While rabies kills approximately 50,000 people a year globally, there’s no reason anyone should die from rabies in places where people have access to a well developed public health system. Rabies is almost invariably fatal, but is also almost entirely preventable with appropriate and timely response to an exposure. The weak link is getting people to recognize that there’s a risk that needs to be addressed.

Once someone reports a potential rabies exposure (and it is assessed as a significant risk), the response should be fairly straightforward, resulting in the person receiving highly effective post-exposure prophylaxis (PEP). But if the exposed person doesn’t realize the risk, they won’t take the basic steps needed to save their life.

That’s what happened with a woman from California who recently died of rabies. She was a teacher who found a bat in her classroom which she handled while trying to carefully remove it, and she was bitten in the process. It was a minor bite, which makes it easy to dismiss because of the limited amount of trauma. You wouldn’t need to go to a doctor to address the physical damage from a bat bite, but that tiny bite can transfer enough rabies virus to a person to cause infection. Any bite from a bat is a potential rabies exposure.

What should have happened?

  • If she’d realized the risk, she would have gone to a healthcare provider or called public health, and a rabies risk assessment would have been done (and concluded that this was a high risk exposure).
  • If the bat was still available, it would have been humanely euthanized and tested for rabies, and if positive (as it no doubt would have been in this case) she would have started PEP right away.
  • If the bat was not available (e.g. flew away), it would be assumed that the bat could have been rabid (erring on the side of caution) and she would have started PEP right away.
  • The PEP (which typically includes an injection of antibodies then a series of 4 rabies vaccines over 2 weeks) almost certainly would have prevented rabies, and this tragedy would have been averted.

What actually happened?

Presumably the teacher did not know about the risk from bats and did not recognize the tiny bite as a major risk, so she did not seek a risk assessment and did not get PEP. That allowed the rabies virus to work its way through her body to her brain. By the time disease developed (typically several weeks to months later) it was too late to save her, as rabies it almost 100% fatal, even with aggressive medical care.

This shows that we need to continue to educate the public about the risk of rabies. It’s rare, but these deaths are entirely preventable.

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The second case of a rabies death I want to mention is one that is a lot less clear-cut. A 53-year-old woman from Vietnam died of rabies after an encounter with a feral cat. Cats are not a rabies reservoir species (i.e. there’s no cat-variant strains of rabies like there are in dogs and certain wildlife species) but they are an important source of rabies exposure for humans because cats can get rabies from other animals and they also have close contact with people.

The woman in this case was “scratched” by a cat in May, and the developed signs of rabies and died at the end of November. The time frame fits, but the history of a scratch (versus a bite) is unusual. Rabies virus is shed in saliva, so when it comes to exposure we focus on bites and other ways that saliva can be inoculated into the body (e.g. a cat spitting in someone’s eye, or licking an wound). Scratches alone are low risk since because animals do not carry rabies virus on their nails. However, if there’s saliva flying around at the same time, such as a fractious cat spitting and scratching simultaneously, the scratch could drive saliva that was deposited on the skin into the body. The cat in this case was killed by the family after it scratched the woman and bit her sister, and it wasn’t tested.

So, how did she get infected? Should this change our approach of not typically giving PEP after a scratch?

  • She might have been infected via the scratch if saliva had been deposited on her skin at the same time. A more detailed history of the encounter would be needed.
  • She might have received a small bite at the time and didn’t notice or pay attention to it. As with bat bites, a really minor bite is all that’s needed.
  • The victim (or the report) could have mistaken a “scratch” from a tooth (which would certainly be a risk for rabies exposure) for a scratch from a claw (which would not be a risk by itself).
  • She might have had another exposure to a different animal that wasn’t reported.

We’ll likely never know unless more details about the encounter (and possibly the rabies strain) are reported.

This shouldn’t change our approach to scratches, which are incredibly common, but shows the importance of a good history and a proper risk assessment, especially when the scratch is from an animal that has a greater chance of being infected (e.g. an unvaccinated feral cat that roams outside, versus a well vaccinated indoor cat).

