There are lots of SARS-CoV-2 variants out there. The virus changes a bit all the time.  However, there’s a lot of, well, concern about a few particular “variants of concern” (VOCs).

VOCs are “OC” because they have mutations that could increase their infectivity (i.e. ability to infect people), their virulence (i.e. severity of disease they cause) or decrease the effectiveness of current vaccines or antibody-based treatments. There are a few main VOCs currently circulating, but the B.1.1.7 variant that was first detected in the UK has received the most attention. In people, it seems to be much more transmissible than other “normal” strains. There’s also been some some suggestion in media from the UK that B.1.1.7 might be more virulent as well as more infectious, but that’s still not clear.

So, how infective are these VOCs to animals?

We have no idea. It’s possible that increased infectivity in people could also mean increased infectivity in animals. It’s also possible that increased infectivity in people could mean less infectivity in animals.  We just don’t know at this point.

How will we find out how infective these VOCs are to animals?

Some experimental study is presumably underway, and the WHO has indicated a need to test SARS-CoV-2 VOCs in experimental animal models so we can learn more about them.

We’ll also have to see what results come from field studies, but one of the issues is there are still only relatively small numbers of infected animals (outside of mink farms) in which we’ve been able to find the virus before it disappears.

  • Based on antibody detection, infection with SARS-CoV-2 in pets, at least, seems to be pretty common when their owners have COVID-19.  Yet, in our surveillance work, we’ve only picked up a few animals shedding the virus, in large part because of logistics and timing of sampling.
  • We’re working with our national lab to sequence the few samples in which we’ve found the virus, but the small numbers limit what we can say.  If we find a VOC, we found it.  If we don’t, we can’t say much more, since you need either luck or a high prevalence in the population to detect something with a small number of samples.

Could VOCs (or other variants) infect animal species that are not susceptible to the “normal” strains of SARS-CoV-2?

Probably not, but we can’t rule it out completely.  To start infecting other species altogether would require a much larger change in the virus, which isn’t likely to happen all of a sudden. We still have to pay a bit of attention to species that we think aren’t susceptible, because we can’t really guarantee how fast or how much the virus will change.

What is the best way to limit the impact of VOCs in animals, and the impact of animals spreading VOCs?

  • Control SARS-CoV-2, and all its VOCs, in people.
  • Limit contact of infected people with animals.  (Sound familiar?)

We know cats are susceptible to SARS-CoV-2, and it appears that human-to-cat transmission may be pretty common in households where people have COVID-19. In the big picture, that’s probably not a huge issue, since most cats that get infected show no signs or develop only mild disease, and most infected cats have limited opportunity to spread the virus outside their own household. However, we still need to understand more about infection in cats and other species, to make sure we understand the true risks (if any) and how to mitigate them.

Expanding on their earlier work, a research group from Kansas State University looked at susceptibility of experimentally infected cats to re-infection with SARS-CoV-2.  The study has been posted as a pre-print on bioRxiv (Gaudreault et al. 2020).

  • When they re-exposed cats to the virus 21 days after their initial infection, the cats got infected again, but infection was less common and mild.  Also, while infected cats could pass the virus to other cats during their initial infection,  the re-infected cats were unable to infect others.
  • So, while the cats were susceptibile to re-infection, the infection was mild and they didn’t seem to pose a transmission risk on the second go-around.
  • Therefore, natural infection is expected to provide some, but incomplete, immunity in cats (which is not too surprising, given what we know about infection in people).

An important aspect of this study to keep in mind is that the cats were re-infected quite soon after the first infection.  The study showed some protective effect after 21 days, but we don’t know how long this incomplete immunity may persist.  Duration of immunity after infection (and after vaccination) is a big question is humans as well. We’re hoping that natural infection or vaccination provide reasonably long-term immunity, but that may not always be the case. That will have a major impact on how this pandemic progresses, and how we approach vaccination in the long-term.

