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Yesterday I wrote about a FDA notice regarding H5N1 contamination of RAWR pet food that killed a cat in California (and likely sickened others, but that’s a guess). A sharp reader pointed me to the manufacturer’s response that must have gone up shortly after I looked at their website. I’ve seen lots of responses from pet food companies after events involving contaminated products (both raw and kibble-based diets); the good companies acknowledge, apologize, indicate what happened (if they know), and what they are doing going forward. Others unfortunately deflect, deny or gaslight.

Let’s look at RAWR’s posted response (“Safety Alert”) to this incident of H5N1 contamination of one of their products. I’ll put on my professor hat and critically assess their document. Italicized text is from the company’s response:

If you know us you know that transparency and integrity are paramount to who we are.

  • Okay, but then why did you only mention this after the FDA released its public notice? That’s not transparency, that’s damage control.

Unfortunately, FDA waited weeks before providing us with any real information that would help guide us to understanding their investigations. When we finally did receive test results, those results were not tied to specific lot codes.

  • (That ticking behind me is my bulls*t meter warming up). I don’t know the details, obviously. Slow follow-up could be a real issue. However, it’s not a reason to do nothing until forced. I’d also be quite surprised if specific details regarding lots tested weren’t provided.

Our reasonable questions regarding the cat, the lot codes, testing methods, and chain of custody have gone unanswered. Instead, FDA declined to provide the information directly and advised us that the only way to obtain these vital records was through FOIA (Freedom of Information Act requests) — a slow process that can take weeks, months or even years.

  • Fair complaint. Although the cat’s information would be confidential, as that’s private medical information.

But if protecting the public were truly the priority, why was critical information delayed for weeks, provided in fragments, and not shared with us until after FDA had already posted a public warning? This approach undermines the very goal of public safety by creating confusion and blame instead of clarity.

Because of this, we did not bring this to your attention sooner; we ourselves have only been receiving snippets of information in an extremely slow and piecemeal fashion. In fact, as I was preparing this alert to you, FDA notified us that they had already posted their public notice – despite us still waiting for our requested information to be provided.

  • Pick a lane. We’re told they didn’t get any information until the FDA released it, that they got piecemeal information and that they were preparing a response when the FDA released their notice (which would require them to know). All these can’t be true. I cannot fathom a situation where FDA would provide no information to a company before a release, and the company’s own verbiage suggests that’s not really the case.

Redirecting blame onto a single small manufacturer does not bring us closer to understanding avian flu, nor does it help prevent future issues in the food supply chain.

  • So? The issue at hand is contamination of this diet, that killed a cat.

Investigations into the death of cats from Avain (sic) Flu seem to only occur when that cat is on a raw food diet.

  • Nope. Investigation is usually started when we find out the cat has H5N1, and we look at how it might have gotten it. Knowing the cat was fed a raw food diet makes us more suspicious, but we don’t just focus on cats fed raw diets.

To date FDA has only two requirements regarding H5N1 in raw pet food: 1. Use only USDA-inspected and passed meat and 2. Include H5N1 in the company’s Food Safety Plan. We are in full compliance with both requirements.

  • Yes, but those requirements don’t prevent contamination, they only help reduce the risk. There is no way to completely prevent contamination in raw poultry.
  • Also, being in compliance doesn’t negate their responsibility to act, inform and take other appropriate measures when a problem is identified.

RAWR has not adulterated any food.

  • That doesn’t matter, as unadulterated food can still be contaminated. This starts throwing terminology around that the consumer won’t understand to make it look like there are no issues with properly handled raw meat.

H5N1 is a naturally occurring virus found in wild and domestic birds. If it is present, it exists in the entire poultry supply chain, as we use only USDA human-grade, inspected, and passed ingredients. If FDA finds this to be an issue then it should be addressed at the USDA level, and not made to be a problem created by raw food companies.

