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I’m on the way home from ESCMID Global, a clinical microbiology and infectious disease conference. Although the conference didn’t include much veterinary-specific content, it did include a good collection of abstracts about zoonotic diseases, including a couple about diseases in veterinarians, one of which described an infection with Brucella canis.

I’ve written about B. canis periodically on this blog. While it’s endemic in dogs in many parts of the world, it’s not well studied. Despite being quite common in some dog populations, disease can still be pretty rare. In Ontario, B. canis has been found in numerous commercial dog breeding operations (puppy mills) whose puppies are sold widely, but most of the clinical cases we see are in imported dogs (which makes me wonder if there are differences in virulence between the strains we have here and those that come from abroad).

From a human health standpoint, there’s sometimes a lot of (somewhat misplaced) concern because the Brucella species found in food animals cause a lot of disease in people in areas where they’re endemic. In contrast, B. canis in dogs often flies under the radar, because despite lots of infected dogs, human infections are rare. Last year we published a scoping review of B. canis cases in people (Weese & Weese, Can Vet J 2025), and we were only able to fine reports of 68 human infections. That’s certainly an underestimate of the true number of cases, since many affected people are likely not diagnosed (or misdiagnosed), and not all cases get published. However, when I talk to colleagues in the human health field about this disease, their response is usually “haven’t seen one” or “Brucella what-a?” In other words, Brucella from dogs really isn’t on their radars.

Nonetheless, it’s still important to keep the risk from B. canis in mind, because rare doesn’t mean never, especially for people handling high risk dogs (e.g. imported dogs, puppy mill dogs) and in high risk situations (e.g. assisting dogs with whelping and contact with the associated maternal or fetal fluids or tissues).

There was a nice abstract at ESCMID from the Royal Liverpool University Hospital about a British veterinarian who became infected with B. canis. This bug has gotten increased attention in the UK in recent years, particularly with regard to imported dogs, but it’s still probably not high on the list for most physicians even there.

  • The affected patient was a 36-year-old companion animal veterinarian who had regular contact with dogs of unknown origin and imported dogs. The lead author (Dr. Firas Maghrabi) said this person also had contact with breeding dogs, which further increases the risk of B. canis exposure.
  • Over the course of two weeks, the veterinarian developed forearm blisters, severe back pain, joint pain, and then fever, headache, chest pain, rash and conjunctivitis. After an extensive workup targeting a wide range of infectious diseases, she was ultimately diagnosed with B. canis infection through identification of the bacterium by PCR in blood and cerebrospinal fluid (CSF), and detection of antibodies against B. canis. She was treated with a combination of antibiotics for 6 months, and fortunately fully recovered in the end.

One of the biggest challenges with B. canis in people is that it’s usually not on the radar, and if you don’t test for it, you’re not likely to find it. The only way you’d find it without a targeted test is if the bacterium grew on a blood culture, which generally isn’t very sensitive for something like this. Specific testing for B. canis is needed, and it’s not widely available for people (and antibody tests for the food animal-associated Brucella species won’t detect B. canis).

Education of physicians is obviously needed, but it’s also a bit unrealistic to expect general practitioners to be read up on every oddball infectious disease that’s out there. More realistically, the focus needs to be on getting infectious disease physicians involved in these case, and ensuring those specialists have adequate awareness of B. canis.

The flip side, which is often overlooked, is patient awareness. While I’m sure physicians dread patients who come in with a “Dr. Google” diagnosis as much as veterinarians do, people can still advocate for themselves and raise issues that might otherwise be missed, particularly if they’re aware of high risk exposures that might not be queried in a typical history. People who handle imported dogs or dogs of unknown origin, particularly for any type of reproductive procedure, should be aware of B. canis. They can then play a role in getting it on the radar earlier in the diagnostic process if they’re ill.

“I work with imported dogs and assisted with a birthing last week. Is it possible I have Brucella canis?” is a clear and fair question to ask a healthcare provider. For many physicians, their answer may be “I have no idea,” but it’s the starting point to think about it, and consider whether testing or referral to a specialist is indicated.

Words matter. Inconsistency and inaccuracy with terminology can result in misinterpretation, poor communication and creates challenges when discussing cases, interpreting research and developing guidelines.

This has been particularly evident when it comes to urinary tract disease in dogs and cats. For example, “urinary tract infection (UTI)” is a very generic term that has been commonly used to describe everything from bacterial cystitis to subclinical bacteriuria, a positive urine culture, positive urine cytology, pyelonephritis and a few other conditions, or often even indistinct combinations of those. This creates a lot of challenges since those conditions can have vastly different clinical issues. When we’re not speaking the same language, or when we mix completely different diseases into the same bundle, we create the potential for error, misdirection and misunderstanding.

