris, and clean the pool.

  • Since the response to a positive or negative test is the same (clean the pool), testing seems unhelpful. It adds cost, hassle and a time delay, and with a negative, I still wouldn’t rule out that the critter was infected since testing isn’t 100% sensitive. So, I’d skip the testing and just assume the critter was positive.

For cleaning the pool, they provide two options:

Option 1:

  • Filter the pool for a minimum of 24 hours and then backwash the pool filter.
  • Put on disposable gloves to replace the material doing the filtering (if possible). Double bag the discarded material in plastic garbage bags. Remove gloves and place them in the garbage bags. Wash your hands thoroughly with soap and water afterwards.

Option 2:

  • Backwash the pool filter.
  • Drain and hose down the pool.
  • Put on disposable gloves to replace the material doing the filtering (if possible). Double bag the discarded material in plastic garbage bags. Remove gloves and place them in the garbage bags. Wash your hands thoroughly with soap and water afterwards.
  • Refill the pool.

I think changing the filter medium isn’t very high yield, and depending on the filter type, it can be a pain. They include an “if possible” disclaimer, but I’d go farther and say “don’t bother unless you’re really worried.” The odds of a pool filter being a source of infection for this parasite, from my perspective, are basically zero (and if there’s a risk to worry about, it’s probably greater from handling the filter than leaving it in place).

Anyway, it’s fine to take that approach, but the main steps that are both practical and effective are:

  • Remove any visible feces (rinse whatever was used to do so after).
  • If there was a chance of contamination of hands while cleaning, wash hands thoroughly.
  • Keep people out of the water for 24 hours with the filter running.
  • Don’t stress about it.

While you’re at it, it never hurts to take a look at your yard to identify and eliminate anything that might be encouraging raccoons to visit (e.g. accessible food sources or garbage).

I had an interesting discussion yesterday about the “antimicrobial pipeline” as part of the Global Leaders Group on Antimicrobial Resistance. When we talk about the antimicrobial pipeline, we’re referring to the dwindling number of new antimicrobial drugs that are currently in development. Antimicrobial research and development (R&D) has fallen by the wayside over the past decades as pharmaceutical companies focus on higher-profit drugs – typically those that are more likely to be used for chronic or lifelong conditions, not critically important antibiotics that will be used as sparingly as possible.

So, as antimicrobial resistance (AMR) continues to increase, we don’t have a wealth of new drugs to compensate for older drugs that are becoming less and less effective.

Discussion of the antimicrobial pipeline usually revolves around funding to support new drug development. That’s a complex area that I won’t get into much, but it’s a huge part of the issue. We need money to support new drug development, to get more drugs into the pipeline.

However, increasing the flow into the pipeline is only part of the solution. Another big problem is the holes that are in the pipeline.

Pumping more into the pipeline helps to some degree, but if we don’t plug the holes, we can’t maximize the benefits of all the time and money that go into the R&D of new drugs. If we put a few hundred million dollars into supporting a new drug without plugging those massive holes in the system, we may end up right back in the same position in the not-too-distant-future… more resistance and a need for more new drugs.

Yes, we need more funding for new drugs, to develop them, license them and get them distributed everywhere they are needed.

At the same time, we need to fill the holes in the pipeline. There are lots of them. For example:

  • Inappropriate antimicrobial use in humans
  • Inappropriate antimicrobial use in animals
  • Inadequate healthcare access
  • Inadequate animal/veterinary healthcare access
  • Poor animal management
  • Inadequate use of preventive measures (e.g. vaccination, infection control, biosecurity)
  • Inadequate development and use of alternatives to antimicrobial drugs
  • Inequitable access and distribution of antimicrobials (leading to poor or ineffective use)
  • Defensive medicine

And the list goes on.

Yes, we absolutely need to better fund antimicrobial research and development. But, we can’t rely on that alone to solve the problem. We need to fix (or at least minimize) all the holes in the pipeline at the same time, to reduce the need for new drugs, to reduce the emergence of resistance to new drugs, and to maximize the effective use of new drugs (including for how long they remain effective). If we don’t fix the holes, our efforts to feed more R&D into the pipeline will simply be a waste. In the end we’d only slightly delay the bigger crisis, rather than fixing the problem long term.

If we know one thing about influenza A, it’s that there will always be something new with this virus.


A recent study out of China (Meng et al. 2023) describes what seems to be a new canine flu strain. Is it a concern? It’s hard to say at this point, but having more flu strains in a species with which we have close contact is never a good thing.

This was a surveillance study of dogs in an area of China where there’s a massive amount of pet dog breeding and trading. Our familiar H3N2 canine influenza is endemic there, and avian flu strains circulate in wild birds, creating the potential for spillover of avian flu viruses into dogs and/or emergence of new strains from virus reassortment.

