Over a year ago, I wrote a few posts about changes to Clinical and Laboratory Standards Institute (CLSI) veterinary antimicrobial susceptibility testing guidelines. When a bacterium is grown in a lab and tested for susceptibility to different drugs, the lab looks to these CLSI guidelines to determine whether they should consider the bug susceptible or resistant to each drug. That’s critical information for choosing an effective drug to treat a patient with an infection.

In January 2024, some major changes were made to these guidelines, particularly with reporting susceptibility to enrofloxacin and marbofloxacin in Staphylococcus, E. coli (and related Enterobacterales) and Pseudomonas, as well as chloramphenicol susceptibility in Staphylococcus and E. coli/Enterobacterales from dogs.

I was hoping veterinary diagnostic labs would be able to implement those changes fairly quickly. I had a lot of empathy for labs given the challenges of sourcing different testing panels and making a big change to their methods and IT workflow. Some labs made the change fairly efficiently. However, the labs that likely account for the majority of veterinary diagnostic testing in North America still haven’t made the switch.

I’m still empathetic to their challenges, but I’m seeing too many treatment failures because veterinarians are using drugs that the lab reported should work, when in reality the updated guidelines tell us the won’t (or we can’t interpret the test results properly because of what they tested or reported). That’s a problem, and I have no doubt that animals have died because of it.

So, in addition to my detailed posts from last year about the CLSI breakpoint changes, here’s a (hopefully) quick and easy reference for interpretation of bacterial culture and susceptibility test results:

test

I get variations of this question not uncommonly from veterinarians:

A client just came in and said they/their kid was diagnosed with Dientamoeba fragilis infection and their physician said to test/treat their dog. What should I do?

On one hand, it’s nice to see physicians thinking about animal exposures. On the other hand, it sometimes ends up with the physician making a testing or treatment suggestion (or directive) for an animal that doesn’t make sense (or at least needs to be considered with a lot more nuance).

Here’s the basic need-to-know about D. fragilis:

  • It’s a microscopic, protozoal parasite that lives in the large intestine. It’s shed in feces, and people get infected through fecal-oral exposure (aka eating poop, albeit in minute quantities).
  • It’s found in humans worldwide, and people are its normal host. Compared to many other intestinal parasites, it’s actually fairly common in people even in high-income countries. For example, a study of children in Toronto daycares found that 8.6% were shedding the parasite, along with 4.0% of the daycare workers (Keystone et al. 1984).
  • Many, if not most, people carrying this parasite in their intestine are healthy. It’s role in causing disease (if any) isn’t clear. If it does cause any illness, it’s pretty non-specific things like diarrhea, abdominal pain, nausea, fatigue and loss of appetite.
  • It’s been found in a few animal species, including non-human primates (e.g. gorillas), budgies and pigs. However, it seems rare and data are quite limited.

One study (Chan et al. 2016) reported finding D. fragilis using PCR in a single dog and a single cat . Whether the dog and cat were truly infected or the test just cross-reacted with a different protozoan isn’t clear. If it was true infection, the low prevalence in dogs/cats compared to humans and the lack of evidence that infected dogs/cats have much of a parasite burden make it pretty unlikely that dogs/cats are a significant source of human infection. The aforementioned daycare study from Toronto (Keystone et al. 1984) reported an association between the parasite and cat ownership, but it’s far from certain that there was any causal relationship; the analysis was pretty basic and the relationship between cat ownership and other identified risk factors wasn’t explored. (The authors indicated that the association could have even occurred by chance.)

I would consider D. fragilis a parasite that’s not normally found in dogs and cats, and is not well adapted to them if they are exposed. If a parasite infects people and is shed in feces, there’s a reasonable chance dogs and cats would be exposed (one way or another), but not necessarily that they’d get infected. Even if infection did happen, it could very well be at such a low level that transmission wouldn’t occur (i.e. a dead-end infection).

At most, dogs and cats are rarely infected with D. fragilis, and there’s no evidence that they’re infectious to people. I never say never with diseases that we haven’t studied much but, it clearly spreads quite commonly human-to-human, so pets are not likely to play a relevant role in the transmission cycle. If anything, the risk is human-to-pet transmission, not the other way around. 

Can we test pets for D. fragilis, if requested?