Overall, this study provides some useful information, but it doesn’t change anything we do at the moment. The key messages remains the same:

  • If you have COVID-19 or have been exposed to the virus, limit contact with animals (just like you would with people).
  • Cats are people too, at least from a disease control standpoint. If your household is isolating, that should include all the non-human critters. It makes no sense for me to lock down all the people in my house but still let my pets have contact with other people and animals.
  • SARS-CoV-2 is (now) a human virus, but it still has an affinity for certain other species. Our goal should be to keep this a human virus and try to prevent it from infecting other animals.
  • If you’ve had COVID-19 once, hopefully you won’t get it again – but you might. Previous infection isn’t an excuse to change your behaviour or stop using basic prevenative measures around other people or animals.

At the start of the COVID-19 pandemic, many major agencies took a head-in-the-sand approach to concerns about the potential for SARS-CoV-2 to infect different animal species. Fortunately,  over the last year a considerable amount of work has been done to help figure out the range of species that are susceptible to this virus, and shed some light on how animal populations might ultimately impact control of the virus, based on the potential for for infecting wildlife in particular (which comes with the risk of creating  wildlife reservoirs, and potential sources of new virus mutants). We now know of a few wildlife species that are susceptible (and can transmit) SARS-CoV-2, but there are so many wildlife species that our knowledge still just scratches the surface.

A recent study in pre-print posted on bioRxiv (Bosco-Lauth et al. 2020) looked at SARS-CoV-2 susceptibility in deer mice, bushy-tailed wood rats, striped skunks, cottontail rabbits, fox squirrels, Wyoming ground squirrels, black-tailed prairie dogs, house mice and raccoons. They did this by catching wild animals and experimentally exposing them to the virus, and then monitoring them in captivity. The study was pretty small (2-9 animals per species) but provides some useful information.

  • Deer mice, bushy-tailed woodrats, and striped skunks were susceptible to infection and shed the virus after infection, but they didn’t get sick (i.e. all infections were subclinical).
  • Cottontail rabbits, fox squirrels, Wyoming ground squirrels, black-tailed prairie dogs, house mice, and raccoons were not susceptible to infection.

That’s a bit of a mixed bag of results. The more wildlife species that are susceptible, the greater the potential problems.  We’re also more concerned about species that may have more contact with people (e.g. urban wildlife), those that live in large groups (where an infected individual can spread the virus to lots of others, potentially leading to sustained transmission in the population and creation of a reservoir), and those that can travel long distances (and could thereby carry the virus to new areas).

One highlight of this study for me is that raccoons were not susceptible, because they’re a very common, social wildlife species that lives in large urban centres where COVID-19 is (at the moment typically) rampant in people. Raccoons are one of the species I’ve been most concerned about in terms of a jump to wildlife.

The authors sum things up nicely “… we will undoubtedly continue to discover more susceptible species as the search for zoonotic reservoirs continues. COVID-19 is just the latest in a series of examples of how the human-wildlife interface continues to drive the emergence of infectious disease.”

I got a question about an old post on this topic, so I decided to add a bit of information and re-post it. Not much has changed since it was written in 2018, apart from more reports of people and pets getting sick from raw pet food and raw treats.

Is freeze-dried raw pet food any different than fresh or frozen raw diets, from a microbiological standpoint?

We don’t have much pet food-specific research, but there’s little reason to believe there would be much difference between these types of diets when it comes to the microbes we’re concerned about. When I want to preserve bacteria, I freeze them or freeze-dry them – those are actually the preferred methods for long-term storage of bacteria. Freezing or freeze-drying is a pretty hospitable process and state for most bacteria. Some, such as Campylobacter, don’t tolerate freezing (or especially fresh-thaw cycles) as well as others, so freezing or freeze-drying might have some impact on those specific bugs. For the higher profile pathogens like Salmonella, E. coli and Listeria, it probably doesn’t have much of an effect. I can see there being some reduction in bacterial numbers but probably nothing substantial, and certainly not enough that I’d consider it when deciding whether it’s an appropriate diet for a particular pet and household.

The story is quite different for some parasites. Many parasites and parasite eggs don’t tolerate freezing – that’s why fish for sushi is typically frozen at some point before it is served. Some are hardier than others, though. Toxoplasma, a potentially important foodborne parasite, is susceptible to freezing, but only if the temperature is low enough and the time is long enough (e.g. -12C for 3 days will kill most Toxoplasma cysts.  To put that into context, typical household freezers run around -20C).

So, the take home message is that for of the microbes that we’re worried about with raw meat,  freezing or freeze-drying is NOT a food safety practice. It’s food preservation, not bacterial control.