  • Yes, H5N1 flu is widespread. Human grade and inspected are more terms that are used to  mislead people to think that means pathogen-free. There’s a reason people cook raw meat bought from the store before eating it: to help prevent all the various illnesses we can get from pathogens that are not uncommonly present in raw meat.

Sample Lot CCS 25 093, Sell By 10/03/26 was the lot code in question and the only test done on this was from an open household bag that had been opened prior to July 13th. Testing a product 6 weeks after it has been opened makes it impossible to know whether those results reflect the product as made, or contamination from the home environment.

  • The odds of contamination of raw meat with H5N1 flu from household sources are extremely low. There would have to be another source. When we have a high risk product (raw poultry) AND a genetic match for the virus in the cat was also found in unopened food sold by the same company, there’s no reasonable argument that the food wasn’t the source.

Other testing was performed on a different lot Lot CCS 25 077, Sell By 9/18/26 produced a month earlier with entirely separate poultry sources, which does not prove a direct connection to the complaint nor have any other customer complaints been filed.

  • Maybe they haven’t clued into the fact that they are raising major issues here. If H5N1 with a genetic match was found in lots from separate production batches and dates, there was either repeated introduction from their sourced meat (of the same strain) OR they have a cross-contamination issue in their facility OR they have record keeping issues and those weren’t actually separate lots. All of which are bad.
  • The “no complaints” statement is a joke. For a complaint to happen, a sick cat would have to be taken to a veterinarian (when some cats die too quickly from this virus for that to happen, and lots of cats don’t go to a veterinarian when sick), testing would have to be done (that’s probably only going to occur in a small subset of cases), a proper sample would have to be collected (usually not a problem but can be tough with some cats) and the lab used must be able to test for H5N1 flu (not always done). Then, the result has to be reported and investigated, and someone needs to identify the link with the food so the company can be notified. We could have a lot of sick cats that were not diagnosed. I expect reported infections to be a minority of the total infections.

Another piece that is concerning and worth noting is that the initial test results we received, despite not being linked to any specific lot code showed non-H5N1 Influenza A. Only later, after retesting one of those samples did FDA report HSN1 (sic).

  • As above – pick a lane. You can’t say critical information was “not shared with us until after FDA had already posted a public warning” and also make the statement above.
  • I’m not sure what the non-H5N1 statement is about. It could be that the first result was a pan-influenza test that had to be followed up to determine if it was H5N1 flu. I’d be surprised if they told the company they found flu that wasn’t H5N1, then changed the story.

In regards to the cat in question no necropsy was performed. There is still no definitive medical determination of the cat’s cause of death.

  • But they say above that the FDA didn’t answer their questions about the cat. How can they know this? We don’t need a necropsy to have a solid diagnosis (it’s nice, but not mandatory). A positive H5N1 PCR with consistent clinical signs is enough. The FDA report says the cat “became ill with H5N1” so I’d trust they had enough clinical and testing information to make that call.

Out of an abundance of caution, we proactively removed the lots in question (CCS 25 077 and CCS 25 093) from circulation weeks ago.

  • (That big boom was my bulls*t meter exploding. Rest in peace old guy. I know I’ve worked you hard over the years.)
  • So, obviously the FDA reported the affected codes a while ago.
  • I wonder how this was done with no information on the website. They could have had sellers remove product from shelves, but that doesn’t protect people who have purchased the food already. That’s why public recalls are needed. People could still have these lots in their freezers.
  • Also “weeks ago” doesn’t fit with “we only found out last night when the FDA issued their notice.”

If you have a bag from Lot CCS 25 077 or Lot CCS 25 093 and would prefer not to feed it raw, please know that simply cooking the food to an internal temperature of 165°F will neutralize any potential virus.

  • !!! If you have a bag of food that’s been implicated in the death of a cat that ate that batch, this isn’t an “if you would prefer not to feed it” scenario. It’s a clear, firm recommendation to dispose of or return it.

It’s okay to try to protect your company, but don’t insult us in the process. There was clearly an issue with the food that killed at least one cat. Giving us a bit of a mea culpa and a here’s what we’re going to do about it would be good.

