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

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

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

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

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

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

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

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

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

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

So, what now?

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

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

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

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

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

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

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

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

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

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

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

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

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

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As part of our upcoming revision of the 2019 ISCAID guidelines for diagnosis and management of bacterial urinary tract infections (UTIs) in dogs and cats, we recently did a systematic review to determine if cranberry supplements reduce or help treat urinary tract infections (UTIs) in dogs and cats. Our conclusion was… we have no idea.

There’s very little regulation of nutraceuticals like cranberry supplements. If products are not being marketed as drugs, there are few to no requirements to prove efficacy (or even safety). So budgets for these products tend to go to marketing, not research, resulting in many products that are widely used with no supporting data whatsoever. Some might work. Most probably do nothing (except maybe make the owner feel better because they are doing something).

Our systematic review aimed to answer four questions:

Does cranberry or cranberry component administration

  1. reduce the incidence of bacteriuria in dogs and cats?
  2. reduce the incidence of bacterial cystitis in dogs and cats?
  3. improve resolution of bacterial cystitis or bacteriuria in dogs and cats?
  4. reduce the recurrence of bacterial cystitis or bacteriuria in dogs and cats?

We found that little has been published. That either means little research has been done on these products, or that research has been done and not been published, possibly due to publication bias.

Publication bias is a significant concern. People are more motivated to publish “positive” studies (that show the effect they were hoping for), and manufacturers are more likely to bury studies that didn’t show the effect they wanted, or showed no effect. We recently evaluated publication bias in regard to probiotics for gastrointestinal disease in dogs and cats (Weese 2025) by looking at research abstracts on probiotics that were presented at conferences, compared to which ones were ever published in a journal. Overall, 5/7 (71%) abstracts that reported a clinical effect were published, compared to 1/5 (20%) that did not. We also have no idea how many studies may have been done and never presented in any form.

Regarding cranberries, we found three studies, but they were of variable quality. One was quite good and looked at cranberry for prevention of urinary tract infection in dogs with spinal cord disease. The other two were quite weak and only included a small number of animals (12 and 16 respectively).

So to answer the questions in above with respect to administration of cranberry or cranberry component, does it:

1) reduce the incidence of bacteriuria in dogs and cats?

The stronger study looked at this in dogs with spinal cord disease. The study was stopped early because there was a numerically higher incidence of bacteriuria (positive urine cultures) in dogs that got the cranberry supplement. Clearly futile.

2) reduce the incidence of bacterial cystitis in dogs and cats?
4) reduce the recurrence of bacterial cystitis or bacteriuria in dogs and cats?

One weak study with only 6 dogs per group looked at cranberry for prevention of recurrent cystitis, so it covered both of these questions. It didn’t show an effect as no dogs in either group developed cystitis during the study period.

3) improve resolution of bacterial cystitis or bacteriuria in dogs and cats?

One study investigated the impact of a cranberry and orange supplement plus an antibiotic (enrofloxacin) compared to antibiotic alone in cats with cystitis The sample size was small (8 cats per group) and no conclusions could be drawn because all cats in both groups responded to treatment (not surprising since they all got an antibiotic).

For any review of an intervention, safety is always an outcome that is evaluated as well. No studies reported safety data.

For those interested in meta-analysis and data, the overall Forest plot is below:

This does NOT necessarily mean cranberry supplements don’t work. It means we don’t have any data showing that they do work.

  • Cranberry might be effective, but the right studies haven’t been done.
  • Cranberry might be effective in certain animals and certain situations, but those haven’t been studied.
  • Cranberry might be effective at different doses or with different preparations.

…Or it might in fact be that cranberry is not an effective aid in any way for UTIs in dogs and cats.

We have no idea if any commercial supplements work since none have any published supporting data, so it’s buyer beware. These products are probably harmless, but it’s hard to say if they are useful at all.