Another point to add… advertizing around pet diets is variable and sometimes quite dodgy. I just checked two websites selling freeze-dried raw diet. One had good info. The other… well… not so much.  Don’t let company advertizing be your infection control guidance.

More information on raw diets and toxoplamsosis are available on the Worms & Germs Resources – Pets page.

I usually link blog posts to Tweets, rather than re-hash my Twitter musings (weese_scott) on the blog, but two things I posted on Twitter today may be of interest here.

COVID-19 in captive gorillas

Not surprisingly, COVID-19 has been identified in captive gorillas, in this case at the San Diego zoo.  It’s suspected that the gorillas were infected by an asymptomatically infected keeper, despite the intense precautions that have been taken to try to protect the animals since the pandemic began. It’s not at all surprising, since we assumed gorillas (and other non-human primates) that are relatively closely related to humans would be very susceptible to the SARS-CoV-2 virus, just like we are. With COVID-19 running rampant in California, it’s also completely unsurprising to have had an asymptomatically infected keeper at the zoo.

The more interesting aspect might be how the virus was actually transmitted from person to gorilla. Zoos tend to have very strict control measures in place to prevent this from happening (even when there isn’t a global pandemic), and the San Diego Zoo is an excellent facility. Figuring out how this occurred (e.g. inadequate practices, inadequate compliance) will be important to guide control measures at other facilities.

Toxoplasma gondii associated with brain cancer

Toxoplasma gondii is a protozoal parasite that has been linked to lots of issues in people, often with somewhat questionable evidence. Cats are the definitive host of this parasite, for which they get a very bad rap, but most human exposure is from the environment or food.

A recent paper has made some interesting but tenuous links between Toxoplasma infection and glioma, a type of brain cancer. It was interesting research, involving a large prospective study in which they collected blood samples from cancer-free people, and then followed them over time. After 13 years, they looked at the risk of gliomas in those who did or did not have antibodies against T. gondii prior to diagnosis (probably no real reason for picking 13 years… long enough for cancer to develop and it happened to be when they were ready to look at that).

There were some weak associations between one type of Toxoplasma antibody and development of glioma and glioblastoma. The data aren’t too convincing, but there are some similar results from elsewhere, which shows the subject needs more study.

What does this mean for cat owners?

  • Very little. Gliomas are a rare cancer, and while Toxoplasma exposure is quite common, it’s not usually from someone’s pet cat. Toxoplasmosis is a “don’t eat poop” disease, so there are lots of simple, routine things we can do to reduce the risk from pet cats (like not touching cat feces and washing your hands after cleaning the litter box).

More of my comments are posted on Twitter here:

We have more information about Toxoplamsa on the Worms & Germs Resources – Pets page.

Here’s the latest version of our pandemic guidance document for Ontario veterinary clinics, produced in collaboration with the OVMA.  Previously entitled “A guide to reopening veterinary medicine in Ontario” it has been retitled “A guide to mitigating the risk of infection in veterinary practices during the COVID-19 pandemic (04-Jan-2021)“.

Previous versions of the guidance and other related documents can be found on the Worms & Germs COVID-19 Veterinary Resources page.


We continue to track cases of canine infectious respiratory disease in various parts of Canada, for what it’s worth. The data are obviously a bit dodgy because it’s primarily from self-reporting, but I think we’re getting some interesting information. Cases seem to be slowing down, but we continue to get reports from the two main areas in Canada (and a trickle from the  US). Part of the clustering we’re seeing is probably due to local increased awareness and reporting, but I don’t doubt that a couple of reasonable-sized outbreaks have been ongoing.

Click here for the latest version of our canine infectious respiratory disease complex (CIRDC) map (December 31), now with the ability to display cases reported by month.  A snapshot of the map is also shown below.

Here are some additional details from the data we’ve collected via the reporting survey:

65% of affected dogs had been vaccinated against “kennel cough” in the past year.

  • That’s not too surprising. Kennel cough vaccines protect against one, two or three of the many potential causes of CIRDC, but not all of the causes, by any means. Furthermore, no vaccine is 100% effective. These data don’t tell us anything about how well those vaccines work (they actually work quite well).

