test

Veterinarians sometimes ask me, “Can I give a half dose of a vaccine to small breed dogs?” But more often they say, “An owner wants me to give their small dog a half dose of a vaccine because they are worried about adverse effects. Should I do that?”

The short answer is there is no evidence that decreasing the vaccine dose will have any impact on adverse events, and no data to know what impact it will have on the desired immune response.

Here’s a bit on the longer answer. The key issues are:

  • We don’t know if lower doses of vaccine work in dogs and cats.
  • We don’t know if lower doses of vaccine reduce the risk of adverse events.

It’s possible that lower doses would work and be could carry a lower risk of adverse effects. It’s also possible that lower doses would not provide good protection against the disease for which the vaccine is being given, and would still carry a similar risk of adverse effects, meaning we’d be getting little benefit from the vaccine while maintaining risk. That’s not good.

Why are vaccines dosed per dog (or cat, or person), rather than based on size like other medications?

Vaccines are not like drugs that are dosed to try to reach a certain concentration in blood or tissue, which requires higher doses for larger individuals. Vaccines predominantly work locally in the body, at or near the vaccination site. It doesn’t matter if the individual is big or small, the vaccine still does its work in a small location. We get similar immune responses to the same dose in large or small individuals.

That said, there are some data on the impacts of different vaccine doses on vaccine response and adverse effects. There’s no consistent association, as the vaccine type, target disease and age of the vaccinated individuals all play important roles in response. While we often focus on animal size, age may be a bigger factor and one that’s not usually on the radar.

  • In humans, the approach to vaccination sometimes varies based on age (so indirectly on size, but age is the focus). Vaccines designed for older individuals sometimes have higher antigen loads because the immune response weakens with age. For example, there’s a high dose flu vaccine for seniors, and an older shingles vaccine had 14 times the antigen load of the version used to vaccinate kids against chickenpox (both caused by the same virus). Those products were designed based on concerns that older individuals need more antigen to properly stimulate the immune response, not that we want to use lower doses in smaller individuals.
  • In contrast, the Tdap (tetanus, diphtheria, pertussis) vaccine for young kids actually has more antigen compared to that for older kids and adults. Lower doses for older individuals are meant to reduce adverse reactions, but that’s based on age, not size.

Do lower vaccine doses work, and do they reduce adverse events in pets?

We don’t know, since it hasn’t been studied properly in dogs and cats. While we have to remember that dogs are not people, and that vaccines used in different species also differ, as do the approaches to vaccination (especially frequency of vaccination), we can gain some insight on this from human studies.

A small study of pre-term infants looked at the effects of some physicians using half-dose vaccines (Bernbaum et al. 1989). They showed that 96% of pre-term infants that got the full dose of diphtheria/tetanus/pertussis vaccine responded adequately, while only 45% that got a half dose responded adequately (even after 3 doses), and an extra full dose was required to generate an adequate response.

In contrast, there are a few studies looking at half doses of COVID-19 vaccines, but it’s important to bear in mind that these use different vaccine technology to what is currently used for animal vaccines. COVID-19 vaccine developers also may have erred on the side of extra antigen because of the need to get these vaccines to market ASAP during the pandemic. So it’s a bit of an apples-to-oranges comparison, but shows that it’s fair to look at what happens with lower doses. A few studies showed that lower doses are likely protective, but that there’s no clear evidence that there’s an impact on adverse events.

  • One study (Valim et al. 2022) was a non-inferiority trial that aimed to see if a half dose of the ChAdOx1 COVID-19 vaccine was no worse than a full dose. (That’s the Astra Zenica vaccine that was rolled out initially but was largely phased out when RNA vaccines became available). They showed that the half dose was non-inferior (23.7 vs 25.7 cases of illness per 1000 people/year). The frequency of adverse events was also similar. So, this the lower dose of the vaccine was similarly effective as the full dose, with no difference in safety profile.
  • Another study of the same vaccine (Galvao-Lima 2023) showed that two half doses were similarly protective as two full doses, in terms of prevention of moderate to severe COVID-19 disease. There was no reporting of adverse event rates, so we can’t really interpret much from this.
  • A small study of the Pfizer COVID-19 vaccine (Batmunkh et al 2024) looked at antibody response and adverse effects to full or half doses in people who had already received an initial COVID-19 vaccine series (any type). They found that the half dose was non-inferior to the full dose in terms of the antibody response for most individuals, but it was not as good for those who had received the Gam-COVID-Vac (Sputnik vaccine) for the initial series. Safety data were pretty limited, and the analysis was weak, so I don’t think we can conclude anything about that particular aspect, but it’s more evidence that COVID-19 vaccines can be effective at lower doses.

The first take-home message is that lower doses of vaccines probably work quite well – at least for some vaccines in some populations (I wouldn’t be as confident about the effectiveness of lower doses in seniors or other individuals who might have a harder time responding to a vaccine).

  • That makes sense, since manufacturers don’t aim to find the absolute lowest antigen load that will work in the average person. They want their vaccines to work for the vast majority of the population, across the gamut of immune responses. Many or most individuals would response to less antigen than what is in the vaccine, but some probably do require the full dose – we just can’t easily tell who needs what.

