Around here, infection in dogs caused by Leishmania infantum typically comes up in the context of imported dogs, particularly those from countries around the Mediterranean (e.g. Greece, Israel, Spain).  This parasite is usually transmitted between a variety of mammalian species, including dogs and humans, by certain species of sandflies.  We’re quite lucky here in Ontario because the kinds of sandflies that transmit Leishmania don’t live here (yet), and we have yet to identify any local insect vectors that can do the same job.  There is still some risk of transmission from an infected dog to others, but it’s much more limited (e.g. direct handling of infected tissues by veterinary staff).  The other really concerning aspect of this disease is that it is very hard to completely clear the infection – so while acute episodes can often be treated, infected dogs are prone to recurrent bouts of illness throughout their lives, and remain a potential reservoir of infection for others (including people), even when infection is subclinical.

Despite the blood-borne parasite’s typical reliance on its favorite insect vectors, there have been instances of transmission within groups of dogs, possibly from breeding or fighting or other very close contact.  One outbreak in foxhounds in the early 2000s affected dogs in 18 states in the eastern US and even spilled over into dogs in Ontario and Nova Scotia, but fortunately there was no evidence found of infection in people in contact with the dogs.  Another report described a rather convoluted web of contacts between five dogs in Finland, two of which were infected with Leishmania while abroad, and resulting in infection of the other three.

Most recently, a case of leishmaniasis was described in a young Boxer dog born in California that had never been overseas (de Almeida et al. 2020).  There are a few notables from the case report:

  • The dog was 1.3 years old when it first presented, and while it had never been overseas, its dam had been imported from Spain, where canine leishmaniasis is endemic. (The dam reportedly died of an “unknown cause” the following year.)
  • It took a year and a half to finally determine that the dog’s illness was being caused by Leishmania (in part, no doubt, because it wasn’t on the radar for a dog that had never been to a high-risk area).
  • Despite multiple courses of antibiotics and other treatments, the dog’s condition gradually deteriorated and it eventually developed neurological signs as well. It was euthanized just over a year later, a little less than three years after it initially presented.

The authors concluded that the dog was likely infected through vertical transmission from its dam, since California is not currently considered an endemic region for this disease.  There are now several studies that have examined the ability for various species of sandflies that are found in certain states to transmit this parasite, which makes it all the more important to avoid creating a canine reservoir in the US through increased scrutiny and testing of imported dogs (and in this case their puppies as well).

I get a lot of emails about vet clinic access from a wide spectrum of individuals. This includes:

  • Owners who are upset they aren’t allowed in the clinic with their pet
  • Owners who are worried that their vet clinic isn’t doing enough to prevent transmission of COVID-19
  • Vets who want to know how to increase owner access to clinics safely
  • Vets who want to keep people out of the clinic as much as possible for safety
  • (And still some that just yell at me regardless what I say)

There’s no “one-size-fits-all” approach to veterinary medicine in the COVID-19 era. I‘ve written about different approaches before but since I get so many questions, here are some more thoughts.

Why can’t someone just say “here’s what all vet clinics should do”?

There’s too much variation between clinics. This includes things like the degree of COVID-19 activity in the region, local rules, staff and management risk tolerance, clinic size, waiting room and overall clinic layout, exam room numbers and size, and ventilation, among others.

What are the basic concepts of COVID-19 prevention in a clinic?

  1. Restrict access as much as possible
  2. Choreograph movements in the clinic
  3. Restrict close contact situations, especially in small rooms
  4. Use appropriate PPE

1. Restrict access

I’ve said to keep owners out “as much as possible” in the past. This has led to issues since “as much as possible” is very subjective, but I can’t really say more. There’s a cost-benefit consideration. Every time someone new comes into a clinic, there’s some risk. The more that happens, the more the risk. The better our other control measures are, the lower the risk (i.e. we can get away with more people in the clinic by doing everything else right).

We can limit access but still allow some people into clinics, with some preventive measures. There may be logistical reasons to let people in (e.g. owner walks to the clinic and would have to wait outside in -20C weather) or patient care reasons (e.g. something needs to be shown to the owner that can’t be done well remotely, euthanasia, patient for which curbside transfer might be risky) that are worth the limited increase in risk. There are many other situations where it’s not worth the risk. We can still do a lot with telemedicine, curbside drop offs and hybrid appointments (e.g. telemedicine appointment followed by a drop off for a quick in-clinic procedure like vaccination or blood sampling) where the owner doesn’t need to be present.

