Various times, I’ve asked audiences “What percentage of antimicrobial resistance in humans do you think it attributable to antimicrobial use in animals?

  • Answers pretty much range from 0-100%.

The actual number is probably on the low end of that range, but we really don’t know. It’s such a complex system that a simple number can’t be generated.  In fact, we don’t have the data to even get close to an accurate overall estimate.

However, better estimates can be made for certain resistant bacteria, for which more specific data are available. The estimates are still pretty dodgy given current gaps in surveillance, so the numbers have to be taken with a big grain of salt, and we have to take care extrapolating to other bacteria or different geographic ranges. Regardless, the information can be interesting and useful if we are careful not to overinterpret things.

A recent paper in The Lancet Planetary Health (Mughini-Gras et al. 2019) investigated multidrug-resistant E. coli, specifically E. coli that produced extended spectrum beta-lactamases (ESBLs) or that harboured the AmpC gene. These E. coli are resistant to 3rd generation cephalosporins (an very important drug class for treatment of infections in people) and are often resistant to various other antimicrobials as well. The study evaluated data on ESBLs and AmpC E. coli from different Dutch sources, and developed a transmission model to estimate how people were becoming infected (outside of hospitals).

Here are some highlights from the study:

  • People carrying resistant E. coli likely most often (61%) got it from other people, followed by food, animal and environmental sources (in that order).
  • The graph below shows how common resistant E. coli are in various sources (size of the bar to the left of midline) and how important each source is to humans in terms of potential exposure (size of the bar to the right). As you can see, for some sources (e.g. chickens – the birds, not the meat), resistant E. coli are very common but they are not thought to be important sources of exposure to people, while for others, the likelihood of resistant E. coli is low but the sources pose a disproportionately high risk of exposure to humans (e.g. raw vegetables). The impact on people varies with the overall amount of exposure and how we handle potentially contaminated sources. For example, even though the rate of contamination of raw vegetables is low, we encounter those very frequently and we often don’t cook them. In contrast, the contamination rate in surface water is high, but we don’t have a lot of direct contact with untreated water.
  • Companion animals came up higher than I would have guessed, being estimated to account for 7% of human infections, most often from dogs (3.9%) (although it reinforces why I’m concerned about ESBLs in dogs and cats, and why we’re studying it).

The over-riding conclusion was that humans are the main source of community-acquired resistant E. coli, but that non-human sources still play important roles. They also concluded that, even though non-human sources accounted for a minority of infections, it would be difficult for these resistant E. coli to be maintained in people without transmission to and from non-human source. So, addressing the problem in people alone will help, but won’t eliminate the problem.

We have to remember that these are just estimates and they may just (or at best) apply to the Netherlands. However, it’s an interesting story and should keep us thinking about the multi-disciplinary (One Health) approach that we need to take to combat antimicrobial resistance.

Despite daily updates to spam filters and contact blocking, I wake up every day to a variety of invitations to submit to journals.

  • No good journal does that. They have lots of submissions.

The spam emails highlight the wild west of predatory journals, often with names that try to imitate real journals. Today’s was the “New American Journal of Medicine”, a not-so-subtle variation of the New England Journal of Medicine or the American Journal of Medicine. It looks like that journal has published a total of 8 papers in 2019. I looked at one of them and “crap” is my generous assessment. It’s a paper that recommends a treatment for pregnant women and it’s one page long, does not disclose the funding source, fails to fulfill pretty much every standard reporting requirement for a clinical trial and reports essentially no specific data or analysis. But, it’s “published data” and therefore now on someone’s CV.

The state of the scientific literature is pretty messed up. “Show me the study” has been a common refrain, but it’s not as useful these days because anything can get published.


  • Too many journals.
  • Predatory journals.
  • Profit.

Good journals screen out the weak articles. High impact journals publish a minority (5-25%) of the articles submitted to them (and bear in mind most often people only send their best papers to those journals). Some journals that are still good quality take lower impact papers that are still good science. Some journals take whatever they can get, just trying to screen out the bad science.

Others will take whatever they can get, as long as the authors can pay. Sadly, there are literally thousands of those, and they’re the worst kind.