Were they apologetic? Not really.

Did they accept that there’s an issue? No.

Did they indicate what they are doing in response to this problem to prevent problems in the future? No.

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H5N1 avian influenza has dropped of the media radar lately (apart from the BC ostrich farm debacle, but that’s a different story), but that doesn’t mean it’s gone away (and with the fall wild bird migration season looming, we need to stay on alert). The same applies to H5N1 infections in pets from contaminated raw diets: there hasn’t been much press about it, but it’s still an issue, as highlighted by another US FDA notification about a cat death linked to a commercial raw diet, namely RAWR Raw Cat Food Chicken Eats. The cat developed severe H5N1 infection and was euthanized. The open package of the raw diet was tested and it was positive for H5N1 flu as well, and it was a genetic match with the virus from the cat. That’s all pretty clear-cut, unfortunate and sadly not surprising.

Some raw pet food companies have tried to deflect responsibility in such scenarios by claiming an open package could have been contaminated by the cat or owner. In this case there was further investigation which included testing two additional retail (unopened, for sale) samples of a different lot of the same food, and they were also positive for H5N1 flu virus. Genetic analysis was done on one of the two, and it was also a match with the virus from the cat and the other batch of food. It’s even more concerning to have two separate batches contaminated with the same virus strain, as it either means they have repeatedly used contaminated ingredients for separate batches, or they have cross-contamination of batches during production. Both point towards risk that might extend beyond the two lots that were tested.

There’s no word about a recall and nothing on the company’s website about this incident. Affected batches have probably already been consumed (and quite likely killed other cats that weren’t diagnosed) but with sell-by dates of September 18, 2026 and October 3, 2026, it’s possible there’s still some of this food out there in pet owners’ freezers. People who have purchased this diet should check the lot numbers: CCS 25 077 and CCS 25 093 are the known affected lots (but I definitely wouldn’t rule out others being contaminated, either linked to this event or separately). Affected lots (or, really, any lots in my mind) should be discarded, preferably in a manner that also prevents them from being scavenged / eaten by wildlife or any other animals.

Raw pet foods, particularly poultry-based raw diets, will continue to be a risk for as long as H5N1 flu continues to circulate (and that might be a long time). Avoiding all poultry-based raw diets is the best avoidance measure. High pressure pasteurized raw diets should pose much lower (but non-zero) risk, and should be sought if someone’s determined to feed their pet raw poultry. If any cat (or dog) that’s eaten raw poultry develops flu-like illness, respiratory disease or neurological disease, the pet owner should consult a veterinarian ASAP.

For more information on H5N1 flu, including H5N1 infections linked to raw pet food, check out all our previous Worms& Germs posts on avian influenza.   We also have a general infosheet on raw meat based diets available on the Worms & Germs Resources – Pets page.

Cat colonies present some interesting infectious disease challenges. Anytime we have animals congregating, there’s an increased risk of disease transmission, and when they’re outside, it also increases the risk of diseases from wildlife. Thus cat colonies can become a bridge for diseases between wildlife and people.

I’ll pause here to add a perspective that I’d often put at the end of the post, and which people often miss (and then email me asking why I hate cats or cat colonies or people who manage cat colonies). I have no issues with cat colonies. Yes they create some risks, but life is full of risks. I’m writing this with a formerly completely feral cat curled up beside me. Yet we should neither ignore nor dismiss issues with cat colonies, but rather try to optimize the cat health and human health components as much as possible.

Back to rabies and cat colonies…

Rabies is always a concern in cat colonies. Any outdoor cat in a rabies endemic area has a risk of encountering rabies from a bat or other reservoir species (e.g. raccoon, skunk, fox). Colonies just amplify the potential impacts: a solitary rabid cat poses much less risk than a cat that has close contact with a large group of other cats, and if it’s a managed colony or the colony cats have other contacts with people, then the risk to humans increases as well. Vaccination of colony cats is a great control measure. It’s hard to get them all, but getting vaccine coverage in a large percentage of the cats will greatly reduce the risk, including to those that can’t be caught. But this method (trap-vaccinate-release (TVR)) takes time and money and people, which are not always available.

