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It’s fair to say that raw pet foods have clearly been source of H5N1 influenza infections in cats, some of which have been fatal – even though sometimes it’s impossible to make a definitive link between the food and infection because of when and how the infection occurred, and what could or could not be tested in timely manner. Sometimes raw pet food companies and their supporters use that missing link as a way to claim that there’s no risk or that the risk is overblown. Confusing (and let’s just say “opportunistic”) communication around test results also adds to consumer confusion – for example, understanding the meaning of “non-negative” test results.

The two most common ways in which the term “non-negative” is used with regard to test results are:

  1. Borderline positive: The test result was not quite strong enough to say it’s positive, but there’s a strong enough signal to make us very suspicious that there’s something there (i.e. the virus of interest). Since we can’t call it a positive or a negative, “non-negative” indicates that the sample could be positive, but we can’t say for sure.
  2. Reportable disease that requires government laboratory confirmation: For some diseases (usually really important ones, like reportable diseases), only the government lab gets to have the final say on the test result. If another diagnostic lab gets a “positive” result (even if it’s a really clear positive), they’re only allowed to call it “non-negative” until the result is confirmed by the government lab. That might mean running the same test, a similar test, or a complementary test. Sometimes, that confirmatory test might actually be less sensitive (i.e. less able to detect a positive), but is nonetheless the test used to provide the definitive answer to determine what response is required.

When we were doing our SARS-CoV-2 surveillance of pets in households with people with COVID-19, we had a few results that were positive/non-negative in our lab but were very close to the cut-off level, and were ultimately just below the cut-off at the federal lab. Those had to be called negative, even though we were pretty confident the virus was present in those animals, such as when we had a clearly positive dog (confirmed by the federal lab) and a non-negative dog in the same household. Odds are very high that the second dog with the borderline result was just shedding less virus than the first dog. But I digress…

Savage Cat Food has issued a recall of some of its raw chicken diets (lot code/best by date 11152026) following infections that were linked to the food and “non-negative” test results for H5N1 flu. . The food was distributed to California, Colorado, New York, Pennsylvania and Washington (not Canada).

  • In February, the company was made aware of a cat in Colorado that developed H5N1 flu and that had been fed their food. The cat fortunately recovered.
  • Sealed packages of the food were sent to the Colorado State University Laboratory and were tested “non-negative” by PCR for H5N1 flu.
  • A sample was then sent to the National Veterinary Services Laboratory in Ames, Iowa for virus isolation testing, which was negative. However, virus isolation is less sensitive than PCR, so PCR positive/virus isolation negative results can definitely occur with a contaminated sample, especially as flu virus is likely to die over time sitting in the food (virus isolation requires the virus to still be viable, whereas PCR can detect “dead” virus).
  • While this was being done, the manufacturer contacted retailers to have them pull the product from shelves.
  • A week after the negative virus isolation result was obtained, the company got a report of another cat with H5N1 flu that had eaten the same lot of food – in New York.

Some people will point to this and say “there’s no definitive proof” that the cats were infected by eating the food. Yes, that’s true, it’s not definitive, but it’s still solid. If they are able to sequence virus from both cats (meaning they find the same virus in two cats from two different states that were fed the same diet that had a PCR positive result) that makes it an even more solid presumptive link. If they are testing other food samples and get a positive, or even just more non-negatives, it reinforces the link further. If they are able to sequence the same virus from the food as they found in the cats, that would essentially be a slam-dunk.

The pet food company has a pretty straightforward influenza alert link on the home page of their website. They’re not saying the food was contaminated, since they indicate it tested negative at the Ames lab, but they are also (unlike some others) not trying to downplay the risk or deflect, so I give them credit for their response. (That said, I still take issue with various statements in their their general FAQ about food safety.)

This company does not high pressure pasteurize their diets. On with website, they say “No, our cat food is not subjected to High Pressure Processing (HPP). HPP can damage helpful bacteria and can change the taste and texture of foods, often times making it unappealing for cats.” That’s likely a big risk factor for why the food is contaminated and why these cats got sick. High pressure pasteurization isn’t perfect, but it’s a good tool to reduce contamination and (despite what the website says) there’s no real argument not to high pressure pasteurize raw pet food, especially high risk poultry-based diets.

The response of raw pet food companies to H5N1 influenza has been really variable.

  • Some have taken it seriously, talked about their risk reduction plans, and not tried to deflect.
  • At least one has started cooking their poultry diets.
  • Some have deflected and tried to downplay any risks.
  • Some are not saying anything.

