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We call rabies “almost invariably fatal” in people. Rabies kills an estimated 50,000 people a year globally, mostly in Africa and Asia. Even with very intensive care, the prognosis is grave. Only a very small number of people have survived rabies: there are approximately 34  documented cases of survival, but an even smaller number of people have survived without serious longterm neurological deficits.

In 2004, a treatment regimen coined the “Milwaukee protocol” was used to successfully treat rabies in an unvaccinated 15-year-old girl (Jeanna Giese), after she was infected through direct contact with a bat. It involved giving anesthetic drugs (ketamine and midazolam) to put her in a coma and slow down her brain function, and two antivirals (ribavirin and amantadine), along with very intensive care to support her vital body functions. The idea was to try to protect her brain and try to reduce the rabies virus levels long enough to give her immune system time to fight off the infection. Remarkably, she survived. Even more remarkably, while her recovery was prolong, she ultimately seemed to have limited longterm neurological problems and 20 years later is a mother of three.

The success of the protocol was published (Willoughby et al. 2005) and it became the foundation for future treatment attempts. Unfortunately, while it attracted a lot of attention and optimism, its success has not been reproduced. That has lead people to question whether Jeanna survived because of the treatment, or simply because of a very fortunate confluence of exceptional factors (that we don’t know) and intensive supportive care, which resulted in her body being able to fight off the virus with few lingering effects, despite not having been vaccinated.

A recent commentary entitled Demise of the Milwaukee Protocol for Rabies (Jackson et al. 2025) highlights these issues, including that there have been no subsequent proven successes (anecdotes, but no hard evidence) and at least 64 documented failures, and that critical care is likely the most important component, as opposed to the specific drug cocktail that was used in Jeanna’s case. The author calls for abandonment of this protocol (which has been echoed by others too) and consideration of new treatment approaches.

The letters to the editor section got a little testy, with a response from Dr. Willoughby (the doctor who oversaw Jeanna’s case and published the Milwaukee Protocol), including a  disappointing comment akin to “well, how many rabies survivors have you had?”   Willoughby claims there are more survivors, but provides no details or links to any peer-reviewed data. Now not all useful data are published, so we shouldn’t dismiss the response based solely on that, but for such a high profile disease and for a protocol that’s been challenged over the past few years, if there were solid data it would be strange for none of it to be published. There might be more evidence of patients surviving, or there might just be weak anecdotes, incomplete stories, questionable data and survival of patients that didn’t actually have rabies – all of which are mentioned in Dr. Jackson’s response to Dr. Willoughby).

Dr. Willoughby states “We do not change a successful protocol even if mechanistically mysterious.” But while we shouldn’t dismiss things that might work out of hand, but we need to objectively assess them, and make sure we are not blinded by single successes, personal biases or hope.

  • Sometimes we don’t understand things that work. We don’t want to make clinical decisions solely on mechanistic aspects and proxies that don’t necessarily apply in the patient.
  • At the same time, we shouldn’t perpetually use treatments that are lacking solid proof of efficacy. We have lots of unsubstantiated dogmas in medicine (both human and veterinary) that persist for decades because they are not critically evaluated, despite no evidence to support them or even evidence against them.

In the case of rabies, one might think “Even if it doesn’t help, it can’t hurt, and we should try something.” That’s understandable, but if people think we have a possibly effective treatment, there’s less impetus to develop and evaluate other treatments that might be more effective. Clinging to a futile treatment can be harmful.

Is the Milwaukee Protocol futile?  Medicine seems to be leaving this protocol behind, but we can still learn from it, and some of the concepts remain potentially useful. Efforts to control the neurological impacts and providing intensive supportive care to keep the patient stabilized while their body gradually fights the infection are probably still key. However, the reliance on the specific drug cocktail used in the Milwaukee protocol, which has not necessarily worked apart from that first case, might be stifling more research.

Twenty-two years from this highly published success, rabies remains almost invariable fatal, and successful treatment is beyond the grasp of the vast majority of people who get infected, as most are in resource limited areas where the degree of required intensive care is not available. The search for an effective treatment continues, and hopefully we’ll find one someday that will be accessible across the world, and not just to those who can access (and afford) highly specialized care.

More important is rabies prevention. That’s still our first and most important defence against this deadly disease, including vaccination of domestic animals, vaccination and sterilization campaigns in areas where canine rabies is endemic, education to avoid bites and how to respond to bites, and improved access to and uptake of rabies post-exposure prophylaxis. Like most problems, prevention is better than treatment, but we still need an effective treatment as rabies isn’t going away.

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Antimicrobials are often used at the time of surgery, but it’s widely accepted that there is tremendous overuse of antimicrobials in this context in both human and veterinary medicine. Antimicrobial prophylaxis is indicated in some surgical patients to reduce the risk of surgical site infection, but in a large percentage of cases use of antimicrobials is actually unnecessary and is based more on habit or fear (i.e. more to make the surgeon or pet owner feel better, versus actually helping the patient).