Some cat colonies are managed, meaning there are people who attempt to capture and spay/neuter and/or vaccinate the cats, feed them, keep an eye on them and interact with them regularly. In contrast, some colonies are unmanaged – they’re basically just a group of cats that live amongst people. They’re less likely to be the target of spay/neuter and vaccination efforts, and health issues are less likely to be spotted.

A recent report in Morbidity and Mortality Weekly Report (MMWR) about a rabies outbreak in an urban unmanaged cat colony in Maryland highlights some of the issues with these populations. It started with a rabies diagnosis in an aggressive cat that was part of an unmanaged group of about 20 cats. This particular cat was caught and tested because it had bitten or scratched 2 people. Because it’s hard to know who else might have had contact with a feral / unowned cat, they had to go searching for other potential human contacts. A complicating factor here was that the cats were near a hotel, and there was concern that hotel guests might have been exposed. Persons experiencing homelessness in the area were also a concern. So, this was a lot more complicated than many investigations. They had to coordinate with health departments in the US and Canada to track down hotel guests, who were asked if they had any exposure to cats during their stay. Reverse 911 messaging was also used, whereby all local cell phone subscribers got a text that described the situation and what to do. Community-based support programs for individuals experiencing homelessness were engaged to reach other potentially exposed people. They also contacted local healthcare facilities to have them flag people coming in for recent animal bites or scratches.

The investigation was wide reaching. Risk assessments were completed for 197/309 hotel guests from 27 US states and Canada (that’s pretty impressive). In the end, three potentially exposed individuals were identified, all of whom started rabies post-exposure prophylaxis (PEP) within 10 days of exposure (also impressive).

A kitten from the colony was seen to have been acting abnormally around the same time, raising concerns about the potential for a cluster of rabies cases within the cat population. It’s not clear whether the kitten was caught and tested, but it seems like it wasn’t. That’s not too surprising as a sick feral cat can be hard to find and catch. If it had neurological disease from rabies, it wouldn’t have survived more than a few days, so it may have died before anyone could find it.

Three other cats from the colony were caught, euthanized and tested. It’s not clear if they were sick or why these three particular cats were tested, but it sounds like they just wanted to catch and test whichever cats they could (not a great strategy). All three cats were negative for rabies.

Rabies vaccination of feral cats living in close proximity to people takes time and money, but so does an investigation like this. Estimates of personnel time required from just 17 of the 29 jurisdictions involved totaled 450 hours. Three people got PEP, which typically costs thousands of dollars per person in the US. The CDC has estimated that approximately $33 million is spent annually in the US on PEP for people exposed to potentially rabid cats. That would buy a lot of rabies vaccine for cats.

Vaccination and better management of colonies won’t eliminate rabies or drop all the costs to zero. However, like most things with infectious diseases, there’s a cost savings argument to be made for putting more resources into prevention via cat colony vaccination and monitoring. Ideally, we’d have effective oral rabies vaccines, like we do for wildlife, to make it easier to vaccinate large numbers of cats. However, conventional trap, vaccinate and release (TVR) approaches can still achieve good population-level vaccine coverage in these groups. Education of people about interacting (or more specifically, not touching) feral cats, and reporting any bites or scratches from feral cats promptly is also important.

Cat colonies aren’t going away, but with good spay/neuter and TVR programs, they can be managed to reduce the risks to both cats and people.

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I suspect that people in every decade since the 1940s have said “we really shouldn’t have to talk about why raw milk is bad anymore, should we?” …but apparently we do still have to talk about it, and with certain high-profile characters in the US pushing raw milk, the topic isn’t going away anytime soon. So here we go again…

Pasteurization of milk was one of the biggest public health successes in history.  No matter how well animals are raised and how hygienically milk is collected, there’s some degree of risk of contamination with various pathogens. Pasteurization takes care of that risk for us, while maintaining the nutritional value of milk.