2. Choreograph movements

I was in a clinic the other day looking at traffic flow, and it’s a good exercise to try. It’s not usually too hard to come up with a logical flow system that creates one way traffic and avoids mixing of people… if numbers are limited. Minimizing the number of people who come into the clinic helps us optimize other preventive measures in the clinic. In combination with some floor markings, furniture re-arranging, designated direction of movement and designated entry/exit points, we can significantly limit contacts and decrease the risk of virus transmission.

3. Restrict close contact situations

Close contact. Closed spaces with poor ventilation. Droplet generating procedures like talking. Those are the high-risk situations for COVID-19 transmission, and they also happen to describe a vet clinic exam room. Time plays a big role in the amount of risk. Fifteen minutes isn’t a magical number, but it’s the one typically used to indicate the time that risk goes up. The smaller the space and the worse the ventilation, the higher the risk and the less time you should spend in it.

All those factors together show how the normal exam room visit needs to be rethought. To me, exam rooms are now “owner waiting spaces.” If the owner needs to accompany the animal into the clinic, they check in and are admitted directly to an exam room (again, the number of people in the clinic needs to be limited to some degree for this to work). Vet personnel come in and retrieve the animal, keeping chatting to a minimum, distance to a maximum, and everyone’s masked. A little conversation is fine and is good for patient care and the vet/owner relationship, but it should be distanced and short. The pet is then taken to a treatment area for examination and whatever needs to be done. Vet personnel can pop into the exam room or connect electronically to ask more questions or talk about things. The owner and pet are re-united in the exam room, and a short conversation can be had to explain or demonstrate things. If a demo is needed that requires restraint of the animal, someone from the clinic joins in so the owner does not have to help out, and can maintain distance from staff. (That’s still a potential issue because of the reflexive nature of owners jumping in to help hold, but that just needs some communication to head it off.)

4. Use appropriate PPE

As much as they are annoying, masks are critical. Masks need to be worn for any close contact situation, by owners and clinic personnel alike.


Lots of questions remain, I know. I’ll touch on a couple of them here but I’m sure there will be more to follow.

What do we do with the exam room after the owner leaves?

The room is ideally minimally stocked with easy to disinfect surfaces. Routine disinfection, focusing on owner contact surfaces (vs our previous focus on things like the examination table) is straightforward. A sign on the door indicating the room has been disinfected is useful and is good for clients to see.

What about the airspace in the exam room? Can the next person go right in?

That’s a tough one. We focus on droplet transmission and direct contact when it comes to SARS-CoV-2, but there is likely some risk from accumulated aerosols in closed spaces with poor ventilation (like an exam room). It’s probably limited in time and degree of risk, but we just don’t know. Most aerosols settle quickly out of the air so they’ll be taken care of with surface disinfection. However, should we leave 1 minute, 2 minutes, 5 minutes, or more between owners? Who knows. There are no recommendations for this kind of precaution in similar human healthcare situations, and I haven’t seen any real evidence of risk. A few minutes between occupancies, with disinfection performed after this brief waiting period, is probably reasonable, based on what we know (especially with good mask compliance, as masks reduce aerosol release).

How important is ventilation in the exam room?

More is better. Looking at how much airflow can be achieved in the clinic is useful, as better ventilation disperses and dilutes any aerosols that may be present. Ventilation rates of less than 3 L/s per person have been suggested as being high risk, and 8-10 L/s per person as being low risk. If you don’t know what your ventilation rate is and can’t figure it out, go with the “more is better'” approach.

Just some quick thoughts that I’m sure I’ll add to soon (and get more questions about).

Last spring, we posted about a report of alveolar echinococcosis (AE) in a child in Quebec from 2018.  This very serious parasitic infection is caused by the intermediate stage of the fox tapeworm, Echinococcus multilocularis (EM), which despite its common name is often also found in coyotes (including right here in southern Ontario), and it can infect dogs as well.  Canids typically become infected by eating small mammals like rodents that carry the intermediate form of the parasite in their organs, and then the infected canids pass the tapeworm eggs in their feces, which then infect more small mammals when they’re ingested.  The big problem is people can also become infected by accidentally ingesting these tapeworm eggs and go on to develop AE. In most cases of AE, parasitic cysts start to develop in the liver, and the cysts grow and spread like a malignant tumour.  The cysts can also appear in other parts of the body, but in any case it often takes years for a person to start showing any signs of illness.  By the time AE is diagnosed, treatment can be very difficult, and it may be impossible to remove the cysts.  Occasionally dogs can also develop the AE form of infection.