The second take-home message is that there’s not really any clear evidence that reducing the vaccines dose reduces adverse effects. It seems logical that it would, if adverse effects are linked to the magnitude of the immune response and if the magnitude of the immune response varies with dose. However, since vaccines largely work locally, there’s nothing indicating that size is a component of this, and age probably plays more of a role. In dogs, breed does too. While we know that certain things may increase the risk of an adverse event after vaccination, we don’t have much supporting data that dropping the vaccine dose by a half helps to decrease the risk.

Do we have any data regarding using lower vaccine doses in dogs and cats?

No. Some people point to a 2015 study by a controversial veterinarian (who has been cited for practicing without a license on multiple occasions, markets unvalidated tests and pushes various narratives that are well away from the mainstream) (Dodds, AHVMA 2015).  It looked at half dose distemper/parvo vaccination vs full dose in 13 adult dogs (with only 8 dogs tested at some points because they somehow “inadvertently discarded” many samples). The study is small, very weak, doesn’t mention any ethics approval, and it’s unclear if validated tests were used – so it really can’t tell us anything. Even if the data are valid, we have to remember that this involves older (3-9 year-old dogs) that had been previously vaccinated with vaccines that are really effective, so they have a very well primed immune response.  But even then the data aren’t convincing. They showed that some (not all) dogs had increased titres after half dose vaccination, but there’s no control group that received the full dose vaccination, no group that was unvaccinated, and no statistical analysis. They also didn’t look at adverse events. So, I don’t think we can say anything at all from this study, which leaves us with no real data about half vs full dose vaccine administration in dogs and cats.

Is there liability for veterinarians if they don’t administer a full vaccine dose?

Veterinarians are expected to act professionally and reasonably, which includes communicating with owners and discussing options about their animals’ care. However, veterinarians are not expected (and in fact are expected NOT) to simply do what owners request if it’s medically (or ethically) inappropriate. Regulations and legalities vary by region but in general, owners cannot consent to malpractice, so client consent is not an automatic “get out of jail free card” if a veterinarian does something wrong. Even if the client thinks it’s a good idea and specifically requests it, the veterinarian is the professional and must use their expertise to assess the situation and what is or is not appropriate for the patient, so there is a professional risk to the veterinarian as well. Is giving half-dose vaccines malpractice? I’m not a lawyer so I can’t say, but I can think of some important considerations:

  • If a veterinarian gives a half dose of rabies vaccine and issues a rabies certificate or indicates the pet is “properly” vaccinated against rabies (according to the manufacturer’s instructions, which is part of the regulation in Ontario), I’d consider that fraud and malpractice.
  • If a veterinarian gives a half dose of another vaccine and implies that it will work equally well as a full dose, that’s a big concern. It’s using a vaccine off-label without consent.
  • If a veterinarian gives a half dose of another vaccine and tells the owner it may or may not work, that’s probably defensible, but it would be a grey area. If the dog later had a problem (e.g. got sick) and the owner complained, the question might be how well the veterinarian really discussed the issues and risks. Owners can’t give informed consent if they are not adequately informed. If the veterinarian made the recommendation (versus giving into the owner’s request), then I suspect the liability increases, since a veterinarian’s recommendation/suggestion would reasonably be taken by an owner as an indication that the approach is safe and effective.

What should veterinarians do when pet owners are concerned about adverse events after vaccination?

The first and most important step is communication – that’s where things often fall apart. We have to acknowledge that vaccine adverse events are real and can happen to any dog, but are more common in certain breeds (especially small breeds). However, these event are still uncommon, and serious adverse events are quite rare.

A very large study of dogs reported an adverse event rate of 0.19% (19.4 adverse events per 10,000 visits) within 3 days of vaccination (Moore et al. 2023). The serious adverse event rate was even lower, around 2.9/10,000. Rare isn’t zero so we still have to be aware of the risk, but we also have to keep it in perspective. If reducing the dose of vaccines reduced adverse events by let’s say 15% (just to pick a number), that would drop the serious adverse event rate to 2.5/10,000. That’s an absolute risk reduction of 0.4/10,000 visits. We’d need to give 25,000 dogs a half-dose vaccine to prevent one severe reaction, but it’s possible we’d be trading that for an equal or greater increase in risk from the disease we’re trying to prevent with the vaccine. We just don’t know.

If an owner is concerned but their pet has never had a vaccine reaction before, talking about the overall low risk and the measures that can be taken to detect and address vaccine reactions is a good start.

If the individual animal has had a vaccine reaction in the past, then we should do a risk assessment and tailor the vaccination program for that pet to help decrease the risk. That could entail no longer vaccinating against all diseases, no longer vaccinating against some diseases (e.g. stop distemper/parvo vaccination but continue for rabies and lepto), changing vaccination regimens (e.g. splitting vaccines over multiple visits), vaccinating after pre-medication, or continuing to vaccinate as per usual, but being ready to respond if there’s a problem.

Is the issue of vaccine reactions in small breed dog actually related to size or breed?

That’s an important question, since I think many people often think “the dog is smaller, so the dog should get a lower dose,” like we do for drugs. It’s a logical inference, but if we look at the Moore study, breed played a big role. The table below shows the differences in adverse event rates between breeds. Small breeds dominated the highest risk breeds, but whether that’s because of their size or genetic factors is far from certain. Since some larger dogs cracked the top 10 list as well, we have to consider that genetics play an important role, and that size may just be along for the ride.

We can say that small breeds are higher risk for adverse events, but that’s not necessarily because they are small, it might be because of their genetics. Disentangling those is tough. If anything, we probably should explore safety and efficacy of lower doses in higher risk breeds (not just “small dogs”), and look at the impact of age on vaccine response too.