Clinical guidelines are an advancement in care, and the field of antimicrobial guideline development has progressed significantly in recent years. We’ve moved from primarily expert-opinion-based guidelines to evidence-based, structured guideline development, which should yield stronger, less biased and more defensible guidance, but guidelines are never perfect, since there are typically still lots of evidence gaps. Also, guidelines are meant to cover the majority of situations, not every possible case, so there are always exceptions to the “rules.” Nonetheless, good guidelines help support good clinical decisions.

The European Network Optimization of Veterinary Antimicrobial Therapy (ENOVAT) has just released their new 2025 guidelines for surgical antimicrobial prophylaxis in dogs and cats. These guidelines are the culmination of several years of work, and are underpinned by a thorough scoping review of antimicrobial prophylaxis in companion animal surgery (Sorensen et al. 2024) and a systematic review on the same topic (coming soon).

The guidelines have a heavy emphasis on when NOT to use antimicrobials, since that’s what the evidence supports, but they also highlight situations where antimicrobials are recommended, and they provide details about optimal approaches for when they’re needed.

The guidelines used a GRADE-based approach, which culminates in a strong or conditional recommendation for or against each intervention (or a conclusion that we can’t make a recommendation either way).

For strong recommendations, the guidelines say “we recommend…”

  • Strong recommendations for an intervention (i.e. antimicrobial prophylaxis) are made based on moderate to high certainty evidence of the effect of the intervention, plus supporting value amongst various other domains (e.g. importance of the problem, benefits, harms, cost:benefit, equity, acceptability).
  • Strong recommendations against an intervention can be made based on similarly moderate-high certainty evidence or where there is lower certainty evidence about the effect but moderate/high certainty evidence about potential harms. The default is not to use the intervention, so a strong recommendation against can be made without solid data showing it doesn’t work.

For conditional recommendation, the guidelines say “we suggest…”

  • Conditional recommendations are made when the recommendation is based on low certainty evidence or when there is a lot of uncertainty or variability about acceptability, applicability, equity or other factors that indicate it might not be an ideal or preferred approach for most. (For example, we’re not going to make a strong recommendation for a treatment that’s so expensive only a small subset of the population could ever use it.)
  • A conditional recommendation doesn’t mean that the treatment is less effective than one with a strong recommendation, it simply means the confidence and certainty behind the recommendation is lower, and/or that its value is more situational, being a preferred choice in some situations but not others.

Below is a quick synopsis of the recommendations (in tiny print). Check out the full text article (which is open access) for more details on each recommendation and the evidence behind them all.

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We’re in the midst of a pretty bad human flu season. That’s a problem by itself, as it also means severe flu cases and hospitalization rates are high, and likely to increase. High flu activity in people also amplifies concerns regarding H5N1 avian influenza, because it creates more opportunities for an infection with both a human flu virus and the H5N1 avian flu virus to occur in the same person (or animal) at the same time. That could lead to recombination of the two viruses creation of a new flu strain that is more severe and transmits effectively person-to-person.

H5N1 avian flu has spilled over into a large number of mammals. Among domestic animals, cats and cattle have attracted the most attention, but there is also some risk to dogs. The number of infections in dogs has been very low (especially considering how often dogs are likely exposed to infected wild birds, other wildlife, cats or livestock), but in a couple of cases infection has been shown to be quite serious. Case in point was a recent fatal H5N1 infection in a dog in Alberta.

In November 2025, a 10 year old golden retriever / poodle cross dog (better known as a goldendoodle) was infected with H5N1 influenza after exposure to a snow goose, and subsequently died. The dog had a compromised immune system (it was being treated for an immune-mediated disease), and that could have contributed to severity of the disease caused by the flu virus. It’s similar to the case that occurred in an Ontario dog in 2023, that died from H5N1 flu after being exposed by chewing on a Canada Goose that died from the same infection.

This case is more of a reminder of the risk that’s already been present for a while, versus anything new, but it’s part of the reason we put a lot of effort into H5N1 influenza control. Currently circulating H5N1 flu strains are poorly adapted to infect and spread between people (and dogs, and most other mammals with a few exceptions), but every time the virus spills over into a mammal, it creates more opportunity for the virus to change and adapt to infect more mammals, which is definitely bad.

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That headline might get some people worked up, but hopefully they’ll read the whole post before firing off an angry email.

Antimicrobial resistance (AMR) is a huge problem in humans and animals, which means we need to improve or optimize how we use antimicrobials, but this is not synonymous with reducing use. Most of the time, improving and optimizing antimicrobial use (AMU) does focus on reduction, because we greatly overuse these drugs in general. Most of the national and international discussion around AMU also focuses on reduction, typically based on one quite crude measure: mass (kgs, tonnes) of drug used in animals over time (e.g. annually). Overall mass of drug used is usually one of the easier numbers to get (though even that can take considerable work depending on the system), and sometimes its useful, but it’s not always the best. Other times it’s simply not helpful, and other times it’s downright misleading.

I wrote a more detailed commentary on this same topic that was recently published in the Canadian Veterinary Journal, but here is a quick summary of some of the reasons why we need move beyond looking at simply reducing the mass of drugs used when it comes to improving antimicrobial stewardship.