Researchers tested dogs from November 2018 to April 2019, and identified influenza virus in 60 of 534 dogs (11%) by PCR. Follow up testing resulted in isolation of live influenza virus from 12 dogs. Isolation of live virus requires culture techniques. We expect to get less recovery with culture compared to PCR, since PCR will detect lower viral loads and does not require the virus to still be viable by the time of testing.

Five of the flu viruses that were isolated were H3N2.

  • That’s not surprising, since H3N2 is a well established canine flu strain in China.

Interestingly, seven of the viruses were H3N6.

  • Looking at the genetic makeup of the virus, it appears to be a mix of H3N2 canine flu and an H5N6 avian flu strain that was circulating in birds in China in 2017 and 2018.
  • It was hypothesized that this was a result of a dog being co-infected with H3N2 canine flu and H5N6 avian flu, resulting in creation of this new H5N6 strain.

Does this mean there’s a new canine flu strain circulating in China?

That’s unclear. Positive samples were from dogs in one shelter at one time point, which could happen for a few reasons:

They found the first dog with this strain, and picked up transmission in the shelter that burned out, making this a one-off event.

  • It’s very unlikely they would have gotten that lucky and captured the very first emergence of this virus. Some of the in vitro characteristics of this virus suggest it should be well adapted to mammals, so full containment is probably unlikely. There’s also some genetic variation in the H3N6 isolates, which we wouldn’t expect with a single point-source exposure.

This virus is rare in dogs and there was cluster in that shelter at that time.

  • Possible, but odds are low that researchers would pick up a rare event like that. As above, the genetic variation in strains suggests that this was more likely from multiple introductions of the virus into the shelter.

H3N6 is circulating in dogs and this study detected a strain that’s been present in the region for a while.

  • This seems most likely.

The lack of clear sampling information is a big limitation in terms of interpreting the study results (e.g. were the dogs sampled on admission to the shelter? Were the positive dogs housed together? Were they sick?).  That’s very basic information that needs to be in a paper like this, but that weak journals may let slip or don’t think to query.

The main things I take away from this report are:

  • We need more surveillance to see if this strain is still present and where it is distributed. H3N6 is probably a relevant new-kid-on-the-block. It’s probably established given it was found in an area like this with massive dog breeding.
  • Changes in importation rules will reduce the risk of this virus hitting North America, but there are enough loopholes that there is still a very reasonable likelihood that it will be introduced here at some point.
  • We need to continue to watch for influenza A infection in various animal species. That includes dogs, which often fall between the cracks because it’s usually VERY hard to get support for disease surveillance in companion animals (compared to food animal). Lots of agencies want to know the results, but rarely do they want to foot the bill. It’s a significant gap in One Health surveillance.

What will we see if H3N6 flu hits Canada (or another country)?

Assuming it causes disease similar to other flu strains, we’ll see large numbers of dogs with typical flu-like disease (which will be lumped together with routine occurrences of “kennel cough”). The number of cases will be the dramatic thing, not the severity; however, with lots of cases, we’ll see more severe cases just based on percentages.

Since dogs will presumably have no existing immunity to this strain, the main thing I’m looking out for is big outbreaks. We see “kennel cough” outbreaks all the time, caused by our usual suspects like canine parainfluenza virus, Bordetella bronchiseptica and canine respiratory coronavirus. However, if/when a new flu virus hits, it will likely be much more and obvious. Rather than an outbreak that affects a lot of dogs in a group (e.g. kennel, shelter), it will affect almost all of them. Rather than a single outbreak in a town, there will be many. I suspect it will be pretty obvious pretty quickly if this virus makes it here.

Raccoon dog (Nyctereutes procyonoides), Finland.
Photo credit: Jukka A. Lang

I would have hoped that the issues with SARS-CoV-2 in mink would have been (yet another) wake up call, but I guess not. Some changes have been made in some areas, but it’s status quo in most places. Given our pretty crappy baseline, status quo is not a good state to be in.

The latest issue, as per the latest WOAH report, is H5N1 influenza on multiple fur farms in Finland, raising Arctic foxes and raccoon dogs (yeah… because nothing bad has ever been associated with farming raccoon dogs!).

The response? Apparently, basically nothing:

Currently no control measures are applied as HPAI is not “listed disease” in fur animals.”

What could possibly go wrong with some 1500 raccoon dogs and 3500 foxes in close quarters on a farm with H5N1 and a response that seems to be mainly surveillance? Don’t get me wrong, surveillance is important. However, surveillance is not a mitigation tool. It provides clarity on what’s happening and helps guide further response. Great surveillance without mitigation is akin to filming a sinking boat in 4K but not bothering to send in any lifeboats. We get great video of the disaster but don’t save any lives.

Large groups of susceptible species create risk for virus transmission and mutation. That’s sometimes unavoidable. There’s a cost-benefit side to consider, and we can’t eliminate all animals or all human-animal interactions.

However, we can look at situations that create more risk (e.g. susceptible species, dense housing, poor management) and have limited benefit. There’s really no societal benefit of fur farming. Fur production is not essential, the benefits of fur farming are for a miniscule percentage of the population, yet the risks are borne by all of us, are real and could be substantial.