That should be all we need to say, but unfortunately it’s not enough. Raw (i.e. unpasteurized) milk continues to be promoted and sold (sometimes legally, sometimes not). Some people who consume raw milk know the risks and chose to drink it anyway. Many presumably don’t know the risks, or have been misled to assume there are no risks.

I could write posts for days about cases of raw milk associated illnesses and outbreaks, but I’ll spare you that. However, since money drives a lot of the raw milk industry and anything that impacts profits will get attention, I want to talk about a recent lawsuit from a Florida woman who is suing a dairy farm that produced raw milk she purchased, after she developed E. coli and Campylobacter infections and suffered a miscarriage. Her toddler also got seriously ill. She claims that she didn’t know about the risks of drinking raw milk.

Whose responsibility it this? Governments that allow the sale of raw milk? People who sell it? People that gloss over the risks and push it as a healthy choice? Consumers who should be expected to do some degree of due diligence?

Yes. All of them. There can be different ratios of responsibility (e.g. a consumer that was misled by false advertising vs someone who knows the risk but chooses to dismiss it), but everyone in that list has some role. That’s often a challenge with infectious diseases: no one can fix the problem alone, and many players are involved in preventing or causing disease. I’ve had lots of discussions with lawyers who get frustrated when I won’t paint a black and white picture of the lawsuit they’re planning or defending, but it’s the truth.

You could say that the consumer has a responsibility to understand what they’re purchasing and eating. The milk container label apparently indicated that it was only fit for animal, not human, consumption (more of a way to deflect liability than to warn people off, I assume). At the same time, you could say that it’s fair for a consumer to assume that someone who is legally selling a food product is selling a safe product.

The woman in this case apparently asked about the label warning, and according to a news article was told that it was just a technical requirement so sell “farm milk.” That definitely amps up the “someone’s really liable” meter.

Consider an analogy using a car accident: Should I sue a car manufacturer if I get into an accident that was an inherent risk of driving?

Is this akin to a a raw milk-associated infection? Or is it more akin to a manufacturer that sold a car despite knowing it had a correctable manufacturing defect that increased the risk of an accident? With raw milk, it’s probably more of the former, since raw milk that has been otherwise handled and produced appropriately may still be contaminated from the start.

What about the regulator? What if the government allowed a car on the road despite knowing it was unsafe and could be made safer using a practical method? I can make a stronger argument for responsibility here.

Ultimately, many people bear responsibility, and the lack of regulation against the sale of raw milk in some regions is a staggering deferral of responsibility by governments. Sale of raw milk is not legal in Canada but there’s a surprising number of US states that allow it. There’s absolutely no public harm or negative impact on food security, food production or farm income through mandating pasteurization, and one huge benefit (safer milk). So, apart from the overused “freedom” excuse, there’s little compelling reason to allow sale of raw milk. I’m not saying we need a nanny state and that freedom concerns are invalid, but it’s clear that many people (and animals) get sick from raw milk, many of whom don’t realize the risks that they are taking, and there’s an easy way to prevent all those infections.

Maybe this lawsuit will at least stop some of the blatant marketing misinformation that’s out there about raw milk, but there’s so much other misinformation circulating that it might not have much of an impact.

Universal Ostriches. It’s been a ride.

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I was involved early in the saga of the H5N1 influenza outbreak on this ostrich farm in BC, answering some questions about the situation and potential options, but eventually stepped back from commenting much as things went off the rails, in part to avoid the flurry of threats that come along with challenging the narratives from their supporters.

To recap briefly, H5N1 influenza hit the birds on this large farm in December 2024 and subsequently killed 69 of their more than 400 ostriches. They didn’t report the sudden onset of deaths to the Canadian Food Inspection Agency (CFIA), which was legally required since avian influenza is a reportable disease and in this situation was very likely the cause of the deaths. Someone else apparently anonymously reported the situation to the CFIA, who then investigated. So right from the start there were indications that responsible animal ownership was lacking.