All antimicrobials are not created alike

We have a lot more concerns about resistance to some drugs (higher tier) compared to others (lower tier). That’s why antimicrobials used in animals are categorized based on their potential impact on AMR in humans. Simply measuring the mass of all the drugs used together doesn’t consider which drugs are being used. It’s also important to account for differences in dosing. Newer, broader spectrum, higher tier drugs tend to be more potent, so they are used at lower doses (see table below), but the consequences of resistance to these drugs is much higher.

Based on this, we could significantly drop the mass of antimicrobials used in animals by using more higher tier drugs in place of lower tier drugs – but that is exactly what we don’t want to do! If a country is pressured to reduce AMU, the risk is they may simply substitute higher tier drugs for lower tier drugs, and then say “look how much we’ve reduced our antibiotic use, good for us!” while ignoring the disaster in the making.

Related to this, an increase in the mass of antimicrobial use might be good in some situations. Let’s use dogs with urinary tract infections as an example. In the table below, the “pre-intervention” column is based on 1000 dogs treated as per a study of AMU practices in dogs with urinary tract disease in the US and Canada. If we implement an intervention to move practices to 100% compliance with ISCAID guidelines for treating urinary tract disease in dogs, it would increase the use of three lower tier drugs, which is good. But, it would also increase the overall mass of drugs used by quite a bit, based on how they are dosed. Looking at the effect on mass of drugs used alone makes this look like a harmful intervention, when in fact the change would be good from a stewardship standpoint, since it would mean using the lower tier, recommended drugs.

Increased animal production

The world is growing. Populations in some countries are expanding greatly, and overall wealth is increasing, leading to more need for food, and more demand for meat. We can debate the ecological aspects of meat production, but ultimately we can’t expect countries to stop increasing their own food production to satisfy a numerical target for antimicrobial use. If a country expands its meat production by 100% but only increases their AMU by 25%, it means they are using less drug per animal or per kilogram of meat. That’s a step in the right direction and a big win in my mind, as it’s often accomplished through improving overall animal health, which provides many other benefits beyond improved AMU. If a country is expanding meat production, they’re not going to sign onto any agreement that limits the overall mass of antimicrobials used, but instead we should be working together to optimize animal health in order to optimize antimicrobial use, so we maximize the benefits and minimize the risks.

Increased access to antimicriobial drugs

“Use as little as possible but use enough”. That’s my mantra when it comes to antimicrobials.

We can use too little. Animals get sick, and sometimes they need antibiotics (just like people). Internationally, a lot of animals that would be helped by an antibiotic don’t get one because the antibiotic is not available or not affordable, or there’s limited or no understanding of how/when to use it. This is most common in low income countries, but access issues in different countries vary. Improvements in drug availability, less poverty, increased literacy, improved transport infrastructue (e.g.roads), better access to veterinary care and other factors can reduce underuse of antibiotics. That can lead to a short term increase in antibiotic use, but it’s better for animal health and welfare, and hopefully is ultimately combined with improvements in animal management, preventive medicine, vaccination and other basic care.

All that said, we still need to reduce antimicrobial use

We massively overuse antibiotics (in animals and in people). However, AMR is a complex problem, and complex problems can’t be addressed with simplistic, sound-bite approaches, like picking a random number and an arbitrary date and saying “let’s reduce antibiotic use in livestock by X% by the year 20XX.” We need more nuanced discussions to maximize animal health, use antibiotics when needed, choose the right drug and duration in each case, and stop using them when they are not needed. Some of that will reduce AMU, but some might increase AMU (at the mass level or even overall), but ultimately improve overall health of animals (and people) and reduce the impacts of AMR.

We also need to think about what we really want to measure. As you can tell, I’m not a fan of measuring overall mass of drugs used. It’ better than not measuring use at all, and it can be useful in some situations, but it’s mainly used because it’s a relatively easy number to calculate. We’re better off focusing on metrics for appropriate use of antimicrobials, such as:

  • The percentage of animals of a certain age or health status that are treated with an antibiotic therapeutically or prophylactically
  • The percentage of treatments that are consistent with available AMU guidelines
  • The percentage of treatments that use lower tier drugs
  • The percentage of animals that are treated based on the advice of a veterinarian

These metrics take a lot more time to develop but are more understandable, more actionable and ultimately lead to better surveillance-to-action, and impact.

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Change is tough. Repeated changes are even tougher, especially when it takes a lot of time and effort for each one to be understood and implemented. But change is also good – and important – when it improves how we do things.

In 2024, the Clinical and Laboratory Standards Institute (CLSI) changed some important breakpoints for antimicrobial susceptibility testing in dogs. Breakpoints are what labs use to to report whether a bacterial isolate is susceptible or resistant to different antimicrobials. As we learn more about the bugs and the drugs and how they interact, sometimes those breakpoints need to be adjusted, so that the veterinarian receiving the report is getting the most accurate information possible to make better treatment decisions for the animal. That’s good. But it also involves change, which can be slow. It’s taken close to two years for some labs to fully implement the 2024 changes.