Routine fecal flotation would detect this parasite if there was a reasonable burden. PCR could also be used, but there are no commercially available tests for animals (although a human PCR test would presumably work – but few human labs will accept diagnostic samples from animals).

Should we test pets for D. fragilis, if requested?

The key question for me with any test is, “what would I do with a positive vs a negative result?”

If a pet tests positive for D. fragilis, I’d say “Interesting. Your dog presumably got this from you or another person with whom you have contact. Odds are really low that the dog will infect anyone. It’s a don’t-eat-poop disease, so let’s just focus on basic hygiene and safe fecal handling, and it will go away on its own.“

If a pet tests negative for D. fragilis, I’d say “It’s probably negative, but testing isn’t 100% sensitive. Regardless, we don’t want you to give it to your pet and we don’t want your pet to give you any of the many bacteria and parasites that might be in its intestine, so let’s just focus on basic hygiene and safe fecal handling.”

Not a lot of difference either way.

Should we just treat pets for D. fragilis is someone in the household has it? 

If I had to treat a D. fragilis infection in a dog – where we found the parasite AND had reason to believe it was causing disease (both pretty unlikely) – I’d most likely use metronidazole. If the parasite isn’t causing disease I’d want to avoid using an antibiotic like that, because it’s not an innocuous drug and it will negatively impact the dog’s normal intestinal microbiota, potentially for weeks.

Time is the cheapest, safest and ultimately most effective treatment in a healthy dog that happens to be infected with this parasite. More than that though, if people in the house are infected, they’re better off focusing on their hygiene (i.e. not eating poop) and eliminating their own infection, rather than worrying about the pets.

test

We don’t talk a lot about antiviral resistance in animals, particularly compared to antibacterial resistance, primarily because we don’t use antivirals a lot in animals – but we do use some.

When we use any anti-infective medication, we have to think about the risks of resistance developing to that medication, and how we can try to optimize use in order to maximize clinical benefits while minimizing resistance risks. I say “minimizing,” not “eliminating,” on purpose, because we can rarely guarantee that there will be no risk. Usually we’re aiming for a risk that is low enough to justify use of the drug, and ideally we can lower that risk even further through some basic infection control practices.

I’ve written a lot over the last year about antivirals for the treatment of feline infectious peritonitis (FIP) in cats, since we now have incredibly effective options (now in Canada) for what was previously an almost invariably fatal disease. The antiviral drug GS-441524 (a relative of the COVID-19 antiviral drug remdesivir) is what we can now use in most regions to treat this disease. It’s a complete game changer.

However, anytime we have a revolutionary new anti-infective (be it for bacteria, viruses, parasites, fungi or other nasties), we need to take steps to try to maintain its effectiveness long term – primarily through good antimicrobial stewardship.  

Are there scenarios where GS-441524 resistance could emerge in cats and be a problem? Yes.

Does our routine treatment of FIP pose much of a risk for emergence of antiviral resistance? No.

Those statements seem to conflict, but let me explain:

Feline infectious peritonitis is caused by feline coronavirus (FCoV), whichbis very common in cats, especially especially cats living in large groups. It infects the intestinal tract and then cats shed it in their feces, usually with no signs of illness The virus is spread cat-to-cat through fecal-oral exposure. The clinical disease (FIP) develops when an intestinal-dwelling FCoV mutates into a tissue-infecting FIP virus (FIPV) within that cat.

While FCoV is highly transmissible, FIPV is not traditionally considered to be transmissible between cats (though I’m not sure we can actually say there’s no risk of transmission; I think there is some cat-to-cat transmission risk, but it’s probably very low).

Antiviral resistance can emerge when a virus is exposed to an antiviral. Random mutations occur that allow viruses to resistant the action of the drug, and then the mutated virus multiplies while the susceptible version may die out. The key is what happens next, and that varies a lot depending on the disease.

A critical component of the risk assessment for GS resistance is that is that we don’t consider FIPV to be transmissible (or at least we consider it really rarely transmissible). So if GS resistance develops in a cat with FIP, while it could be very bad for that cat (because the infection won’t respond to the drug), the odds of that cat transmitting the resistant virus to another cat are very low, so the resistant virus would likely die out with the first host.

The main concern is if cats with intestinal FCoV infections are treated with GS, then resistance could develop in FCoV in the gut of a cat, and that resistant virus would be shed in feces and be transmitted cat-to-cat (like FCoV normally is) through the cat population. Then, if any of those cats develops FIP, the virus would already have GS resistance and wouldn’t respond to treatment.