Some people don’t realize most researchers don’t get paid to write scientific papers, and in some cases it’s quite the opposite. Some journals still publish at no cost, but increasingly, there are publication fees that may range from a few hundred to a few thousand dollars. That, itself, isn’t necessarily the problem. Some journals charge fees so that the papers can be open access (available to anyone, without a need for a subscription). However, some journal charge a couple thousand dollars, make a nice profit and don’t particularly care about the science.

As someone who’s an associate editor, editorial board member and frequent reviewer for many journals, I see the good and bad.

  • I see papers that should be published accepted.
  • I see good quality papers rejected by good journals, knowing they’ll still end up in another good journal.
  • I see bad papers rejected.

However, I also see…

  • Horrible quality papers rejected that I know will (unfortunately) still end up published somewhere else.
  • Published papers that clearly didn’t undergo any/much peer review, or at least peer review of any quality and/or editors that paid any attention.

It’s frustrating to be reviewing a paper that’s complete crap, knowing it will find a home in a journal eventually and still become part of the “published literature.” Yes, it will most likely be in a bottom-feeder journal that many of us in the scientific community know is dodgy, but not everyone will realize the difference. Sometimes that’s just frustrating, because poor quality science shouldn’t be published and just “muddies the water” of what’s out there. However, when it deals with clinical matters (e.g. diagnosis, treatment of disease) it can actually be harmful, because poor quality or invalid data shouldn’t form the basis of decisions. Yet, it happens.

There have been a couple “stings,” where fake (and clearly garbage) papers have been submitted to journals. The highest profile was one that was published in Science (Bohannon, 2013).  The author submitted a paper to several journals.  It was later said of the study that “Any reviewer with more than a high-school knowledge of chemistry and the ability to understand a basic data plot should have spotted the paper’s short-comings immediately. Its experiments are so hopelessly flawed that the results are meaningless.” More than 50% of the open access journals to which it was submitted accepted it.

There are many reasons these dodgy journals are used.

  • “Publish or perish” as they say in academia isn’t quite true, but it’s pretty close. Junior faculty need to show productivity to keep their positions or move into the increasingly elusive tenured positions. Published scientific papers is a key metric, because it’s easy to count.
  • Some people get taken advantage of, not realizing the journal is predatory (or that fees are so high, until after the paper is accepted).
  • Commercial profit. Companies want to say their products are supported by published data. If the data aren’t actually any good, the amount of money that it takes to get something published is inconsequential for most companies (and cheaper than going back to the drawing board).

Open access isn’t inherently bad. There are excellent open access journals that charge a couple of thousand dollars per paper for publication but have high standards. Open access is actually ideal as it means the science is available to everyone. It just has to be acceptable science, and that’s where things start to fall apart.

Anyway… enough ranting. I always like to say “don’t talk about a problem without talking about a solution” but I don’t have an easy solution. More awareness is key, which is why sites that track predatory journals, such as Beall’s List, are important. It’s a good update on a sad state of affairs.

As an Associate Editor for CDC’s Emerging Infectious Diseases journal, I get an early look at some interesting articles (and have to read things that I wouldn’t necessarily get around to otherwise). The December edition just came out, and it had a variety of interesting articles. I’ll try to get to a few over the next couple of days, but this first one is an interesting case report of Mycobacterium bovis infection associated with cats (O’Connor et al 2019).

Mycobacterium bovis is a bacterium that’s closely related to the bug that causes most human tuberculosis, Mycobacterium tuberculosis. Mycobacterium bovis is linked primarily to cattle, but can be found in a variety of wild and domestic animal species, and it can infect people. Classically, human infections with M. bovis are associated with consumption of unpasteurized milk, but direct contact with infected animals can also result in transmission.

M. bovis is an issue in the UK, where it’s found in a variety of animal species, including cattle and wildlife (such as badgers).  This case report report from the UK involves two separate incidents of human M. bovis infection linked to cats. M. bovis is a rare cause of disease in cats, but it can happen in areas where the bacterium is present, through exposure to infected domestic animals or wildlife (or from eating contaminated raw meat).

The human cases were linked to a cluster of infections in cats in Dec 2012-Mar 2013. Seven confirmed feline cases were identified, with at least three more suspected. All of the cats were from households in the same area (less than 250 metres apart), and they had severe disease, consistent with tuberculosis. Presumably, they were exposed while tangling with infected badgers in the neighbourhood.