So as part of our ongoing revision of the International Society for Companion Animal Infectious Diseases (ISCAID) 2019 urinary treatment guidelines, we recently completed an initiative to develop consensus-based definitions for these conditions using a broad group of international participants.

  • The guideline field has advanced a lot in recent years. We’re getting past the time where you could just get a few smart people together to create a guideline based on their knowledge and experience. While those past guidelines were often quite good, and they were really important stepping stones, they lacked broad representation, involvement of stakeholders, consideration of biases and had other limitations. The same applies to developing definitions, which requires a more rigorous process to be done right.

We started off with a steering committee of 5 people from 4 countries, then had a review by the ISCAID guideline working group members (19 people), and then two broader rounds of input from 90 people from 19 countries. The goal was to engage a broad range of people with expertise, through multiple rounds of review and suggestions, to arrive at a consensus.

  • All the methodological details of how we came to our definitions are now published online (Weese et al 2026) for anyone that wants to see them. We tried to be as transparent as possible, explaining what was done each round, how and why decisions were made (including some terms/definitions that we abandoned). It wasn’t easy, but I think it yielded some solid results, with a lot of good discussion along the way.

The final definitions and associated footnote are in the images below. For more information and context (and maybe easier reading), check out the complete open-access paper.

Are these definitions perfect? Probably not.

Did we include everyone who might have had useful input? Definitely not.

That said, they’re a step along the way (in the right direction).

As we said in the paper’s conclusion: “Standardisation of terminology is a foundational component of clinical communication, clinical research, surveillance and guideline development. This initiative has allowed for the creation of terms and definitions based on broad stakeholder consensus. The study’s output should assist with ongoing and future efforts to improve the evidence base pertaining to infectious urinary tract disease and foster improved clinical guidance.”

As the weather (slowly and inconsistently) gets nicer here in Ontario, dogs start to go swimming more. My dog, Ozzie (pictured below), is an embarrassment to the Labrador breed as he will not swim, but he’ll happily wade through water, as long as his feet don’t leave the ground (but he still manages to get thoroughly soaked).

It is also the time of year when the question inevitably comes up (yet again): Do topical parasite preventatives need to be re-dosed more frequently in dogs that swim or get bathed over the summer?

No, they don’t. (An easy answer, for once!)

We have lots of options for parasite control in dogs and cats, including oral, topical and injectable products. There are lots of different pros and cons to each, and I won’t wade into that quagmire but here’s the scoop on the topicals:

  • Topical antiparasitics don’t “coat” the animal and stay on the skin or fur; topical is just the route of administration. These products are rapidly absorbed through the skin, and exert their effects through the body, not on the skin’s surface. A lot of of the absorption occurs within a couple of hours of being applied, and the drug can adhere to the skin and haircoat as the rest is absorbed, with peak serum drug levels occurring 2-7 days later. Once the drug is in the skin (even if it’s not yet in the bloodstream), it can’t be washed off.
  • A 2016 study (Kilp et al.) evaluated “repeated intensive shampooing” starting 3 days after administration of a topical parasite preventative, and there was no effect on the ability of the drug to kill fleas or ticks on the dogs. In another study, (Taenzler et al. 2016) researchers “water immersed’” dogs 3, 21, 49 and 77 days after treatment, shampooed them for 6-8 minutes or did nothing (control group). There was no apparent difference in the efficacy of the anti-parasitic treatment between the three groups.

I just checked the labels for a couple products available in Canada: One said to keep the dog out of water for 72 hours after treatment, and another said that exposure to water (including swimming) starting 60 minutes after treatment, or bathing 90 minutes after treatment, doesn’t impact efficacy.

  • I don’t know if the difference is because some products are absorbed quicker than others, some manufacturers are more conservative than others or because the products were simply studied / evaluated differently.
  • It’s important to pay attention to those product labels though. If anything, they’re probably quite conservative, so if they say that the dog can get wet X hours after treatment, I’d follow that guideline, but if the dog gets rained on earlier than that, it’s likely not a problem. If the dog goes for a swim immediately after the product is applied, I’d be concerned the dog would need to be retreated.

In the absence of specific guidance, it’s reasonable to avoid water immersion or bathing for 48-72 hours after treatment; 24 hours is probably lots in most cases, but 48-72 hours gives a bit more margin of safety.

