Rat bite fever (RBF) is an uncommon disease in people, but one that I nonetheless spend a lot of time talking about with owners, veterinarians, and physicians (and sometimes lawyers). It’s a bacterial infection spread by (you guessed it) rats. The causative agent of RBF is an obscure bacterium called Streptobacillus moniliformis, which lives in the mouth of most healthy rats.  It’s typically introduced into a person’s body via a bite from a rat. Usually people don’t get an infection after such a bite, but sometimes they do, and the consequences can range from mild to fatal. Most cases aren’t too bad and respond to treatment, even though treatment is often started later than it should have been (because many physicians don’t ask about animal contact and many patients don’t mention if they’ve been exposed to a rat).

It’s not clear how common RBF really is, especially because it’s not reportable (so no one formally tracks it) and it’s probably under-diagnosed anyway.

A recent study in Open Forum Infectious Diseases provides a bit more information about RBF, but it’s still pretty limited. The paper, “Rat bite fever in the United States: an analysis using multiple national data sources, 2001-2015” (Kache et al. 2020), concludes that it’s a rare disease. That’s presumably true; however, what they looked at were hospitalizations and emergency room visits. So, they can conclude that it’s a rare cause of hospitalizations, but that’s not necessarily the same as telling us how often it causes milder disease. Regardless, the study still provides useful information about the more serious cases of RBF.

Here are a few highlights:

Rat bite injury visits were 10.5 per million people. Hospitalization for rat bite injury was 0.27 per million.

  • That’s rare, but not unexpected.  Visits to an ER after a rat bite would be unusual since they don’t cause the same degree of trauma as for example, a dog bite.

Rat bite injury hospitalization rates were highest in females, people over 60 years of age and Blacks, as well as people from the Northeast.

  • It’s maybe easiest to explain the higher rate for older individuals, as they may be more likely to seek care after an injury. The others are tougher to explain. Knowing more about the type of rat bites would help. Pet rat vs wild rat exposures weren’t differentiated, and it’s certainly plausible that someone bitten by a wild rat would be more likely to go to an ER than someone bitten by their pet. There could be socioeconomic-related reasons for racial disparities in exposure to wild rats in urban areas.

The ER visit rate for RBF was 0.33 per million.

  • Again, that will be an underestimate of RBF, since it only includes people with RBF that go to the ER and are diagnosed and properly documented in the medical record (both potential issues).

RBF hospitalization was most common in people 19 years of age or younger.

  • That’s fully expected and consistent with the cases with which I get involved. One reason is that kids are presumably more likely to be bitten, based on how and how often they interact with animals. Young kids are more likely to get sick after exposure. Put those together, and an age predisposition is expected, as with many other pet-associated diseases.

Outcomes weren’t reported. Rat bite fever is typically easily treatable, but serious disease can occur. Sometimes that’s because the diagnosis is missed, but it can also cause rapidly progressive severe disease in rare cases, and even death.

For anyone interested, the paper has a lot more data about hospitalization rates, duration of hospitalization and costs, but I won’t get into those here.

The conclusion states: “For the medical community, clinical recognition involves enhancing awareness of RBF and the implications of this disease among pediatrics.” That’s a critical point, since RBF is a niche disease that can be overlooked by physicians (and veterinarians counseling owners about zoonotic disease risks). One of my typical talking points is about the need for physicians to query animal exposure ALL the time. This disease gets missed time and again because rat bites and rat contact get missed. Rat bite fever won’t jump to mind for most physicians examining a kid with a fever and rash, but if they ask about animal contact or the parent mentions it, there’s a good chance the diagnosis will be made. If not, it’s very unlikely. Asking a question about animal contact is free and takes a few seconds – there’s no reason not to do it.

As things change, both in the epidemiology of COVID-19 and our approach to containment, re-assessment of how we practice veterinary medicine and COVID-19 protection is important. The latest iteration of our guidance document has been released: COVID-19: A Guide to Reopening Veterinary Medicine in Ontario, Stage 3. As for the previous versions, this is a guide, not a standard – meaning it’s a document of recommendations and considerations, not a “standard of care.”

The guidance is designed for Ontario veterinary clinics, but much of it applies more broadly as well. Balancing the need to reduce SARS-CoV-2 transmission risk and the need to deliver practical, effective and efficient veterinary care is a challenge (I assume, as always, that I will get an earful of complaints from both sides of the spectrum).  A lot of factors need to be considered when deciding what to do in a particular clinic, including the epidemiology of COVID-19 in the region, clinic layout, clinic size, presence of high-risk individuals in the clinic, and risk aversion just to name a few. This document outlines the issues and some of the possible approaches, and hopefully will help clinics tailor their practices to find the right balance for them.

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

I’ve been away and need to catch up on some posts.  I was planning a nice non-COVID post, until a few seconds ago when I saw the CNN headline “Chinese officials say chicken wings imported from Brazil tested positive for COVID-19.”

My response… oh crap.

Not because I fear a wave of foodborne COVID-19. Rather, I fear a wave a paranoia about foodborne COVID-19 (and an overstuffed email inbox today).

According to the report, testing identified SARS-CoV-2 in a sample of chicken wings from Brazil. We have to realize that it’s most likely the testing was done by PCR, which is a very sensitive method that detects the nucleic acid building blocks of the virus (the RNA). That means it can detect live OR dead virus.  This virus does not live long outside its host, so it’s almost certain the virus (or more specifically pieces of virus) detected in the chicken wings wasn’t infectious.

How did the virus get there?

  • Likely from people handling the food. While research is still limited, this virus has not been identified in poultry, so a human origin is almost certain. That would fit with other recent reports from China of detection of SARS-CoV-2 on packaging of imported food. Infected people contaminate surfaces they touch.

Is there any risk?

  • Presumably no. Small amounts of this virus are probably common of surfaces in areas where the virus is circulating. The more infected people, the more contamination is likely. Yet, transmission risk still seems to be mainly from droplets and direct contact. The presence of viral “bits” on surfaces does not mean the presence of risk.
  • The risk from handling chicken wings is mainly from our run-of-the-mill foodborne bugs like Salmonella.

What should people do?

  • Pay attention to measures that we use to reduce the risk from our run-of-the-mill foodborne bugs like Salmonella, such as handwashing after handling raw meat, and cooking meat properly, and avoiding cross-contamination of food and surfaces in the kitchen. (If you want an extra level of protection, avoid sticking raw chicken wings up your nose.)”

There are a lot of things regarding SARS-CoV-2 to be concerned about. This isn’t one of them.

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).