Of that 65% of affected dogs that were vaccinated in the past year:

  • 40% were vaccinated orally: The oral vaccine only covers Bordetella bronchiseptica, which consistently comes in as the #2 cause of CIRDC in Canada. It’s a good vaccine for that bacterium but has less coverage than intranasal vaccines.
  • 29% got an intranasal vaccine: Intranasal vaccines in Canada cover Bordetella bronchiseptica and canine parainfluenza virus, giving protection against the top 2 causes or CIRDC. Some also include protection against canine adenovirus type 2.
  • 35% received an injectable vaccine: Injectable vaccines are less protective when it comes to CIRDC. Oral and intranasal vaccines provide better protection where the infection occurs – in the upper respiratory tract.
  • 26% were unsure of the vaccine type: So whether these dogs were truly vaccinated against kennel cough is unclear.

Over half of affected dogs had visited a dog park shortly before they got sick.

  • That’s not surprising at all, since CIRDC is spread dog-to-dog, and parks are a place where dogs congregate.  Groomers came in as the #2 most common previous contact, followed by doggie day care.
  • Since we just looked at sick dogs, we can’t say anything about risk factors (e.g. we don’t know if visiting a dog park was more common among sick dogs since we couldn’t compare them to healthy dogs).
  • There were a couple specific parks that were frequently named, so it’s likely there were some true hot spots of transmission at those parks.

Diagnostic testing was performed on 17% of sick dogs, but nothing remarkable was apparent in terms of diagnosis.

  • That’s actually a pretty high percentage for testing in cases like this. Testing isn’t commonly recommended for routine cases of CIRDC since the cost is hard to justify where there’s little impact of test results on individual patient care.
  • Testing is more useful when there’s an outbreak (to figure out what the culprit is and see if there are any control measures that might be applied), with imported dogs (worried about bringing in influenza strains), kennels (outbreak potential) and breeders (outbreak potential, risk of more severe disease in young and pregnant dogs).
  • Limited test results were provided on the survey but nothing remarkable was present.

Most of these outbreaks of CIRDC die out over time and we never find the cause.

  • Canine parainfluenza is always high on my list since it’s common (common things occur commonly) and can be missed with routine testing because the virus isn’t shed for long. By the time the dog is taken to a veterinarian and sampled, PCR tests looking for the virus may be negative (and other approaches like antibody-based testing aren’t usually done).
  • A “new” or (more likely) established but unknown cause of illness is certainly possible. There are undoubtedly many canine respiratory viruses out there that we don’t know about.
  • Introduction of canine influenza from imported dogs is always a concern. It’s a “foreign” disease, but canine influenza was introduced to Ontario a few years ago, and was ultimately eradicated (as far as we can tell).  Here, since there haven’t been any positive test results, it’s unlikely to be the cause. That virus is shed for a while in infected dogs, and I’d expect to see a positive result with a reasonable number of tests. Introduction of influenza into areas where few to no dogs have immunity to the virus would almost certainly result in more widespread disease. So, I think flu is pretty unlikely here, but the potential for flu is a reason to test. We’ve shown it can be controlled when it’s caught early, but if it’s not, it can cause a lot of damage.

Disease tracking like this won’t provide clear answers, but helps identify and refine things we need to look at, so I think there’s a role for it  as an easy, low-cost surveillance tool.

The new SARS-CoV-2 strain circulating in the UK (technically called SARS-CoV-2 VUI 202012/01, or B.1.1.7 – see “what’s in a name” below) has raised a lot of concern internationally. The fact that we have a mutant strain of the virus isn’t surprising. There are countless mutant strains out there already. Viruses like this naturally change over time. Usually the changes are fairly irrelevant in terms of how the virus behaves, though they can still be useful for tracking purposes. However, depending on the type of mutation and location on the virus genome, it can impact what the virus does in either a good way, or a bad way. Mutations are random, but if a certain mutation helps the virus survive and spread, those mutant strains tend to become more common.

What’s the deal with B.1.1.7 (or whatever you want to call it)?