So, while it can take a little bit of planning and attention to make sure you don’t waste a dose of your dog’s topical preventative (particularly for dogs that swim every day), they only need to stay out of the water for a few days, after that swimming or bathing won’t have any detrimental effect on the treatment.

If you’re a companion animal veterinarian practicing anywhere in Canada, please take 10 minutes to contribute to a University of Toronto–led study on antibiotic prescribing practices for common conditions like urinary tract and respiratory infections in dogs and cats!

Your anonymous responses to this survey (available in English and French) will help guide antimicrobial stewardship efforts and inform future veterinary practice across Canada.

English survey: https://www.surveymonkey.com/r/RM8SGR6

French survey: https://www.surveymonkey.com/r/PBFWW5M

The short answer: I don’t know, but probably not, and it could potentially do more harm than good.

I get asked a lot about splitting vaccines for pets, that is to say giving different vaccines at different visits instead of giving a bunch of vaccines all at the same time. The questions are often related to small breed dogs, which are more prone to adverse events following vaccination. Sometimes the questions are because a particular dog has had an adverse reaction to a vaccine in the past, and sometimes they’re because the owners are concerned about adverse reactions, even though their dog has never had one.

The theory behind the supposed benefits of splitting vaccines is that less antigenic stimulation would lead to a lower risk of adverse events. On one hand, that’s true. Data from a really large study of vaccination adverse events in dogs (Moore et al. 2023) showed that as you add more vaccines, the adverse event rate goes up (see graph below).

So, why do I say I don’t know if splitting vaccines helps avoid adverse events? Because we have to think about what happens to the dog over time, not just what happens after each vaccination visit. If we give only one vaccine today, we have a lower risk of an adverse reaction than if we gave two, but if the dog still needs the second vaccine, it will need to come back for again for another vaccination visit, that also comes with its own risk of an adverse event.

Looking at the numbers from the graph above, let’s approximate the risks for a small breed dog that is due for DA2PP (distemper, adenovirus 2, parvo, parainfluenza, which are given together as a single injection) and rabies vaccines.

  • That’s two vaccines. Based on the crude estimate from the graph, the risk of an adverse event would be roughly 27 in 10,000 if they are given at the same visit.
  • If we only give DA2PP vaccine, the risk would be lower, at around 21 in 10,000, but the dog will still need to get a rabies vaccine.
  • When the dog comes in for its second visit and we only give the rabies vaccine, the risk of an adverse event is once again 21 in 10,000.

If we look at the risk for a single vaccine visit, the risk is lower if we only give one vaccine (21 vs 27 in 10,000). However, if we look at the cumulative risk to this dog to receive both vaccines on separate days, (21+21= 42 in 10,000) it’s actually higher than if we’d given them both at once.

How solid are these numbers? It’s hard to say. The data are crude, but they are the best we have. It makes sense, though. Splitting vaccines would have to drop the risk by at least 50% to achieve a net benefit when we have to add extra vaccination events to ensure the dog gets all the vaccines it needs. This also doesn’t consider the added stress, hassle and normal general malaise the pet can get after vaccination, which happens twice if the vaccines are split. I got my flu and COVID-19 vaccines at the same time this year. I did that on purpose because I’d rather have one episode of having a sore arm and maybe feeling crappy than two episodes. The same presumably applies to our canine patients.

It’s not that there are no valid reasons for splitting vaccines. It’s possible that some dogs that are particularly reactive to vaccines would benefit more from this strategy. We just don’t know.

The main benefit of splitting vaccines is to understand which vaccine may be causing a reaction in the dog if they have one. If I give DA2PP one day and the dog is fine, then follow up with rabies vaccine and the dog has a reaction, that’s useful because it suggests we have to focus on issues with the rabies vaccination. However, even that isn’t a guarantee of the cause, as many vaccine reactions are just random, non-repeatable events that don’t indicate long term risk.

So, split away if you want, but realize that’s it’s a bit more complicated than it might seem at first glance. It might not be reducing the risk to the dog, and it may actually be increasing it.

When it comes to disease surveillance and communication, we have a tendency to throw lots of stuff at the wall to see what sticks. Some things stick around (like this blog!), others things not so much… like our first attempt at WormsAndGermsMap about ten years ago. It was a good idea, but the technology wasn’t ready for it yet (at least for a low budget operation like ours). But technology advances, diseases continue to spread, and informal disease mapping can still be useful, so we’re giving it another try with the launch of our new and improved WormsAndGermsMap.