The CFIA tested the birds, and a novel assortment of H5N1 influenza virus was identified, which made the situation even more concerning. As per standard practice and international disease codes, a quarantine order was issued and a cull was mandated (which includes financial compensation for the birds destroyed).

However, the farm refused to euthanize their remaining birds, and challenged the decision in court – unsuccessfully – at various levels. They took to social media to spread the word, rally support and ultimately ask people to come to the farm to protest (peacefully). They essentially had an ongoing public campout at a farm that was under a quarantine and cull order. That’s pretty much exactly what we don’t want to do at a farm with a high-consequence zoonotic pathogen that we’re trying to contain.

Despite the large number of deaths, many birds survived, but many of those were probably infected and infectious, whether they were sick and survived or or simply healthy carriers of the virus. That’s expected, because although the mortality rate with H5N1 flu is extremely high in many domestic poultry flocks, it isn’t always 100% and can vary in different bird species. So there were still potentially infected birds around as all this was slowly winding its way through the legal challenges. Especially because they keep their birds outside, there was (and still is) concern about the farm being a source on infection for wild birds and other animals, which could lead to further spread of the virus. Ostriches are classified as poultry, and Canada’s international obligation through animal health codes is to cull infected birds unless there are strong mitigating circumstances and control measures.

From the start, the story moved very quickly from any concern about animal health to a mix of anti-regulation, anti-government, anti-PCR, anti-[insert lots of other things] fringe elements, and a lot of changing stories from the farm. Add on Rebel “News” (my quotes) embedding itself on site, rage baiting and coming up with bizzare stories such as murder drones taking out birds, the constant pleas for donations, as well as the trucker convoy elements who tried to recreate that disaster on the farm, and you can see how it devolved (the summer schedule even included a concert by convicted convoy leader Tamara Lich). An anti-vax far right pastor was also baptizing people in a river downstream from runoff from the ostriches and convoy campground (multiple levels of “yuck” here). Dr. Angie Rasmussen has a much more interesting and comprehensive discussion on the whole situation.

I have to admit, it was kind of funny watching the “viruses don’t exist,” “masks are harmful” and “antivax” crowds do the mental gymnastics in online chats to support a farm that has said they’ve played a role in developing products for masks and that they were involved with injecting birds with SARS-Co-2 antigens to produce antibodies (aka vaccination).

This week, the Federal Court of Appeal rejected the farm’s appeal to block the Canadian Food Inspection Agency (CFIA)’s cull order. That should be the end of all of this, although the farm is calling on people to come to the farm and “sit with the birds.”

There are multiple issues and levels of concern here. Ultimately, it’s a matter of national and international health regulations, and whether we are going to follow them or not, and whether there are repercussions for blatantly ignoring them.

If I drove home drunk and nearly ran over someone in the process, but made it to my driveway after a high speed police chase, I wouldn’t have much luck saying “no harm, no foul. I made it home ok. You need to let me go.” No, I’d rightfully get raked over the coals in a court of law. It’s the same thing here.

From the standpoint of further spread of H5N1 flu, has something really bad happened because of what the farm did? Not that we know of (at this point).

Does that mean we should drop everything and move on? Absolutely not. There’s a rule-of-law issue and a critical precedent here. We may have gotten lucky here. We may not the next time.

  • We can’t effectively control diseases if we allow anyone who just doesn’t want to follow the rules to weaponize the court system to draw things out.
  • We can’t let people blatantly ignore quarantine restrictions (while posting evidence of these breaches online).

The tough part is the birds. The last thing I want to see is animal culls, unless there’s a clear requirement, which I wrote about in an earlier series of posts. I assume all these surviving birds are flu-free at this point, so the protective value of culling them at this point is probably very limited. The bigger issue is the farm, their actions and future risks considering H5N1 flu is still around.