Key points:

  • Half dose vaccines likely work in some, if not most, animals, but we don’t have any data to provide any confidence in that hypothesis.
  • We have nothing to suggest that lower vaccine doses reduce adverse events.
  • Higher adverse event rates in small breed dogs might be in part due to their size, but genetic factors likely play a big role.

Ultimately, I think using half doses of vaccines is bad medicine, since we are creating risk (potential for a poorer response, albeit low, which creates higher risk of disease) in the absence of any reasonable evidence that there’s a corresponding benefit (of any sort, let alone one that results in a net benefit).

test

If I’m talking to veterinarians or veterinary students about infectious diseases and I mention Capnocytophaga canimorsus, I usually get a blank stare (or “capno-what?”). If I’m talking to physicians, it’s usually the same response, unless they’re infectious disease physicians or trainees (but I still get “capno-what?” from some of them on occasion).

Capnocytophaga canimorsus is a bit of a niche zoonotic bacterium, but it’s an important one. It can be found in the mouths of most dogs, so people are really commonly exposed, but human infections are rare. However, when infection does happen, it tends to be very severe or even fatal. Not having a spleen (e.g. if a person had to have their spleen removed at some point) is a huge risk factor for infection. Other types of immunocompromising disorders and alcohol abuse are other known risk factors.  For more details on Capnocytophaga, check out the infosheet in Worms & Germs Resources – Pets page.

A recent case report (Sorensen et al, 2025) reminds us that the risk of infection with this bacterium is no solely from dogs; the report describes a severe Capnocytophaga infection in a person linked to a cat bite.   Cats can also carry Capnocytophaga in their mouths, but it’s much less common than it is in dogs.

The affected patient was a 53-year-old man who (unsurprisingly) didn’t have a spleen and was heavy alcohol user (two big risk factors for infection). He had a two-day history of fever, chills, diarrhea and lethargy, with progressive weakness and decreased mental acuity. He then developed a purplish discolouration on his face, back, arms, legs and abdomen. He was taken to the emergency room, where a small cat bite was noticed. He then deteriorated quickly.

It’s not clear whether seeing the bite wound changed their initial approach, but he got the infectious disease kitchen sink treatment: ceftriaxone, vancomycin, azithromycin and atovaquone.  Despite this, his disease progressed to severe septic shock, DIC, purpura fulminans and multiorgan failure. Blood cultures were negative, so antibiotics were changed to meropenem, vancomycin, doxycycline and penicillin, and molecular testing was done to look for a fastidious bacterium. That’s how they detected C. canimorsus.

Although the patient gradually improved, the severity of infection resulted (as is common with this disease) in the need for multiple amputations. Both his legs were amputated below the knee, along with multiple fingers. (There are photos included in the case report.)

The authors concluded “Although C. canimorsus is typically associated with dog bites and scratches, it can show up after exposure to cats, as seen in this case, and should be considered along with more common pathogens such as Pasteurella multicoda and Bartonella henselae.”

A common issue with C. canimorsus infections is not considering it until it’s too late. I’ve talked to many family members of people who had this infection, and a common theme is that there was no querying of animal contact or animal bites until after the diagnosis was eventually made, and the family didn’t think to report any animal bites (when they knew about them).

Animal contact and bite history can be really important when someone gets sick, and is takes seconds to ask, but too often the question is never asked. That’s a healthcare gap. At the same time, we need better education of the public so that people can advocate for themselves and know to tell healthcare providers about animal contacts, especially animal bites.

I’ve written a lot in general about the risks of rabies and other infectious diseases from imported dogs. However, we have to remember that borders are political, not biological, and that rabies (like certain US presidents) doesn’t respect such borders, whether they’re between countries or between provinces. 

Whenever we move animals or people, we risk moving diseases with them. In 2021 and 2022, we detected two rabid dogs in Ontario that were both imported from Iran. However, there are also risks with movement of people or animals from different risk areas within the same country, particularly very large countries like Canada. Arctic fox-variant rabies is present right across the north in Canada (see map below), and there is always a risk of it spilling over into dogs in northern communities. Then sometimes, those dogs get moved south and bring rabies with them. It’s happened before, and it’s just happened again, this time involving a dog from Nunavut that was moved to Winnipeg MB, where is subsequently developed rabies. Here are some of the highlights of the case:

  • A 1.5-year old dog in a community in Nunavut was seen chasing a fox, along with some other dogs (which is not an unusual occurrence in the north) on February 27. It wasn’t clear (or at least not reported) whether there was any direct contact with the fox. If a dog has contact with an unusual fox and/or there is a chance the dog was exposed to saliva from such a fox (which is how rabies is transmitted), the typical recommendation would be to keep the dog under observation or confined for up to 6 months depending on its vaccination status and whether it’s able to receive a rabies vaccine within 7 days of the exposure. However, this isn’t always feasible in northern communities where dogs are often allowed to roam extensively and access to veterinary services and vaccines is very limited. It’s also important to remember that there is always a risk that dogs allowed outside unsupervised (even in the south) can have unobserved contact with wildlife, which puts them at risk for rabies exposure.
  • The dog was then moved by a dog rescue group from Nunavut to Winnipeg on March 31 where it was quarantined for 2 weeks. This kind of quarantine after transport is a good general infection control practice for other disease that may come to light after the stress of travel, but it’s not long enough to rule out the risk of rabies. After arrival in Winnipeg, the dog was vaccinated against rabies and then spayed a couple of weeks later.
  • The dog began showing signs of rabies on April 18, two days after the spay. Signs included hypersalivation, stargazing and aggression. It died two days later, and tested positive for rabies. Typing of the virus will presumably confirm the Arctic fox variant.

