TL;DR: There’s no proven premedication strategy that reliably prevents adverse reactions to vaccines; instead focus on patient risk assessment, appropriate vaccine selection, close monitoring, and prompt treatment if an adverse event occurs.  

Vaccine adverse events (AEs) in pets are uncommon, but that doesn’t mean their inconsequential. Clients (and veterinarians) worry about them a lot. Adverse events following vaccination can range from very mild (like feeling crappy for a day or two after getting a flu shot) to life-threatening anaphylaxis.

Some worry about pets that have had an AE in the past. Others worry even when the animal doesn’t have a history of an AE. In either case, premedication is sometimes used to try to reduce the risk of an AE – but does it actually make a difference to the animal, or does it just make us feel better?

For both prevention and treatment, it’s important to be aware of the different mechanisms that drive different types of AEs. For the purpose of this post, we can group these into four broad categories:

  1. Inflammatory reactions: These include localized pain and swelling around the injection site, and systemic signs like fever and malaise. These are essentially exuberant “normal” responses to a vaccine, based on what we would expect the body to do. These reactions are typically mild and self-limiting, but can still make the animal feel pretty rough the day after (as many people experience after their own vaccines).
  2. Anaphylaxis: This is the most sudden, dramatic and life-threatening type of reaction. It’s a rapid-onset, immune-mediated reaction driven by immunoglobulin E (IgE), which leads to profound systemic mast cell and basophil degranulation, releasing massive amounts of histamine into the body.
  3. Localized / non-anaphylactic allergic reactions: These are true allergic reactions that develop minutes to hours after vaccination, but they’re actually quite rare. They are likely a response to non-target antigens in components of the vaccine (e.g. trace components, stabilizers), not the actual vaccine antigen itself.
  4. Immune mediated inflammatory reactions: There are a few types of these, the onset of which typically occurs several hours to days after vaccination. They can vary in severity, from little nodules at the site of injection to severe systemic consequences to widespread immune complex formation.

Below is a list of some of the strategies that are commonly used to try to prevent or treat vaccine AEs, and whether they do or don’t make sense, depending on the mechanisms involved.

Non-steroidal anti-inflammatory drugs (NSAIDs)

Anti-inflammatories are usually the first approach to treating reactions that result in inflammation and pain. For pain, malaise or fever after a flu shot, many people would likely take ibuprofen (an NSAID). The same is generally true for dogs and cats: if they feel rough after vaccination, an appropriate dose of an NSAID will help them feel better. This is something we do in response to a problem, it is not something we should be trying to use as a preventative. The US CDC’s Epidemiology and Prevention of Vaccine-Preventable Diseases (also known as the “Pink Book”) includes a chapter on vaccine administration, which states: “The prophylactic use of antipyretics (e.g., acetaminophen and ibuprofen) before or at the time of vaccination is not recommended. There is no evidence these will decrease the pain associated with an injection. In addition, some studies have suggested these medications might suppress the immune response to some vaccine antigens.”

Antihistamines

As the name suggests, these drugs are meant to address histamine-based reactions that cause issues like hives (but not anaphylaxis – that requires epinephrine). In dogs and cats, diphenhydramine (Benadryl) is the most frequently used antihistamine. Unfortunately, oral absorption (bioavailability) of this drug is poor and unpredictable in dogs, and the half life is short, so it’s effects can be unpredictable, limited and short term, which makes it an unreliable choice for treatment and particularly bad for prophylaxis (because there’s a good chance if you give it in advance that it may be gone by the time a reaction starts). The short half-life also increases the risk of “rebound” signs, e.g. if the histamine release persists after the drug concentrations fall. Intravenous diphenhydramine is useful for initial short-term treatment of severe reactions. Cetirizine is a better choice for an oral antihistamine, since it’s more potent, has better bioavailability and lasts longer.

Nonetheless, as for NSAIDs, antihistamines are for treatment of AEs, not prevention. In humans, they specifically recommend against pre-treating with antihistamines before vaccination. There’s no evidence that they help prevent AEs. The US CDC’s guidance for preparing for the potential management of anaphylaxis at COVID-19 vaccination sites addresses this quite clearly: “Administration of antihistamines to COVID-19 vaccine recipients prior to vaccination to prevent allergic reactions is not recommended. Antihistamines do not prevent anaphylaxis, and their prophylactic use may mask cutaneous symptoms, which could lead to a delay in the diagnosis and management of anaphylaxis.”

Corticosteroids

These drugs have potent anti-inflammatory effects, and at higher doses they can even suppress the immune system. They are a core component of treatment of immune-mediated diseases. However, at both anti-inflammatory or immunosuppressive doses, they can cause a variety of adverse effects. We’re not going to prevent an immune-mediated reaction with an anti-inflammatory dose of steroids, and it makes no sense to give an immunosuppressive dose of steroid prior to a vaccine (as it would inhibit the good immune response the vaccine is trying to induce). While corticosteroids are critical for treatment of vaccine AEs, they have no role in prevention, and quite realistic could do more harm than good if used prophylactically.

Epinephrine

Epinephrine is an essential emergency drug for treating anaphylaxis, but there’s no role in prevention. It’s a short term treatment of imminently threatening, active anaphylaxis.

Anti-nausea medications (e.g. maropitant)

                  This anti-nausea medication is sometimes used, particularly in cats and there’s no real downside. If the animal was going to get nauseous in response to a vaccine, it might help, if it is given shortly before vaccination. Is nausea likely enough to make it worthwhile? Probably not unless the animal has a known history of repeated nausea events after vaccination. There’s no real downside, though.

So, what can we do to reduce the impact of vaccine AEs?

I focus on two things…assessing vaccination needs and being ready to treat AEs.

We have standard approaches to vaccination that are meant to cover the general population and that usually err on the side of more vaccination. If an animal has a true increased risk of an AE, the cost:benefit calculus changes…the potential risks of vaccination increase and if the value of the vaccine is low, it might be worth skipping the vaccine. In some situations (e.g. DAPP in a dog that has gotten a dose at 16+ weeks of age) I’m happy stopping. In other (e.g. leptospirosis), the value of vaccination is higher so I’ll push it more. Consideration of the risks, benefits and owner’s preferences are key aspects since there’s no one-size-fits-all approach.