The new site lets users report disease events (cases) directly using a very simple submission page (see screenshot). The cases are then plotted on the map, randomly within a 5 km radius of the location provided (to protect privacy). The exact locations are retained on the back end of the site it case they’re needed, for example for looking more closely at a potential local outbreak.

The map can then be filtered by animal species, disease and dates. Clicking on a point provides some basic information on the case, but we also keep a bit more information on the back end of the site, and submitters can add comments in case there’s additional relevant information we should have.

There aren’t a lot of cases on the site yet (as you can see from the screenshot above) as we’re focusing on ongoing crowd reporting, but I’m also adding some data points we have that I think will be useful.

Why are we trying this again?

Because I get emails every week along the lines of “I think I’m seeing more of this disease.” I also get lots of questions about what diseases are where. I also get questions like “we saw something unusual. To whom can we report it?”

Informal, crowd-based disease reporting and mapping can help with all of these issues, but it’s important to remember that it also has lots of limitations. It’s based on what people happen to report, so it doesn’t capture all infections, or even a structured subset collected as part of a formal surveillance program. It also relies on the accuracy of the diagnosis, since we aren’t assessing the case ourselves to confirm the disease is what the submitter says it is. We also need to keep in mind that a disease that develops / is diagnosed in one area might have actually been picked up in an entirely different region (because animals travel too).

But the limitations also shouldn’t overshadow the potential educational and surveillance value. We’re not trying to say “the incidence of this disease is X in this area” or “there’s been an increase in disease in that area.” We’re just trying to help raise awareness about regional diseases risks, identify and track high risk incidents (e.g. canine influenza outbreaks), and give people a way to report unusual observations that might warrant more investigation or communication. Most of the time, an unusual observation is a typical disease acting atypically. Somethings, though, it’s the sign of something new. We can also sometimes pick up emerging issues or local clusters of disease. Ultimately, we have to interpret the data with caution, but the data can still be useful.

We’ll see if WormsAndGermsMap sticks better this time. I think there’s a need, but it’s only useful if we can get people to use it and submit cases. Time will tell.

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I haven’t written about raw diets lately (beyond risks from H5N1 influenza, particularly in cats), but that doesn’t mean the risks from these diets have gone away, and they are still really popular in some areas, and some messages are worth repeating.

Potential problems with raw diets for dogs and cats include infections (e.g. Salmonella, E. coli O157) in animals that eat the food or in people who handle the food or animals, nutritional imbalances (particularly problematic in growing animals), and intestinal foreign bodies (e.g. from diets containing pieces of bone). As usual, I’ll focus on the infectious disease aspects since that’s my turf.

A recent surveillance study from the UK looked at bacterial contamination of commercial raw diets for dogs and cats. The results were predictably disappointing. They tested 380 raw pet food samples (277 canine diets and 103 feline diets), and found one or more pathogenic bacteria in 35% of samples:

  • Salmonella: 21%
  • Multidrug-resistant Salmonella: 9%
  • Campylobacter: 14% (and 21% of C. jejuni were multidrug-resistant)  
  • Shiga-toxigenic E. coli (a bad one): 12%
  • Antimicrobial-resistant E. coli: 20%
  • Colistin (an antimicrobial of last resort) resistant E. coli: 1%
  • Methicillin resistant Staphylococcus aureus (MRSA): 10%

Overall, 29% of the diets were not compliant with what is allowed to be sold in the UK because of the presence of Salmonella or the level of E. coli present (over 5000 CFU/gram). Those are pretty loose limits too, as I’d be worried about Campylobacter or any level of colistin-resistant E. coli… Regardless, a large percentage of the diets were of concern based on potential human and/or animal health risks.

Another interesting finding was that 8% of samples leaked through the packaging while being defrosted. In a household, that means potential contamination of the fridge or countertops, creating more human exposure risk.

None of that is really surprising. It’s consistent with what we’ve known for years about contamination of these diets with things like Salmonella and Campylobacter, and adds to more recent evidence that raw diets are a major source of multidrug resistant E. coli. Multiple studies have now shown that eating a raw diet is a big risk factor for dogs to be shedding multidrug resistant E. coli, with potential for disease in the animal or transmission to people.

Would I like people to stop feeding raw diets to their pets? Yes.
Do I think for a second that they’ll actually all stop feeding raw diets to their pets? No.

So my focus is on situations of greatest concern, where there are high risk people or animals in the household, including the very young, elderly, pregnant or immunosuppressed. I’d also like people who are adamant about feeding raw diets to move toward using high pressure pasteurized (HPP) raw diets. The HPP process doesn’t eliminate the risk from these diets, but should decrease it considerably.

