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

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

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

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

Why are we trying this again?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

1. Treatment of enteric feline coronavirus

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

    2. Treatment of other diseases

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

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

    What does this tell us?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

    So, what now?

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

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

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

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

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

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

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

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

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

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

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

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

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

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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.