Beyond that, I focus on treatment of AEs, not prevention. If they look like they are feeling a bit rough after vaccination, an NSAID is reasonable. If they have what looks like a true histamine-based reaction (e.g. hives), an antihistamine is indicated. I’d start with injectable diphenhydramine for a quick effect and then use oral cetirizine for a more reliable and prolonged effect (compared to oral diphenhydramine).

If it’s a rare immune-mediated disease, then we need immunosuppressive doses of steroids…necessary for immune-mediated disease but not something we want to do unless we have to because of potential complications.

If there’s any hint that anaphylaxis might be present, they get epinephrine.

The greater the concern about the risk of an AE and the greater the risk of a severe AE, the closer I want them monitored. That might mean vaccinating them in the morning and keeping them under close observation in the clinic during the day or ensuring that they are at home with someone to observe them. If there’s thought to be a really high risk of anaphylaxis (but enough of a need for the vaccine to go ahead), the approach might include having an IV catheter in place and having an epinephrine dose readily available, along with close observation and a review of what we’d do if the animal crashes after the vaccine.

Another question that comes up is about splitting vaccines. I’ve covered that before and will rehash it soon for another part of this series, but splitting vaccines doesn’t likely help.

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Picture this: An owner takes their dog to a veterinarian for routine vaccines. The veterinarian recommends a DAPP vaccine (distemper, adenovirus, parvovirus, parainfluenza), as well as vaccination for rabies and leptospirosis. After some discussion, the owner declines the lepto vaccine, but proceeds with the others. The next day, they call back after doing some reading, having decided they’d like to have the dog vaccinated for lepto after all. When can the dog receive the additional vaccine?

A lot of veterinarians would likely recommend waiting at least two weeks, because that’s the minimum interval for boosters for many of our canine vaccines. It’s a pretty well entrenched dogma that’s been propagated through teaching, continuing education talks and reviews for years, but if you try to trace back that recommendation, you eventually hit a dead end.

  • It’s sometimes stated that the immune system can get overwhelmed or overloaded if too many vaccines are given close together, but there’s no hard evidence that happens. People and animals are bombarded by antigenic stimuli every day, so out immune systems are designed to be ready to go 24/7.

There’s actually no clear immunological basis for a universal 14-day minimum interval between administration of different vaccines (vs boosters of the same vaccine) in dogs and cats, or that giving different vaccines closer together than this results in clinically relevant vaccine failure. In human medicine (where they have a lot more data), there’s no recommendation for a minimum interval between most vaccines, with a few exceptions that don’t apply to pet vaccines.

  • According to the US CDC guidance on Timing and Spacing of Immunobiologics: “There is no evidence that non-live vaccines interfere with the immune response to other non-live vaccines or to live vaccines. Any non-live vaccine can be administered either simultaneously or at any time before or after a different non-live vaccine or live vaccine. The 2 exceptions are a 4-week interval between PCV13 and MenACWY-D in a person with anatomic asplenia and the separation of doses between PCV13 and PPSV23. (These exceptions are not applicable to dogs and cats of course).
  • Regarding live vaccines, the CDC guidance goes on to say: Limited data are available regarding interference between live vaccines used in the United States. The immune response to one live-virus vaccine might be impaired if administered within 28 days (i.e., 4 weeks) of another live-virus vaccine. In a study conducted in 2 U.S. health maintenance organizations, the risk for varicella vaccine failure (i.e., varicella disease in a vaccinated person) among persons who received varicella vaccine within 28 days of MMR vaccination was threefold higher than among persons who received varicella vaccine >28 days after MMR vaccination. Another study determined that the response to yellow fever vaccine is not affected by monovalent measles vaccine administered 1–27 days earlier. The effect of nonsimultaneous administration of rubella, mumps, varicella, and yellow fever vaccines is unknown.”

Based on this, the concern is only with serial administration of multiple injectable modified live vaccines, and it likely only affects some of these vaccines, not all of them. Combination core vaccines for pets (DAPP for dogs, FVRCP for cats) include modified live components, but the other vaccines we use (for lepto, Lyme disease, feline leukemia, and some rabies vaccines) are non-live vaccines. There are some modified live feline chlamydia vaccines, but those are typically part of FVRCP vaccines. (If there was a chlamydia-only live vaccine, I’d consider spacing it by at least 4 weeks from an FVRCP vaccine, but I don’t know if that would actually be necessary). We don’t otherwise need to worry about giving different modified live vaccines close together because the products don’t exist.

So in my opinion the dog in our initial scenario can be vaccinated for lepto at any time with no additional concerns about “interference” or poor response because of the vaccines the dog received at the initial appointment. If the owner is told to wait, there’s a good chance life will get in the way and a later appointment won’t get booked. I wouldn’t want to miss an opportunity to vaccinate the dog, so I’d have them come back as soon as they are able. That also helps the dog get protection as soon as possible.

Now let’s think about non-injectable vaccines. Picture this instead: Same dog, same owner, same recommendations. This time the owner calls back the next day and says they will be boarding the dog later this year, so they want to get it a “kennel cough” vaccine. You recommend a mucosal (oral or intranasal) vaccine, since they are more effective than injectable kennel cough vaccines. When can the dog receive an oral or intranasal vaccine?

Mucosal (oral, nasal) vaccines that we use for “kennel cough” (typically Bordetella bronchiseptica, canine parainfluenza virus, canine adenovirus in various combinations) in dogs are modified live vaccines, so there might be some issues to consider with regard to minimum vaccination intervals, but we have a complete lack of data on the impact in pets.

  • In humans, the CDC guidance says “Two or more injectable or nasally administered live vaccines not administered on the same day should be separated by at least 4 weeks, to minimize the potential risk for interference. If 2 such vaccines are separated by < 4 weeks, the second vaccine administered should not be counted and the dose should be repeated at least 4 weeks later. On the day a live injectable or intranasal vaccine will be administered, providers should ensure that no live injectable or intranasal vaccine was given in the previous 28 days.”

This is the one situation where there might be a biologically plausible argument for a minimum interval between different vaccines, but whether it actually has a clinically significant impact is another question. We have no idea if it’s an issue for pets, but this scenario could occur with dogs given a modified live core vaccine and then a modified live intranasal or oral vaccine less than 4 weeks apart. I’ve never really considered this to be a big concern, as I’d typically be more concerned about missing the opportunity to protect the dog against a vaccine-preventable disease, but I don’t think we can ignore it completely.