Overall, these cases are reminders that rabies is still here, and will likely always still be here. While we have tools to effectively prevent infections, the human factor is the weak link. We need to be able to get these tools to those who need them for them to be effective, and the entry point for that is better public understanding of rabies risk.

Always remember that the best prevention for rabies it to avoid exposure in the first place, which means avoiding direct contact with wildlife and unfamiliar animals whenever possible.

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Recently, the American Animal Hospital Association (AAHA) designated leptospirosis vaccination to be a “core” vaccination in dogs. That means it’s recommended for all dogs. I’ve had a lot of veterinarians asking questions about this, since traditionally leptospirosis vaccination has been positioned as “optional” based on an individual dog’s risk of exposure.

I’ve considered this vaccine to be a core for dogs in much of North America for years. Lepto is a very nasty (and sometimes fatal) disease with a safe and effective vaccine, so a large percentage of the dog population would benefit from vaccination. I’ve been adamant I want all dogs around here (in southern Ontario) vaccinated.

But is it necessary for all dogs everywhere? That’s a tougher question, because the risk of exposure to lepto varies regionally:

  • In some areas, it’s a major issue.
  • In some areas, it’s uncommon but there’s an ever-present low risk of exposure.
  • In some area, it’s largely (or completely) non-existent.

As is unfortunately still typical with many veterinary guidelines (we’re working on improving that ), they didn’t describe any clear evidence basis, evidence synthesis and formal guideline development process that lead to this change. Making lepto a core vaccine for dogs is consistent with the recently updated ACVIM consensus statement on leptospirosis in dogs, but even that statement similarly lacks formal evidence synthesis and clear differentiation of what’s based on hard evidence and what’s based on expert opinion.

Overall, this is a well-meaning change that works for dogs in most areas and could be very useful to help drive better vaccine coverage in higher risk areas. But we still have to acknowledge that variability in risk and the fact that lepto is rare in some areas, where the cost-benefit for vaccination may not add up the same way.

Here are my take home messages on lepto vaccination for dogs:

  • Dogs in areas where lepto is endemic: Core vaccine for all dogs.
  • Dogs that might travel to areas where lepto is endemic: Core vaccine for all dogs.
  • Dogs in areas where there is enough information to confidently say lepto is rare (to non-existent): Non-core vaccine, but consider vaccinating based on the individual dog.
  • If there’s any doubt about the risk of exposure, vaccinate.

We don’t want to leave at-risk dogs unprotected, but at the same time, I’m wary of suggesting to veterinarians and dog owners that everyone needs to follow this change. Veterinarians have concerns about liability if they don’t recommend vaccination, even in areas where they’ve never seen a dog with lepto in decades. We should use guidelines to guide us, not tie our hands. Well-developed guidelines are important and useful, but they will never cover every situation, and are not meant to be blindly followed 100% of the time (and I write that as someone who is extensively involved in guideline development).

People in areas where the lepto risk is truly low shouldn’t feel bound to vaccinate their dogs. It’s something to consider and discuss, but not mandate.

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Earlier this year, our ability to treat feline infectious peritonitis (FIP) in Canada was revolutionized through legal access to imported GS-441524. I don’t use “revolutionized” lightly. This drug has changed FIP from an almost invariably fatal disease to one with a 90+% cure rate in cats.

People have (illegally) imported black market versions of this drug over the past few years, which created tough ethical issues for veterinarians. While the black market drugs often worked, it was still illegal use at a few levels, and safety was always still a big concern. Access to legal drug produced with good manufacturing practices with proper quality control was huge challenge.

Starting in February 2024, Canadian veterinarians were able to import GS-441524 via Canada’s Emergency Drug Release (EDR) process. Although actually pretty straightforward and efficient, this process adds some cost and hassles as a specific request must be made for each patient. The bigger concern was the added time; even though the turn-around time for EDR requests by Health Canada’s Veterinary Drug Directorate was really good, the need to get approval, then order the drug, then have it shipped from the UK, meant 7-10 day between when the patient was identified to actually getting the drug. For cats that are critically ill with this terrible disease, that delay could often be the difference between full recovery and death.