While sporadic cases in cats wouldn’t necessarily get much attention, the number of cases in a short period of time in close proximity to each other led to an investigation of human contacts. Close contacts were offered TB screening, and 24 people agreed to be tested. Three were positives for latent TB, meaning they were infected but didn’t have signs of active disease and were not shedding the bacterium. Essentially, these individuals had become infected and the bug had gone dormant in their body. That’s good, in that they’re not sick, but there’s always the potential for the bug to re-activate and cause active infection later on (and make the person a risk for transmitting the bacterium to others). Treatment was offered and one person accepted. One of the two that declined treatment then developed active TB six months later. A contact of that person (who also had an infected cat) had initially declined screening but then developed chest pain and fever…

What’s the take-home?

Beyond being an interesting story, the main thing to consider from a disease prevention standpoint is how to reduce human exposure to M. bovis in such a case. Here are some key points to take away from this report:

  • While rare, M. bovis is a risk to cats in areas where it’s present in wildlife. Outdoor cats have greater risk of exposure to a lot of things, including this bug in some parts of the world. Whether or not to allow your cat to go outdoors requires assessment of the risks (e.g. disease, trauma, wandering, environmental impacts) and benefits (e.g. cat’s behaviour and welfare).
  • All of the people who were infected had contact with cats with active disease, including discharge from visible lesions. Contact with infected sites logically increases the risk of exposure to whatever’s causing the disease. Avoiding contact with infected site, particularly pus, and good attention to hand washing and other basic hygiene practices probably reduce the risk of exposure and infection.
  • Diagnostic testing of your pet might help protect your health. There are instances where we can find something in an animal that poses a human health risk. Knowing that can be important (e.g. so you can tell your physician you were exposed to the bug if you get sick, speeding up your diagnosis / knowing what precautions to take when handling the pet). That’s the One Health concept that gets talked about a lot (but actually used much less commonly).

Encouragingly, the conclusion of the article points out some actual One Health actions:

Public Health England now advises that all close contacts of household companion animals with confirmed M. bovis infections should be assessed by a public health professional and receive guidance on how to best minimize zoonotic transmission. In addition, as part of an enhanced surveillance system in England and Wales, newly diagnosed human case-patients with M. bovis infection are now also asked explicitly about contact with pets with suspected or confirmed M. bovis disease.

Two reports came out this week, both detailing the scourge of antibiotic resistance.

They’re both comprehensive, with a combined >400 pages explaining that this is a big problem.

I’m not going try to summarize the reports. I’ll just pick out a few interesting tidbits.

From the CCA report (Canada):

  • According to their modelling, first-line antimicrobials (those most commonly used to treat routine infections) helped save at least 17,000 lives in 2018 while generating $6.1 billion in economic activity in Canada. “This contribution is at risk because the number of effective antimicrobials are running out.”
  • Antimicrobial resistance was estimated to reduce Canada’s GDP by $2 billion in 2018. That’s only going to get worse unless we get our act together. It’s estimated that by 2050, if resistance rates remain unchanged, the impact will be $13 billion per year. If rates continue to increase, that stretches to $21 billion. Remember, that’s just for Canada, a relatively small country from a population standpoint.
  • Healthcare costs due to resistance (e.g. drugs, increased length of stay in hospital) accounted for $1.4 billion in 2018.  But remember that people who die from resistant infections can actually cost less. If I get a serious resistant infection and die quickly, my healthcare costs are pretty low since I didn’t get prolonged care. All that to say that dollar costs alone don’t capture all the human aspects. Regardless, this cost will likely increase to $20-40 billion per year by 2050.
  • In terms of human health, resistant infections were estimated to contribute to 14,000 deaths in Canada in 2018, with 5,400 of those directly attributable to the resistant infection (i.e. those deaths would not have occurred if the bug was susceptible to first line drugs). That makes resistance a leading killer, and it’s only going to get worse.

I’ll stop there. The document has a lot of good information and it’s worth reading if you’re interested in the topic.  They also provided a handy 2-page “infographic” summary if you can’t quite stomach the complete 268-page report (also see image below).

From the CDC report (US):

The document’s dedication says a lot. “This report is dedicated to the 48,700 families who lose a loved one each year to antibiotic resistance or Clostridioides difficile, and the countless healthcare providers, public health experts, innovators, and others who are fighting back with everything they have.”