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Boehringer Ingelheim (BI) has issued a voluntary recall of one lot (serial #18665) of its IMRAB 3 TF rabies vaccine that was distributed in the US, because some vials in the lot were found to contain sterile water instead of vaccination. That’s a big oops, but it’s also good to see that it was caught and is being addressed.

I’ve only seen information about the IMRAB3 recall on a few state veterinary medical association websites, but not directly from the manufacturer or the US FDA. According the posted information, BI is directly contacting clinics that received vaccine from the affected lot to provide replacement vaccine and support revaccination of animals that may have been affected before the issue was identified.

Why this happened is for the manufacturer to sort out; I assume that will be very closely investigated. But there are also some more questions about how to manage the situation.

What should veterinarians do if they have patients that may or may not have actually been vaccinated for rabies, because a vial from the affected lot was used?

BI is recommending revaccination for any dog, cat, or ferret that was vaccinated with a vial from the affected lot. That makes sense. If we’re unsure if they got a vaccine or sterile water, we need to revaccinate the animal to avoid gaps in protection and to ensure compliance with local rabies vaccination requirements.

Is there a risk from giving a pet another rabies vaccine soon after the first, if the animal actually received an active vaccine the first time?

No. A second dose of rabies vaccination does not pose any higher risk than any other vaccination: the risk of an adverse event is still very low.

Do we need to wait a certain amount of time before giving another dose of vaccine?

No. If the pet got an active vaccine the first time, the timing of a second dose soon after won’t affect the response, whether it’s days, weeks or months later. If they got sterile water the first time, the sooner they’re given an active vaccine, the sooner they’ll be properly protected again.

Are the rabies certificates for animals vaccinated with the affected lot still valid?

No. If the animal was vaccinated with the affected lot, we’d have to consider the vaccination certificate invalid, since we don’t know for sure that they received vaccine.

What do we do about pets that may now be overdue for their rabies booster, because they may not have received an active vaccine?

The label instructions for this vaccine are to revaccinate one year after the initial dose, and then every 3 years for dogs and cats (or annually for ferrets).

If the most recent dose from the affected lot can’t be trusted, we have to ignore it. If that makes the pet overdue for a booster, what to do depends a lot on where the animal is (or to where it may travel).

This vaccine is very good, and we expect solid, long term protection. A few weeks delay for a booster (or even a few months) doesn’t concern me in terms of the animal’s response to the vaccine and duration of immunity. However, in some jurisdictions (or typically when crossing international borders) they are very strict about the revaccination schedule, and if the pet is overdue, there’s no flexibility – they will not accept the 3 year duration of immunity anymore, and you need to start over from the beginning with the 1 year booster. In other jurisdictions, they may consider a grace period (e.g. up to 3 months) that would still allow an animal to stay on the 3-year booster schedule. But it is a grey zone that can depend on a variety of factors, so having a clear understanding of what’s done locally in critical. If in doubt, or if the animal is substantially overdue / beyond the grace period (if applicable), restart the series with a dose as soon as possible and a booster in 1 year, instead of 3.

  • Immunologically, that doesn’t make a lot of sense, since I’d expect a great response to the booster regardless in a healthy animal, but unlike other vaccines, we need to be wary of the regulatory issues when it comes to rabies too.

For ferrets, they need to be revaccinated annually regardless, so they would just need another dose as soon as possible and then carry on with the normal revaccination schedule.

 Are there any similar issues with other vaccines, or other lots of this vaccine?

No. This recall only affects one lot of one vaccine. The lot number is typically included on the animal’s vaccination certificate, so clinics will hopefully be able to contact the owners of any animals that received doses from the lot. Owners can also check the lot number on their vaccination certificate / proof of vaccination themselves if they want additional reassurance.

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Here are a couple of quick H5N1 flu updates about which I’ve been wanting to write. Neither is very surprising, but they highlight (again) some issues of concern.