So in the scenario with the newly vaccinated dog and the owner now requesting a kennel cough vaccine, I’d consider how important the vaccine is in the very short term and over the next several months. If the dog won’t be boarded for a few months, I’d recommend waiting 4 weeks for the kennel cough vaccine out of abundance of caution, to try to get the best response possible on the first dose. If the dog is going into a high risk environment (e.g. boarding) soon, then I’d give the vaccine right away, but also recommend another dose 4 (or more) weeks later based on the theoretical potential for a poorer response to the first dose. That may be overkill, but it’s the one scenario with a plausible basis for setting a minimum dosing interval between different vaccines.

To sum up another very long blog post:

  • There is no scientific basis for a minimum interval between giving different non-live vaccines to dogs and cats.
  • The only scenario in which a minimum interval between different vaccines could plausibly matter is sequential administration of multiple modified live vaccines, which doesn’t come up very often in pets anyway, and the potential for interference it based only on extrapolation from human medicine, with no evidence that it is clinically relevant in dogs or cats.

This also raises questions about vaccination of pets in shelters. Shelters vaccinate frequently using modified live vaccines, including kennel cough vaccines for dogs. Does that mean those dogs may be suboptimally vaccinated in some situations, OR can we consider shelters a natural model that shows this kind of interference actually isn’t a concern? An interesting point for discussion, but shelter vaccination strategies are fodder for a separate post.

Don’t forget to check out the new paired resource from the Ontario Animal Health Network (OAHN): Vaccination Timing and Intervals in Dogs and Cats (infosheet and infotable). If you don’t have an OAHN login, veterinarians and RVTs can sign up for free.

Let’s face it, approaches to vaccination in companion animals are based partly on direct evidence, partly on extrapolation from other species, partly on expert opinion, and partly on “this is what we do because it’s what we’ve always done.” The evidence base for much of what we do is incomplete, and for a lot of things the evidence base is actually sparse to non-existent. We typically have good basic information about most of our vaccines and what happens with them in the specific “textbook” scenarios, but we also need to know what to do when animals and owners don’t follow the textbook (which happens a lot).

Label instructions on vaccines have traditionally described those ideal / textbook scenarios, but more recently they are getting much less specific. That’s useful in some ways, because it provides room for flexibility and gets away from rigorous, dogmatic approaches, but it doesn’t necessarily help someone know what to do instead.

That’s where veterinary vaccination guidelines can be useful too, and these have been critical to the advancement of preventive care over the years, but they also need to evolve. Current veterinary vaccination guidelines have a lot of recommendations that aren’t supported by any data, but sometimes we have to make recommendations even when we have very little evidence. More recent approaches to guideline development use rigourous evidence synthesis (to make sure we are basing decisions on what’s known, not just the parts we like) and provide insight into how certain we are about each recommendation: Some recommendations are very clearly evidence-based and solid; many are reasonable but not strongly supported by evidence; some need to be rethought altogether. If there’s no transparency about what we know versus what we think versus what we’re guessing, it can lead to confusion and other issues (like guesses being treated as fact).

  • That’s me wearing my guideline methodologists hat, but I’ll take that off now, since I’m about to make some recommendations without that degree of evidence synthesis and structured decision-making process. It’s a blog post, after all. But hopefully it might entice some of the groups that make those guidelines to evolve.

Today I’m going to tackle what to do with pets that are overdue for their scheduled vaccine boosters. (I’ll try to cover some of the other scenarios in subsequent posts – this one will be long enough as it is!) Vaccines usually have recommended re-dosing intervals. In the past these have typically been very specific (e.g. every 12 months), but the trend is now toward much looser statements. For example, one Canadian canine vaccine label now reads “Historically, annual revaccination with this product has been recommended. The need for annual booster vaccination has not been established for this product. For advice on revaccination frequency, consult your veterinarian.”

Here’s an example: An 8-year-old Bichon (let’s call him Teddy) was vaccinated as a puppy, and then got core (distemper, parvovirus) and rabies vaccines at approximately 1 year of age, and then again 3 years later (around 4 years of age). He was due for re-vaccination a year ago (7 years old). Teddy was also consistently vaccinated against leptospirosis every year, but missed that one last year too.

What do we do with Teddy?

  • To be honest, my thoughts on this have evolved as I’ve put more time into looking at evidence and thinking about vaccination. I’ll admit I had a lot of ingrained approaches that were based on historical norms and not data and evidence. Changing behaviours is hard for people, and even I’m not immune to that, but we have to evolve.

A common response to this scenario would be to say that Teddy is well overdue for everything, so we need to restart all of his vaccine “series,” meaning a dose now and (for some of the vaccines) as booster in a few weeks. But that doesn’t make sense to me immunologically. Most (not all) of our canine vaccines are quite good at what they do, and the immune system of most animals has an effective long term memory. While protection against some diseases may wane over time (which is why the boosters are still needed), the ability to respond well to a booster vaccine often endures for much longer (a concept sometimes referred to as boostability).

In human medicine, there are very few situations where it is recommended to restart a vaccine series, and none of them apply to the kinds of vaccines we use in dogs and cats. If a person misses their scheduled booster and is overdue – whether by a day, a year, or 10 years – the recommendation is typically to simply revaccinate them. According to the US CDC guidance on Timing and Spacing of Immunobiologics: “Vaccination providers should administer vaccines as close to the recommended intervals as possible. However, intervals between doses that are longer than recommended typically do not reduce final antibody concentrations, although protection might not be attained until the recommended number of doses has been administered. With some exceptions (e.g. oral typhoid vaccine) an interruption in the vaccination schedule does not require restarting the entire series of a vaccine or toxoid or addition of extra doses.”

So for Teddy, I’d recommend simply revaccinating him as usual, with the exception of the rabies vaccine… That exception is due to regulatory issues around rabies vaccine, because regulators don’t like to take any chances when it comes to very deadly zoonotic diseases (which is somewhat understandable).