As is normal, there was an investigation to identify people and animals that might have been exposed to the dog during the short period when it would have been infectious (up to 10 days prior to starting to show clinical signs). “Several” people are receiving rabies post-exposure prophylaxis (PEP), including three who handled the dog when it was sick. Most likely, many of these people had little or no true risk of exposure, but understandably public health tends to very much err on the side of caution when it comes to rabies exposure in people. 

It was reported that “One dog in the foster home received post-exposure vaccination but does not require a quarantine as it was fully vaccinated prior to its exposure.” That’s because if the dog was vaccinated and received a booster within 7 days of the potential exposure, it would typically only be subject to an observation period, which is much less strict than a quarantine or confinement period which is used for higher-risk dogs.

Two other related dogs were moved from the community over a six-week period, but they were transported at different times and had no contact with the affected dog since February. So while those dogs would have the same risk of exposure to an infected fox as any dog in the community, there was no increased risk due to exposure to the dog that developed rabies, because there was no contact during the dog’s potential infectious period (starting from approximately April 8).

We can’t eradicate rabies from wildlife across Canada, particularly in areas like the north where populations are so widely dispersed and often inaccessible. Wildlife-to-domestic animal contacts always carry some degree of disease transmission risk, and the risk of rabies is particularly high in endemic areas when reservoir species like foxes are involved. When we move at-risk dogs, we then create additional risks for others. 

That isn’t to say we shouldn’t move dogs at all, as there are sometimes compelling and compassionate reasons to do so. But we need to take some basic precautions and always be aware of those risks. Ideally, we’d start by improving rabies vaccination of dogs in northern communities, which not only helps keep the dogs safe, but also protects community members who live in close contact with free-roaming community dogs. However, there are a lot of barriers to providing vaccination and other basic veterinary care in the North. Cases like this, and like the recent cases of confirmed rabid foxes in northern Ontario, highlight the importance of working together as a society to help overcome these long-standing barriers.

Distribution of rabies virus variants in Canada, 2016 to 2020 (Public Health Agency of Canada)

Last week I wrote about the recently updated ISCAID antimicrobial use guidelines for canine pyoderma, specifically regarding surface pyoderma. The full guidelines are freely available online (Loeffler et al. Vet Derm 2025). Today I’m going to cover the highlights about the “big one”: superficial folliculitis. I call it the big one because it’s so common in dogs, and it’s the one where we can have a big impact by convincing more people to using topical treatment as the first option, instead of reaching for systemic antimicrobials.

The three most important points to remember about superficial folliculitis in this context are:

  • It’s a staph-driven disease.
  • It basically always has an underlying cause, particularly allergies (e.g. food, flea, atopy). If we don’t address the underlying cause, the infection will inevitably come back. Too often, the underlying cause doesn’t get addressed, or doesn’t get addressed until multiple rounds of infection have occurred.
  • It’s a superficial infection, so we can approach it from the surface (topically). 

Here are the main treatment recommendations from the new guidelines. For full details, as well as information about diagnosis and other issues, check out the complete document.

  • Diagnosis is based on clinical signs and cytological analysis (cocci and neutrophils)
  • Topical antimicrobial therapy as the sole antibacterial treatment is the treatment-­of-­choice. The best evaluated treatment is 2-4% chlorhexidine.
  • Response to topical therapy should be re-­assessed by a veterinarian after 2–3 weeks of treatment.
  • Topical treatment should be continued until the lesions have resolved and underlying problem has been addressed (when possible).

When are systemic antimicrobials indicated for superficial folliculitis?

This choice is mainly based on owner and patient factors, not the disease. There are no clinical reasons to use systemic over topical antimicrobial therapy alone. However, if the owner cannot or will not treat the dog topically, then systemic antimicrobials are indicated. Systemic antimicrobials can also be considered if there has been no response to 2 weeks of topical treatment, but other causes (e.g. uncontrolled underlying disease, or a different disease) are more likely if compliance with the topical treatment was actually good and there was no response.

Culture and susceptibility testing is recommended if systemic antimicrobials are used. It’s particularly important if there are risk factors for resistance, such as previous rounds of antimicrobial treatment. 

  • The authors of these guidelines had a lot of debate about this. Ideally, we culture every time we’re thinking about using a systemic antibiotic. If the animal is not at high risk of having a resistant infection, culture is less valuable, and cost becomes an issue, so it’s fair to not culture cases where the risk if resistance is likely low. However, it’s best practice to culture whenever we can.

Additional treatment recommendations from the new guidelines include:

Clindamycin, cefalexin, cefadroxil and amoxicillin-­clavulanate are the recommended first line options for superficial follicultis if systemic antimicrobials are warranted. 

  • If there’s a suspicion (based on cytology) that the infection is not caused by staph, then a culture would be indicated because these drugs focus on staph.
  • Adjunctive topical treatment should be used in addition to systemic antimicrobials whenever possible. 

How long should systemic antimicrobials be given?