(Presumed) fatal H5N1 influenza infection in a cat

An outdoor cat in Washington State tested positive for H5N1 influenza. Spillover of H5N1 infection into cats isn’t new. It occurs sporadically, most often in cats with outdoor access or fed contaminated raw poultry-based diets from potentially infected birds. In this case they specifically mentioned that the exposure was thought to be from contact with wild birds and not contaminated food.

Although the article doesn’t specify, presumably the cat died and was tested thereafter. That outcome seems to be the norm for cats with H5N1 flu. It’s possible that there are milder cases that go undiagnosed because a dead cat is more likely to be tested than a slightly ill cat that recovers on its own after a few days. Regardless, whether it’s almost always, most often or regularly fatal, infection in cats is bad. Trying to limit cats’ outdoor access (especially when flu is active in birds in the area) and not feeding cats raw poultry-based diets are two key preventive measures.

H5N1 influenza in cattle in the Netherlands

Back in December, I wrote about a litter of kittens from a dairy farm in the Netherlands that likely died from H5N1 influenza. At the time, none of the other animals on the farm (including the dairy goats and other cats) tested positive for flu. More recently, it was reported that one cow on the farm tested positive for H5N1 flu antibodies, which is consistent with the cow having been previously infected. The latest update is that five cows on the farm have now tested positive for H5N1 flu antibodies. That’s noteworthy for a few reasons:

  • The infection went relatively unnoticed in cattle. Whether they were all completely healthy or only mildly ill such that it wasn’t flagged isn’t known. This demonstrates that cattle can have relatively silent infections that may be difficult to detect clinically. It also shows (again) that cats may be great sentinels on farms, i.e. unexplained cat deaths should trigger an investigation to see if flu may be present.
  • Five positive cattle also gives us more confidence in the diagnosis. A false-positive test in five cows is much less likely than a false-positive in one. It also fits with some degree of cow-to-cow transmission. It’s unlikely (but not impossible) that there were five separate bird-to-cow transmissions, but much more likely that the virus went bird-to-cow-to-cow, as has been seen on US dairy farms. As I’ve mentioned many times before, any mammal-to-mammal transmission of this virus is a concern in terms of increasing the virus’ potential to jump to and spread among humans.

I periodically get calls from concerned veterinarians (none recently from Ontario, thankfully) along the lines of “We did surgery on a dog with a liver mass that was diagnosed as Echinococcus multilocularis (EM). What is the risk to the staff and what do we do to decontaminate the clinic?”

Depending on how well I know the veterinarian (and my mood), I sometimes start my reply with “Unless your staff are secretly canids AND snacked on the dog’s liver, everyone will be fine.”

The reason for this is based on one key aspect of the biology of EM: infection in dogs can occur from two different life stages of the parasite. (For more basic background on EM (aka the fox tapeworm), check out our Worms & Germs Echinococcus infosheet, or the Ontario Animal Health Network EM infosheet).

Dogs are primarily definitive hosts for EM:

  • As definitive hosts, dogs harbour adult worms in their intestinal tract, which are effectively harmless to the dog (they are very tiny!), but result in parasite eggs being passed in the dog’s feces, which are infectious to other animals, including people.
  • This form can also occur in other canids (e.g. foxes, coyotes) and rarely in cats.
  • Dogs get this form of infection by eating an intermediate host (usually a rodent) that was harbouring immature tapeworms in the form of cysts its body (known as alveolar echinococcosis (AE).

Sometimes dogs develop alveolar echinococcosis, which is the form of EM infection typically seen in intermediate hosts:

  • Intermediate hosts develop AE after ingesting E. multilocularis eggs from feces of a definitive host.
  • The immature form of the parasite migrates through the body and ultimately forms large budding cysts, most often found in the liver, that can spread like a malignant tumor. The disease can be fatal.
  • AE can occur in a wide range of species, including people.

It is relatively unique that dogs are a definitive host but they can also develop the intermediate host form of the infection, and that’s where the confusion typically lies. Only one form poses a risk to people.