  • Rabies vaccine works very well, and many animals respond extremely well to a booster vaccine even if they’re overdue by several years (Moore et al. 2015), but it’s impossible to know (in advance) which animals will and which won’t respond well to a booster, or how long an animal may be protected beyond what has been tested by the vaccine manufacturer. But even rabies vaccines labels have become less prescriptive; for example, one such label now says “Duration of Immunity is at least 3 years after a repeat dose” but does not specify an interval for the repeated dose.
  • A pet’s rabies vaccination status therefore impacts what happens if that animal is potentially exposed to rabies. Different jurisdictions have different rules about this; Ontario’s rabies management guidelines for domestic animals are one example. If an overdue dog like Teddy was revaccinated today, I would have absolutely no concern about the dog being protected for at least the next 3 years, but some regulators would only consider that booster valid for 1 year. So if Teddy was exposed to a bat or an abnormal raccoon 18 months from now, that could mean a long confinement period (instead of easy observation).
  • Knowing what the rules are in your local area is important. Some jurisdictions now may worry less about the previous vaccination intervals (but knowing the pet has had previous rabies vaccines at some point), and focus mainly on the interval from the last dose (e.g. within 3 years). Some will accept a 3-year duration of immunity if there are only short lapses in the history (e.g. as long as the dog was boostered within 3 months of when it was due). Some remain very strict, meaning as soon as a pet is overdue, it’s next rabies vaccine is only good for 1 year, and only after getting another booster within 12 months can the pet go back on the 3 year revaccination schedule. While it could be helpful for regulators to have some more flexibility, “regulation” and “flexibility” are difficult concepts to marry along with “consistency”.
  • Animals that travel overseas may encounter the strictest rabies vaccination requirements. Border authorities may look very closely at vaccination history, any lapse in vaccination (even by a day) could invalidate a claim to a 3 year duration of immunity (meaning if it’s been more than 1 year since the pet’s last vaccine, it will be stopped at the border).

Knowing what rules may apply to a certain pet (based on where it lives or where it may travel) is key. If in doubt, I’d revaccinate Teddy now and give a booster in a year, even though it’s likely overkill for many pets (but better than a rabies quarantine or interrupting the owner’s vacation plans).

Even if we get veterinarians (and owners) on board with the immunological basis for not needing to restart vaccine series in overdue pets, some veterinarians will still worry about liability and vaccinating “off label.” But consider that giving a single dose now is no more off-label than restarting a series, because neither of those scenarios is described on the label (or even in the R&D from the vaccine manufacturer). Yet we convince ourselves that the historical norm (e.g. what we did before, as per the label) is the safer / better approach, but we don’t know if that’s actually true.

For me, at this point, overdue animals are easy: Vaccine them as you normally would, but also think about (and discuss with the owner) if the pet might run into any regulatory issues if it’s not revaccinated again in 1 year (instead of 3 years).

I’ll be a little more concise (I almost promise) when I cover other vaccination scenarios (stay tuned). For more information (and a sneak peak of what’s to come), check out the new paired resource from the Ontario Animal Health Network (OAHN): Vaccination Timing and Intervals in Dogs and Cats (infosheet and infotable). If you don’t have an OAHN login, veterinarians and RVTs can sign up for free.

I doubt I’ve posted anything here about hairballs in cats before, despite having cats that sometimes leave them around the house, as it’s not really an infectious disease issue. However, Dr. Samantha Taylor, a feline and internal medicine specialist who’s been at the forefront of navigating the new realities of antiviral use for feline infectious peritonitis (FIP) in cats, is coordinating a short survey looking at grooming and hairball behaviour in cats, to help answer understudied questions about how common hairballs are and factors that might be associated with them. So I figured we could help by sharing the survey link with our many cat-owning readers.

I’m not involved in this survey, but I completed it as a cat owner myself. Fellow cat owners can access the survey as well through the link below:

The Fur Report 2026: Survey on grooming behaviour and hairballs in pet cats

No hairballs yet from Franklin, my daughter’s new cat (pictured above)… but he looks like he’s planning something.

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Two separate stories regarding Salmonella contamination of unrelated pet products have been in the news lately.

The most recent one was a recall of Salmonella-contaminated pet supplements from Fi, a New York based company (see the link for specific products and lots affected). Details are pretty sparse, but the recall was apparently triggered because of contamination of an ingredient supplied to the company. It’s not clear whether the contamination of the ingredient was detected by the supplier during routine testing, by Fi during routine testing, or based on an investigation linked to sick pets. The FDA notice doesn’t mention anything about sick animals (or their human contacts), so hopefully this recall was made out of abundance of caution prior to any known cases of illness (while noting that “no known cases” doesn’t mean “no cases”, as illness from contaminated food, treats or supplements is vastly underidentified and underreported).

While contamination is concerning, the response seems very appropriate: A problem was identified, the FDA was notified, and a recall was initiated. That’s how it should be.

…But at the other end of the spectrum is Darwin’s Pet Food.

I’ve written about Darwin’s before as they’ve had multiple contamination problems with their raw pet food in the past, including E. coli in contaminated pet food resulting in severe disease in a child, follow a few months later by more issues with contamination of their products with Listeria and Salmonella. A common theme with both stories (beyond the biohazardous pet food) was the company ignoring FDA requests to recall the implicated diets. It boggles my mind that a company can just ignore an FDA recall request, both based on the legal aspects and basic ethics. But, they did.

More recently, the US Justice Department filed a complaint to “to permanently enjoin a Washington state pet food manufacturer [Darwin’s] from manufacturing and selling adulterated pet food.”

It shouldn’t take a Justice Department lawsuit to make a company stop selling contaminated food but that seems to be the case with Darwin’s. In the FDA notice, Timothy Schell, Director of FDA’s Center for Veterinary Medicine stated “Despite repeated FDA warnings, this company continues to manufacture and distribute products contaminated with harmful bacteria. When a company does not take responsibility for product safety, FDA will intervene to protect public health.”

In some ways, I’m surprised they acted, as contamination of raw pet food is a niche issue that has largely avoided regulatory attention in the past. It’s a good sign, though. Our archives have lots of information on the broader issues around whether or not feeding raw diets to pet is a good idea, so I won’t get into those again here. Suffice to say, if raw diets are fed to pets, people need to realize there’s an increased risk to both pets and people, and they need to take appropriate precautions. Companies need to do that too. For example, some raw pet food companies use high pressure pasteurization to reduce (not necessarily eliminate) bacterial contamination in their products, which is a very useful measure.