We are now having the FIP Treatment Revolution 2.0 in Canada! A Canadian pharmacy (Trutina Pharmacy) is now producing GS-441524 legally, with pharmaceutical grade drug and proper quality control, in collaboration with BOVA, the UK pharmacy from which we’ve been importing this drug with EDR approval since earlier this year.

This is huge, because it means veterinarians can now order this life-saving drug and get it within a day or two. It also means that we don’t have the same drug ordering, stocking and distribution restrictions that are in place for drugs obtained by EDR. The net result is much quicker access to the same high quality product, and likely saving more cats in the process!

We typically avoid talking about specific products and companies on this blog. This is an exception since Trutina is the only company that can legally compound GS-441524 in Canada. I’ve been in touch with them regularly as they’ve been gearing up for this, but have no financial or other relationship with them. Similarly, I was in regular touch with BOVA, their partner in this venture, as we worked to get access to this drug via EDR a year ago, but have no financial or other relationship with them either.

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The ongoing H5N1 avian flu pandemic in wild birds (and all its various spillovers into domestic poultry, cattle, wildlife and sometime people) has led to a lot of questions about how we handle situations that increase human or domestic mammal contacts with wild birds. This includes a range of activities and animals, including:

  • Backyard bird feeders
  • Backyard chickens
  • Hunting dogs
  • Off-leash dog walks in areas with waterfowl
  • Indoor-outdoor cats
  • AND petting zoos / public farms

There aren’t a lot of petting zoos where people can have direct contact with birds (birds can be pretty flighty, and there’s the pecking risk among other things) but some operations do allow it. Even when direct contact is not permitted, people at petting zoos or on these open farms can certainly be in close proximity to birds, and have contact with mammals that live with birds.

What’s the risk of exposure to avian flu at a petting zoo or open farm?

It’s hard to say. It’s probably quite low but non-zero. A recent outbreak of H5N1 avian flu on a petting farm in British Columbia has highlighted some of the issues. The outbreak resulted in approximately 50 ducks and chickens being euthanized (presumably after one or more got sick or died, and were tested and found to be infected with the flu virus). Local public health is “advising anyone who visited the farm on Oct. 26 or 27 to monitor for symptoms associated with avian flu, including but not limited to cough, fever, sore throat, runny nose or red, watery, itchy or painful eyes”.

Anyone with signs of illness should contact public health ASAP for testing. The health unit has also been in touch with school groups and other known visitors who were on the property during this time period.

Bird-to-human transmission of this virus is still pretty rare, and is typically associated with direct close contact with (usually a large number of ) birds. Given the low incidence of transmission, likelihood that there was no or limited direct contact with the birds, and maybe limited risk of people and birds being in small enclosed airspaces together, the risk to the public is probably still very low even in this situation. The risk for farm personnel would presumably be higher. Regardless, the risk still isn’t zero so it’s good to raise awareness and have testing available to see if there was any transmission to farm visitors or staff.

The risk of severe disease in people in this case is very low, since the currently circulating H5N1 strain has typically caused mild infections in people. But, every bird-to-human (or bird-to-any-mammal) transmission creates more risk for adaptation of the virus to mammals. We want to limit that as much as possible, and identify transmission to better understand the virus and help reduce the risk of subsequent human-to-human spread.

At this point, we should be past the risk period for human illness since it’s been over 2 weeks from the last potential exposure to the birds on this petting farm. Hopefully no news is good news. (The recent case of H5 influenza infection in a teenager in BC does not appear to be linked to this petting farm, as it was later reported that the individual had no known exposure to any infected animals or birds.)

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A presumptive case of H5 avian influenza has been reported in a teenager from British Columbia. Confirmatory testing is underway. Very little additional information has been released, so it’s hard to say how surprising and concerning it is. Information vacuums like this often lead to excessive speculation, but information sharing has to be balanced with privacy of medical information, and we don’t have an automatic right to know everything about a case immediately. It also takes time to properly investigate a case, and there’s often (understandable) reluctance to release very preliminary findings where there are still a lot of unknowns. Hopefully some reliable details will be released soon as the investigation continues.