That means that appropriate treatment of cats with FIP poses an exceptionally low risk of causing resistance issues. For there to be a significant problem, it would require rare cat-to-cat transmission of FIPV (or emergence of resistance of FCoV from a concurrent, unrelated FCoV infection in the intestine). The benefits of treatment massively outweigh this small theoretical risk.

Empirical treatment of cats for FIP (without a solid diagnosis) is also generally low risk of resistance. If the cat doesn’t have FIPV or FCoV, there’s no risk. It’s not like the situation with bacteria where there’s always a massive and diverse pool of bacteria in the body that could develop resistance through exposure as “bystanders” and where resistance genes can then be transmitted between different bacteria. If the cat doesn’t have FCoV or FIPV to start, it can’t develop resistant FCoV or FIPV. The only risk would be (as above) if there was a concurrent incidental intestinal FCoV infection.

Does use of GS in cats with enteric FCoV pose a risk of resistance? That’s a big “hell yeah!” from me. We don’t have data to prove it, but the last thing I want is to be treating lots of cats with highly transmissible enteric FCoV infections, because spreading resistant FCoV through the cat population is how we end up with a lot of dead cats from resistant FIP.  The cost-benefit just doesn’t add up in this scenario. Enteric infections are mild or cause no disease at all, and we are not going to eradicate FCoV from the overall cat population, or likely even from a local cat population (e.g. cattery), using antivirals (the virus is just too common and transmissible to be thinking about eradication). So we’re talking about treatment with little to no clinical benefit and no eradication benefit, while posing significant risk of selecting for resistance to a game-changing drug that is currently saving countless feline lives. That makes no sense to me.

Are there any human health issues related to use of GS in cats?

GS is related to remdesivir, a drug used to treat COVID-19 in people, but transmission of antiviral resistance from FCoV to SARS-CoV-2 isn’t a risk. The only theoretical risk would be if a cat had FIP AND a SARS-CoV-2 infection at the same time, AND resistant SARS-CoV-2 emerges in the cat during treatment AND the cat then infects a person with it. That’s a really unlikely scenario, so the risk is negligible compared to risks from direct use of remdesivir in humans.

Use as little as possible but use enough. That’s my line for antibiotics, and it applies equally well to antivirals. We don’t want to miss treatment opportunities, but can’t be reckless either and jeopardize this incredible new opportunity to be able to treat this terrible disease.

Details have now been released about the information that was briefly posted then removed from the US CDC website a couple weeks ago regarding suspected household transmission of H5N1 flu to and from cats. It’s great to have more details, but (as is common with emerging diseases) the full story probably raises more questions than answers. The gist of the story is similar to what we inferred from the leaked information, but the full report is now available online (Naraharisetti et al. MMWR 2025), and includes some useful details. Here’s the more complete rundown:

Household 1

  • This household contained 2 adults, 2 kids and 3 indoor cats. One of the owners worked on a dairy farm that was not known to have infected cattle, but there were infected farms in the area.
  • Cat 1: One of the adult indoor cats developed loss of appetite, lethargy and disorientation, then worsening neurological signs.  After a few days, she was euthanized because of rapid and severe disease progression. H5N1 influenza virus (genotype B3.13) was detected in the cat’s nasal passages and brain tissue; this is the predominant strain currently circulating in US dairy cattle. 
  • Cat 2: One of the other cats then developed signs of respiratory disease four days after the first cat got sick – that timing is generally consistent with what we’d expect for transmission of a flu virus. The owner was asked to collect a nasal swab from the cat because it was too sick to be taken to a veterinary clinic, but this wasn’t done. Fortunately, the cat recovered after 11 days.
  • Cat 3: The last cat just watched everything unfold and appeared healthy the whole time.

The household investigation:

The owner who worked on the dairy farm didn’t have direct contact with cattle. He reported that he took off his farm clothes and boots when he returned home and that they were stored in an area that the cats could not access. The cats were not fed a raw diet or raw milk.

One of the kids had mild upper respiratory tract disease (cough, sore throat, headache and muscle pain) six days after the cat got sick. The other kid had a dry cough around the same time that was attributed to allergies. 