This strain has multiple mutations (compared to other commonly circulating strains), and many of those mutations affect the spike protein. The spike protein is what the virus uses to attach to ACE2 receptors, which are found on the surface of human and animal cells. The better the match between the spike protein and the ACE2 receptor, the greater ability of the virus to attach to and infect cells. Differences in the ACE2 receptors impact species susceptibility (e.g. a person’s ACE2 receptor is a good match for the virus, so people can be infected. A bird’s ACE2 receptor is a very poor match so birds are resistant). The mutations in B.1.1.7 seem to make the spike protein a better match for human ACE2 receptors.

That’s likely why this strain seems to be much more transmissible to people than other strains, and it’s rapidly become a common strain the UK. It’s also been found in various other countries (typically with an epidemiological link to the UK).

How did B.1.1.7 emerge?

The ECDC’s Threat Assessment Brief mentions three main potential mechanisms for the emergence of this particular strain. They considered gradual accumulation of the collection of mutations in the UK to be unlikely, since this strain is a big jump from other strains in that country (i.e. intermediate generations of the virus with smaller numbers of these mutations weren’t found in the population before B.1.1.7 suddenly appeared). That left the following main considerations:

  • Prolonged infection of a single patient with SARS-CoV-2, which allows more mutations to occur quickly, with subsequent spread back into the general population.
  • Infection of an animal, with mutation in the animal and then transmission back to people.
  • Gradual emergence of the strain in another country that has little sequencing data, and then introduction of the strain to the UK.

I assume this strain originated in a person. However, movement of viruses between species can foster selection of mutants, and that’s why we’re paying close attention to how SARS-CoV-2 behaves in animals, especially large groups of animals like mink farms where there can be a lot of transmission. It’s also one reason we’re worried about infection of wildlife, as sustained spread in wildlife could potentially create lots of new strains.

What is the impact of B.1.1.7 on animals?

Increased affinity for human cells doesn’t necessarily mean increased affinity for other species’ cells. It might, or it might result in decreased affinity. Hopefully someone’s looking into that.

  • If this virus is equally transmissible to animals as its predecessor, we still have more human cases and that means more animal cases, just from more human-to-animal exposures.
  • If this strain can more easily infect certain animal species, we could see even more human-to-animal transmission, i.e. a higher occurrence of the spillover infections we’re already seeing.
  • Another concern is whether any new strain could infect species that are resistant to the current SARS-CoV-2 virus, including livestock and wildlife species. I doubt this set of mutations is enough to change the host range, but it needs to be considered.

How can we find out how B.1.1.7 affects animals?

Experimental studies are one way, but they’re not ideal in this case for a number of reasons. Field studies can be useful, looking at transmission of the new strain to animals in contact with infected people, as well as ongoing surveillance of animals in settings like mink farms. The issue is there are very few researchers doing things that way. Logistical challenges, as well as lack of coordination with the human health measures and testing, hamper timely testing of in-contact animals. We need to test animals when infection in their human contacts is first detected if we want to recover virus from them. Cooperation of local and provincial health authorities has been a challenge here, an understandable one though given the stress the system is under trying to manage the pandemic. It’s another example of why planning for this type of thing needs to be done in advance (as I said repeatedly post-SARS-CoV-1, and as I tried to address with the province in January 2020, with no response). The odds are good that animals won’t play a role in dissemination of this virus, but it would be nice to base that on data, not hope.

Will this new strain impact the most impressive vaccination development drive in human history?

Hopefully not. There is confidence that this mutation will not impact the efficacy of the current vaccines. However, it’s a reminder that we still have to control transmission as much as possible while vaccines roll out. Less transmission means fewer illnesses, fewer deaths and fewer mutations. We need to buy time until vaccines are available to everyone, everywhere, to reduce disease and the risk of significant mutations.

What does it mean for Canada (or the US, or any other country)?

It means we need to:

  • Control the spread of SARS-CoV-2, whatever the strain
  • Sequence more viruses to understand the presence and spread of different strains
  • Investigate potential animal sources
  • Vaccinate, vaccinate, vaccinate

What’s in a name? When it comes to a virus…

Just like we quickly tried to move away from calling SARS-CoV-2 the “Wuhan coronavirus,” we are trying to avoid calling this new strain a “UK variant.” It’s best referred to as a strain first found in the UK, or by its technical name (which unfortunately isn’t particularly short or catchy).  We shouldn’t be “shaming” countries that find pathogens or their variants and report them. Just because this new strain was first found in the UK doesn’t mean it originated there. We don’t want fear of blame, travel bans or things like that to be a disincentive for countries to test and report. Even if the virus emerged there, it’s not the UK’s fault (beyond the fact that more virus spread overall means more risk of a mutation like this occurring).  A mutation like this could have happened anywhere in the world and been imported to the UK, and then spread rapidly there after it arrived.