The forward has some great messages too:

To  stop antibiotic resistance, our nation must:

  • Stop referring to a coming post-antibiotic era—it’s already here. You and I are living in a time when some miracle drugs no longer perform miracles and families are being ripped apart by a microscopic enemy. The time for action is now and we can be part of the solution.
  • Stop playing the blame game. Each person, industry, and country can affect the development of antibiotic resistance. We each have a role to play and should be held accountable to make meaningful progress against this threat.
  • Stop relying only on new antibiotics that are slow getting to market and that, sadly, these germs will one day render ineffective. We need to adopt aggressive strategies that keep the germs away and infections from occurring in the first place.
  • Stop believing that antibiotic resistance is a problem “over there” in someone else’s hospital, state, or country—and not in our own backyard. Antibiotic resistance has been found in every U.S. state and in every country across the globe. There is no safe place from antibiotic resistance, but everyone can take action against it. Take action where you can, from handwashing to improving antibiotic use.

The reports take different approaches but ultimately have a lot in common, and none of it is good in terms of the story they’re telling. There are lots of things that can be done, if there’s support (including morale, logistical, financial, etc. – all of which tend to be lacking when it comes to actually doing something).

Some might say it’s alarmist. However, I don’t think it’s alarmist when someone really should be raising the alarm. We need to talk about it more, not less. We need to get people (including the general public, healthcare workers, farmers, veterinarians, policymakers) on board, to realize it’s a big issue that needs to be addressed now. “Short term pain for long-term gain” certainly applies here. We can keep delaying and the numbers will keep going up, or we can invest in solutions.

The numbers are scary but specific numbers don’t really matter in many ways. “Lots” is all we should have to know to get motivated. However, decision-makers like numbers, so these numbers hopefully will be useful to show the impact and potential benefits of investing in this problem, and motivate them to put money into antimicrobial stewardship. Saving lives should be enough, but that often doesn’t cut it. Antibiotic resistance doesn’t have a good marketing campaign. Everyone knows why people were wearing pink last month and why there are some pretty dodgy moustaches this month. Those are important issues, for sure. However, considering the overall impact, antibiotic stewardship needs to get more people behind it if we’re going to effect change.

A colleague sent this leading in with “you can’t make this stuff up.”  He was right.

Here’s the Cole’s notes version of the story of a couple’s visit to a Louisiana truck stop.

  • A Florida couple stops at a roadside rest stop that has some animals on display as attractions.
  • Their (apparently poorly restrained) small dog enters a pen with a camel, where there are numerous signs warning visitors to keep out.
  • The woman nonetheless crawls into the pen and somehow ends up with the camel sitting on her.
  • Her method of getting the camel up is to bite it… on the genitals.
    • Well, I guess that would work.
    • And, to top it off, it occurred on a Wednesday (hump day).

Part of me just wants to post this to tell the story.  The other part wants to use it as a lead-in to discussing when antibiotics are needed after a bite.

The camel in question got prophylactic antibiotics. That’s actually a reasonable plan for a bite over higher-risk area like the genitals. However, it appears that the antibiotics were started five days after the bite, well beyond the window for preventing infection, so they were unlikely to be of any benefit.

So, when are antibiotics indicated after a bite (for any species, by any species)?

  • In general, antibiotics are indicated when there’s high risk of an infection or a high risk that an infection would cause serious problems.
  • Typically, that includes bites to individuals who have compromised immune systems, ncluding (especially) those who don’t have a functional spleen. They’re at greater risk of developing a serious infection.
  • Situations where infections are potentially of greater consequence would include bites over tendons, joints or nerves (so, pretty much any bite over the hands, wrists or ankles), bites over prosthetic devices, bites to the face and bites to the genitals.

Avoiding getting bitten is an even better approach.

Getting sat on by a camel, or biting a camel…. well, that brings in a whole different set of issues.

I was flying home from Vancouver the other day and there was a lot of barking from the holding area near the baggage carousels. It sounded like a lot of dogs were back there, which obviously got me thinking about from where they had come, to where they were going and what risks might be involved. We have hardly any idea of the number of dogs that fly within or into Canada and where they go, and I haven’t been able to get any information from airlines about how dogs are generally handled in transit (e.g. how closely cages are kept together, which is important because a dog flying a short distance domestically could potentially be placed close to a dog that’s just come in from overseas).