Eleven days after Cat 1 got sick, samples were collected from three of the people in the household. That’s a bit later than ideal, but still reasonable (logistics often dictate when samples can be collected). All the people tested were negative for flu. The sicker kid had a positive test result for rhinovirus/enterovirus, which could explain the illness, but it doesn’t rule out flu completely. 

Unfortunately, the person who worked on the dairy farm declined to submit a sample. He reported a day of vomiting and diarrhea before Cat 1 got sick… Was that potentially related to flu infection? Maybe, since flu can cause gastrointestinal disease, but it’s far from classic, and most that episode was unrelated. The unanswered question is whether the person had a mild or asymptomatic H5N1 flu infection and was responsible for infecting the cat(s).

The people who were tested for flu also got oseltamivir prophylaxis (antiviral medication) because of their close contact with the infected cat (and potentially the initial source of the virus in the household…); the farm worker declined prophylaxis.

Putting Household 1’s story together:

  • The most likely source of H5N1 flu exposure of Cat 1 was the farm worker. Whether he unknowingly tracked the virus home from the farm or whether he had a mild infection that he transmitted to the cat can’t be discerned, but that’s a really important thing to figure out in future cases.
  • It would also be really useful to know if the farm where the person worked had confirmed H5N1 flu in the cattle. Hopefully follow up testing of the cattle was done. If flu wasn’t present, that raises more concerns about how the farm worker might have gotten infected, or if the farm worker was not the initial source in the household, then how did an indoor cat with no other apparent risk factors get infected? 
  • It’s unclear whether there was cat-to-cat transmission of flu. Spontaneous, transient upper respiratory tract disease is uncommon in adult indoor cats. Maybe stress caused a recrudescence of feline herpesvirus infection in Cat 2, but it sounds like the cat was a lot sicker than we’d expect for that. We therefore have to consider Cat 2 to be a strong flu suspect; based on the timing of illness relative to Cat 1’s illness, if it had flu, it presumably got it from Cat 1.

Ideally, serological testing would be performed to detect anti-H5N1 antibodies in blood from individuals (cats and people) in the household, to determine which individuals ultimately were infected, even though serology can’t tell us the when or how.

  • If the farm worker was seropositive, it still wouldn’t tell us if they infected the cat directly or if the cat was exposed to virus on clothing or other fomites (though the former seems more plausible, and would be concerning). If the farm worker was seronegative, that suggests that clothing or fomites was the source (which is a good reminder of why infection control measures like wearing and changing personal protective equipment are so important).
  • If Cat 2 was seropositive, that doesn’t confirm cat-to-cat transmission, though that would still be most likely.
  • If the kids or other adult were seropositive, then there was almost certainly either cat-to-human or human-to-human transmission, neither of which would be good news.

Household 2

This household consisted of a dairy worker and two indoor cats. It’s not clear whether the person had contact with cattle, but he collected raw milk from farms and reported being frequently splashed with milk. He didn’t remove his work clothing before returning home, and one of his cats liked to roll on his work clothes (that were presumably contaminated with milk).

  • Cat 1: The worker’s six-month-old indoor cat was taken to a referral veterinary hospital with a one-day history of progressive neurological disease. It was seriously affected and died in hospital within 24h. H5N1 influenza virus (genotype B3.13, the dairy-associated type) was confirmed in this cat. Whether it was a coincidence or not, this was the cat that liked to roll in the work clothes.
  • Cat 2: The other cat remained healthy, and swabs collected from this cat the day after Cat 1 got sick were negative for flu. 
  • The worker reported signs of eye irritation that began 2 days before Cat 1 got sick. The person was not tested and declined antiviral treatment. So we don’t know if the person had H5N1 flu, but eye inflammation is consistent with the conjunctivitis seen in other human cases of H5N1 infection in the US in the last year, and would be a likely presentation in someone getting splashed in the eyes with influenza-contaminated milk.

There was little further follow up because the owner shut down contact with public health officials, stating a fear of losing his job. 

As with Household 1, timing of sample collection is always a challenge. While we’d ideally get serial samples over time, it’s simply not possible in many cases. Testing Cat 2 at the start was logical and useful, but if there was cat-to-cat transmission, that was probably too early to test. We’d need at least one more sample a few days later to account for the incubation period if Cat 1 infected Cat 2. The initial sample only tells us that Cat 2 likely wasn’t exposed at the same time as Cat 1.