And, as always, a little hygiene (and some common sense!) goes a long way to reduce the risk of contamination and transmission of / via kitchen surfaces, food bowls and the pets themselves. More information about risk reduction with regard to raw diets can be found on the Worms & Germs Resources – Pets page.

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Maureen’s going to give me grief over the length of this post, but the use of antivirals in cats is important topic with a lot of issues to consider, so let’s dig into it once again.

Access to effective antivirals to treat feline infectious peritonitis (FIP), particularly GS-441524 (a relative of the anti-COVID-19 drug remdesivir), has been a game-changer in the truest sense in veterinary medicine: it has changed FIP from an almost invariably fatal disease to one that has a 90% or greated cure rate. It’s truly amazing how it has impacted the care of affected cats.

BUT we have decades of history in human and veterinary medicine of screwing up the use of remarkable, game-changing anti-infective drugs.

I sometimes tell students that my biggest concern with FIP now is that in 10 years, we’ll be saying that we used to have great drugs for treating FIP, and we had really high cure rates and saved countless cats, but FIP became resistant to all these drugs, so once again FIP is almost invariably fatal. That’s a bit dramatic, and I don’t think we’ll get there (I really hope not!), but it’s not unreasonable to be concerned about resistance, as more cats would end up dying from this infection.

Drugs like GS-441524 (and remdesivir) as well as molnupiravir (and its relative EIDD-1931) need to be managed as highest-tier anti-infectives, in the same way we need to manage highest-tier antibiotics. We need to avoid squandering them, so we have to use them carefully and appropriately.

There is lots of additional discussion about FIP and these new treatment options in previous blog posts, so I won’t rehash everthing again, but here’s a quick reminder of some key points:

  • FIP is caused by a very common cat visus, feline coronavirus (FCoV).
  • FCoV is carried in the intestinal tract; infection rates are high in some cat populations, but most of the time it does not cause any significant illness.
  • Some cats can shed FCoV in their feces for prolonged periods of time.
  • FIP occurs when FCoV mutates within a cat into a strain that can cause disease.

My main concern is development of antiviral resistance in the normal intestinal FCoV that is widespread in cats, because it’s common, transmissible and the origin of FIP. If we brew resistance in some cats and it gets transmitted through the population via resistant FCoV, we would end up with antiviral resistant FIP, which could kill a lot of cats.

Anytime we use an antiviral, there’s some chance for resistance to emerge. It’s a race between the drug killing the virus and the virus randomly mutating in a way that makes it resistant to the drug. Usually, the drug wins and the virus is eliminated, but sometimes, it doesn’t. If a resistant strain of the virus emerges, and the cat potentially spreads that virus to another cat, and then it spreads to another cat, and then another and another… and the more cats that are carrying the resistant strain, the faster it spreads.

The more we use antivirals, the more risk of resistance emerging, and spreading.

When we treat cats with FIP, the risk of resistance emerging in the virus is low. If the virus in an individual cat becomes resistant, it’s not a huge issue beyond the individual because after the FCoV mutates to to the FIP form, it’s not typically shed in the feces, so the risk of transmission to other cats is limited. The bigger risk is if the cat has a concurrent intestinal infection with “regular” FCoV that becomes resistant, since the FCoV form is much more transmissible and some cats will shed the virus for prolonged periods of time. We accept this risk when we treat cats with FIP, because the risks are hopefully low and the rewards (saving the cat’s life) are very high.

However, when we use these critical drugs in other situations, that risk/reward ratio can be very different. The two main scenarios of concern for me at this point are:

1. Treatment of enteric feline coronavirus

    Intestinal infection in cats with FCoV is common, but it doesn’t cause disease in most cases, and when it does, it’s usually mild disease in kittens. Antivirals will likely have an impact on intestinal infections, and there are data showing GS-441524 will reduce FCoV shedding in cats. But intestinal FCoV infection isn’t much of health risk. With lots of FCoV in the intestine, where antiviral levels may not get as high as they need to to kill the virus effectively, and the risk of long-term shedding of the virus, the risks of resistance emerging AND spreading to other cats are concerning. Treating cats with mild intestinal infections doesn’t provide much benefit, but it could create a lot of risk regarding these critical drugs.

    2. Treatment of other diseases

    This is something that’s becoming a major concern. GS-441524 and EIDD-1931 are approached by some as “miracle” drugs. And they are miracle drugs – for FIP. That does NOT mean they will work well for other conditions, or work well enough to justify the risk. There’s been a lot of talk lately about antiviral treatment of cats with feline chronic gingivostomatitis (FCGS). It’s a nasty disease (often requiring extraction of all the teeth in the mouth), so I can understand the desire to try just about anything, but there’s not much evidence yet that either of these drugs will help.