  • “An initial 2-­ week course may be dispensed, and an appointment for re-­examination by a veterinarian should be scheduled before the end of the course to determine whether systemic treatment can be stopped or whether longer treatment is required.”
  • “Clinical resolution of superficial pyoderma can be assumed, and systemic antimicrobials stopped when primary lesions of pyoderma (papules, pustules and erythematous epidermal collarettes) are no longer found.”

Long-term management of superficial folliculitis

  • Addressing the underlying disease is critical. It can take time and money, but will reduce disease (and also ultimately save time and money).
  • Regardless of whether systemic or topical treatment is used, “topical treatment can be continued longer than systemic therapy, and is potentially life-­long, where the primary causes cannot be resolved and the risk of recurrence remains.”
  • “There is no evidence to support extending systemic antimicrobial therapy beyond the resolution of clinical signs associated with infection; instead, underlying primary causes must be identified and addressed.”

Up next: recommendations on the nastier and more complicated condition, deep pyoderma.

test

Most people don’t realize the massive number of dogs that are imported into Canada every year, for all kinds of reasons: from people moving with their own pet, to importation of large shipments of dogs from puppy mills or rescues (the latter ranging from really good operations to really dodgy). Moving animals (or people) from one place to another always creates some degree of risk of moving diseases along with them, but there are things that we can do to reduce that risk. Vaccination is one of those things.

Rabies vaccination is a pretty standard requirement for international movement of dogs into many countries. In Canada, we require (kind of) vaccination of dogs that are entering the country. (I say “kind of” because in practice an unvaccinated dog coming as a personal pet may be permitted to enter Canada with a promise to get it vaccinated within a few weeks.) The vaccination requirement hopefully helps reduce (but does not eliminated) the risk of a rabid dog being imported, and, just as importantly, helps ensure that dogs that arrive are protected from exposure to rabies in Canada, where we have endemic rabies in bats and some terrestrial mammals. 

This vaccination requirement is not a guarantee that rabid dogs won’t be imported, though. The last two rabid dogs in Ontario were imported dogs, and both had a history of rabies vaccination. Most rabies vaccines are really good, but still not 100%, and vaccine quality (especially in come other countries) and vaccine record veracity (i.e. did someone falsify the vaccination certificate) are also concerns. 

Dr. Catherine Belanger coordinated a recent study looking at rabies antibody titres in imported dogs. There is no established “protective” titre for rabies in dogs, but there’s an international standard of 0.5 IU/mL that’s used to indicate what we assume to be a proper response to vaccination. 

For this study, dogs that were being imported into Canada and arriving in Ontario were enrolled (not an easy task, especially during a pandemic).

  • From October 2021 to November 2022, blood samples were collected from 67 dogs, mainly arriving from Egypt (46).
  • Concerningly, almost half (32/67, 48%) had antibody levels below the 0.5 IU/mL cutoff, and 14% had no detectable titres at all (despite all dogs presumably having a rabies vaccination certificate to get through customs).

Whether the poor results are because of poor quality vaccines, problems with vaccine handling (e.g. degradation because of cold chain issues), falsified rabies vaccination information or poor response to the vaccine can’t be determined. Any or all are possible contributing factors. 

These results highlight concerns with rabies immunity in imported dogs. In Ontario, there’s a legal requirement for all dogs over 3 months of age to be vaccinated against rabies by a vet licensed in Canada or the US, with a vaccine licensed in Canada or the US. Many people don’t realize that means dogs imported to Ontario from places other than the US are considered unvaccinated and need to be vaccinated upon arrival, even if they were vaccinated abroad – but that only applies in Ontario. Canada allows dogs to enter based on vaccination in other countries and other provinces do not have the same requirement to re-vaccinate dogs for rabies on arrival. Even so, revaccination is a good general practice for imported dogs unless there’s very good confidence in the vaccination history. Titres can also be tested, but that’s more expensive than another vaccine, and rabies vaccines are very safe. 

Another interesting aspect of this study was the availability of pre-exportation rabies titres for a subset of 29 dogs from Egypt (from a rescue that puts in extra effort and tries to ensure dogs are protected before they leave).  

  • All of those were reported to have a titre above the desired cutoff based on an ELISA test.
  • However, upon arrival, 38% of them had titres less than 0.5 IU/mL based on the RFFIT.

The RFFIT is approved by the World Organization for Animal Health (WOAH). The ELISA that was used prior to importation is not, and the differences between the two test methodologies are important. There could have been a decrease in antibody levels between when the two tests were run, but there wasn’t much of an interval (median 7 days apart), so it’s more likely the tests themselves or lab issues that account for the different results. This highlights the challenges that exporters face even when they want to do the right thing by testing prior to shipping the dogs.

To try to put that 48% of dogs with a titre less than 0.5 IU/mL in perspective, a comparison was made to test results from non-imported dogs in Ontario that had rabies antibody titres tested for other reasons.

  • 14% of non-imported dogs tested (9/65) had titres less than 0.5 IU/mL. That’s a lower proportion compared to the imported group, but still not great.

A more direct comparison was with 49 local dogs that were tested for export purposes, since they presumably were on a regular rabies vaccination schedule, and would be expected to have a good titre.

  • Only 8% of dogs tested in Ontario for export purposes had titres less than 0.5 IU/mL.