Now we have data suggesting more things need to change. CLSI hasn’t updated any mrore breakpoints (yet), but published data indicate that we should probably be rethinking how we’re interpreting certain antimicrobial susceptibility test results for cats.

A recently published study (Papich et al. 2025) came to the conclusion that that breakpoints for fluorquinolone antibiotics for some bacterial isolates from cats should be lowered. That means some bacteria that would currently be reported as susceptible should actually be considered resistant. It’s very similar to the changes that were made in 2024 for isolates from dogs; I suspected at the time a similar change would eventually be needed for feline isolates, but it hadn’t yet been studied enough.

The researchers examined pharmacokinetic data, pharmacokinetic-pharmacodynamic (PK/PD) analysis and susceptibility data from a large number of bacterial isolates to determine the appropriate breakpoints for enrofloxacin and marbofloxacin when it comes to Enterobacterales (E. coli and related bacteria), Pseudomonas aeruginosa, Staphylococcus spp., Pasteurella multocida and Streptococcus. Skipping to the punchline, what they found indicated that we should be using lower breakpoints for these bug-drug combinations in cats. The current breakpoints would classify certain isolates as susceptible to these drugs, when in fact the likelihood of achieving adequate inhibitory drug levels in the target tissues using standard dosing was very low.

Here is a summary of the old (technically still current) and suggested new breakpoints for these bug-drug combinations in cats:

They also suggested a “susceptible dose dependent” (SDD) breakpoint, as was done for dogs. This means that the bacterium can be considered susceptible when a higher dose of the drug is used in the patient. For marbofloxacin, isolates that meet the SDD breakpoint are only considered susceptible when the cat is dosed at 5.5 mg/kg (the high end of the label dose for this drug). There are no SDD breakpoints for enrofloxacin because we don’t want to use higher doses in cats due to the risk of causing blindness (retinopathy). Personally, I have no use for enrofloxacin in cats at all because of this risk. but if it’s going to be used, we don’t want to go beyond 5 mg/kg regardless, so there’s no SDD breakpoint.

What do we do now?

  • We have data suggesting that we need new breakpoints, but the CLSI standards haven’t yest been changed.
  • Personally, I’ll start using the new breakpoints right away. I trust the research group and the data, and the new breakpoints are consistent with the change that was made for canine isolates.
  • When we get MIC data directly on our lab reports, it’s easy to apply the breakpoints ourselves. The challenge is when labs only test a narrow range of drug concentrations or don’t report MICs (i.e. the report doesn’t provide the number, just susceptible intermediate or resistant (S-I-R)). Then we’re a bit stuck, and my confidence in using enrofloxacin or marbofloxacin would decrease.

Pradofloxacin, the newest licensed fluoroquinolone in cats (and dogs in some countries), was not included in this study. The breakpoints for this drug were not changed for dog isolates in 2024 either. Whether that’s because the newer breakpoints for pradofloxacin are fine, or there isn’t enough data to re-assess them, or it was just lower priority to study isn’t clear, but it raises questions. If I see an isolate that is resistant to marbofloxacin and enrofloxacin based on the new breakpoints in dogs (or the suggested new breakpoints in cats), and it’s classified as “susceptible” to pradofloxacin but right at the breakpoint, I’d be wary of using it. It might work perfectly fine, but it gives me a bit of pause, and I’d be inclined to look at other options.

I’ve been meaning to write about this for a few days, but a case from today prompted me to finally do it. It was a cat with an E. coli infection that was reported as susceptible to fluoroquinolones, but looking at the MICs and this paper, I’m not confident that it actually is. So, I recommended a different drug. I actually would have recommended the different drug anyway, since it was a lower tier option that should nonetheless be effective, but this paper changed my assessment; had my options been more limited, I would have searched for a non-fluoroquinolone option.

This paper and the new suggested breakpoints add more complication to an already complicated area, but while it can be a hassle, and change is still tough, it’s important progress. It will help veterinarians provide more effective patient care and improve antimicrobial stewardship, by avoiding using drugs that aren’t likely to be effective against specific infections in cats.

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I’m on my way back from Copenhagen where we had a very productive meeting to update the ISCAID pyelonephritis antimicrobial treatment guidelines for dogs and cats. As the process for developing guidelines like these has matured, it’s no longer about simply getting some very smart people in a room and agreeing on recommendations; it’s now a much more structured, evidence-based process. As part of that, we think about more than just “would this drug work?” We also think about factors like adverse effects, cost, acceptability, feasibility, equity and others. One of the newer consideration is now “planetary health,” which is applicable to a lot of things, including antimicrobial use guidelines.

Antimicrobial production, distribution and use have carbon footprints and require other resources that impact more than the individual who gets treated with the drug. (And yes, I fully recognize the irony of talking about carbon footprints while flying across the Atlantic in a plane, but sometimes in-person meetings are important too.) While we’re not going to dramatically alter our guidelines based on a drug’s carbon footprint, it’s something we need to at least think about for awareness. A side benefit of good antimicrobial stewardship resulting in less antimicrobial use is smaller footprints of this sort. But, are those footprints really relevant? It’s always hard to figure out what the contribution of something like a drug (or a flight) is to the big picture, and individual events have near negligible impacts. But, when we do something over and over and over again, the cumulative impact starts to become more relevant.