    A lot of the discussion about treatment of FCGS with these antivirals revolves around a research abstract that was presented at the 2025 ACVIM Forum (Colon et al.). The researchers looked at 8 cats with FCGS. All the cats were negative for feline leukemia virus and feline immunodeficiency virus. Five were treated with molnupiravir and three were “untreated” (it’s not clear if these three got other “standard” treatments, but they did not get antivirals). By week 4, four of the five treated cats had improved lesion scores (it’s important to know the degree of improvement to put the response into context, but unfortunately abstracts have limited space so this detail was not provided). Decreased (note that they did not say “elimination of”) FVoC shedding was also noted in two of these five cats. There was no change in the 3 control cats.

    What does this tell us?

    • It doesn’t tell us molnupiravir is effective for treating FCSG.
    • It doesn’t tell us that molnupiravir is superior to standard approaches for treating FCSG.
    • It doesn’t tell us the benefits of molnupiravir treatment in these cats outweigh any risks.
    • It does tell us that a proper clinical trial would likely be worth doing to see if this drug really is effective compared to standard approaches, and to investigate potential risks (e.g. emergence of resistance, adverse effects in the cats, human exposure risk). As the authors said “Further research is needed to confirm [molnupiravir’s] efficacy and broader applications in cats with FCV.”

    Unfortunately, this abstract has been jumped on as evidence that molnupiravir works to treat FCGS. People want another treatment option for this awful disease. Some are also looking for a cheaper treatment option than expensive dental extractions (I understand that too, especially when it comes shelters and rescues). But, we need to consider the big picture:

    • A cat with FCGS may also have a concurrent intestinal infection with FCoV. Given the high shedding rates in cats, it’s a very realistic concern. While it’s possible antivirals might help with some cases of FCGS, the abstract only tells us someone needs to do a much more thorough study on this. Such a study would need to include testing treated cats for concurrent FCoV infection before and after treatment, and looking for resistance mutations in the virus.
    • I also really don’t want to see these drugs used in lieu of full mouth dental extractions when that is clearly needed. It’s just like I wouldn’t use meropenem (a highest-tier antibiotic) in an animal if there was a definitive (or at least critically important) concurrent treatment that wasn’t being done (like removing an infected implant). 

    Another important consideration is the potential impact of this use on access to these lifesaving drugs for FIP. This is mainly a concern in the US, where these drugs are currently accessible, but not licensed for use in cats. The US FDA has allowed them to be used based on the benefits for treatment of FIP outweighing the potential risks of allowing use of an unlicensed drug. The more we deviate from what they based their decision on (use for treatment of FIP), the greater the risk that they will change their permissive stance, and we could lose access to these drugs altogether. Losing access to these antivirals for FIP would be devastating, and it’s not implausible. The FDA’s risk assessment for use in cats with FCGS could be very different, since it’s a non-fatal disease that has other established treatment approaches (even though it’s still nasty and treatment isn’t easy). One pharmacy in the US is now selling a molnupiravir product specifically marketed for FCSG (and it also contains doxycycline (an antibiotic) which just adds more “ugh!” to the picture). That’s just asking (not in a good way) for FDA intervention. The pharmacy has a notice on their website saying the product is meant for stomatitis associated with calicivirus, but few people read notices at the bottom of the page, many people won’t care about that, nor that there’s no evidence that molnupiravir is effective against feline calicivirus. I assume they’re trying to build in a viral infection justification for a new product, versus a product based on evidence of efficacy and need.

    Let’s not repeat decades of failures with how we handle antimicrobials by taking chances on how we use these critical antivirals for cats. I’m fine with exploring their use for other conditions, but before we start risking the efficacy of or access to these miraculous FIP treatments (which saves the lives of countless cats), we need to have solid evidence of efficacy for other uses AND risk : benefit analysis that points convincingly toward “benefit.”

    Many countries have import requirements for dogs based on rabies control (among other things), primarily based on the dog’s rabies vaccination history, plus or minus rabies antibody titre (RAT) testing. A few years ago (with support from the Ontario Animal Health Network), we studied RATs in dogs imported into Ontario by rescues (Belanger et al. 2025). I also wrote a bit about this study last year when it was first published online. It wasn’t easy to recruit groups to participate, but we ultimately were able to test blood samples from 67 dogs. The results were… disappointing, and concerning, but not surprising.