Hopefully more of these companies are exploring high pressure pasteurization as a risk reduction (though still not risk elimination) method for customers who are still intent on feeding raw diets to their pets.

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A recent opinion article in the Washington Post about how to protect cats from H5N1 influenza includes some good considerations, but alongside some bad information. It’s prompted me to write a bit about pet food preparation and how it does (and does not) affect the presence of infectious pathogens (but please keep in mind while reading this that I’m an infectious disease veterinarian and not a food safety specialist!).

In the article, there’s a statement from a professor at a school of public health who said they were avoiding canned pet food “…largely because the pet food industry is not as closely regulated as the human food industry,” …Coleman has not been giving her cats canned food, as it might contain unpasteurized milk. Kibble, on the other hand, is heated at very high temperatures, which, like pasteurization, would kill H5N1.”

However, canned pet food is actually likely the lowest-risk form of pet food when it comes to pathogens. Processing conditions are very different for different forms of pet food, and the processing significantly impacts pathogen survival:

Canned pet food

These diets are heated to high temperatures (235F/115C or above), akin to sterilization. If it wasn’t, cans would spoil quickly and often explode because canned food is otherwise a great culture medium for bacteria. Canning will absolutely kill H5N1, full stop. No question, no concerns. Move on please.

Kibble / dry pet food

These diets are also thoroughly cooked prior to being made into kibble. The temperatures used are not standardized, but are well above the recommended temperature for cooking poultry (165F/74C). Heat is also generated during extrusion process (forming the food into kibble) and desiccation (being dry food) will also decrease pathogen survival. The food isn’t sterile, but as long as the finished product is kept away from raw ingredients (a pretty standard food safety step), I have no concerns about flu contamination in dry kibble.

Lightly or gently cooked diets

These diets are in the grey zone. They’re marketed as diets that are cooked but are not to the same extent as kibble. Killing pathogens in food is a function of temperature and time. If they reach the recommended cooking temperature for poultry (165F/74C), any flu virus in the product should be long gone. At lower temperatures, there’s more variability and more need for a longer cooking time (e.g. 60C/140F for 30 minutes). A challenge with these diets is the lack of information about the “gentle” cooking parameters (temperature and time). I suspect they likely all hit a high enough temperature to at least kill flu viruses (which are easier to kill than some food borne bacteria) but that’s a bit of a guess. I’d consider them low risk overall, but if I was going to feed a diet like this I’d ask the company how they cook the food, to be sure.

High pressure pasteurized raw diets

High pressure pasteurization (HPP) uses pressure (instead of heat) to inactivate microorganisms. However, the effectiveness is dependent on the amount of pressure and how long it’s maintained, as well as the food matrix itself, and volume of food undergoing HPP. If the method is validated and performed properly, the risk of flu virus surviving the process should be really low. However, we’ve seen at least one report of fatal H5N1 influenza in a cat that was eating a HPP-treated diet. Recalls of HPP treated diets for Salmonella contamination are also far from rare (and if the process doesn’t kill Salmonella in a certain product, we’d be concerned it might not effectively kill flu virus either). I consider HPP a risk reduction method, not a risk elimination method. If a company can show that their method kills flu (or a proxy virus), then I’d be more confident the diet is safe (at least from a flu standpoint). 

Raw diets with “natural preservatives”

Preservatives are used to reduce spoilage. That means they reduce growth of bacteria that are already in the food. They are not designed to kill pathogens (bacteria or viruses) in the food. So, whether or not there are preservatives (and whether or not they are considered “natural”) likely has no impact on survival of and risk of contamination with H5N1 flu in the diet.

Freeze-dried pet food

These diets are frozen, and then the water is removed under vacuum. Freeze drying is actually great method for preserving viruses for long-term storage in laboratories. I’m not aware of any evidence of any impact of freeze drying on survival of flu viruses, so until then I would assume that freeze dried diets are the same risk as fresh diets.

Raw (fresh) poultry

If H5N1 flu is present in a bird, it will be present in the meat from that bird. If there are no steps to kill it, flu virus can persist for a while in that nice moist environment, even after the bird has been slaughtered or died. Refrigeration probably helps with survival of the virus. Freezing probably has a bit of impact, since freeze-thaw cycles can impact viral viability, but I have no confidence in simply freezing the meat to significantly reduce viral contamination, and would not consider frozen raw diets to be any different than fresh in terms of risk. Untreated raw poultry is undoubtedly the highest risk pet food when it comes to H5N1 flu (not to mention a lot of other pathogens as well).

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:

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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.

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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.

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