Now a new report has been released about an unusual case of AE in a child from northern Manitoba (Joyce at al. 2020).  There are several noteworthy points about this case:

  • The patient was only 12 years old. Cases of AE in children are uncommonly reported – only 4 of 559 patients in a European registry from 1982-2000 were children. Although children are generally more likely to have fecal-oral exposure due to poorer hand hygiene, because of the long incubation period for AE (5-15 years) people exposed as children might not be diagnosed until they are adults.
  • The patient did not have any parasitic cysts in the liver. In the same European registry, only 13 of 559 patients lacked liver involvement. The authors speculate that this could be due to the fact that the patient also had a large portosystemic shunt (an aberrant vein that allows blood coming from the intestine to bypass the liver).  However, the patient did have lesions in the kidney, lungs and brain, all of which were presumed to be parasitic cysts once the diagnosis was made.  It’s an important reminder that what usually happens doesn’t always happen.
  • The boy had a history of latent tuberculosis which was treated 10 years earlier, so initially the masses seen on CT and MRI were thought to be due to tuberculosis, until more tests were completed. You can see how this would be a challenging diagnosis to make.
  • The authors also report that two years later the child does not have any clinical signs of disease from the cysts, and/but regular imaging shows that the lesions have not changed for better or worse.

The paper also provided a very brief summary of recent epidemiological findings regarding EM in Ontario and western Canada.

Since January 1, 2018, EM infection in animals in Ontario is reportable to public health.  In 2019 there were three cases of fecal shedding of EM in dogs reported in Ontario, in Niagara, Durham and Kawartha Lakes regions (though one dog was recently imported and was likely infected before coming to Ontario).  No cases of AE in people in Ontario were reported in 2019.  Nonetheless, this is definitely a parasite for veterinarians and dog owners to keep on the radar.  Dogs that hunt and may consume small mammals, or that have a lot of contact with coyote feces, may be at increased risk of exposure.  The best way for people to avoid infection is (dare I say it again) don’t eat poop (in other words, wash your hands and practice good hygiene around food and drink), and try to reduce the risk of infection in dogs in the household.

More information about Echinococcus multilocularis can be found on the Worms & Germs Resources – Pets page, or check out the EM infographic from the Ontario Animal Health Network.

As reports of animals testing positive for SARS-CoV-2 continue to trickle in (as expected), it’s clear that some domestic animal species are susceptible (at least to some degree) to this virus. A recent article in National Geographic about “Buddy,” the first dog in the US to test positive for SARS-CoV-2 back in May, has flooded my inbox with emails about the story and the broader question about whether we need more testing of pets.  Here’s my take:

Do we need more testing?
  • Yes. We know little about human-to-pet transmission , pet-to-pet transmission and the clinical implications for animals or people.  More testing – along with good data collection about clinical signs, contacts, timelines etc. – could provide important information.
Do we need more patient testing done in veterinary practices?
  • Not really.  At this point we know pets can be infected, and there are some risks (e.g. to clinic staff) when it comes to testing of potentially actively infected animals. Whether 10, 20 or 200 pets have been diagnosed, it doesn’t tell us more unless we know the context, i.e. we have accurate information about the cases, including other clinical data to help figure out whether the test result means the animal was actually infected with +/- sick from SARS-CoV-2, and we have accurate information about the animals that test negative as well.

From a clinical standpoint, I think of three questions when it comes to testing pets:

  • Is there a realistic chance that the pet was exposed to the virus?
  • Does the pet have clinical signs that could realistically be due to infection with SARS-CoV-2?
  • What would I do with the result? More specifically, would I do anything differently if the result is positive vs negative?
    • The answer to the third question is almost always “no.”  The hassles and risks involved with taking a pet to a clinic for testing only make sense if we are going to learn something useful from the the result. That’s rarely going to be the case now.