What do we know about the ecological impacts of antimicrobials? I’m far from an expert in this, but it’s interesting, so I’ll just toss out a few points – food for thought.

That’s a random collection of studies on the topic, and ultimately we don’t really know the full downstream effects of antimicrobial use, but it’s fair to say that these drugs have a big carbon footprint, and we can reduce it through antimicrobial stewardship: using fewer antibiotics, using them better when necessary, and, most importantly, optimizing health so we don’t have sick people or animals to treat in the first place.

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It’s nice to finally be able to talk about H5N1 influenza without discussing ostriches, but unfortunately, we still have things to talk about.

1) Peacocks. Specifically peacocks that don’t have influenza and aren’t going to be culled.

Last month I posted about an animal sanctuary in BC (Critteraid) that was dealing with an outbreak of H5N1 influenza in poultry on the property. The outbreak lead to investigation of the risk to other animals on the same premises, including their peacocks. My understanding is the peacocks were physically well removed from the infected birds, so there was clear rationale to try to avoid culling them. It was a great example of how to respond to H5N1. Critteraid was transparent, worked with CFIA and followed their guidance, and took appropriate measures to contain the infection and decontaminate the affected areas. As a result, CFIA was able to assess the situation through their established processes, the peacocks were tested and were negative for the virus, and they were therefore able to avoid culling them.

2) More sick cats with the flu. This story doesn’t have such a good ending. We know cats are susceptible to H5N1 flu and often develop fatal neurological disease. Recently a lot of attention has been paid to exposure of pet cats to the virus via raw diets and raw milk, but cats can also get infected through contact with infected birds. A recent cluster of fatal H5N1 infections in a group of kittens in the Netherlands reminds us of that risk:

  • On November 19, a kitten from a dairy goat farm was found dead and tested positive for H5N1 flu. Samples were collected from other animals on the property the next day as part of the investigation. Three adult cats (including the kitten’s mother) were tested, as were the goats (the goats probably being the main concern, given the issue with H5N1 in dairy cattle in the US). All of the animals were healthy at the time, and all tested negative.
  • However, the other 7 kittens from the litter weren’t on the farm anymore as they had all been adopted. Further investigation revealed that they had all died; none of them were tested, but it’s quite likely they all could have had H5N1 flu as well.
  • The source of the virus in this case couldn’t be identified, but the mother cat was seen with a dead bird October 27, and it would be logical to assume that the kittens may have eaten part of the bird or been exposed to it it some way. The timing doesn’t quite fit though, as that was 23 days prior to the one kitten being found dead on the farm, which is a very long timeline for flu. I’d have to wonder if there might have been exposure from another dead bird, since the mother cat likely caught birds on more than one day, or she may have been infected by the bird caught on October 27, and then the kittens were subsequently infected by her.

This case is a good reminder of the potentially devastating impact of this virus on cats and one of the reasons why we’d prefer to keep cats away from wild birds. If cats have outdoor access, flu must be a consideration in any cat that develops acute neurological disease or dies suddenly.

We don’t know what’s the risk is to people from infected cats. I think we have to assume there’s some degree of risk since there is evidence to support that cat-to-cat transmission can happen. Fortunately the risk to people seems to be low, given the lack of identified cat-to-human transmission. However, we can’t rely on that to say there’s no risk, both in the present and in particular in the future, as this virus continues to evolve.

It’s World Antimicrobial Resistance Awareness Week. Did you know that? Probably not. Antimicrobial resistance (AMR) is a huge global health threat with an unfortunately crappy marketing plan.

I’m on my way back from the BC One Health and Zoonoses Symposium where I was talking about AMR. It’s a complex issue and there are a lot of things we need to do to address the problem. One is development of clinical guidelines for antimicrobial use (including when not to use them), but a major challenge with guideline development in veterinary medicine is a profound lack of high-quality evidence to guide us.  We have few clinical trials, and even fewer that are properly designed and executed. That doesn’t mean we can’t create guidelines, after all we have to start somewhere, but it limits the certainty we have in the evidence that underpins our recommendations.

Fortunately, we are making progress in this field. Slowly. Trials are difficult to do and can be expensive, and it’s often very hard to find funding for this type of work, but progress is being made.

Peri-operative antibiotics are commonly used (and overused) in veterinary medicine to prevent surgical site infections. Sometimes they are needed, but often they aren’t. Continuing antibiotics post-operatively is still common too for some procedures, but there’s likely little to no reason to do so. We want antibiotics on board during the “period of risk” when contamination of tissues related to surgery is most likely: that starts with the surgical incision and ends soon after the surgical wound is closed. So we want antibiotics in the tissues at good levels during surgery, and potentially for up to 24 hours after, but that’s it. Once the period of risk is over, the benefit of antibiotics plummets and the costs (e.g. adverse events, selection for resistance) outweigh the risks.