Beyond the issue with imported dogs, the 14% of non-imported dogs with low titres is a concern, since that suggests we might already have a reasonable pool of dogs with poor titres here in Ontario. This highlights the importance of a proper response to potential rabies exposure. If a dog is potentially exposed to rabies, we want to give it a rabies vaccine booster within 7 days. Even if a dog has a suboptimal titre, if it’s been previously vaccinated, odds are probably quite good that it will have a strong response to the booster, meaning that while its initial antibody levels are low, its immune system will still be ready to go and can ramp up antibody production quickly, because of the previous vaccine(s). With a proper (and prompt) post-exposure response, we can still keep the risk of rabies in the dog very low.

While somewhat unsurprising, this study highlights various issues and challenges with imported dogs, and the need to scrutinize when and how we import them, and how to manage them after arrival. 

Check out our new webinar about H5N1 influenza in pets that has just been posted as part of a collaboration with Trupanion’s new Pet and Public Health Early Warning and Protection System. There are actually two versions of the webinar:

test

The updated ISCAID antimicrobial use guidelines for canine pyoderma have just been published (Loeffler et al. Vet Derm 2025). This is the first major update since the guidelines were first published in 2014. The document is a bit of a monster, so I’ll break down some of the key points in my next few posts.

Let’s start with the guidelines for treating surface pyoderma, which includes pyotraumatic dermatitis (aka acute moist dermatitis aka “hot spots”), intertrigo (skin fold dermatitis) and bacterial overgrowth syndrome, each of which is pictured below:

A big advantage of treating skin is that it’s on the outside of the animal. We can treat superficial infections topically, and that can be a lot easier, safer and more effective than systemic treatments, and lets us save systemic antimicrobials (e.g. oral or injectable) for when we absolutely need them. This simple figure sums it up nicely: if it’s surface or superficial pyoderma, we want to treat topically if at all possible. We can’t always do that, but if the patient and owner are amenable to it, that’s the recommendation..

Here are the main treatment recommendations from the new guidelines. For full details, as well as information about diagnosis and other issues, check out the complete document.

  • Topical antimicrobial therapy is the treatment-­of-choice for surface pyoderma. The first option is 2-4% chlorhexidine. It’s the most proven treatment and is readily available.
  • A combination of topical antimicrobial therapy with topical glucocorticoids or with a short course (5–7 days) of systemic glucocorticoids (at anti-inflammatory doses) or antipruritic medication may be helpful in cases of pyotraumatic dermatitis or intertrigo where an inflammatory or pruritic primary cause is involved.
    • Dose is the key. Corticosteroids like prednisone can be a great help with treating certain infectious diseases, since inflammation is often what’s driving disease. We just need to make sure we stick with anti-inflammatory doses, not immunosuppressive doses.
  • Antiseptic treatment can be continued proactively on previously affected skin, potentially life-­long, where the primary underlying causes cannot be resolved (e.g. skin folds) and the risk of recurrence remains.

Here are a couple of case examples from the guidelines:

The next post will be the big one on superficial folliculitis. Stay tuned.

test

Last week, I wrote about the use of oseltamivir in dogs and cats infected with H5N1 influenza. We have to be aware of the risk of drug resistance risks whenever we use anti-infectives, especially when the same drugs (like osteltamivir) are used in people, and assess the risks and benefits in order to “use as little as possible, but use enough.”

That’s lead to some questions about use of the antiviral GS-441524 in cats. This drug has been a game changer in the management of a previously almost invariably fatal disease in cats called feline infectious peritonitis (FIP). 

When considering use of oseltamivir for treatment of H5N1 flu, there are a few things to our advantage:

  • It’s a narrow spectrum antiviral 
  • H5N1 infection and virus shedding are short term 
  • There’s no endemic H5N1 flu virus circulating in the cat and dog population
  • Cats and dogs are not common (if ever) sources of H5N1 transmission to people
  • We can implement infection control measures during the short treatment course required and estimated virus shedding period to contain the risk of spread of any resistant virus

The risk of a resistant H5N1 virus emerging during use of osteltamivir in a pet is therefore low, and the risk of any such virus spreading is even lower. While there’s some risk, with basic precautions, I think we can justify its use in infected pets under the right circumstances.

When considering use of GS-441524 (GS) for treatment of FIP, there are some very important differences:

  • GS is a broader spectrum antiviral
  • Enteric feline coronavirus (the virus that mutates to ultimately cause FIP in cats) can be shed by infected cats for months
  • Enteric feline coronavirus is a cat-adapted virus that can spreads very efficiently from cat-to-cat via fecal-oraltransmission

The risks of resistance when using GS in cats therefore differ according to the scenario.

1. Using GS to treat a cat with FIP

    • There’s a risk of emergence of resistant FIP virus within a treated cat. This would be bad news for the cat, but probably of limited broader risk since once enteric feline coronavirus becomes a cause of FIP, it’s not readily transmitted anymore. Odds are that the cat would not transmit the resistant virus further. We can’t say there’s no risk, but it’s low risk.
    • If the cat had concurrent intestinal infection with feline coronavirus, then there would be a risk of that virus becoming resistant and then spreading. One study reported fecal shedding of feline coronavirus in 61% of cats with FIP that were being treated with GS . Shedding dropped fairly quickly in most cats, which shows some likely impact of the drug, but it also shows that there’s some plausible risk of resistance emergence and transmission.
    • Since FIP is devastating, GS is highly effective, and the risk of resistance spreading is low, this is clearly a high-benefit / low-risk use situation. However, it’s not no risk so we need to study it more and optimize our treatment approaches.