It’s also hard to say if the owner had H5N1 flu or if his clothing was the source of virus for Cat 1. Ideally they could have done serological testing after the fact to confirm whether or not the person was infected, but it doesn’t sound like the person would have been willing to come back to provide a blood sample.

What about the veterinary staff involved in these cases?

Twenty-four (24) veterinary clinic personnel were potentially exposed to the two confirmed H5N1 flu-infected cats from the two households, 18 of which were contacted and monitored for signs of flu. They were all deemed to have had limited exposure. Hopefully that’s a win for routine infection control practices and quick identification of higher-risk situations warranting use of enhanced personal protective equipment (PPE). Because they were all deemed low risk, they were not offered antiviral prophylaxis. Seven individuals reported signs or symptoms of illness after exposure, of which five were tested for flu, and all were negative.  

To sum up:

  • Was there direct human-to-cat transmission of H5N1 influenza? Maybe.
  • Was there direct cat-to-cat transmission of H5N1 infleunza? Maybe.
  • Was there transmission of H5N1 influenza via contaminated clothing? Maybe.

Unfortunately, we need to learn more about transmission by investigating disease events. It’s almost certain there are undiagnosed infections, and maximizing our recognition of H5N1 flu spillovers between species (including humans) is critical, as it helps inform proper care and management of people and animals (including antivirals, when indicated) and helps us figure out transmission patterns and risk factors to prevent more infections. The more we understand this virus, the better we can control it, all the while trying to walk that ever-changing fine line between protection and practicality.

If I asked 100 random people on the street “should we be giving antibiotics to healthy animals?” I’m pretty sure most or all of them would say “no.“

That makes sense in a lot of ways. We should save antimicrobials to treat sick individuals (especially people), and we shouldn’t use antimicrobials in healthy individuals… except when we should.

If I asked to the same 100 people “Should your dog get an antibiotic if it eats something it shouldn’t have, and then needs to have surgery to open up the intestines to remove the object?” I’m pretty sure most would say “yes!” – even though that dog doesn’t have an infection. That’s prophylactic use of an antimicrobial.

Like most things in the antimicrobial resistance (AMR) space, this issue of prophylaxis is complicated and messy. Too often, the sound bites we hear about approaches to antimicrobial use (AMU) in animals miss the nuances and complexities that play a huge roll in the necessary discussions. 

  • We don’t want to overuse antimicrobials.
  • We don’t want to use antimicrobials unnecessarily.
  • We don’t want to use antimicrobials to compensate for poor animal management or lack of veterinary care.
  • But, there are situations where antimicrobial prophylaxis makes sense and logical prophylaxis can improve animal health and animal welfare, and reduce the need for therapeutic use of antimicrobials (that might be higher tier drugs) with limited risk.

There’s always some risk with the use of antimicrobials in any animal or person, but part of optimizing antimicrobial stewardship (AMS) is using them when we should, and avoiding them when we shouldn’t. Use antimicrobials as little as possible, but use enough.

Because we keep running into the same misconceptions and misunderstandings about AMR and AMU at various levels (including high level international discussions) we teamed up with the World Organization for Animal Health (WOAH) and the quadripartite‘s AMR Multi-stakeholder Partnership Platform to write a primer on antimicrobial prophylaxis in animals. The document discusses when antimicrobial use is bad, when it’s clearly indicated, and a few levels in between.

Prophylaxis can include scenarios such as:

  • Routine administration of antimicrobials to groups of animals in the absence of evidence of need, largely because of historical practices. 
  • Routine administration of antimicrobials for a prolonged period of time to a group of animals because of a high endemic rate of a specific disease in the group.
  • Routine administration of antimicrobials to most or all animals at a specific stage in life or production to reduce a specific disease or syndrome (e.g. tetracycline treatment of pigs at the time of weaning to prevent post-weaning diarrhea, administration of intramammary antimicrobials to dairy cattle at the end of lactation to prevent mastitis, tetracycline with ITM vaccination for prevention of East Coast fever).
  • Targeted administration of antimicrobials to a group of animals in response to a specific, defined disease threat that is known to be mitigated by antimicrobial prophylaxis.
  • Administration of antimicrobials to a specific animal at a specific and well-defined high-risk time (e.g. peri-operative antimicrobial prophylaxis for prevention of surgical site infection).