We’re continuing to track informal reports of canine infectious respiratory disease in a number of areas.  Click here for the latest version of our canine infectious respiratory disease complex (CIRDC) map (December 17).

We’re still getting lots of reports of sick dogs in Edmonton and Calgary, both via cases reported through our survey for the map and through emails that I get from various people.

The cause of illness in these dogs is currently still unclear. There have been a few positive tests for canine parainfluenza virus (our most common cause of canine infectious respiratory disease) and Mycoplasma (something I’m not convinced is truly a primary cause of disease in dogs), but nothing consistent. Limited testing and testing late in disease affect our ability to figure out what’s really going on.

Nonetheless we are seeing some clustering around specific parks and some cases linked to groomers, which is not uncommon in situations like this.

There are various reasons we’re paying attention to SARS-CoV-2 in domestic animals. One important one is the potential for transmission of the virus from domestic animals to wildlife (because animals tend to have more direct contact with wildlife than people do). More specifically, we’re concerned about transmission to wildlife and then persistence of the virus in wildlife populations. For that to occur, you need susceptible wildlife species in large enough numbers and in close enough contact with each other for transmission of the virus to be sustained over time.

There is emerging information about the susceptibility of a few common wildlife species, so there is basis to those concerns and a need for more study.

A lot of the concern about SARS-CoV-2 in animals has revolved around mink. They’re highly susceptible and farmed mink are kept close together in large numbers. That’s a recipe for virus transmission (and potentially virus mutation, but that’s a different story). Farmed mink are also good at escaping. “Wild” mink found around mink farms tend to be escaped mink, or the offspring of escaped mink.  Escaped farmed mink and wild mink can often be distinguished by certain physical characteristics including size (larger) and coat color (some farmed mink are bred for coat colours that don’t commonly occur in wild mink) .

When it comes to SARS-CoV-2, escaped mink create a few concerns. One is they could take the virus with them when they escape if they’re infected, creating another potential exit point from the farm for the virus. We don’t want that. The virus getting onto the farm is bad, but if it stays there and burns out, it’s not as big deal compared to the farm becoming a source of infection for other animals. Mink don’t shed the virus for long, so there would only be a short window of time after escape that a runaway mink would pose a transmission risk to other animals. Another concern is that if escaped mink continue to hang around the area (e.g. coming back to find food), they could become a longterm bridge for infectious diseases (e.g. SARS-CoV-2, and others) from the farmed mink to wildlife.  Or worse, if escaped mink move between properties in areas where mink farms are close together, they could spread diseases from farm to farm.

That’s my long-winded introduction to the latest concern with mink, identification of SARS-CoV-2 in a wild mink in Utah, USA. Some mink farm outbreak investigations have included testing of wildlife around the farm. Infected cats have been found in Europe, and testing of wild mink around an affected farm in Utah identified an infected animal there too. They’re considering it the first case in a “free ranging, native wild animal,” which I guess is correct, but I’m not sure it’s much different than the spillover to cats on and around mink farms that’s been seen before. Not surprisingly, the viral sequence from the affected mink was identical to that of virus from mink on the nearby farm.

What does this mean?  It’s too early to tell. One good thing about the SARS-CoV-2 virus is there’s no long-term carrier state, that we know of (at least outside of bats… that’s yet another story that still needs to be sorted out). If the virus makes it into wild mink or other wildlife, the relevance depends on whether that species can maintain and spread it. Infection of solitary species, species that have low population density, or species that aren’t very susceptible and don’t shed a lot of virus likely ends quickly. The concern is infection of large groups of susceptible animals, where infection might be self-sustaining in the population, circulating within and between groups (just like it does in people). At this point, we have no idea if that’s a realistic concern in wildlife, but it’s better to look and find out than just hope for the best.

Still, the best way to prevent this from becoming an issue is to prevent exposure of all animals as much as possible, especially wildlife. The best way to prevent that is to control it in people.