Unfortunately, it can be difficult to convince people to stop giving antibiotics post-operatively, because it’s what many have gotten used to doing, and people are resistant to change. Post-op antibiotics is more psychotherapy for the veterinarian or owner…. it make us feel better if the animal gets an antibiotic, but it doesn’t make the animal feel any better (and may in fact do more harm than good).

A new study published just a couple of months ago (Vlhäinen et al. 2025) provides some good new evidence regarding the use of antimicrobials to prevent infectious complications following pyometra surgery in dogs. Good data like these can help convince people to change their habits and helps support our guidelines. Pyometra is an infection of the uterus that is not uncommon in unspayed dogs. In these cases, the uterus basically becomes a big pus-filled bag, and the most effective treatment is removing it (hysterectomy).

In this well-designed randomized controlled trial, 152 dogs undergoing pyometra surgery were enrolled and received an intravenous antibiotic (trimethoprim-sulfadoxine) pre-operatively. Then, they were randomized to either receive 5 days of oral trimethoprim-sulfadiazine (TMS) or a placebo. It was a non-inferiority study, so all they were aiming to do was to determine if no treatment was no worse than antibiotic treatment.

  • Surgical site infections developed in 7.8% of dogs that got post-operative antibiotics and 2.7% of those that didn’t, so not giving post-op antibiotics was definitely no worse than giving them.
  • Post-operative urinary tract infections developed in 2.7% of the treated dogs and none of the untreated dogs, so antibiotics didn’t help prevent these infections either.

In another interesting component, they looked at bacteriuria (bacteria in the urine without infection) of a subset of 43 dogs that were known to have been bacteriuric pre-operatively. They found 14/20 (70%) in the placebo group and 2/23 (8.7%) in the treatment group were still bacteriuric post-operatively.

  • That’s not too surprising, since TMS is a great urinary drug, and 5 days of post-op treatment would be more effective for clearing bacteria from the lower urinary tract than a single dose (single dose treatment for urinary infections works for some drugs but not something I’d have a lot of confidence in for TMS). But remember that only 2 of those dogs had signs of cystitis, and both of them were dogs in the treatment group.  None of the dogs that had pre-operative and then post-operative bacteriuria had any clinical signs of infection. This supports the notion (and our guideline recommendations) that bacteriuria in the absence of disease (subclinical bacteriuria) doesn’t need to be treated.

This study provides some nice evidence supporting the lack of need for post-operative antibiotics in pyometra surgery, which is something we can also likely extrapolate to a range of other “clean-contaminated” procedures.

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The mention of fur farming can evoke some pretty strong reactions from some people, but this industry largely flies under the radar most of the time. The industry itself is dying out in much of the world, as people turn away from raising animals solely for their coats, but large numbers of animals are still farmed in some countries.

Recently, the Federation of Veterinarians of Europe (FVE),  Federation of European Companion Animal Veterinary Associations (FECAVA) and World Small Animal Veterinary Association (WSAVA) released a joint position statement on fur farming. It’s pretty straightforward, and consistent with various other statements, but further highlights concerns about fur farming and pressure from professional groups for countries to take action. The statement calls for:

  • A legally-enacted complete phase-out of fur farming globally in the next decade.
  • A phase-out of farmed animal fur and products containing such fur being placed on the market.
  • A ban on importing farmed animal fur and products containing such fur from countries that have not phased it out.

The position statement supports its call for a ban on fur farming by highlighting the inability of confinement rearing to meet the complex behavioural and physiological needs of species commonly farmed for fur (e.g. species like mink and fox, which naturally range over wide areas and don’t live in large groups), health and welfare problems from common rearing conditions (e.g. wire-floored cages), concerns about euthanasia methods commonly used for these species, the impact of escaped non-native animals on local ecosystems and native species, and zoonotic disease risks.

Some people will point to arguments like “If we ban fur farming, then we should ban all animal farming,” for two different reasons. Some will say it because they want all animal farming stopped. Others will say it to argue that we shouldn’t restrict one type of farming if we aren’t going to restrict others, and to let consumers decide which industries should survive.  

Like most things, there’s a middle ground. The cost:benefit also comes into play, but it can be tough to calculate for multifaceted issues like this where the costs and benefits are not easy to quantify (especially animal welfare) and where a component of the “cost” involves the potential for future infectious disease outbreaks. The societal component is also part of the consideration.

  • The societal benefit of fur farming is likely negligible. Yes, some people make a living from it, and some people like the products, but that’s a very small group. There are less than 100 known fur farms in Canada.  Given the small number, it could be more practical to fund transition plans for fur farms to close or move into other types of agricultural activities, if the main concern is those who rely on the industry for their livelihood.
  • The societal risk from fur farming could be substantial (though it’s hard to predict) since some farmed species are potential reservoirs of a variety of infectious diseases, including some that can infect wildlife or even people. Mink, in particular, are good hosts for a few concerning viruses, like influenza and SARS-CoV-2. Mink farming was eliminated in some countries during the COVID-19 pandemic when it was recognized that mink were getting infected, and the farms had potential to act as viral reservoirs and increase the risk of viral mutations. While the odds a problem developing are really low, the implications if it happens could be really high. The position statement adds “Despite biosecurity measures, fur farms remain a persistent potential reservoir of zoonotic risk, requiring disproportionate disease surveillance, culling, and resource investments.”