A few key things that we’d like to know include:

  • What was the source of the virus in this person? The government release indicates “The source of exposure is very likely to be an animal or bird, and is being investigated by B.C.’s chief veterinarian and public health teams.” The lack of a specific statement that this was linked to a known poultry infection has led some to questionable messaging. A ProMedMail report said “Based on the details provided, it would seem the individual did not have direct contact with infected cows or poultry” which seems to be a questionable (bordering on irresponsible) overstatement at this early point in the investigation. It might be true, but it’s way to early to raise concerns about unknown exposure routes, especially given there are active cases of H5N1 in poultry in this region.
  • What strain is the virus in the person? Presumably it’s the circulating wild bird strain (vs the strain circulating in dairy cattle in the US, or another strain from wild birds, or imported from overseas), but knowing more details about the strain and whether it has any relevant mammalian adaptations is important.
  • Have there been any additional human cases? This takes time to determine, but it’s important to know whether this was a single isolated event with no human-human transmission, part of a cluster associated with common animal contact (e.g. on a poultry farm), or whether there was any downstream human-to-human transmission. So far, no other human infections have been identified.
  • How serious was the illness in this person? The press release only indicates that the person “is receiving care at BC Children’s Hospital.” While there’s public interest in knowing how severe the infection is, that’s personal medical information, but hopefully some information will be released at some poiny. Infections in people associated with the H5N1 strain in the US have been mild, and hopefully that’s the case here too.

Ultimately, it remains to be seen if this was a rare but expected spillover to a person with known direct contact with infected birds (the most common and most reassuring scenario) or something else. The less it fits that scenario and the harder it is to explain the infection, the greater the concern.

As usual, social media has a big camp amplifying “the end is near” messaging. While it’s not good news, there’s nothing here yet that raises a lot of concern, beyond the fact that every human exposure and human infection is playing with fire, as it creates more opportunities for this virus to change and adapt to people. As I’ve said before, I’m not really concerned about the currently circulating strain of H5N1 from a human health standpoint, since it rarely causes disease in people, typically causes mild disease when it does, and is not well adapted for human-to-human spread. I’m concerned about what this virus could do if it becomes more adapted to humans, with an ability to spread effectively between people and cause more severe disease. We need to do all we can to contain it, limit spillover infections and address those that occur promptly, but we need to maintain some perspective at the same time.

Presumably more information will be released soon to help us better understand this situation.

Our latest WormsAndGermsPod episode is a chat with Andy Gibson and Ian Battersby about canine rabies and, in particular, the work of Mission Rabies to help achieve the goal of zero canine-mediated rabies deaths by 2030.

Find all our podcasts on most major podcast directories, or access them here directly through your web browser.

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This week US officials reported a case of H5N1 influenza in a pig in the Oregon. While it’s certainly a noteworthy finding, as is unfortunately now typical, a lot of the social media buzz is overblown. This is a concerning situation that we need to watch, and yet another indicator that we need to continue to up our game when it comes to H5N1 influenza, but this finding is neither unexpected nor a harbinger of doom.

Here are some of the key points from the report:

  • H5N1 influenza was detected in a pigs and poultry on a small non-commercial backyard farm in Oregon.
  • There were only five pigs on the farm; they were healthy but were tested as part of the response to the infected poultry. Initially only one of the five tested postive.
  • The pigs were euthanized as part of the response (along with the poultry). From some standpoints that makes sense as a precaution against further spread. However, it also means euthanizing animals (that may have even been pets) that possibly could have been effectively isolated and would have recovered from infection (as most pigs do with flu), thereby also missing an opportunity to see what happens in pigs after exposure to better understand risks.
  • More testing was done after the pigs were euthanized. Two pigs tested negative, one was still positive, and results are still pending for the other two.