We do need more research testing to answer questions about prevalence, clinical implications and transmission, as we can’t answer those by piecing together clinical testing results from haphazardly tested pets. Getting a data dump from a lab that says “this many” cats tested positive tells us a lot less than a research study that looks at positives and negatives, and can put the story together about things like how often human-to-pet transmission seems to occur, how often infected pets get sick, what risk factors increase the odds of transmission or illness, how long infected pets shed the virus and, ideally, help us determine the risk of subsequent transmission from an infected pet to other animals or people.

A variety of research studies are underway to answer these very questions, but it’s not easy. Our own studies have run into the “problem” (which in other ways is a good thing) of declining numbers of potential participants, since case numbers for COVID-19 in people are now very low in our region. Few people are getting infected so few pets have the chance of being exposed. That said, if there’s any study I’d like to see compromised by low case numbers, it’s this one. I really want us to be able to answer some of those interesting questions, but I can live with study enrollment hassles if it’s because the virus stays under reasonable control.
Time will tell.

A colleague asked me about scent detection dogs the other day. My response was that I hadn’t heard much after all the initial buzz, which might suggest things weren’t going well. However, as opposed to the horrible pre-print about COVID-19-sniffing dogs I wrote about previously, a paper in BMC Infectious Diseases (Jendry et al. 2020) provides some more robust and interesting information. It’s a pilot study, so it’s small, preliminary and underpowered, but it shows potential. Whether that’s “potential for dogs to be able to detect SARS-CoV-2 under certain circumstances” or “potential for dogs to be an effective detection tool” isn’t clear, but that’s the big question.

Here’s a breakdown of the study and some commentary:

The researchers collected saliva samples and respiratory secretions from hospitalized COVID-19 patients, and healthy people who were PCR-negative for the SARS-CoV-2 virus.

  • This may not be ideal, depending on the goal. My vision is using these dogs in the community to rapidly detect infectious people in high risk situations (e.g entrance to transit stations, public buildings, schools). In that case, people who are hospitalized with severe COVID-19 are likely not the best test population. A dog isn’t going to replace a PCR machine in the hospital.  It’s simply not practical in most cases to collect a sample from a patient, take it to a dog as a quick screening test, and then submit the sample for definitive testing.  We want dogs that can detect a mild case in the community, long before the patient needs to be hospitalized.
  • They didn’t test samples for other human coronaviruses, like those that cause the common cold. It’s a potential limitation, but I don’t think it’s a big deal in this case.
  • They also don’t explain where they got their negative samples. A clear description of the study populations is critical and it’s somewhat lacking here.  We want to be sure the dogs were detecting SARS-CoV-2 and not something else unique to the positive sample population, like a smell associated with being from a hospital.

Because of the potential susceptibility of dogs to the SARS-CoV-2 virus, samples were inactivated prior to exposing them to the dog.

  • That’s a reasonable step, but raises more issues of practicality and how the dogs could ultimately be used (e.g. can the dogs only be used to screen specimens collected from high risk patients, or can they be used to detect infection in someone walking by).

Eight dogs were trained using standard methods. They had a 2-week habituation process for the training system, then had 5 days of training until their rate of detection was greater than what would be expected by chance alone. They then started the study

  • The sample size was small, but reasonable for a proof-of-principle study.

The ability of dogs to detect positive samples increased over time. There was some variation between dogs, but all of them were pretty good. The overall sensitivity (percentage of positive samples that the dogs correctly identified as positive) was 83%, ranging from 70-95%. The specificity (percentage of negative samples that the dogs correctly identified as negative) was 96%, ranging from 92-99%.

  • For a screening test, we’d actually want the reverse, that is to say higher sensitivity at the expense of specificity. That would mean the dogs would catch most of the positives. Lower specificity is okay initially if the screening test (i.e. the dog sniffing) can be followed up with a more specific test, and if the implications of an initial false positive aren’t high. If a dog calling a person positive results in that person being sent home to self-isolate for 14 days, then a high false positive rate is a problem. If it just results in the person being pulled aside to have a swab collected for a lab test, that’s not as big of a deal (perhaps a bit of a hassle but maybe not a deal breaker).
  • A low sensitivity and high specificity means you run into fewer hassles with false positives, but the test will miss more positive people. The fact that 17% of prime samples from people hospitalized with active COVID-19 were called negative is a concern in terms of the dogs being able to detect the virus in less severely affected people and from less voluminous and close samples (e.g. detection directly in someone walking by).