  • A dog with intestinal infection sheds tapeworm eggs in feces which are infectious to people and other animals that ingest the eggs.
  • The AE form is only infectious to other definitive hosts (generally dogs and other canids) and only if they eat parasitic tissue from the dog. A person could snack on a raw sample of that dog’s liver and they’d be fine (at least in terms of the parasite, but still… yuck).

We can’t say dogs with AE are completely zero risk, because if the dog has been exposed to EM eggs, then it’s also possible the dog could have ingested an infected rodent with the intermediate form of EM in the same area, and may therefore have a concurrent intestinal infection. We really can’t say zero risk for shedding of EM eggs in any dog that lives in an endemic area (including southern Ontario) and spends time outdoors (because dogs will be dogs…). The fact that the dog has AE doesn’t influence that risk or make it higher risk than any other local dog.

We often test or empirically treat dogs with AE with praziquantel (an anti-tapeworm drug that is effective against the adult worms only) out of an abundance of caution, but other dogs from the same area (and with the same lifestyle risk factors, like catching rodents) are likely at just as much risk.

So… if you’re in contact with a dog with AE, relax. If you’re in contact with a dog with intestinal EM infection that may be shedding parasite eggs, then don’t eat poop and you’ll be fine. In Ontario, EM (in any form) in a definitive host (i.e. cat or dog) is immediately reportable to the local public health unit, and they will assess the risk to anyone who has been in contact with the dog (or its feces). Understanding and differentiating the different types of infections, how they occur and the different risks they pose is a key aspect of EM control and communication.

Life cycle diagram below from US CDC DPDx website.

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A few months ago, there was a cluster of kittens from a dairy goat farm in the Netherlands that likely all died from H5N1 influenza (only one kitten was tested). That wasn’t too surprising since the H5N1 virus is circulating in wild birds internationally, and we know that cats are highly susceptible to the virus, and can develop very severe (and not uncommonly fatal) disease. Being from a dairy goat farm, there was concern the kittens could have been infected via milk from the goats, because that’s what’s been seen / suspected in cats on dairy farms with infected cows in the US. When the H5N1 virus spilled over into daily cattle in the US in 2024, it spread rapidly and widely amongst dairy farms, often infecting (and killing) the farm cats. Initially it was reported that the goats and several other cats on the Dutch farm were also tested at the time and were negative for H5N1 flu. It was therefore assumed that the kittens had been exposed to the virus via wild birds, possibly indirectly through the mother cat.

More information about this case has recently been released. It turns out the farm was a dairy cattle farm (or at least had cattle as well as goats). When they tested the cattle – which were all clinically healthy – they found one cow that had antibodies against H5N1 influenza. If the test isn’t a false positive (which is always a consideration with rare outcomes and antibody tests), that would mean at least one cow was infected with the virus at some point, but wasn’t sick enough for it to be noticed, and then eliminated the infection without spreading it to the other cows, and leaving antibodies in the bloodstream as evidence.

It’s a good news/bad news situation.

The H5N1 influenza outbreak in dairy cattle in the US has been a mess, both in terms of the impact and the approach to control. We’ve been watching to see if the virus would spread or cross over into cattle again in another country. Sporadic wild bird-to-mammal transmission of the virus in wildlife especially is not uncommon, but the infections don’t lead to further mammal-to-mammal spread. Hopefully that’s what happened on this farm. However, every time H5N1 flu jumps into a mammal, it creates more opportunity for the virus to adapt to spread more easily in mammals, or the strain that jumps could already be adapted to this kind of spread. The more domestic animals get infected, the greater the risk of human exposure, and the more risk of further adaptation or recombination with human flu viruses to make another strain that could be worse for us.

The good news is that this seems to have been a one-off situation on this farm. The virus spread to at least one cow but didn’t cause overt disease, didn’t seem to spread further in cattle, and the situation seems to have resolved itself with no damage beyond the initial cluster of infected kittens.