    Dogs were sampled at the time of arrival to Canada or shortly after (before any additional rabies vaccines were given), and blood samples were sent to Kansas State University for the rapid fluorescent focus inhibition test (RFFIT), which is the gold standard for RAT testing. The standard cutoff for an “acceptable” titre (demonstrating response to vaccination) is 0.5 IU/ml.

    • 48% of these dogs had RATs less than 0.5 IU/ml.
    • 19 (28%) had no detectable titre at all.

    Rabies antibody titres had been test prior to shipping in 29 of these dogs, all of which came from Egypt. The Egyptian lab used an ELISA test to measure the titres 30-40 days after vaccination. While all 29 dogs had “adequate” titres based on the ELISA, only 11 (38%) had adequate titres when they arrived in Canada, based on the RFFIT. There was a median of 7 days between the pre- and post-import testing in these dogs, so it’s unlikely that a natural drop in antibody levels would account for the difference in testing. This raises questions about the accuracy of the pre-import testing in other countries, and highlights why countries that have RAT requirements for dogs are quite strict about what labs can perform this testing.

    Close to 50% of imported dogs in this study had poor (or no) RATs. That’s a concern, especially considering this group may actually be better than than average, since they agreed to participate in the study (selection bias). We know some dogs get imported with false rabies vaccination documentation, and those using faking documents would be unlikely to volunteer to participate.

    These results weren’t actually too surprising compared to other studies though. A study of dogs imported into Finland reported no detectable antibodies in 39% of dogs (Kaila et al. 2019). Another European study reported inadequate titres in 53% of imported dogs (Klevar et al. 2015).

    Why did so many imported dogs have “inadequate” rabies titres, even though they all had to be vaccinated prior to arrival?

    It’s hard to say. There are a few possible explanations:

    • Poor vaccine response: Not all animals respond well to a vaccine, particularly a single dose. Rabies vaccine is a really good vaccine in this respect, but we know that not all dogs will respond well, even with the best vaccine. For example, a study of dogs less than 1 year of age in the US that received a single rabies vaccine showed that 12% of dogs failed to reach the 0.5 IU/ml RAT (at various time points, mostly within 6 months of vaccination) (Wallace et al 2017). A study of dogs in Sri Lanka showed that a single rabies vaccine failed to produce a titre of over 0.5 IU/ml in 40-57% of dogs a year after vaccination (Pimburage et al. 2017), which tells us about both the magnitude and duration of the antibody response. These studies suggest that we can’t necessarily count on good protection in all dogs (in some situations) after a single dose, but many of these dogs with poor titres may still respond well to a booster dose, which is why revaccination is critical.
    • Vaccine quality and handling: Vaccine quality varies internationally, and perhaps more importantly, vaccine handling (maintaining cold chain) can play a role in whether a vaccine is effective or not. It’s possible that poor responses in some situations were from questionable or mishandled (and therefore ineffective) vaccine. In our study, 46% of the dogs were reportedly vaccinated abroad using a rabies vaccine licensed in Canada, but only 46% of those dogs had a titre of 0.5 IU/ml or higher on arrival. Using a Canadian licensed vaccine gives us confidence that it was high quality product when it was manufactured, but if there were handling issues (e.g. not kept cold), that could compromise vaccine efficacy.
    • They were vaccinated too soon before testing to detect titres: Vaccines stimulate the body to produce antibodies, but that’s not an instantaneous process. When a dog gets its first rabies vaccine, it can take a little while for antibodies to reach detectable levels, and then levels will rise for a short time. (With subsequent boosters, the response is much quicker). The median time from vaccination to sampling in our study was 42 days, which is lots of time to see the antibody response if it happens, but ranged as low as 3 days. It wouldn’t be surprising to find low or undetectable titres in a dog vaccinated for the first time 3 days earlier, but the vaccine response ramps up quickly, as shown in the graph below from the Wallace et al. 2017 paper. So, I doubt timing of testing played a significant part in most of the dogs with low titres.
    • The dogs weren’t actually vaccinated: This is probably less likely in our study, since groups that falsify vaccination certificates are not likely to agree to participate. It’s a big concern in general, though, since falsified rabies vaccination certificates have been detected and are a recurrent issue.