I’d file this in the “interesting but preliminary” folder. Anything that can help identify infectious people is useful. If dogs can do it, that’s great, but they also have to be able to do it from a distance, because a handler and a dog getting very close to large numbers of people might cause more problems than they fix.

In my perfect world:

  • A SARS-CoV-2-sniffing dog would be parked at the entrance of schools, office buildings, transit stations, etc.
  • The dog would be able to detect infected people from a short distance away (i.e. without direct contact).
  • The dog would signal its handler when it detected a positive person.
  • That person would then (discretely) be pulled aside for testing, which would (in my perfect world) be done quickly, right there (there is lots of work being done to develop a more rapid test like this that can be done on the spot, but we don’t have one yet).
  • If positive, the person would be told right away and sent home to self-isolate. If negative, the person would be good to go (though maybe wondering why they smell like a coronavirus).

As I’ve said, it’s an interesting and useful preliminary study that shows potential. The key is to follow up preliminary studies with more detailed, rigorous work, which unfortunately often doesn’t get done. Nonetheless, I suspect media headline writers will jump on this and over-interpret the results. It’s also another example of the remarkable things a dog’s nose can do, but the potential practical applications (if any) are still very much up in the air.  I’ll be a bit surprised if this ever becomes a common/useful tool, but I’d love to be wrong about that.

Taking a break from the latest pandemic microbe, there have been a couple of recent items about another very old pandemic bug that’s never really completely gone away – Yersina pestis, known commonly as plague, and the cause of the Black Death of the mid 1300s, aka the deadliest pandemic recorded in human history.

Even though we now know what causes plague (a bacterium) and how its transmitted (primarily by fleas, but also some routes of direct transmission), its various forms (bubonic, pneumonic and septicemic) and even how to treat it (antibiotics), this disease still rears its ugly head periodically in various parts of the world, including North America.  Make no mistake, it is still a serious and potentially fatal disease, particularly when its signs are not recognized and appropriate treatment is delayed.  This was the case in two dogs from Colorado that were described in a recent report in BMC Vet Research (Schaffer et al. 2020).  Both dogs presented with fever and vague signs of illness, but within 24 hours they were coughing up blood (hemoptysis).  In the first dog they suspected a possible pulmonary contusion or rodenticide toxicity, and the dog was euthanized the next day.  The true cause wasn’t confirmed until 9 days later when the dog’s owner was also hospitalized with signs of pneumonia.  The second dog underwent surgery to have part of its lung removed, thinking it may have had a foreign body/aspiration pneumonia.  When the removed piece of lung yielded Y. pestis five days later, that dog was also euthanized.

There are a few noteworthy points about these two cases:

  • The dogs were both from an endemic area where plague is known to circulate in the wildlife population, but clinical infection in dogs is uncommon, and infection with the pneumonic form in dogs is exceedingly rare.
  • The pneumonic form of the disease is particularly dangerous for others, as infected animals (or people) can expel the bacteria in their sputum when they cough.  Four cases of plague in people were detected due to exposure to one of these dogs, but the public health investigation involved contact tracing of over 100 people in each case.
  • The lobar pattern seen on radiographs in both dogs is also atypical, so these animals had an uncommon presentation of an uncommon disease that is even more uncommon in this species, and in one case it was also outside of the typical transmission season for plague – not an easy diagnosis to make right away. The automated bacterial identification systems used in these cases also delayed the diagnoses.
  • It is really important to rule out plague in animals with compatible signs, even if they’re not “typical” or at the typical time of year, when they live in (or have visited) an endemic area – for the health of the animal and the people handling it.

More recently, on the other side of the world in Mongolia where this same bacterium is also endemic, an outbreak of bubonic plague in people has been linked to marmots (a kind of large rodent, similar to a groundhog).  Marmots are considered a local delicacy, and in the process of hunting, butchering, preparing (but likely not thoroughly cooking) and eating marmots, there are lots of opportunities for transmission of Y. pestis when it is present, but the highest risk is still from the fleas on the animal.  At least 4 cases of bubonic plague have been reported in the area so far, including one fatal infection in a 15-year-old boy, all associated with consumption of marmot meat.  Several areas in the region are now under quarantine, contact tracing and testing is being conducted, and authorities are discouraging hunting and consumption of marmots.