Good companies have good facilities and food safety practices. Others deflect responsibility and ignore warnings and reports of sick animals or people. The problem is, consumers often can’t tell which companies are doing (or not doing) what. Government action is important in this kind of scenario in particular; naming-and-shaming can be a big part of it since, ultimately, if consumers stop buying dodgy products, those companies will either go out of business or have to improve.

Here’s some other info from the Justice Department notice:

The complaint, which was filed in the U.S. District Court for the Western District of Washington, alleges FDA found the presence of pathogenic bacteria, including Salmonella, Listeria monocytogenes (L. mono), and Shiga toxin-producing E. coli (STEC) in the company’s finished pet food products in samples collected from 2017 through 2025. In 2024, FDA investigators also found Salmonella in the company’s Tukwila facility. Infections from L. mono, Salmonella, or STECcan cause symptoms such as diarrhea and vomiting in healthy adults. For vulnerable consumers — including pregnant women, the elderly, and the immune-compromised — L. mono, Salmonella, and STEC can each cause more serious effects including death. L. mono can cause stillbirths and miscarriages.  

The complaint further alleges Arrow Reliance’s products have repeatedly infected consumers over several years. After multiple Arrow Reliance customers complained of humans or pets suffering from health problems, FDA investigators detected the presence of pathogenic bacteria in unopened samples of the company’s product. In 2024, a four-year-old child fell ill with a STEC infection and developed Hemolytic Uremic Syndrome after the family dog was fed Arrow Reliance’s products. Third party laboratory testing of the family’s unopened pet food from Arrow Reliance confirmed the presence of both Salmonella and STEC bacteria. 

Here we have the juxtaposition of one company that seems to have initiated a recall of its products because an ingredient was contaminated, without evidence of disease but acting appropriately to reduce the risk (yay!), compared to another company that has chronically and repeatedly ignored FDA recall requests, has clear evidence of long term quality control and contamination issues, and shows no interest in the health of consumers or their pets (boo!).

I hope that people who feed Darwin’s diets will pay attention to what this government action is saying.

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Antibiotics get used a lot in dogs and cats (and other species) that undergo surgery. A lot of the time, the antibiotics are unnecessary. I suspect in many cases veterinarians know it’s unnecessary, but they still use them out of habit, fear of complications, fear of complaints from owners, lack of consideration of the potential downsides, and because we are programmed to want to “do something” to avoid adverse outcomes, even when not doing anything may be the best approach.

A big challenge with developing reliable veterinary antimicrobial prophylaxis guidelines is the lack of good studies. There are lots of small observational studies in animals for various types of surgery, which are useful but only provide quite low-certainty evidence. We’d love to have randomized controlled trials for each type of surgery in each species, but such trials are expensive and complex. Another major challenge for any surgical site infection study is enrolling enough cases (i.e. sample size). Since surgical site infections are uncommon after most procedures (which is a good thing!), studies usually need very large sample sizes (e.g. hundreds to thousands of animals) to detect differences between treatment groups, or to confidently say there’s no difference (i.e. non-inferiority trial). I frequently have discussions with people who want to do studies looking at use of antimicrobials and surgical infections. Once we go over the numbers, they tend to quickly get turned off because sample size calculations show the required size would be way too big for what they can manage (or afford) to do. Unfortunately, there simply is not enough funding in this area, so we’re not likely to get these kinds of large trials anytime soon. That doesn’t mean we’re stuck with no evidence at all on which to base our guidelines, it just means we have to rely on different types of evidence that have less certainty.

That can be disheartening to feel like the kinds of studies we want to do are constantly out of reach, but it doesn’t mean that smaller studies are futile even if they can’t answer all the questions. “Don’t let perfection be the enemy of the good” as they say. We just have to have realistic expectations (and avoid over interpreting the results).

We recently published a commentary highlighting this, entitled Small sample sizes in clinical trials: a pragmatic approach to clinical research in veterinary medicine (Weese et al. J Small Anim Pract 2026). A single small study may not be able to answer our big questions, but we can put data together from multiple small studies (if they’re well designed) using meta-analyses to draw stronger / broader conclusions. The concept is that there are no underpowered studies, there are only underpowered analyses.

  • Small studies may not be amenable to much or any statistical analysis on their own, yet weak or futile analyses are often attempted, likely because the authors feel it’s expected. However, improper conclusions from underpowered analyses can range from useless to even harmful in some cases.
  • We still want small studies to be published, but they may just be data with no analysis, and that can be hard for researchers and readers alike to wrap their heads around.

I raise this concept in the context of a nice recently published little study about bacterial endocarditis in dogs that underwent balloon dilatation because of congenital pulmonary stenosis (Zeedijk & Szatmári et al. 2026). The authors evaluated dogs that underwent this procedure and that had adequate post-operative follow up, with focus on the 83 dogs that didn’t get peri-operative antimicrobials. None developed an infection. There was a smaller group of 11 dogs that did antimicrobials. None of them developed an infection either.  We could run a rather futile statistical analysis and conclude that there is no statistically significant difference, but we’d have no confidence in that analysis. The study was not adequately powered for that comparison, so it’s great they actually did not try to do it, but we still have those data for a future meta-analysis.

The 83 dogs that didn’t get antimicrobials can also provide some additional insight. With zero infections in 83 dogs, the 95% confidence interval for the true infection rate would be 0-3.6%, i.e. the true incidence of infection could be between 0 and 36 infections per 1000 dogs that underwent the procedure without antimicrobial treatment.

  • Based on this low rate of infection, the potential severity of disease if infection occurs, the ability to treat such an infection, and the potential for complications from prophylaxis, we can consider the balance between risks and benefits of antimicrobial use in these patients. That’s still challenging, but the point is it’s important to consider all these different factors and not just the infection rate.

We can take it a step further, too. Consider that not all infections are preventable, even when antimicrobials are used, so we shouldn’t base our calculations on the assumption antimicrobial use would eliminate all these infections, it would only lower the infection rate.

  • Using an infection rate of 3.6% (the upper limit of the confidence interval) and an estimate that antimicrobials would reduce the infection risk by 25% (remembering that we don’t know if they will in fact reduce it at all), the calculated absolute risk reduction would be 0.9% (i.e. 9 infections per 1000 treated dogs).