So, what do we do? Do we want the government to surrender, ignore their rules, ignore international standards and move on? Do we want a response that’s probably no longer necessary? Is there even an acceptable middle ground?

What would I like to see done?

I have no power in this regard (that’s probably a good thing most of the time) but I’d love to see this response:

  • Test all of the birds (at the farm’s expense)
  • If they are all negative, and they can be rehomed, seize the group and rehome them. This farm has clearly shown it should never be allowed to raise livestock.
  • Fine the farm substantially (again) to make it clear to others that they can’t act this way.

Dr. Oz has offered to take the birds, so I say test them and let the American’s figure out how they want to import birds from a quarantined flock and deal with them. That could be entertaining.  The farm declined the offer earlier, saying they want to keep the birds in Canada (which might just mean they don’t want to give the birds away for free, as there’s no profit in that).

I’d also review the response to H5N1 flu to see where we can improve (and internationally, discussions to re-classify ostriches as non-poultry might help). There are potential ways to bring in non-culling options for special populations, but only with proper and usually intensive infection control measures, as this is still a very serious virus that is a major threat to human and animal health.

The stories change regularly on this ostrich farm, but one thing they talk about a lot is the massive research value of these birds, and that they are part of a study of some sort that involved producing anti-SARS-CoV-2 antibodies. That’s interesting, but I doubt there’s any true value here. I’ve seen no publications, abstracts or other research outputs from the Japanese lab with which they have reportedly been working to suggest these birds have been useful or that they harbour anything unique or critical. I’m not saying not to study them, but we can inject lots of ostriches or other species with SARS-CoV-2 antigens (vaccination) and harvest antibodies. I’ve not seen any independent experts suggest the research value of these birds is anything special, so that aspect should be removed from any discussion.

In response to the recent verdict, the farm has once again appealed to the public to come to the farm. To do what? Physically prevent CFIA personnel from entering? Get more attention? Have one last party (or fundraiser)? Regardless, it’s one more example of a lack of respect for the law and due process, and shows to me that they shouldn’t be allowed to keep livestock. I’m all for exploring options to avoid culling the birds, but not to keep them in the hands of this group.

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Tritrichomonas blagburni (formerly T. foetus) is a frustrating cause of diarrhea in cats. This parasite causes chronic diarrhea that will most often ultimately resolve on its own, but it can take months (or longer). During that time, most cats are largely healthy but with very messy feces (and they’re infectious). Some cats do feel sick, and can have a range of problems such as abdominal pain, vomiting, weight loss and complications from having a constantly diarrhea-stained rear end, or from straining. So while many cats may seem fine, we’d rather treat them, both for the cat and to reduce transmission risks.

There are no licensed treatments for this disease, and no drugs that are licensed for use in cats for other diseases are effective. Traditionally, we’ve treated these cats with a drug called ronidazole, which was obtained from compounding pharmacies (a valid approach when there’s no approved product). However, there’s currently a global issue with access to the base drug, so it’s no longer accessible in most areas.

Tinidazole is plan B in these cases, but it’s not great for a few reasons. The drug has not been well studied and doesn’t seem to work as well as ronidazole. It probably helps infected cats, but is far from a preferred option. However, we are now also have problems accessing tinidazole (and I haven’t been able to find a source in Canada).

Are there any other options? I’ve wondered about using secnidazole, and would consider it. We know nothing about efficacy (or safety), which is a significant concern, but it could be an option in some countries where a human oral version is available… which does not include Canada, so we have to keep moving down the options.

Most often, we end up trying to manage these cases with diet to try to minimize diarrhea and keep things tolerable until the cat ultimately gets rid of the parasite on its own. Sometimes, the diarrhea is pretty bad though, so we’d really like to try something more in those cats in particular.