Some of these are good uses of prphylaxis, some are bad, and some are situational. But it shows the wide range of possible prophylaxis scenarios. We need to make sure we use antimicrobials when they are needed, but not prophylaxis as an excuse to overuse them or try to avoid scrutiny. It can be challenging to have discussions about why we need prophylaxis when some people think we’re just being apologists for the agriculture industry.

Do we need to improve antimicrobial prophylaxis?  Yes, especially in agriculture.

Can we massively reduce antimicrobial prophylaxis without negative impacts on animals? Yes, if we do it right, and if we do the other things we should be doing to prevent infections and optimize animal health.

Do we need to use some antimicrobial prophylaxis in animals? Yes, but we need to find that “use as little as possible but use enough” sweet spot. That’s not easy, but it’s clear we can reduce what we currently use a lot.

We need to have informed discussions about prophylaxis, not dogmatic debates with “all prophylaxis is bad” as an entrenched starting point. 

The Washington State Department of Agriculture and the Oregon Department of Agriculture have issued a public health alert because of H5N1 influenza virus contamination of another brand of raw pet food, following the deaths of two more indoor cats from separate households linked to consumption of the pet food.

Details are sparse, but both cats were euthanized due to severe disease from H5N1 influenza. Authorities tested the cats and the food from open containers in the household as well as unopened food samples, and found H5N1 flu virus in all of them. This shows that the food was truly contaminated at the source, and removes the potential that the food got contaminated in the household by the cats or some other source. (In a previous raw food-associated cluster of H5N1 flu infections in cats, the manufacturer of the implicated food tried to suggest the diet was contaminated in the household and was not the source of the virus, which was a very weak argument, and definitely not the case here based on the additional testing).

The recall involves Wild Coast LLC Boneless Free Range Chicken Formula, lots 22660 and 22664, Best Buy day 12/25. However, given that we have multiple instances of fatal raw poultry associated H5N1 infections in cats from multiple companies, the risk probably extends beyond this product.

To avoid the risk of H5N1 influenza from raw pet foods:

  • If raw diets are to be fed, use a non-poultry based diet, and choose one that’s high pressure pasteurized to reduce (though it will not eliminate) the risk.

Image from https://agr.wa.gov/lookuptypes/recallfile/131

I think it’s fair to say H5N1 becoming seemingly endemic in US dairy cattle in the past year caught us off guard. The virus has spread widely within and between US dairy herds, has caused mild infections in a number of people in close contact with infected cows, has killed a lot of cats on farms (and a few from drinking raw milk from infected cows)… and it isn’t likely to go away any time soon. 

Dairy veterinarians are one of the higher risk groups for exposure from infected cattle because of their close and frequent contact with these animals, particularly when cattle are ill. Surveillance testing of people at high risk for exposure to H5N1 influenza can help us get a handle on how much (if any) under-the-radar cow-to-human transmission may be happening, so it was great to see the release of the results of just such a surveillance study in dairy veterinarians in the US (Leonard et al. MMWR 2025).

In this study, researchers tested blood samples from 150 veterinarians with cattle contact and tested them for antibodies against H5N1 influenza. The presence of antibodies would indicate previous infection, whether or not the person was ever sick from the virus.

Three of 150 (2%) dairy veterinarians were positive for H5N1 flu antibodies, but none of those reported having had signs of illness that could have been attributed to flu, and none reported working with dairy cattle that were known to have been infected with H5N1 flu. If that’s accurate, it could indicate a few things, including possibly:

  • working on farms where there was mild disease in cattle from H5N1 flu that was not recognized
  • working on farms where there was disease in cattle from H5N1 flu but the cattle were not tested for it
  • veterinarians were exposed to H5N1 flu in some other way from animals or the environment, such as through contact with other animals or raw milk. (One of the veterinarians who tested positive also had contact with infected poultry, so that’s another potential source of exposure)
  • veterinarians were exposed through unrecognized human-to-human spread of H5N1 (which would be the most concerning possibility)

One of the seropositive veterinarians worked with dairy cattle in Georgia and other cattle in South Carolina. Neither of those states is known to have H5N1 in dairy cattle (see map above from the report), but the degree of surveillance and (more importantly) reporting is variable across the US. This would suggest that testing of cattle in Georgia needs to be ramped up to see if they have unrecognized infected herds.