But this is yet another reminder of why we need to pay attention to H5N1 flu and try to control it as best we can. This situation didn’t cause a problem, but a nationwide outbreak in dairy cattle will likely start with a single spillover on a single farm, so we need to remain vigilant so that we can hopefully stop it before it spreads further from there.

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Whether it’s dealing with an individual patient or developing international antimicrobial use guidelines, one of the bigger challenges we face in regard to antimicrobial treatments for dogs and cats is determining how long different infections need to be treated.

Unfortunately the treatment durations most commonly used are not evidence-based. We have very little data to go on, but well-established dogma that’s often largely based on something someone said or wrote (without evidence) possibly decades years ago. (This phenomenon is also not unique to veterinary medicine!)

It’s not that the traditional (old) approaches are inherently wrong, but we have to realize they’re not necessarily right, and we have to be open to change. Most antimicrobial treatment durations currently used in dogs and cats (and sometimes other species) are probably way too long; when we compare them to what’s done in human medicine for comparable conditions (for which they have a lot more large-scale studies), some of the differences are striking. But people are often (understandably) reluctant to change, even when there’s little or no evidence to support current practices, and we have circumstantial evidence (and basic principles) that suggest we’re treating patients for too long. We’re afraid of the risks of not treating long enough, but treating for too long also has risks, especially when it comes to antimicrobial resistance.

As the clinical antimicrobial treatment guidelines field advances, we’re underpinning new guidelines with evidence syntheses, particularly systematic reviews, to help change people’s minds and ultimately (hopefully) prescribing practices.

A new systematic review entitled “Shorter versus longer durations of antibiotic treatment for pneumonia in dogs and cats: a systematic review and meta-analysis” (Emdin et al. 2025) should help us revise our treatment guidance for pneumonia in dogs and cats. Veterinarians sometimes make recommendations for very long treatment courses for pneumonia in pets, which is in stark contrast to what’s done in humans and other species such as cattle.

Unsurprisingly, the systematic review only found a small number of studies (3) for dogs and none for cats. Two of the canine studies were randomized controlled trials (yay!) and one was an observational study (which provides lower level evidence and is more prone to bias, but still important to consider since we have such limited data in veterinary medicine). Meta-analysis showed no significant difference in outcomes (both clinical cure and recurrence) between animals treated with shorter (10-14 days) versus longer (21-28 days) courses of antimicrobials (see tables below or the full review for more details).

BUT there are lots of provisos. There were only 3 studies, and they were fairly small (only 74 dogs in total), so the assessment of the certainty of evidence was deemed very low (details in table below).

Despite the limitations in the data, this study suggests that we can use shorter treatment durations for pneumonia in dogs. It also highlights yet again that we need more data and better studies. We also need to study even shorter treatment courses to see if they’re effective. In humans with community-associated pneumonia (i.e. not acquired in hospital), there are numerous controlled trials showing 3-5 days of antimicrobials is just as effective as longer courses (check out Dr. Brad Spellberg’s “Shorter is better” website for more details). In cattle, we also we use much shorter treatment courses, typically only a few days, or a single dose of a long-acting drug that provides coverage for 3-8 days.

While this review suggests that we don’t need to treat pneumonia is dogs for longer than 10-14 days, but doesn’t tell us if even shorter courses would be just as effective. I suspect that if we had a study looking at 5 versus 14 days of treatment, we’d see they are equivalent. My current standard recommendation for treatment duration in these animals is 5 days; although this is admittedly based on no direct evidence in dogs and cats, we have enough indirect evidence that I’m comfortable with it as long as the patient responds clinically over those first 5 days.

Fortunately, the fields of evidence synthesis and guideline development are advancing in veterinary medicine. Unfortunately, we have many, many areas in which data are still limited or non-existent. That means we have lots of low-hanging fruit for future studies; more data will help us make more robust and reliable guidelines.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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