So, we have little to no broader societal benefit but the potential for serious infectious disease risks, on top of the substantial animal health and welfare concerns when it comes to fur farming, which is why this statement ultimately calls for a ban. We’ll see if more veterinary associations follow suit with similar statements.  

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Canada recently lost its measles-free status, in large part because of a slip in our overall vaccination rate. A lot of that has been driven by vaccine hesitancy. The resurgence of measles in people shows what can happen when we aren’t using one of our best control methods (vaccination) optimally.

Vaccine hesitancy is an issue in veterinary medicine too, and it’s probably increasing. There are known overlaps between vaccine hesitancy in humans and animals; people who are wary of or opposed to human vaccination often have similar approaches to vaccination of animals. It’s a complex issue, though, with many causes, and unfortunately pretty limited data.

  • One study of people in the US (Motta et al. 2023) showed that 53% of respondents reported at least one component of hesitancy, i.e. expressing concern that veterinary vaccines may be unsafe (37%), ineffective (22%), or unnecessary (30%). We don’t have comparative data for Canada; my guess is it’s less prominent here, but still a significant issue.

Vaccines are highly effective disease control tools, in both human healthcare and veterinary medicine. They aren’t perfect, but they are critically important. They can range from useful aids to critical tools to essentially the only line of protection, depending on the vaccine and the disease. Without vaccines, pet life expectancy would be shorter: we’d lose a lot of young animals to preventable diseases. Veterinary care costs would also be higher. We’d probably have fewer people with pets because of these challenges, especially in urban areas where a lot of pets and pet contacts would mean a lot of disease transmission.

Why are people vaccine hesitant?

It’s critical to understand the reasons behind vaccine hesitancy to try to mitigate the problem.

  • Some people have completely understandable and valid concerns.
  • Some people fundamentally do not believe vaccines are safe or effective, and they will not trust anyone or anything that says otherwise.
  • Some people may not really know why they are hesitant – they’re simply unsure.
  • Internal conflicts can be part of the problem too, such as a person who is really worried about the cost of vaccines, but doesn’t want to admit it (openly or to themselves), and might therefore convince themselves that it’s safer not to vaccinate, to avoid feeling like they are compromising their pet’s health by not vaccinating.

Various other complex scenarios occur too. The bottom line is it’s complicated, and often unclear. That makes addressing vaccine hesitancy challenging.  

  • If someone has trust issues, we can educate them all we want about vaccine efficacy and safety. It won’t matter.
  • If they’re terrified that their dog is going to die from the vaccine because of something they read online, that’s a completely different scenario that requires a different approach.
  • If cost is driving concerns, that’s harder to address.

There’s a lot more to discuss about reasons for vaccine hesitancy, but I’ll hold off on that for now. My focus today is on the implications of vaccine hesitancy.

Potential impacts of moderate decreases in vaccine coverage

Less vaccination means more disease at the individual level. It can also increase the risk of outbreaks, increase the risk of well-controlled diseases becoming uncontrolled, and allow for re-introduction of diseases that were previously successfully contained.

For humans, we want really high measles vaccination rates (>95%) to prevent spread, as well as to protect individuals from disease. That way if someone happens to have measles, the risk of spread is low because so many people are already protected. We need a really high percentage of vaccinated people in the population for this to work for a highly transmissible virus like measles, but we were previously able to do that in Canada – until recently. As vaccine rates slip, when there is an introduction of measles virus into a population, there is a higher risk of sustained transmission among unprotected people, sometimes with devastating results.

It’s a bit different for dogs and cats. We don’t have the same level of baseline vaccine coverage for most of the diseases against which we vaccinate pets, and for some diseases, we also have feral and wildlife reservoirs.

Individual animal risk is straightforward, but population risks in pets are harder to understand. Those risks can’t be ignored, but they also shouldn’t be overstated, since we need to be transparent and clear in our communication with pet owners in order to maintain trust. Let’s use vaccination of dogs as an example:

Distemper

Canine distemper virus (a relative of measles virus) is one of our big concerns in dogs. Disease can be really severe, but vaccines are highly effective. However, we’re nowhere close to eradication because we still have a fairly large pool of unvaccinated dogs, and canine distemper virus is also endemic in wildlife in many areas (especially in raccoons). Reduced vaccination in dogs won’t lead to re-emergence of the disease, since it’s already endemic. Reduced vaccination will mean more disease in general.

So, the risks of less vaccination are mainly to the unvaccinated dogs. However, there is a spillover risk. Just like in humans, where we focus on vaccinating as many people as possible to protect those who can’t be vaccinated, the same principle applies in dogs, since some dogs cannot be vaccinated or cannot respond well to a vaccine. An unvaccinated dog that gets distemper poses a risk to those dogs. The more unvaccinated dogs, the greater the risk to puppies especially, and for a potentially devastating outbreak.