Here are the concerning bits:

  • We simply don’t want this virus being transmitted to more animals and more species. Every mammal that gets infected with this H5N1 strain creates more potential for the virus to adapt to mammals, potentially creating more risk to people (and other mammalian species).
  • We really don’t want this virus being transmitted to species that have their own influenza A viruses and/or that are susceptible to human influenza viruses. Both of those apply to pigs. If a pig gets infected with H5N1 and another flu virus at the same time, the viruses can get “mixed” within the pig and recombine to make a new flu virus that might be more transmissible to and between humans, but still far enough removed from the current seasonal human flu strains that no one would have any pre-existing immunity from vaccination or previous infection. That’s how new pandemics start.

Here are the good bits:

  • This is one of many, many spillovers of this flu strain into wild and domestic animals (okay, that’s not really good news but it’s important context). In many ways spillover into these pigs is no different than the countless other spillovers into other animals that didn’t get any press (and the world did not end).
  • This was a small backyard farm with only five pigs, so the odds are exceptionally low that there was a separate strain of flu circulating in the pigs on the farm at the same time.
  • The pigs on the farm shared water sources, housing and equipment with the infected poultry, so in some ways I’d be surprised if they didn’t get infected. How pigs are raised, including co-housing with other species and outdoor access, has many trade-offs, especially from a biosecurity standpoint.
  • This was probably a dead end host situation, whereby the pig(s) got infected from the birds, but there was no onward transmission from the pigs to any other animals or people, and therefore plays no role in further viral evolution.

My guess is that, despite all the doomsday prophesies on social media, this specific event will be a nothing-burger. It’s a spillover to a domestic animal that’s probably not anywhere unique as we think, since we probably miss the vast majority of these and they do not go on to contribute to further transmission of the virus. At the same time, it’s a warning shot that so long as this virus continues to circulate, we have a continual risk of it becoming something worse.

I’m not worried about the current H5N1 virus. It’s not a big deal.

I am wary of what the current H5N1 virus could become, under the risk circumstances. The virus keeps getting opportunities to change. Unfortunately we can’t control H5N1 in wild birds, so it’s clearly going to be around for a long time, if not permanently. I believe we can do a much better job of trying to control it in dairy cattle, and we can (and should) also be more proactive and ready to act (actually act, not just talk about acting…) when there are other spillovers into domestic animals.

I’ve had a few questions about the risks posed by heartworm in imported dogs to local dogs. (This also speaks to just how often we import heartworm-infected dogs, but that’s another story…). Here’s a bit of a deeper dive into the topic based on a fictionalized (but very typical) scenario:

You live in Guelph, Ontario, Canada. Your neighbour imported a dog and just found out is has heartworm. Fortunately they detected the infection fairly early on and are going to treat it, but what’s the risk to your dog?

Here’s a quick summary of some important aspects of heartworm disease and its biology:

  • Heartworm is (most often) caused by the parasite Dirofilaria immitis.
  • Adult worms live inside the major blood vessels leaving the heart in dogs (with very severe infections the worms will be found in the heart as well, hence the name).
  • When at least one male and female adult heartworm are present, they produce microfilaria that are found in the dog’s blood.
  • Mosquitoes ingest microfilaria when they feed on an infected dog.
  • Microfilaria have to develop in the mosquito to the L3 larval stage to become infectious, and can then be passed on to another dog when the mosquito feeds again.
  • Parasite development in the mosquito is temperature dependent.

Larval maturation in mosquitoes stops below 14C, so we can consider “heartworm development units (HDUs)” which are calculated by looking at the mean daily temperature over time. If it’s over 14C, then heartworm development could occur; the amount of development is based on how far above 14C the temperature goes. For example, if the mean (not maximum) temperature was 20C yesterday, that’s 6 HDUs for that day. It takes a total of approximately 130 HDUs for the parasite to develop to the point where it can be transmitted by a mosquito bite to another dog.

Back to our scenario…

You find out that your neighbour imported the dog six weeks ago. They went to their veterinarian a couple of weeks ago and got confirmation that the dog has heartworm last week. He’s starting treatment this week.

Overall, the risk is low. A mosquito would have to bite the neighbour’s dog, get infected, the larvae would have to mature to an infectious state, then that mosquito would have to bite your dog. Unlikely, but not impossible.