All three antibody-positive veterinarians “reported wearing gloves or a clothing cover when providing veterinary care to cattle (including a variety of clinical activities, such as pregnancy checking or surgery)”. That’s strange wording, since those are two distinctly different types of PPE. Virtually every dairy veterinarian is going to wear coveralls (a clothing cover) on farm, so that stat tells us nothing about how many of them wore gloves (nor whether glove use may have been suboptimal, as it often is on farm). There was no use of eye or respiratory protection, which is far from surprising and something the veterinary profession needs to improve, as we do a poor job of using respiratory protection and rarely use eye protection when we’re dealing with animals with respiratory infections, even when they could be zoonotic.

The fact that all three antibody-positive veterinarians reported no obvious consequences of H5N1 flu infection is good news on many levels. However, asymptomatic infections raise some concerns, since if people are asymptomatically infected but still infectious, it may allow the virus to spread silently through the population, at least for a while. We have no idea if infected people shed the virus at levels that can infect others, but it’s something for which we need to be on the look out.

Any H5N1 flu infections in a person is bad, because of the potential for severe disease in the person and, even more importantly, the potential for evolution of the virus to transmit more easily among people. The more H5N1 encounters humans, the more opportunity it has to become adapted to humans. Infection of people concurrently infected with human flu virus strains creates opportunities for recombination of both viruses, which can lead to rapid and significant undesirable changes and emergence of new strains.

This is far from a doomsday report, but it highlights some things that we need to keep watching. It also shows why we need more effort to contain the spread of H5N1 flu in domestic animals. The data here are a bit limited, but they’re an important step in our understanding of this virus. A parallel study of the general population would complement these data, as would more focused study of veterinarians and farmers from affected farms, and veterinarians working with other species.

The more H5N1 influenza continues to circulate in wild and domestic birds around the world, including here in North America, the more we have to be concerned about exposure of pets to H5N1 influenza through raw food diets. Recent documented infections in cats fed raw meat from infected birds have highlighted these concerns. For more information on the risks of H5N1 influenza from raw diets for pets and associated risk reduction measures, check out the latest quick podcast on Worms&GermsPod.

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

Back in March 2024, I wrote a post about a systematic review of the efficacy of antibiotics and probiotics and the associated treatment guidelines for acute diarrhea in dogs from the European Network for Optimization of Veterinary Antimicrobial Treatment (ENOVAT). Now, we have an ENOVAT/WSAVA infographic to put all that into a (hopefully) quick reference for veterinarians.

While we’ve historically used antimicrobials like metronidazole by rote to “treat” acute diarrhea in dogs, a lot of dogs were probably getting better despite what we were doing rather than because of it. Antimicrobials are needed in dogs with severe disease, but that’s to target systemic infection in those cases, not necessarily what’s going on in the intestine.

It’s pretty straightforward, as the infographic shows:

  • Dogs with mild diarrhea: no antimicrobials needed, just basic supportive care like a GI diet.
  • Dogs with moderate diarrhea: fluid therapy first, and if that resolves the systemic signs then no antimicrobials required. If signs persist that might be attributable to sepsis, then it’s considered severe and systemic antimicrobials are warranted.
  • Dogs with severe diarrhea and systemic illness: systemic antimicrobials are warranted.

The standard disclaimer is that guidelines are meant to cover most cases, but there can be nuances to individual cases that indicate the need for a different approach. That’s fine, but we still want to try to use an evidence-based approach as much as we can to determine the default treatment.

Of all the guidelines with which I’ve been involved, this one is by far the hardest to get people (including veterinarians and pet owners) to accept, since we are so conditioned to treating diarrhea with antibiotics. We do it because we’re risk averse, because it’s habit, and because we are conditioned to want to do something – even when there’s no evidence that the something is useful. A large percentage of the metronidazole that is used in dogs is psychotherapeutic… for the pet owners and veterinarians, because it makes the people feel better, but not the dog. In fact, those antimicrobials might actually make the dog feel worse.

We’ve made big strides in veterinary antimicrobial treatment guidelines in recent years, and this is one more step in the right direction, but we still have a long way to go.

test

H5N1 influenza has been widespread is US dairy cattle for close to a year, so you might wonder why a recent report of H5N1 in dairy cattle in Nevada is garnering extra attention. Well, it all comes down to the strain. TLDR:

H5N1 influenza isn’t one specific virus. There are already numerous known subtypes and new ones continue to emerge. The “dairy strain” that’s spread among US dairy cattle is called clade 2.3.4.4b, genotype B3.13. 