In this scenario, the number needed to treat (NNT) to prevent a single infection is 111 dogs. (NNT is an underused but very helpful concept to put rates like this into context.) At first glance, an NNT of 111 might seem quite reasonable, especially since infective endocarditis can be a severe disease. However, that’s based on a very conservative assumption that the true infection rate is at the upper end of the confidence interval, and we have yet considered other factors:

  • Some of those 111 dogs will experience adverse effects from the antimicrobial. Most will be minor side effects, but occasionally they can be significant. So we need to weight the benefit to some dogs versus the potential harm to others.
  • Also remember that we’re basing this number on a very (and likely unrealistically) high infection rate. If the infection rate is 1% and antimicrobials still reduce that risk by 25%, the absolute risk reduction would be only 0.25%, or 2.5 infections prevented per 1000 treated dogs. The NNT would be 400. Drop that infection rate to 0.5%, and the NNT is 800.

The endocarditis rate for this procedure in humans has been reported at 0.12%, which would make the NNT 3333. I think it’s pretty safe to say we’d do a lot of damage treating a few thousand dogs to prevent one case of endocarditis (and that’s not even taking into consideration the risks of antimicrobial resistance selection). Yet, antimicrobials are still very commonly being used in dogs for catheter-based cardiac interventions that are very low risk for infection (Blok et al. 2025).

Too often we don’t do the math. We don’t think about absolute risk reduction, NNT, number needed to harm, broader risks like selection for resistance, or even cost to owners. We get tunnel vision about incidence rates and p-values, and act as though they provide the answers, when in reality they rarely tell the whole story, and are sometimes even misleading.

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These days, it’s really easy to identify new viruses. Our technology has advanced so much that you can sequence a vast array of viruses from almost any sample from an animal, person or the environment. Finding the viruses is easy, but understanding what, if any, roll they play in the grand scheme of things is a much greater challenge.

As a reviewer for scientific journals, I see lots of papers describing new viruses. Most of these are probably old viruses that we just recently identified. Often, studies say “look what we found” but don’t take the next step to figure out if the “what” is relevant, or they tend to overstate the potential relevance. I might find a new virus in a sick animal, but that doesn’t mean the virus is causing disease; it might just be part of the normal innocuous viral population that lives on and around even healthy animals.

We don’t want to dismiss new findings, but we also don’t want to over-react. Take amdoparvovirus for example, or more specifically, raccoon dog and fox amdoparvovirus (RFAV). Amdoparvovirus in part of the Parvoviridae family, along with the more well-known canine parvovirus, but is a distinct genus that includes a variety of different viruses that infect a range of mammals, particularly mustelids (e.g. ferrets, mink), skunks and raccoons. One of the most well-recognized members of this genus is the cause of Aleutian disease, a serious disease in mink.

Raccoon dog and fox amdoparvovirus was first reported in 2014 as part of an investigation of an outbreak in raccoon dogs and Arctic foxes on fur farms in China. Disease was most severe in young animals, with signs of decreased appetite, weight loss, slow growth and chronic diarrhea, with histological evidence of gastrointestinal and kidney damage.

A recent preprint (i.e. a non-peer reviewed preliminary paper) (Gajdov et al. 2026) describes an outbreak of disease in dogs attributed to RFAV. Not surprisingly, given the world we now live in, social media in some places has taken it from “here’s a potential spillover of a virus in a single kennel” to “OH NO! A NEW DOG VIRUS!!!” This preprint describes an interesting outbreak with some nice details along with some clear gaps.

  • I try to pay attention to reports of “new” issues, but always with a healthy dose of skepticism. Most of the time, a strange disease is just an unusual presentation of a normal disease. Similarly, a “new” disease event (like RFAV in dogs) is more often a rare event or something that’s happened before but not previously been recognized, versus true emergence of a new problem.

Here’s a synopsis of the outbreak and pathogen investigation described in the preprint:

  • An outbreak of disease was identified in Dobermanns in a kennel in Serbia. Affected dogs had abnormalities such as ocular and nasal discharge, conjunctivitis and weight loss, with some dogs also having “blue eye,” liver disease or, at later stages, neurological disease (which sounds pretty textbook for canine distemper). They tested for distemper, among other things, and results were negative. Samples were submitted initially from a dog and her two puppies, but it’s not clear if only those dogs were tested for distemper or whether other dogs were as well. More details about the testing (e.g. test type, numbers, timing) would be useful to help understand if we can really exclude distemper as the cause. As the old adage goes, common things occur commonly.   However, they mention repeated testing, and presumably they did a pretty good investigation before embarking on sequencing to identify any new pathogens.
  • The authors then went virus hunting, using sequencing to look for viruses present in lung, kidney and liver samples from the dog and puppies. They found “RFAV” — more specifically, they found sequences with 97% genetic similarity to the limited number of known RFAV genomes. We know relatively little about the genetic variation of this virus in nature, which is important for interpreting this finding. If the virus is genetically similar to RFAV strains circulating in wildlife, that would support direct spillover into the kennel from an infected wild animal. If it is substantially different from viruses circulating in wildlife, that suggests that it could be a distinct variant, although that still wouldn’t mean it is a dog-adapted virus. It’s way too early to say. At this point, a spillover of RFAV into dogs seems more likely than the emergence of a distinct canine virus.
  • They then developed a PCR test specifically for this virus. They got positive results from one other epidemiologically-linked dog, and an undefined number of healthy dogs from other locations tested negative. They don’t say if they tested other affected dogs, which is important context. The more sick dogs that test positive and the more healthy dogs that test negative, the more convincing it is that the virus is clinically relevant. But even with these kinds of findings, association doesn’t necessarily mean causation.

Lack of histopathological investigation (both in general and specific testing to look for evidence of canine distemper virus) is a limitation of this paper. I wonder if they’ll get asked to do that prior to peer-reviewed publication, if they still have tissues from these animals.

Another gap is this paper is the limited epidemiological data. No information was provided about potential sources of exposure or transmission patterns. I wanted more details about the kennel, numbers of affected and unaffected dogs, a timeline of how infections developed, kennel management practices and diet, as well as potential opportunities for direct or indirect contact with wildlife. There shouldn’t be farmed raccoon dogs or foxes in the area since that’s been banned in Serbia, but wild fox exposure would be worth investigating.