Plague is a classic example of one of the many pathogens with which we coexist, and which is unbounded by time, space or species.

Image: A female Oriental rat flea, Xenopsylla cheopis. (CDC Public Health Image Library 22259)

I’ve been slow posting in the past few days, so here are a few quick recaps from the animal/COVID-19 world.

Higher quality debunking of crappy dog-SARS-CoV-2 paper

Back in April, a paper (Xia 2020) was released that suggested dogs could be the source of SARS-CoV-2.  Most of us considered it crap at the time (read more about it in our previous post), and most people moved on pretty quickly, but it still left some fear and poor messaging in its wake. Now, a proper dismissal of this paper (in the same journal) has been published.  I won’t get into the details, but it basically says “Everything that was written in that paper… yeah, not so much.”

More formally, here’s what they concluded: “In summary, the proposition of Xia (2020) that dogs are a likely pre-human host for SARS-CoV-2 is not justified by available evidence. Xia (2020) did not demonstrate that the low CpG frequency in the SARS- CoV-2 genome was driven by a unique selective environment in dog digestive tracts. The SARS-CoV-2 is also less virulent than other human betacoronaviruses (SARS-CoV-1 and MERS-CoV), contradicting his assertion that CpG-deficient viruses are more virulent. Furthermore, closely related betacoronaviruses from bats and pangolins have CpG-deficiencies similar to SARS-CoV-2. Dogs are not more plausible than most other potential host species, and based on current data, far less plausible than bats or pangolins. Still, we are missing ~20-70 years of the recent evolutionary history of the lineage leading to SARS-CoV-2, and we must broadly survey a wide range of wild and domestic species to uncover the origin of SARS-like coronaviruses.

More SARS-CoV-2 in mink

Mink are really susceptible to this virus, and human-to-mink transmission seems to occur quite easy.  In the Netherlands, SARS-CoV-2 has infected mink on at least 24 farms, with widespread disease in mink and even some plausible mink-to-human transmission. There was a plan to end the mink industry in the Netherlands by 2024, and this crisis appears to be speeding things up as mink on affected farms are culled.

In Denmark, multiple farms have also been affected. They’re taking a different approach there, now choosing not to cull affected mink farms, but putting strict measures in place to control any outbreaks and monitoring closely for more.

In Canada, so far, so good. Since infection with SARS-CoV-2 in mink was first reported, there’s been an emphasis on biosecurity measures to avoid infecting mink, and relatively low disease rates in people in Canada (at the moment) mean the risk is currently fairly low. However, it’s still a concern. An additional worry is mink farms becoming a source the virus that could spread to wildlife. Feral cats have been infected on at least one affected mink farm in the Netherlands. Spread to wild mink (which are present throughout Canada and the US) is an even bigger concern given how susceptible this species is. We don’t want to create a wildlife reservoir of SARS-CoV-2, either through spread from farms to wild animals or from escape of farmed mink.

Human-to-pets transmission is still a thing

Reports of cases of human-to-pet transmission of SARS-CoV-2 continue to trickle in, and probably represent a small fraction of cases that actually occur. I’m sticking to my promise not to report each new case if there’s not really anything new about it. Infections in pets are still uncommonly reported, but a lot of cases are likely not detected because there’s limited testing. The animal and public health risks of these cases are probably very limited regardless, especially in places where there’s rampant human-to-human transmission. But, we’d still like to contain exposed animals to prevent them from playing any relevant role.

Still no signs of infection in livestock

So far, so good on the livestock front. Fortunately, major livestock species do not seem to be overly (or at all) susceptible to SARS-CoV-2. We still need to pay attention to this though, and I think the message “If you might be infected, stay away from animals” remains important, regardless of the species. However, the risk of significant issues from livestock seems pretty limited right now.

Still looking for the animal origin of SARS-CoV-2

This is still a huge question. It seems a little late, but the World Health Organization has sent a team to China to further investigate the animal origin of the virus. Kind of.  They’ve sent two people there to discuss a larger investigation.  It might be a challenge to find the animal source but we still have to try. We need to know if this virus is still lurking somewhere in the wild, and where. We also need to understand how and why this outbreak happened, to help prevent it from happening again (with this virus or one of many other potentially nasty bugs that are no doubt also lurking in the wild).