    2. Using GS to treat cat with enteric feline coronavirus infection

    • Feline coronavirus is widespread and continually circulating in cats. There’s been some discussion of use of GS to knock that back, and to try to eliminate it from groups of cats (e.g. catteries). Treatment will reduce fecal shedding of the virus, and less shedding would likely have some downstream reduction of FIP, but I have my doubts that we can do much to control spread in the grand scheme with an antiviral. Reducing and eliminating a virus are different, and reducing while creating a substantial risk of resistance isn’t usually a good combination. In general, we are rarely able to use anti-infective drugs for effective infection control approaches in a population, especially for a virus that’s host adapted and endemic.
    • If we are treating cats with enteric infection, there’s a lot of virus, a lot of cats and a lot of chance for resistance emergence. If resistance emerged in a cat, it could shed large amounts of virus for long periods of time, releasing GS-resistant virus into the cat population and hampering our ability to treat FIP when it occurs. That’s a big concern for me.
    • Since enteric feline coronavirus infection isn’t a major health issue, treatment is not likely to have a major impact on enteric virus circulation, GS is so important for cats with FIP, and resistance would result in cat deaths, I have a hard time finding an indication for use of GS for enteric feline coronavirus.

    Dr. Niels Pedersen, a (or The) leader in development of antiviral approaches for FIP has a nice commentary entitled “Inappropriate use of GS-441524 in an attempt to eliminate Feline Enteric Coronavirus (FECV) from healthy cats.” The title gives away his thoughts on the matter. It’s a good, impassioned summary of why we need to be good stewards of FIP antivirals and why targeting feline enteric coronavirus is likely a bad idea.

    test

    For the longer answer to this question, check out the latest podcast episode I just posted on WormsAndGermsPod. For those who prefer to read the summary, here it is:

    If you ask people on the street “should we use the limited antivirals we have available to treat people with flu on dogs and cats?” the common answers would probably be “no,” along with the occasional “hell no!!” On the surface, that response makes sense. We have limited antivirals (both in number and sometimes supply) and they are important for treating people in some situations. However, we shouldn’t completely dismiss the utility of antivirals in animals with influenza infection in selected circumstances with good controls.

    Early treatment with an antiviral like oseltamivir (Tamiflu) could be effective against H5N1 flu in some animals, and there may be a rationale for prophylaxis in high risk situations (e.g. housemate of a cat with known H5N1 flu). Both of these scenarios involve companion animals, and non-reservoir species, and no livestock (including backyard chickens).

    Is there a concern about development of antiviral resistance if we use the drug in pets?

    We can’t ignore the possibility. Antiviral resistance is a concern, and it’s a spontaneous event that can occur as flu spreads, regardless of whether antivirals are used or not. Antiviral resistance markers have been found in influenza virus isolated from poultry (that were never treated with antivirals). The more the virus is transmitted and the more antivirals are used, the greater the risk of selecting for and spreading resistant strains.

    But antiviral resistance is different from antibacterial resistance in some important ways. Antivirals are much more specific in their effects, and viruses don’t swap resistance genes with each other like bacteria do.

    • If we treat an animal or person with an antibiotic, there will be myriad bacteria in that individual that are resistant, can become resistant or can spread resistance genes.
    • In contrast, if we treat an animal with oseltamivir when it doesn’t have the flu, it can’t select for a resistant flu strain.
    • If we treat and animal with oseltamivir when it does have the flu, there is a chance of resistance developing, but it’s only a broader problem if that flu virus is passed on to another individual. We don’t know if dogs and cats can transmit H5N1 flu, but it’s prudent to assume that they can. So, if we’re going to use an antiviral, we need to do all that we can to reduce the risk that any virus from that individual does not get transmitted to anyone else. We can probably do much more effectively in a pet than we can in a person that’s being treated with an antiviral.

    Good antimicrobial (including antiviral) stewardship means use as little as possible but use enough. We need to be prudent, but we also shouldn’t miss opportunities to intervene when we can do so effectively and with minimal risk.

    When does it make sense to use an antiviral to treat H5N1 flu in a dog or cat?

    Use of an antiviral makes sense for early treatment of known or high risk cases of H5N1 influenza where there’s a concern for development of serious disease (i.e. any infected cat, and probably infected dogs) AND when the animal can be properly treated AND when the animal can be kept isolated during and shortly after the treatment period.

    Basically my two main questions are: do they need it? and am I confident the animal won’t be able to infect another individual (human or animal)? If I can comfortably say yes to both of those, I think it’s reasonable to use an antiviral.

    Example 1: An infected cat in a household or veterinary clinic

    • Yes. We can properly treat, isolate, monitor and test the cat appropriately.

    Example 2: An infected cat that goes outside

    • No, unless the cat can be kept inside during the treatment and monitoring period. I don’t want to risk an antiviral-resistant flu strain developing and then the cat spreading it to other cats, or worse, birds.

    Example 3: A potentially infected backyard chicken

    • No (or hell no). These are livestock, so they are approached differently (and in Canada poultry infected with H5 flu must be culled). Poultry are highly susceptible to H5N1 influenza, and can clearly infect people. Also, an antiviral is probably too little, too late for a species that is so susceptible.

    Canine heartworm (Dirofilara immitis) is a nasty parasitic infection of dogs that’s relatively rare in Canada, but it’s still a concern because of how severe it can be and because treatment isn’t easy. It’s transmitted by mosquitos (we have lots of those), but transmission is also influenced by temperature (which varies a lot in Canada over the year).