Finding the B3.13 strain in cattle in Nevada wouldn’t have been surprising, but multiple herds in Nevada tested positive for a stain of H5N1, subtype D1.1. This “new kid on the block” is a recombination of one of the H5N1 strains that moved from Asia to North America in late 2021 and early 2022 and a low pathogenicity avian flu strain that was already present in birds in North America. It was first identified in September 2024 and has now emerged as a dominant strain in wild birds (and spillovers into poultry). 

The first detection of the D1.1 strain in Nevada cattle was from samples collected January 6 and 7, 2025, so (as is typical) we’re playing catch-up. It will be important to see if these farms are linked, and whether there are other affected farms. It will also be important to see if shedding patterns (lots of virus in milk, little in respiratory secretions) and virulence in cats on these farms (lots of dead cats) are similar to B3.13. Obviously the risk to humans must also be tracked(more on that below). 

This is a noteworthy event because it represents a new spillover into cattle from wild birds. Infection of a single cow wouldn’t be too remarkable, since rare spillovers to mammals are expected given how widespread the virus is in birds. However, infection in multiple cattle on multiple farms suggests either effective bird-to-cow transmission on multiple different premises, or another single bird-to-cow spillover that has subsequently been spread cow-to-cow and farm-to-farm like B3.13.

Another concern is the potential for more severe disease in people. Human infections with D1.1 have been previously identified in people who were depopulating infected poultry farms. They had mild disease, like most of the human H5N1 flu spillover infections in the North America to date. But D1.1 is the strain that was involved in a fatal H5N1 flu infection in a person in Louisiana, and that caused very severe disease in a teen from BC. On one hand, we can say any H5N1 strain can cause severe disease under the right circumstances and maybe those were just rare events. On the other hand, those two severe infections show that we can’t sit back and just say but human infections are always mild. When something spreads widely, rare events become more common, so we can’t ignore them. It also raises concerns about what could happen if this strain becomes better able to spread human-to-human. A more transmissible strain that can cause severe disease in people is the big concern.

Highlighting these concerns, a human infection has already been linked to these Nevada dairy cattle. Fortunately, the person had mild disease (conjunctivitis), akin to what’s been seen in dairy workers with B3.13 infections. Still, it shows that this strain also poses a risk to people who work with infected animals. 

There’s also a concern about evolution of this virus in cattle, even over this short timeframe. The Nevada cattle D1.1 strain has already acquired one mutation (PB2 D701N) that makes it more able to infect mammalian cells. Lots of things still have to happen to make this a mammal-adapted virus, and even more for it to become an effective human pathogen, but this is a potential step in that process. Spillover into farm workers raises the stakes further, since any new infection of a person increases the likelihood of human adaptation or, worse, recombination with a human flu virus in someone coinfected with two flu strains at the same time (e.g. H5N1 and a human seasonal flu). A recent CNN article has a nice description of some of the issues related to the H and N changes in these H5N1 subtypes.

More information about the effects of this “new” strain on cattle is also needed. It’s reported that the cows were not obviously sick when the positive results were first obtained as part of a state screening program, but that disease subsequently occurred. That might suggest that disease is mild and only found when someone is really looking for it, or that they just picked up these infected farms very early with their surveillance program. The US recently started a national Milk Testing Strategy surveillance program, which should help detect problems earlier. We’ll also need more information about the spread of this strain within farms and whether it’s spreading between farms (and if so, how). 

The sky is not falling, despite some social media reports, but it’s another concerning development. The more this virus infects mammals and spreads between mammals, the more risk to humans and domestic animals. Surveillance is a key part of our response but there also needs to be a concerted effort to limit mammal-to-mammal transmission and exposure of people to infected animals. 

From a Canadian context, this highlights a few things too. We can’t just focus on preventing H5N1 flu in dairy cattle through movement of cattle from the US. If D1.1 can move from birds to cattle in Nevada, it can do it anywhere.

We have to maintain a robust milk surveillance program to identify early incursions of this virus. We also have to be ready, able and willing to act decisively if/when H5N1 flu is identified in dairy cattle in Canada. That doesn’t mean culling cattle, but it does mean using strict controls to prevent farm-to-farm spread, and reduce the risks to humans on farms.