Following the recent debacle with a large group of imported dogs from Ukraine in early June, the Canadian Food Inspection Agency (CFIA) has cancelled import permits for all commercial puppies under 8 months of age from Ukraine. It will not issue any new permits “until the CFIA is satisfied that import conditions and international transport standards are in place and that animals will travel safely in the future.”

Import permits are required for importation of commercial shipments of dogs less than 8 months of age. They are not required if the dogs are over 8 months of age, or if they are personal pets.  This creates some big loopholes in the system, since it’s easy for people to claim that puppies are older than they actually are, and for people to import batches of dogs that are for sale or adoption (making them commercial dogs) but claiming they are personal pets. It also allows importation of pregnant dogs without a permit, which has been seen in the US as well where people have imported heavily pregnant dogs as a means of bypassing puppy importation restrictions.

The impact of the CFIA restrictions will be hard to measure, because there are various ways people could potentially try to get around them. There are some important questions that would help us gauge the impact, but unfortunately they are virtually impossible to answer right now because of the lack of data collection about personal pet importations, and lack of import permit requirements for dogs over 8 months of age:

  • Will there now be an upswing in “personal” dog imports from the Ukraine?
  • Will we see importation of heavily pregnant dogs as a way to get puppies in the country?
  • Will we see lots of dogs that are stated as being 8 months old when they’re really much younger? (How do you prove a puppy’s age when they don’t have anything like a birth certificate?)
  • Will the total number of dogs being imported from Ukraine actually change? (e.g. if there are fewer puppies imported, will more “older” dogs be imported?)
  • Will we see Ukrainian dogs coming in via neighbouring countries or other transit countries, instead of directly from the Ukraine?

Hopefully it’s a useful step, and it’s great to see some action taken in an area that’s not received much regulatory attention in Canada in the past, but I see lots of potential ways people might get around the restriction. Time will tell, but increased interest and awareness of canine importation issues is certainly a good thing.

Click here to download a pdf of this canine importation infographic from the CFIA.

As we continue to work our way through the COVID-19 pandemic, balancing protection and practicality continues to be a challenge. The desire to return to “normal(ish)” is completely understandable. However, “normal” is a long way away. It’s more a matter of what degree of “abnormal” we’re willing to tolerate (and for how long), and what degree of disease risk we’re willing to tolerate – the two are generally inversely related.

SARS-CoV-2 is a respiratory virus, and it’s becoming clearer and clearer that respiratory droplets are the main risk for transmission. Yet, as more businesses and facilities look to re-open, the focus still tends to be on sanitization of surfaces. Yes, cleaning and disinfection is important; however, it’s not the only (or even most important) preventative measure. Enhancing surface cleaning without taking precautions to prevent droplet spread (i.e. mask policy) is of limited benefit, and is more along the lines of “look, we’re doing something” versus actually doing something effective.

One challenge we face in designing control programs for this (and many other) pathogens is limited definitive information about the source of infections (aka source attribution). It’s impossible to say X% of infections come from this source or that source. What we can say is based on the biology of the virus, lab testing and the patterns of spread, fomites (inanimate objects) don’t seem to be a major concern.  A recent commentary in The Lancet entitled Exaggerated risk of transmission of COVID-19 by fomites” (Goldman 2020) provides a nice synopsis of the issues. The first paragraph sets the scene: “A clinically significant risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission by fomites (inanimate surfaces or objects) has been assumed on the basis of studies that have little resemblance to real-life scenarios.” The article’s a commentary, not a research study, so it’s personal opinion, but it’s a good read.

What’s the downside of excessive concern about fomites?

The concern is making sure people are focused on the right priorities. Cleaning and disinfection is useful. Cleaning and disinfection as the sole or main preventive approach is not good. It’s like saying I won’t worry about wearing a seatbelt, being sober or using headlights when driving at night because I make sure to check my tires before I leave. Yes, the latter is important, but it’s only going to offer a small degree of protection compared to the other items.

Yes, wash your hands regularly.

Yes, clean and disinfect common touch surfaces.

But no, you can’t stop there. Wear a mask.

Businesses that focus on sanitizing surfaces over physical distancing and mask use are doing little to stop the spread of this virus. Customers will like it because it doesn’t require them to do anything and things will feel normal, but it’s increasingly clear that masks are the key to controlling this virus.