If we really want to look into the risk more, we can calculate the HDUs, which can tell us whether there was even a chance for the recently-arrived dog to be a source of infection to others in the neighbourhood before treatment was started.

I can look up the local mean temperature data for Guelph for the last 6 weeks. When I sum up all the daily HDUs, there were only 74 HDUs during that period. That means that even if a mosquito bit the neighbour’s dog on the day of its arrival, there wasn’t enough heat/time combination for the parasite to become infectious in the mosquito. To reach 130 HDUs, the dog would have had to arrive a few weeks earlier. Any mosquitoes the dog may have infected in the meantime are not going to be infectious because we (likely) won’t have enough warm days this fall to continue that development. They are also not likely to overwinter.

If the neighbour’s dog wasn’t treated, the risk wouldn’t start until next summer. In 2024, Guelph hit 130 HDUs on approximately June 20. Our common heartworm preventive medications for dogs will kill L3 and early L4 larvae, so they are effective if started up to 4 weeks after exposure. For example, if a dog was infected on June 20, treatment by July 18 should still be effective at preventing adult heartworm infection (but I wouldn’t want to push that limit too much, earlier is better).

If the neighbour’s dog is treated successfully (as we would expect), the transmission risks are negligible, because the diagnosis was made – promptly – and based on the time of year heartworm development in mosquitoes was limited, and the dog will be treated before the risk starts again next year.

If the dog had been imported earlier in the year or the diagnosis was not made, then the risk increases. That’s why we want to make sure imported dogs are tested – ideally before they arrive, upon arrival and again about seven months later – to get them treated as soon as possible and to reduce the risks of local transmission.

Unfortunately, people don’t always test imported dogs, either before or after arrival. Some people don’t treat infected dogs (and strangely, some will even knowingly import an infected dog and then not treat it). These scenarios create risk of adding to our local heartworm burden, which is still pretty low in most parts of Canada compared to other parts of the world (but is increasing).

I do have some disclaimers. As with most things in infectious diseases, we have to realize that there can be exceptions, loopholes and data gaps.

  • The 130 HDU cutoff seems to be pretty reliable, but is based more on in-lab testing than complex field situations. However, the 74 HDUs accumulated during the time frame in my example is so far away from 130 HDUs that the risk is presumably negligible.
  • Looking at hourly versus daily mean temperatures is a bit more accurate, but hourly temperatures are not always available, and it’s a lot more work for fairly limited extra benefit. In this example once again, the 74HDUs is so far below the threshold that the extra detail wouldn’t make a difference here.
  • We’re also assuming that mosquitoes are not hanging out in warmer microclimates (e.g. inside a shelter or a house). If a mosquito was living somewhere warmer than the mean outdoor temperature, then larval maturation could be quicker.

Take home messages:

  • Test imported dogs for heartworm before arrival, ASAP upon arrival and 7 months later.
  • Start imported dogs on monthly heartworm preventive as soon as possible, and keep them on it at least until all this testing is complete.
  • Treat heartworm-infected dogs as soon as possible.
  • Use a routine heartworm preventive for all dogs during the at-risk (mosquito) season if heartworm is present in the area.
  • Realize that the risk of heartworm from imported dogs is case specific, and depends on dog, mosquito and climate factors.

Image from https://capcvet.org/guidelines/heartworm/

Parasites are pretty gross in general – both the organisms themselves, and the concept of them living in or on you. Some parasites are of limited concern to people and pets, but others not so much… If I made a list of “parasites I really don’t want,” Echinococcus multilocularis (EM) would be high on the list.

Here’s a bit of information about EM if you’re not familiar with it. More information about EM and related Echinococcus parasites can be found on our infosheet on the Worms & Germs Resources – Pets page, or check out the EM infographic from OAHN.