In the end, we’re left asking if this situation is:

  1. A new emerging disease caused by a new virus that may lead to widespread problems in dogs..
  2. An uncommon spillover event that happens periodically but just hasn’t been identified before, because such detailed investigation of kennel outbreaks is rare.
  3. An outbreak cause by a co-infection where RFAV was perhaps a contributing factor in disease but there was something else involved too
  4.  A confluence of factors that allowed a really rare scenario to develop.
  5. A distemper outbreak that was not detected.

I’d like to have convincing details to rule out E before anything else, but by next guess would be B… that this virus is “new to us” versus “truly new”.  

I don’t want to downplay the usefulness of information though. Studies like this form the foundation for further studies to help us figure out if this virus is actually a health threat in dogs and how common it is in the population (sick or healthy). Now that this is on the radar, testing can be done (through research labs) in situations where it might be relevant. We’d also need to have some testing of healthy dogs to provide context.

Raising awareness versus causing panic is always a tough balance with infectious diseases. This report tells us we have something else to consider and to investigate further, not that we have a new concerning problem that’s causing an imminent threat.

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I get a lot of questions about what to do when a healthy dog tests positive for antibodies to Borrelia burgdorferi, the bacterium that causes Lyme disease. It happens regularly because this test is often run alongside blood tests for heartworm, whether we want it or not – it’s really just along for the ride. A small percentage of healthy dogs have antibodies against Borrelia, so when millions of dogs get tested, there will be a lot of positive tests.

The tests are quite accurate too, but there’s a problem with how the test results are framed. Borrelia serology in a healthy dog is not a “Lyme disease test.” These tests alone can’t diagnose Lyme disease anymore than a high white blood cell count by itself can diagnose pneumonia. They just tell us the dog has encountered the bacterium and mounted a normal immune response. Most of the time, Lyme disease did not (and never will) develop. But when people refer to it and use it as a “Lyme disease test,” it leads to a lot of stress, more testing and unnecessary treatment, which can be harmful. When we get a positive test result, all too often our own insecurity makes us over-react.

What should we do when a dog tests positive for Borrelia antibodies?

Data to guide us on exactly what to do are unfortunately pretty sparse. There have been two ACVIM consensus statements on the subject (2006 and 2018), but there wasn’t a lot of consensus in the end, and many recommendations didn’t have much or any supporting evidence (That doesn’t mean they are inherently bad, it just means we need to better understand the issues). We have to look at the data we have now, what we know about infectious diseases and what we know about Lyme disease in humans. Here’s my thought process about the different options for what to do with a dog that tests positive:

Double check the dog’s health status

If we find a dog that is positive for antibodies against Borrelia, my first question is “how is the dog doing?” If the dog doesn’t have any signs that might be suggestive of Lyme disease, that’s pretty much the end of the discussion. I still want to be sure to take a very careful history to be confident that there really isn’t anything relevant going on (e.g. mild shifting lameness that could suggest Lyme arthropathy), but if the dog looks healthy, acts healthy and the owner is happy, I’m happy.

Do NOT reach for antibiotics

Unfortunately, thousands of dogs are treated with antibiotics every year because they have Borrelia antibodies, not Lyme disease. There’s no evidence that antibiotics help in dogs that have no overt signs of illness. A positive test result is an indicator of historical exposure, not necessarily an indicator of active infection. Dogs can remain positive on serological tests for years. Antibiotic treatment of a random healthy seropositive dog is very unlikely to help. Doxycycline, the typical treatment of choice, is generally safe, but there is always a risk of adverse effects. Selecting for antibiotic resistance in the dog’s microbiota (which always contains numerous potential pathogens) is also a concern. The more we use antibiotics (including doxycycline), the less effective they’ll be down the road. The cost:benefit ratio is clearly tipped towards “cost” from my standpoint.

Testing for proteinuria?

There’s no evidence that testing for proteinuria is useful in seropositive dogs either. This was recommended in the older 2006 ACVIM consensus statement (despite little consensus), but it was based on no data. I suspect it was more of “we have to suggest something so let’s suggest something that’s not harmful” versus “we have reasonable evidence to suggest this is useful.”  

The main reason for the recommendation was the concern about Lyme nephritis, which causes severe kidney disease. It’s rare but its often fatal. It also seems to be a very acute disease, in that it hits quickly and very hard. It will cause high levels of protein in urine, but the odds of us finding proteinuria as the initial sign in an otherwise normal dog (i.e. that is just about to crash from Lyme nephritis but hasn’t yet) are exceptionally low. Also, Lyme nephritis is an immune mediated disease, not an infection of the kidneys, so treatment is immune suppression. We’re really unlikely to start a healthy dog on an immunosuppressant drug, even if we do find some proteinuria.

Finding proteinuria means we need to go looking for the cause, not jump to the conclusion that the dog has Lyme nephritis. Testing for proteinuria is never bad, and it’s a very non-invasive test, it’s just of limited benefit; it’s probably no more useful in a seropositive dog than in a seronegative dog.

Skip the quantitative C6 testing

This test puts a number (quantitative) to the positive antibody result. Initially, when it first came out, we were hopeful that it would be useful if higher levels were more indicative of disease and changes during treatment could be used for monitoring response. Unfortunately, none of that has panned out. There have been no data suggesting this test provides any useful additional information, so I don’t recommend it.

Watchful waiting

“Do nothing” sounds dismissive, but it’s largely what’s indicated. It’s fair to have owners be aware that there’s a chance the dog could develop Lyme disease, and that they should watch for compatible signs of disease, but that could also be said about any dog in an area where the disease occurs.

Talk about tick exposure

This is the big one for me. A positive result means there is a need for tick prevention. If the dog is currently on a preventive, it’s worth discussing compliance since the available products are generally very good at preventing ticks from attaching for long enough to transmit Borrelia. If compliance seems to be excellent, we can add other strategies like tick checks and avoiding high risk areas to help prevent exposure. Lyme disease vaccination can also be discussed as a “plan B” approach for when ticks break through preventives. Overall, the positive result is an entry point for a discussion with the owner about the need to up their game in terms of tick control and prevention. That’s valuable for Lyme disease and other tickborne disease circulating in the area too.

Is there any value in routine testing for Borrelia antibodies?

Maybe. There are two things to consider: the patient and the population.