I don’t expect to get answers to any of these questions in the near future. However, there’s a bit more awareness now.  That’s a start.

In the US, the CDC has just released a new flyer about canine importation. It’s being distributed to US Customs and Border Protection, which seems a little late in the process (once you’re at the border with your dog, it’s a bit late to check some of these things). However, if it raises general awareness, it’s still a good thing. It would be interesting to know how widely distributed these fliers end up at border crossings.

“Kennel cough” (now more conventionally termed “canine infectious respiratory disease complex’)  is a fairly common problem in dogs that can be caused by an array of bacteria and viruses. We commonly see it in outbreaks, often linked to kennels, but sometimes we see higher levels of disease in the broader community. What we’re more concerned about is new problems , new patterns or more severe disease.

We may be seeing an increase in respiratory disease activity in dogs in a few parts on Ontario at the moment. It’s always hard to say for sure because it’s based on information from different sources, and whether it’s a true increase, an increase in reporting of the normal amount of disease, or just a misperception is hard to say.

We don’t want to over-react, but we also don’t want to miss the start of something important, so we’re paying attention to the information that’s coming in and trying to make sense of it.

An important limitation to the available data is the amount of diagnostic testing that gets done. Only a small percentage of dogs with “kennel cough” get tested to try to determine which viruses and bacteria are actually involved.

Should all dogs with “kennel cough” be tested?

  • No.  Since a lot of pathogens can cause the clinical signs we see with this syndrome and we can’t test for them all, the test results rarely impacts how we treat an individual dog. It’s nice information to have but it’s usually hard to justify the cost for an average household pet. This recommendation is also part of the 2017 ISCAID  treatment guidelines for respiratory disease in dogs and cats.

When is testing more rewarding?

  • Testing is more useful when something is unusual about the scenario or the patient. From the patient standpoint, testing can be more useful when it involves a kennel or shelter, since the result could affect the infection control response. It also can help differentiate “vaccine breakthrough” from the presence of a bug we can’t vaccinate against.
  • By “unusual scenario” I mean something different in the incidence, distribution or severity of disease. If we think we’re seeing more disease, testing is useful to see if disease is mainly caused by one bug, whether we have a mix of causes, or whether the cause can’t be identified (suggesting something different/new might be present).

When do I really want to test dogs with respiratory disease?

  • When I’m concerned about a foreign disease like canine flu, I definitely want to get testing done. Figuring out when to worry about that comes down to two big factors: high attack rates and links to imported dogs, especially from Asia. When most dogs in a group get sick, I worry about something new like flu and want to test them, so that we find out as early as possible if flu is present and we can take measures to contain it, like we successfully did last year. A high attack rate was what led to identification of the biggest flu cluster we had when canine flu hit Ontario in 2018.

So, what about now in Ontario?

  • I’d like more information but don’t have any money for testing, so I’m relying on information that comes in from various sources. It’s always a fine balance between raising awareness and causing paranoia, so it’s important to put things in perspective. We’re on the lookout for respiratory disease in dogs and want to learn more, but we’re far from panicking about the situation.
  • The average dog owner doesn’t need to do anything more than good routine care and using common sense. However, we’d like to figure out if something new or interesting is going on.

More to come (hopefully).

While it was pretty well documented on the Worms & Germs Blog as it was underway, the full story regarding Ontario’s 2018 canine influenza outbreak(s) has now been published in the latest edition of Emerging Infectious Diseases. You can use the link above to access the full report, but here are some highlights.

  • There were 104 confirmed cases. In most outbreaks, we talk about how that’s likely the minority of true cases. However, here, it probably accounts for the vast majority of cases, given the amount of contact tracing and testing that was performed.
  • Transmission occurred in many ways, including while boarding, at a groomer, pack walking, day care, between neighbouring dogs and at a veterinary clinic.
  • High attack rates were common. In an area where flu is not normally present, when it hits, large numbers of dogs can be affected quickly. Large clusters of disease, or situations where most or all dogs in a group develop respiratory disease around the same time, is a trigger for me to test for canine flu. That’s true even if there’s no initial link to imported dogs. One of our large clusters was first identified because of a high attack rate of respiratory disease in a good kennel. The link to imported dogs was only found later.
  • Outbreaks were the result of multiple introductions of H3N2 canine influenza virus into Canada through dogs imported from Asia (China and South Korea).
  • Two dogs died from complications of influenza. Both were older dogs, which isn’t surprising as older individuals are at greater risk of death from influenza, whether they’re dogs with canine flu or people with human flu. One other death was suspected but not confirmed.
  • Some dogs shed the virus for a long period of time. We were able to collect serial samples from a reasonable number of dogs and some shed for at least 20 days, despite looking healthy after just a few days of illness.