Parvovirus

Issues with parvo are pretty similar to those with distemper. It’s a potentially life-threatening disease in unvaccinated dogs. There’s low level but continual circulation of parvo in the dog population because there are enough unvaccinated dogs (domestic and stray) to maintain it. The risks of decreased vaccination are mainly to the unvaccinated animals. However, as with distemper, when there are more infected dogs, there’s more risk of transmission to other dogs, including puppies that are still to young to be vaccinated.

Leptospirosis

This is an important vaccine in many areas. Leptospirosis is a bacterial disease caused by the spread of Leptospira from wildlife reservoirs (e.g. raccoons, rats). We can’t eliminate lepto from wildlife, so reduced vaccination doesn’t change the overall risk of exposure, but it increases the risk to the unvaccinated dog.

However, there are some secondary risks here too. Dog-to-dog and dog-to-human transmission of lepto seem to be rare, but can happen. If a dog is unvaccinated, it’s at risk of severe disease, and that risk extends (at a low but non-zero level) to its canine and human contacts.

Rabies

There are a lot of interesting aspects to rabies when it comes to dogs. In North America, we don’t have the strain of rabies virus (canine variant) that circulates in dog populations in other countries. Dogs can still get rabies from wildlife reservoirs, such as bats, raccoons and skunks, but we don’t expect strains from those species to result in ongoing transmission of rabies within the dog population. However, canine variant rabies is highly prevalent in some parts of the world, where it causes most of the ~60,000 global human rabies deaths annually. We are at some risk of importing dogs carrying canine rabies. Despite the controls we have in place to prevent it, at least two rabid dogs have been imported into Ontario since 2021, and there’s ever-present risk of it happening again.

If a dog is not vaccinated against rabies, the main risk is to itself. If it tangles with a bat and is exposed to the virus, it’s more likely to develop rabies (which is essentially always fatal). There are other risks, though. When a dog has rabies, there is a short but important window of time when it can transmit the virus through its saliva to any human, domestic mammal or wild mammal contact. There can also be substantial healthcare costs for investigation of human exposures and treatment of exposed individuals. Unvaccinated dogs and cats that are potentially exposed to the virus can be at risk of developing rabies for months, necessitating long confinement periods to prevent exposure of even more people and animals (and sometimes pet are even euthanized because of the risk if they can’t be safely and effectively confined).

The broader population risk from decreased rabies vaccination is much lower. We have eradicated canine rabies in Canada and really don’t want it back. For that to happen, we’d have to import a dog with rabies, it would have to infect other dogs or wild canids, and they would have to keep infecting enough new dogs/canids to keep the disease cycle going. That’s not realistic in a controlled pet dog population, but is a concern with feral dogs (which we don’t have many of in most regions) and wild canids (which are very common in some areas).

The odds of canine rabies virus coming into the country, making it into wild canids and establishing itself anew are really, really low, but they are not zero. While the risk of an unvaccinated pet dog contributing to re-establishment of canine rabies in Canada are likewise exceptionally low, the implications were it to happen, both in terms of health (human and animal) and the costs for control are substantial. So it should not be ignored. Still, the main risks from a dog that is not vaccinated for rabies are to the unvaccinated dog itself and its close contacts.

“Kennel cough” (canine infectious respiratory disease complex, CIRDC)

When it comes to CIRDC, we mainly vaccinate dogs against Bordetella bronchiseptica and canine parainfluenza, with a smattering of vaccination against canine flu. These vaccines are meant to help reduce the risk of infection and reduce severity of illness when it occurs. They’re useful, but they’re mainly for individual health, not reducing transmission or containing the disease. These vaccines are also not as widely used as others, so overall vaccine coverage is pretty low. A moderate reduction in vaccination would not do too much to impact the broader epidemiology of this complex. It would mean that more dogs would get sick, or get sicker than they would have with vaccination.

Do I worry about vaccine hesitancy?

Yes. I hate to see animals dying of vaccine preventable diseases. We can’t prevent all disease, but by optimizing vaccination, we can maximize the benefits to vaccinated animals, and to some degree, other animals and people around them.

How do we address vaccine hesitancy?

That’s way more complex that I can cover in a few paragraphs, but I’ll highlight a few key aspects for addressing vaccine hesitancy (hard core anti-vaxxers and people who spread misinformation are a separate topic):

Communicate communicate communicate

  • We have to listen to why people are hesitant.
  • We have to acknowledge their concerns, even if we disagree.
  • Sometimes we can educate.
  • Sometimes we can work to provide more confidence in veterinary care or vaccines.
  • Sometimes we can allay fears.
  • Sometimes we can just have a good conversation, agree to disagree, and still work to care for the animal.
  • …and unfortunately sometimes it falls apart, or views are so polarized that there’s no moving forward. We just hope those are the minority of cases.

We don’t have the exact same issues in veterinary medicine as human medicine, and approaches to vaccine hesitancy aren’t necessarily going to be identical, but vaccine hesitancy among animal owners is definitely a concern. We need to develop a better understanding of how common it is (and more importantly, the reasons for it), look at ways to address it (including how it’s done in human medicine), have open and honest discussions, and try to optimize vaccination. There’s no one-size-fits-all approach to vaccination and there’s no one-size-fits-all approach to a vaccine-hesitant owner.