  • Echinococcus multilocularis is a vey small tapeworm.
  • Wild canids (e.g. foxes, coyotes) are the natural definitive hosts. Adult parasites living in their intestinal tracts don’t cause them any problems, but they shed eggs that are passed in the feces.
  • When those eggs are ingested by an intermediate hosts (usually small rodents), they develop into nasty budding parasitic cysts, usually in the liver but potentially elsewhere in the body as well. That condition is called alveolar echinococcosis (AE).
  • If a wild canid eats an infected rodent with these cysts, the parasite matures into adult worms in the intestinal tract, and the parasite’s life cycle continues.
  • Dogs can also be definitive hosts for EM, with adult parasites in their intestines and shedding eggs in their feces, though they’re nowhere near as commonly infected as wild canids. In a cruel and confusing trick of nature, dogs can also be intermediate hosts if they ingest enough parasite eggs, developing AE like rodents typically do, which is often fatal (but that’s a whole other issue).

The problem for people is that we can also develop AE if we inadvertently ingest parasite eggs from the feces of infected wild canids or dogs. It’s a very rare but very serious disease in people; the parasitic cysts look like a tumour, act like a tumour, and the condition had a prognosis like a malignant tumour. It usually develops very slowly, and can be quite advanced by the time it’s detected. Untreated, the mortality rate for AE in people is very high. Treatment usually involves surgery to try to remove as much of the cystic tissue as possible, and then life-long drug therapy to suppress any leftover parasites in the body. Even with. treatment, the outcome can be poor.

Communication about are rare but serious diseases is always tricky. It’s important to convey that it’s rare so people don’t freak out. At the same time, it is still a risk and this isn’t something anyone wants to have, so using a few practical measures to avoid it is completely warranted.

The first step in knowing more about the parasite and where to find it. A recent study with which I was involved with provides a comprehensive look at Echinococcus multilocularis in dogs across North America based on over two million laboratory tests from Antech Diagnostics (Evason et al, 2024).

Here are some of the highlights from this study:

  • Echinococcus multilocularis DNA was detected by PCR in 26 of 2 333 797 fecal samples from dogs that were submitted by veterinary clinics in Canada and the US between March 2022 and July 2024. That’s approximately 11 infections per 1 000 000 samples, which highlights how rare the infection is in dogs; however, if you owned or had contact with one of those 26 dogs, there are some important things to think about.
  • Seventeen (17) of the positive samples were also tested by fecal flotation, a commonly used method for detecting parasites and parasite eggs in feces, but the taenid-type eggs shed by EM were only detected in 8 of these 17 samples. That’s not surprising because we know that fecal floatation isn’t very sensitive for detecting eggs from this tapeworm, and it highlights the value of using PCR finstead. Fecal floatation also can’t differentiate EM from Taenia spp., which are other types of tapeworms whose eggs are visually identical to those of EM.
  • Positive samples were submitted by veterinary clinics in both Canada (n=10) and the US (n=16) (see the map below). Some were in areas where we already knew EM is present in wild canids, but others were in regions where this parasite hasn’t really been on the radar – yet.
  • Of the infected dogs, 25 of 26 were treated with praziquantel to eliminate the intestinal infection. Post-treatment testing was performed on these 25 dogs and all were negative. The untreated dog was lost to follow-up.

What do we do with this information?

As I mentions, it’s challenging to message “rare but really bad.” Some people will see the low incidence and therefore dismiss the risk. Some will hear what this parasite can do and freak out. Most people will be somewhere in between.

Preventative measures need to account for a few things:

  1. Geographic risk factors
    • Knowing where the parasite is present in the wild canid population (the natural reservoir). At this point, since wild canid surveillance has been limited in many regions, we should probably assume that if wild canids are present, EM probably is too, at least in North America.
  2. Dog risk factors
    • Dogs get infected by eating infected rodents. As a result, dogs with outdoor access (especially unsupervised access) and dogs that are prone to eating anything (like my dog Ozzie) are at higher risk.
  3. Owner risk aversion
    • Everyone’s different, and the key is giving them enough information to make an informed decision, even if the information we have is incomplete. Cost of treatment and prevention is also an important consideration, especially for large dogs.

Photo credit: Alan R Walker (https://commons.wikimedia.org/wiki/File:Echinococcus-multilocularis-adult.jpg)