For those of you interested in a more detailed read about masks and protection, there’s a recent modelling study of their potential effect (Fisman et al. 2020, Infectious Disease Modelling). Don’t let the equations in the methods scare you off, it’s an interesting and important paper. Here are some highlights:

  • Even if masks don’t offer complete protection, widespread use can reduce the SARS-CoV-2 transmission rate. Importantly, in reasonable scenarios, it can reduce the reproduction rate (R0) to below 1, at which point the virus starts to die out, since the average infected person infects less than 1 other person.
  • Mask use alone doesn’t replace other efforts. There’s no single magic bullet. However, masks are a cheap, easy and effective control tool (now that they are more widely available than they were at the beginning of the pandemic, when there were severe supply shortages).
  • The lower the reproduction rate (R0) in the community, the less effective masks are, and less widespread use of masks can still be enough. However, if transmission in the community is not well controlled (e.g. lots of cases but no distancing or other restrictions) masks will not be enough.
  • As the percentage of the population that uses masks drops, the overall protective effect drops. It can drop to the point that cases continue to increase. So, mask use has to be widespread (typically through mandatory masking), particularly when disease rates are high.

Their somewhat understated but important conclusion is:

In the absence of evidence of harms done by masking, and with even preliminary evidence that they could influence epidemic growth, we suggest that their more widespread use be considered by jurisdictions which have not yet advocated this intervention.

Normalizing mask use is the key.  Mandatory masking does that. In Wellington-Dufferin-Guelph, it’s required. Compliance is pretty much 100%. People don’t have to feel conspicuous wearing a mask, and there’s no drama about who is or isn’t wearing a mask. It feels normal very quickly. I think I’ve seen one person in a grocery store in Guelph without a mask in the past few weeks. In contrast, I was at a grocery store out of town this weekend in an area where masking isn’t mandatory. No staff and probably <5% of customers wore masks. Mandatory masking rules are not meant to focus on penalties and enforcement. They’re meant to encourage everyone to act and to make wearing a mask the socially accepted approach. You don’t need a bylaw officer standing on the corner to enforce compliance – you need to make it feel normal to wear a mask.

I was at our local farm supply store the other day and saw a sign indicating they were out of chicken coops and trying to find more from different sources. I wonder if there’s a run on backyard chickens as people spend more time at home.  There are some positive aspects to that – and then… there’s Salmonella.

I’m not anti-backyard chicken. (In fact, if I wasn’t convinced they’d be coyote-food, and that Heather would kick me out of the house, I’d consider getting some myself.)

I’m anti-diarrhea and anti-preventable death. It’s clear that backyard chickens pose some risk to people. How much of that is non-preventable vs preventable with basic common sense and hygiene is a big question (and one we’re working on, but like so many other things has been stalled by COVID-19).

The CDC’s latest Investigation Notice of Outbreaks of Salmonella Infections Linked to Backyard Poultry (24-Jun-2020) highlights many of the concerns with this trendy practice, and need for better education of the public and management of the birds.

Here’s the really quick version of the report:

  • Since their May 2020 update, another (whopping) 368 Salmonella infections linked to backyard bird have been diagnosed in people. That brings the total diagnosed to 465 (meaning there were probably many thousand people truly infected).
  • 36% of those with available information were hospitalized, and one person died.
  • As is common, young kids appeared to bear the brunt of disease: 31% of cases were kids less than 5 years of age. That’s probably also a reflection of their higher likelihood of close contact with the birds (e.g. kissing them), inadequate supervision and inadequate hygiene (hand washing in particular).
  • Chickens came from a range of sources, such as farm stores, hatcheries and websites.

Risk reduction isn’t rocket science. It’s some basic management and hygiene practices, and some common sense.  (No, putting a diaper on a your chicken does not make letting it run around your kitchen a safe proposition, despite the availability of chicken diapers online).

  • Keep backyard poultry in the backyard – don’t let the birds roam the house.
  • Wash your hands after contact with poultry.
  • Look at where runoff can carry bacteria from manure in the pens (not a good place for a garden).
  • Don’t kiss poultry.
  • Wash your hands.
  • Supervise kids around poultry.
  • Wash your hands.
  • Handle eggs like commercially sourced eggs. (Your home-raised, all-natural, organic, antibiotic-free egg is as likely (or maybe more likely) to have something nasty on it as the eggs you buy in the store.)

Enjoy your chickens, but… wash your hands.