At the patient level, I don’t see any direct value from these tests from a disease standpoint, if the dog is healthy. However, they can be useful from an educational standpoint and initiating (or revisiting) the discussion about exposure to infected ticks and tick prevention practices, including product selection, compliance and duration of administration (the period of risk is now approaching 12 months a year in many regions since ticks are active once it gets a bit above freezing).

  • If we’re going to use these tests, we need to remarket them. They should be considered “tick exposure tests,” not tests that indicate the need for treatment or other diagnostic testing in a healthy dog. A positive result means there’s definitely been tick exposure, but a negative result doesn’t rule tick exposure out, since not all ticks (or tick bites) transmit Borrelia.

These tests are most useful at the population level. I don’t really care what the result is in a an individual healthy dog. However, when we put together results from lots of healthy dogs from lots of regions, and repeat the testing over time, it can give us a very useful picture of the distribution of evolution of exposure risks. That can help us better understand, prevent and manage tickborne disease, and better understand parallel exposure risks in people. We know much more about Borrelia exposure in dogs than in people, because we test millions of dogs over time. If we use that information wisely, it can be useful. If we use it poorly, we cause harm. I suspect we do more harm than good currently, but there’s still lots of opportunity to improve.

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Cyclospora has been in the news a lot lately because of a large, ongoing outbreak of cyclosporiasis in people in the US. Total case counts aren’t clear (and official numbers are always lower than the true number of cases because of under reporting) but it’s estimated that well over 10 000 people have been infected.

For those unfamiliar with Cyclospora, it’s a group of protozoal parasites that can cause gastrointestinal disease. This outbreak specifically involves Cyclospora cayetanensis, which is a well known cause of diarrhea in people. Infected individuals shed the parasite oocysts in their feces, but it takes 1-2 weeks in the environment for the oocysts to sporulate and become infectious, so direct human-to-human transmission is generally not the concern. Transmission occurs from fecal contamination of food or water. Fresh fruit and vegetables are the most commonly implicated sources in food borne outbreaks; the food gets contaminated when they’re picked by hand, and they’re then often eaten raw (and unfortunately not always washed well).  In a typical year there would be about 3000 cases of cyclosporiasis reported in the US (and about 300 cases annually in Canada). Fortunately the mortality rate for this disease is very low, but illness can last for weeks even with proper treatment.

With so many people getting sick, it’s important to consider whether there are also risks to – or from – pets and other animals.

Exposure of dogs and cats to Cyclospora

It’s likely that dogs and cats are being exposed to this parasite as well, but exposure is likely uncommon ad fairly low level when it occurs. Currently the outbreak investigation is focused on a source of contaminated iceberg lettuce that was produced in central Mexico. While this iceberg lettuce may not be the only source, it seems to be the main one at this point. Presumably very few dogs (and even fewer cats) are fed lettuce, so that limits their exposure. Indirect exposure to the parasite through contaminated hands or surfaces, or cross-contamination of other foods that the animal might eat is always a potential risk, but the overall risk of exposure for most pets is presumably very low.

What would happen if a dog or cat ingests Cyclospora?

After exposure, a few different scenarios can occur:

  1. The animal gets sick, including shedding the parasite in its feces
  2. The animal doesn’t get sick, but has a subclinical infection and sheds the parasite in its feces
  3. The animal doesn’t get sick or infected, but the parasite passes intact through the animal’s intestinal tract and winds up in the feces (at very low level)
  4. The animal doesn’t get sick or infected, and the parasite doesn’t make it through the intestinal tract to the feces either.

Some foodborne pathogens can cause disease in a wide range of species (e.g. Salmonella). Others, like Cyclospora cayetanensis, are much more limited in terms of species they can infect. Investigations of both experimental infection and potential natural infection have concluded that it’s predominantly or almost exclusively a human parasite. Experimental infection has been attempted in dogs without success; while that’s not a guarantee that dogs can’t ever be infected (experimental infection models are never perfect), it’s certainly supportive of this parasite not being clinically relevant in dogs. Cyclospora cayetanensis DNA or Cyclospora-like oocysts have occasionally been detected in dog feces, but these findings have not been associated with clinical disease and most likely reflect simple transit through the intestinal tract rather than true intestinal infection. Very limited information is available for cats, but there is currently no evidence that cats develop clinical infection or serve as an important reservoir either. So while we can’t say with 100% certainty that dogs and cats can’t ever be infected with this parasite, the odds are very low.

Can dogs and cats spread Cyclospora to people, even if they don’t get sick? 

Living with a dog was a statistically significant risk factor for disease in one Cyclospora outbreak in the late 1990s, but there are lots of potential confounders, so this doesn’t provide any real evidence that dogs themselves are the risk. Theoretically, we can’t rule out a dog ingesting the parasite, passing it in their feces, and then a person in the household getting infected through fecal-oral exposure, but that’s a stretch. Even if viable oocysts were passed in the dog’s feces, they would still require time in the environment to sporulate before becoming infectious, so basic routine practices like cleaning up dog feces (poop and scoop) and hand washing would reduce the risk even further. Cyclospora is very low on the list of things I’d be concerned about in any random fecal sample from a dog. The risk of exposure for people through contaminated produce is much higher.

If there’s active Cyclospora infection in a person in the household, I’d pay close attention to avoiding fecal-oral exposure to dog feces, but I’d say the same thing for any household with a dog.

There is currently no evidence that dogs or cats play a meaningful role in the epidemiology of human cyclosporiasis. If there is Cyclospora in your household, focus on preventing fecal contamination and food borne exposure. Standard hygiene and feces-handling practices are always important, but there is no reason to be concerned about pets becoming ill or serving as significant sources of infection for people.

Here’s a screenshot of a quick but useful New World Screwworm (NWS) resource for animal shelters that was developed by University of Wisconsin-Madison Shelter Medicine Program in collaboration with a number of shelter organizations and shelter medicine experts. With the continued re-emergence and spread of NWS from Central America back into the southern US, it’s an issue of importance for animal owners and veterinarians in those areas, and for those who take care of animals that are moved from those areas. Domestic animal cases in the US (including cattle sheep, goats and three dogs) have been limited so far, but will no doubt continue to increase, at least in the short term. Basic awareness is a critical control tool to stop further spread.

For the original post (and larger print) use this link: Humane Prevention and Management of New World Screwworm (NWS) in Shelter and Rescue Dogs and Cats