Another wake up call. Will we actually respond?

My own animals provide frequent fodder for this blog, both good and bad. Rumple’s been featured a few times before, and his latest escapade is a great antimicrobial stewardship case.

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.

A week or so ago, we noticed a scab on Rumple’s ear and one on his neck. We 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 ago, 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 has 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.


The H5N1 avian flu outbreak in cats in Poland seems to be slowing down but the cause is still under investigation. While outbreaks often die out on their own (sometimes because of what we do, sometimes despite what we do), it’s still important to figure out what happened, to help understand the disease and ideally prevent future problems.

It seems like the number of confirmed cases has stayed at 16 and I’ve received fewer anecdotal reports from people in Poland about new sick cats. Clear information is still fairly sparse (and my lack of Polish fluency doesn’t help) but there have been reports implicating food as the source of H5N1 infection in these cats. I mused about possible sources of the virus in this outbreak last week, and a food link was on the list, but I assumed it was #2 or #3 on the depth chart).

A few pertinent things have been reported from different sources:

The same or very similar H5N1 strain was found in multiple cats from different areas.

  • That would be consistent with a point source exposure such as food, but could also be because there’s a single dominant strain of the virus that different cats were exposed to through other routes over a short period of time.

H5N1 was found in 1 of 5 samples of raw poultry diets from affected households

  • That’s a critical finding. Most importantly, they found more than just viral RNA (which could be dead virus) – they were able to isolate the whole virus, meaning it was in a viable state in the diet.
  • This adds a lot of weight to the food-source hypothesis, but since it’s retrospective and so far just 1 food sample tested positive, it’s not definitive.

For me, a key question remains: Did all of the cats receive the same diet?

That’s a very basic component of the epidemiological investigation that should be easy to sort out, but unfortunately laboratory components of outbreak investigations often move faster than boots-on-the-ground epi / info collection. If all the cats got the same diet and contamination of at least some samples of that diet can be demonstrated, that’s a pretty solid presumptive link, especially for the affected indoor cats. It’s a bit trickier in outdoor cats because of other potential sources (e.g. birds), and more details about the genomics of the locally circulating virus strains is needed to help sort that out. Ultimately, we’re often left with “most likely” cause, versus “Eureka! We’ve nailed the diagnosis!

So, hopefully we’ll get more details soon but we have to move food up to the top of the list for potential sources in this outbreak for the moment. That raises a few more obvious questions:

Should cats be fed raw poultry?

There are various issues with raw diets and this just adds another dynamic. Without knowing more about the food that’s been implicated here, it’s hard to say too much.

The risks from typical commercial diets prepared from poultry that’s deemed safe for human consumption (the poultry, not the pet food) is very low. Since H5N1 infections on poultry farms are usually pretty obvious (lots of sick and dead birds very quickly), it’s unlikely that infected poultry from commercial operations would make it into pet food manufactured by a reputable company.

If there are pet food diets that do not use typical “human-grade” poultry, the risks could be higher. If poultry from infected farms is (presumably illegally) being diverted to dodgy pet food companies, risks from those would be even higher.

If people are making their own raw diets, the origin of the birds/meat is the key. Poultry purchased at grocery stores should be exceptionally low risk. Other sources (e.g. live birds or meat from small outdoor operations) could pose much greater risks. The less scrutiny and transparency about the poultry sources, the greater the concerns.

The safest way to avoid food safety concerns from raw diets is to avoid them, cook them, or use a product that’s at least high pressure pasteurized (there’s no guarantee the HPP process eliminates all pathogens in the food, but it should at least greatly reduce pathogen levels).

So, at this point, I’d avoid feeding raw poultry to pets if there’s not complete confidence in the source, especially in areas where H5N1 is active in birds. I’d stick with products from companies with strict (and transparent and adhered to) rules about their sources, that use commercially reared poultry and that have a proper food safety program.

Are there related food safety concerns for people?

More information about poultry sources that are linked to this outbreak is critical. If food was a source, was it the same poultry that’s eaten by people, or was it from some other pathway? That’s a big question.

That said, fortunately people don’t tend to (deliberately) eat raw poultry. Cooking will eliminate any influenza virus (and a lot of other pathogens) in the meat. However, there’s always some risk of exposure to foodborne pathogens from improper handling and cooking (that’s how we get things like Salmonella) and H5N1 can survive on meat for at least a few days. So, we can’t ignore the risk entirely.

The risks would be lowest (and approaching negligible) from poultry sold in grocery stores. The risks would be highest from live market-sourced birds where there’s no information about the health status of the flock. There are gradations in between, but overall, the less the confidence in the health status of the flock, the greater the risk of contamination of the birds and the products made from them.

Cooking poultry properly, prevention of cross contamination and good kitchen hygiene (including hand washing) would greatly reduce any risks, even in the unlikely event contaminated poultry was present.