    Another relevant question involves the 0.5 IU/ml titre target, which is not considered “protective” because we don’t actually know what a true “protective titre” is. The cutoff we use basically inidcates that the dog has responded to a rabies vaccine. With that, it probably has some degree of protection and also has an immune system that is primed to pump out more antibodies in response to future exposure or vaccination. A dog with a titre less than 0.5 IU/ml might still have responded to the vaccine and could respond very well to a booster, but we have less confidence in its current status. Dogs with a zero titre are more of a concern since that doesn’t give us any evidence that they have been vaccinated at all or had any form of response to a vaccine. In short, a dog with a titre of 0.4 IU/ml is quite possibly fine, but a dog with a 0.0 IU/ml titre is at far greater risk.

    So, what now?

    We’re going to continue to import dogs and no import rules will be perfect (or perfectly followed). Trying to maximize rabies vaccination and use of good quality vaccine in imported dogs is key. Beyond that, giving a dog a rabies booster at the time of arrival is prudent – and also legally required in Ontario, if the dog was not vaccinated with a vaccine licensed in Canada or the US by a veterinarian licensed in Canada or the US.

    A lot of interesting case reports get published in human medical and veterinary journals, but I always take case reports with a grain of salt. It’s not that I don’t trust the validity of the report, but there are those who may over-react to a single case. A publication about a single case typically signifies that it’s an oddball occurrence, and probably has limited broader significance. However, sometimes case reports can be an early indicator of something emerging, or something that we’ve missed in the past. Sorting out those possibilities can be challenge.

    With that in mind, I want to talk about a recent case report (Bradbury et al. 2026) published in the American Journal of Tropical Medicine and Hygiene, which describes a person in Australia who had an intestinal infection with Ancylostoma caninum, the canine hookworm.

    Ancylostoma caninum is a common hookworm in many areas that can cause disease in dogs (especially puppies) but is more often shed in the feces of healthy dogs with no clinical signs at all. Adult worms live in the dog’s small intestine, where they produce eggs that are shed in dog’s feces. The eggs then hatch in the environment, go through a few larval stages, and if then ingested by another dog, develop into adult worms in the intestine and the cycle begins again.

    Human infections with this parasite are not unusual in some regions either, but in people the infection takes the form of cutaneous larva migrans, where the larvae from the environment penetrate the skin and cause intensely itchy lesions while they migrate around, fruitlessly looking for their natural site of infection (dog intestines).

    The normal life cycle of A. caninum in dogs, with spillover infection causing cutaneous larva migrans in people, is shown below:

    The larvae shouldn’t be able to develop into adult worms in human intestines, but biology is full of exceptions, and rare cases do occur (like the one I wrote about back in 2019). Unusual zoonotic infections / forms of infection are more likely to occur in people with weakened immune systems, but it is noteworthy that the case from this latest report was in a 35-year-old man with a normal immune system. The patient had a recurrent history (over years) of hemorrhoids and bleeding from the rectum, so he had a colonoscopy. Along with some intestinal polyps, they found several areas where the intestinal lining had aphthous erosions (these are similar in appearance to canker sores some people get in their mouths). They also found a live worm within one of these eroded regions, and the worm was identified as A. caninum based on its appearance and DNA sequencing. When biopsies of the erosions were evaluated, they showed eosinophilic inflammation, consistent with lesions caused by a parasitic infection.

    The patient was treated with an antiparasitic (dewormer). They didn’t test his feces for parasites or eggs, because it’s assumed that in these aberrant infections in people the worms don’t develop past the subadult stage, so they don’t produce eggs (but it would have been nice to confirm that). That’s good because it means the person wouldn’t be able to spread the infection, but also makes it harder to detect the infection in the first place. That raises the question about whether intestinal infections like this could be more common that we think.

    It was suspected that the hookworm was more of an incidental finding, as the rectal bleeding was more likely associated with the hemorrhoids. However, it’s possible that the worm could have been causing some disease, as anything that triggers inflammation and erosion in the gut is a potential concern.

    Another interesting consideration is that the worm was found in the colon. In dogs, this parasite likes to live in the small intestine (which is much farther upstream). Hookworms are usually only found in the colon when a dog has a severe infestation. This raises the question of whether the patient might have had a more extensive infection than was not detected, since only the colon was evaluated.

    What does this change? Not much. It’s an interesting case, and a good reminder of the risks from zoonotic pathogens and the potential for underestimating the amount of animal-to-human and human-to-animal transmission of various organisms. The take home messages are the same though:

    • don’t eat poop
    • avoid environments with heavy fecal contamination – and wash your hands!
    • pick up animal feces and dispose of them appropriately, so that any parasites in them don’t get a chance to find their next host (be it human or canine or other).

    More information about hookworms in animals can be found on the Worms & Germs Resources – Pets page.