    Heartworm control focuses on regular administration of preventive medications that are typically given to dogs monthly, either during the heartworm transmission season or all year round. The medication is often combined with flea/tick preventives and/or other antiparasitics.

    We have a seasonal risk period for heartworm in Canada, and it’s pretty short in some areas. We want to maximize use of heartworm preventive drugs during that period, so understanding exactly when the risk is present is important. Since transmission is temperature-dependent, the transmission period will vary across the country, and as out climate changes over the years, we need to keep re-evaluating the timing for giving dogs preventatives.

    Reminder: Heartworm life cycle

    Canids (including dogs and wild canids, like coyotes) are the reservoirs for this parasite . Adult heartworms produce microfilaria which are found in the dog’s bloodstream. These are picked up by mosquitoes when they feed on a dog. They then develop into the mosquito from microfilaria to L1, L2 and then L3 larvae (L3s are the infectious form). At that point, if the mosquito bites another dog, it can transmit heartworm via the L3 larvae.

    Why is temperature important?

    Heartworm larval maturation stops at temperatures less than 14C (57F), so the time that it takes for an infected mosquito to be able to transmit infectious heartworm larvae depends on the time that’s above 14C, and how far above 14C the temperature is. We measure this in “heartworm development units” (HDUs), which are calculated by taking the mean (not maximum) daily temperature in Celcius and subtracting 14. If it’s a positive number, that’s the number of HDUs for that day.

    Today, the mean temperature will be around 0C here. So, if there was an infected mosquito, the heartworm larvae are not developing. Hopefully things will warm up soon. If we get a day when the mean temperature is 17C, then we’ve accumulated 3 HDUs for that day. Once we get a total of 130 HDUs, those larvae should be infectious. That obviously takes time in spring in Canada, but not much time in places like the southern US when mean daily temperature is consistently and substantially higher, and 130 HDUs can be accumulated quickly, any time of the year.

    In Canada, June 1 has traditionally been the recommended starting date for heartworm prevention. That was based on temperature data from Windsor, Ontario (pretty much as far south as you can get in Canada) plus a very safe buffer period. However, since data for this recommendation were from 1957-1986, we figured it was worth rechecking, and we published the results in December in the Canadian Veterinary Journal (CVJ)(Weese & Peregrine, 2024).

    The short answer: our current approach is still good.

    We looked at temperature data from 1996-2023 for a variety of cities in Ontario, and how long it took for 130 HDUs to be accumulated. (I’ve put together data for cities in other provinces too but haven’t done anything with those yet.) The results are shown in the table below. In southern Ontario, the risk typically started mid June. In Windsor, it was as early as May 25, but with a median of June 7. Some years, the risk started quite late, and in some northern cities it didn’t start until August.

    Okay, but May 25 is before June 1, so is it a problem to still use that date as the start of the risk period, at least in Windsor?

    • No. Fortunately, our heartworm preventive drugs will kill L3 and early L4 stages, so they will kill larvae up to 4 weeks after infection. If a dog was infected May 25, preventive administration as late as June 22 would still work.

    If we want to look at the limits for when we should start preventive treatment, it’s actually the date that 130 HDUs are accumulated plus 28 days. I definitely wouldn’t want to cut it too close, and since we don’t track HDU accumulation in real time (and there are some potential disclaimers), we want to give ourselves a good cushion in terms of timing.

    What about climate change?

    Climate change is real, but mean temperature changes are slow and gradual. The graph below shows the trends over time. In some locations, there was a significant trend towards earlier dates of 130 HDU accumulation. In others, there was actually a trend towards later. Overall, there was no significant change. However, it’s fair to expect that there will be gradual changes over time, so we’ll just need to keep checking in.

    Can we trust the 130 HDU requirement?

    Mother Nature’s always a bit unpredictable, but the 130 HDU threshold has been validated pretty well. Even if the threshold was lowered to something like 125 HDUs, it would only change the typical time to accumulation by one or two days. 

    When we’re assessing risk periods, we want to err on the side of over-estimating, not under-estimating risk, so we took a conservative approach with our methods. You can calculate HDU accumulation two ways: 1) simply calculating the time until 130 HDUs is hit in the spring, or 2) using a 30 day rolling window. The latter is based on an assumption that adult mosquitoes only live for a maximum of 30 days, so early warm periods become irrelevant if the mosquito dies before larvae can become infectious. We chose to use the total time, not the 30 day window, since there is evidence that some mosquitoes can live for over 30 days.

    There are also potential issues such as microclimates (mosquitoes living in a warmer local site like a building or sewer) and heat sinks. Whether this is relevant to heartworm transmission is unclear, but it’s probably a minor issue, if it’s an issue at all.

    What does this mean for routine heartworm prevention?

    It means that it’s still fine to use June 1 as the start of the risk period in Canada, even in extreme southwestern Ontario. We don’t need to worry about starting earlier (a question I get all the time), at least not yet. June 1 still provides a good cushion too, for situations where people are late getting or starting the prescribed drug.

    But… don’t forget about ticks!

    Ticks are different. The tick risk season is much longer than the heartworm risk season. We have some risk of tick activity anytime the temperature is above 4C (or maybe even lower). Obviously, that means we have risk of tick exposure well before risk of heartworm exposure, and we have problems with people starting tick prevention too late because they only think about the June 1 heartworm risk date. If ticks are a concern, then tick prevention earlier in the year is important (and if it’s combined with heartworm preventive, the heartworm start date discussion becomes a moot point).