The good news is that canine flu was eradicated. Good, old fashioned infection control was the key.  Some astute primary care veterinarians and responsible dog owners who were willing to quarantine infected dogs or facilities (e.g. kennels, groomers) for 28 days played a critical role.

While we were able to eradicate the virus in 2018, we’re under no illusion that it won’t come back. The large number of dogs imported from Asia and the lack of any quarantine or testing requirements for influenza means another outbreak is likely inevitable. However, we’ve shown that even with the introduction of a new virus to a population of dogs with no pre-existing immunity, it can be contained. It takes time, effort and money (and probably no small amount of luck), but it’s possible and worth the effort.

The map below shows the various clusters of H3N2 canine influenza identified in Ontario in 2018.

A recent CDC expert commentary was recently published on “Animal Lovers and Zoonotic Diseases: 5 Things to Know“.  Regular readers of Worms & Germs will find many of the points very familiar, but the article provides a nice summary of some of the recurring themes that arise when dealing with animals and people and the infectious diseases we share.  The article is great reading for healthcare providers (who are in fact the target audience), with some important reminders about the risks of not only direct contact with animals, but also indirect contact and even contact with pet food.  At the very end is a link to a simple but useful 1-page tip sheet on staying healthy around pets.  While certainly not exhaustive, the tips provided are certainly a good start to decreasing some of the infectious disease risks associated with pets.

There have been a few news reports about an apparent increased incidence of the fungal disease, blastomycosis, in dogs in Minnesota. Blastomycosis is an interesting disease with important “One Health” aspects. It’s caused by the fungus Blastomyces dermatitidis, that naturally lives in the soil in certain parts of the world. The risk is highly variable by region, being an important concern in some areas and a non-entity in others… and sometimes those are not too far apart, which can be a big concern for travellers.

Dogs, cats and people are among the many species that can get blastomycosis.  Infection can cause a wide range of problems from severe lung disease to skin disease. It’s actually not transmitted between infected individuals, but finding it an animal (or person) is still relevant to other species, because they’re all infected the same way: from the environment. Since dogs spend more time with their nose to the ground, they’re at greater risk of exposure compared to people. So, dogs can be useful sentinels for human risk. Having a dog with blasto doesn’t mean you’re at risk from the dog, but it means you might have been exposed from the same environmental source. Knowing that can be important, since it might speed up recognition of the disease if you get sick.

Back to the Minnesota situation. A news report indicated there have been 170 cases of blasto in Minnesota dogs. (Presumably that’s a marked under-estimation, since many dogs are likely infected but not tested, as with many diseases.) While year-to-year comparisons can be a bit dodgy, because things like increased awareness can bias the results, that’s a 50% increase from this time last year, and it’s already well above the record of 155 cases set in 2017. Also, unfortunately demonstrating what I described above, there’s another report from Minnesota talking about a man battling life-threatening blastomycosis, a year after his dog died of the disease.

The situation where I live here in Ontario is less clear. We know there are “hot spots” of blasto in the province. However, unlike in Minnesota, it’s not a reportable disease in animals here. So, there’s no easy way to capture data, compare case numbers year-to-year, identify trends and see if the affected areas are changing. Blastomycosis is now reportable in people in Ontario, but the lack of centralized dog data hampers our assessment of the risks and changes to those risks.

We’ve worked periodically to track blasto in animals, and hope to get back to that shortly with our soon-to-relaunch WormsAndGermsMap. It’s all based on voluntary data, so it has some limitations, but it’s better than nothing.


Image of thoracic radiograph of a dog with lungs heavily infected with blasto (from Weese and Evason, Infectious Diseases of the Dog and Cat, A Colour Handbook).