That leaves the bottom of the barrel option, pradofloxacin, a fluoroquinolone antibiotic. It’s a higher-tier antibiotic so I really hate considering it for this disease, but some infected cats are pretty miserable, so we have to consider it in severe cases. Efficacy data are lacking, so it’s more of a “this might work, you could try it if you really need to” situation, than something based on even preliminary data. If cats are sick enough and not responding to dietary management, I’m okay with that. The treatment duration that’s typically used is 7 days; if there’s not a good response after 7 days, I wouldn’t extend it, at that point we’d just have to accept that we’ll need to wait it out for that patient.

Are there any ways to get ronidazole?

The internet is an interesting place. You can find pretty much anything somewhere, but it’s very much buyer beware. Whether anything you order is actually ronidazole (and at the stated concentration) is always going to be in question. There are also legal issues with importing drugs. As veterinarians, we are able to get permission to import drugs on an emergency release basis. However, that system is focused on licensed drugs that are available in other countries but not here in Canada. It’s not meant for accessing unapproved drugs and compounded drugs. We were able to get permission to import antivirals for the treatment of FIP in cats, but that took some time, the drugs came from a well established company, and due diligence was done on that company as part of the review process. Importing from an established compounder that has clear quality control procedures and testing is different than buying a drug from some random company that provides no information (at least not in English or French). I’d be interested in exploring some of these products more to see if we can get enough information to pitch an Emergency Drug Release request, but I haven’t been able to find anything that would give me confidence to make such a request yet.

So, the answer to the common “how can I treat this cat with tritrich?” question is still currently ”feel free to call around and see if any pharmacies have been able to get ronidazole. If not, and they can’t get tinidazole (or maybe secnidazole) either, try dietary management. If that doesn’t work, consider a course of pradofloxacin. If that doesn’t work, you have to try to wait it out for now.”

I don’t like the “see what happens, it will hopefully get better soon” approach, but that’s unfortunately where we sometimes end up.

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A couple of days ago, I mentioned that Jason Stull and I have done a scoping review of human Baylisascaris procyonis (raccoon roundworm) infections. The paper is published in the Canadian Veterinary Journal, but won’t be open access until October, so I’ll provide a preview of some of the findings here. Here’s a snapshot of what we covered:

  • 60 infections in people were described.
  • 47 had neurological disease, 9 also had ocular disease, 11 just had ocular disease, and there was one case each of eosinophilic cardiac pseudotomour and an incidental finding during an autopsy.
  • Most cases were from the US (52), followed by Canada (5), Germany (2) and Brazil (1)
  • 75% of cases were male, with a median age of 2.9 years (range 9 months to 73 years)
  • 12 (25%) of people had been observed to eat feces, dirt or other potentially contaminated material; 75% of these cases were less than 5 years of age.
  • 5 patients had developmental delay and 1 had Down’s syndrome.
  • Of the people with neurological disease for which an outcome was reported, 19% died, 10% fully recovered and 71% had mild to severe residual neurological deficits.
  • 70% of patients with ocular disease had permanent vision loss.

Hopefully that sets the scene a bit. Today, I’ll focus on sources of infection / exposure. I very often get questions from people asking if “X” creates a risk for B. procyonis exposure. Most often, it’s really unlikely but I usually can’t say “never.” That’s not always well received, since people are typically looking for re-assurance, so the messaging can be tough. “Non-zero but as close to zero as you can get” is my somewhat convoluted but honest answer in a lot of situations.

But, what do the data say to support that answer? Not a lot, unfortunately. Data support what we think of as high risk exposures, but also show that there’s some degree of risk from more casual situations.

The data from our review were limited, since source of infection was only investigated for a subset of cases, and retrospective investigation of sources can be tough – particularly when a large subset of affected people are young children or others who can’t provide a reliable history. Our relatively small number of reported cases (60) dwindled to 37 with an attributed source, and many of those sources weren’t proven, but just logical assumptions.

Prior to this review, I would have said that young kids or people with developmental delay that are prone to eating inappropriate items outside were the highest risk groups, and that casual contacts with the environment (and even raccoons) were low risk. That still largely holds true. The presumed sources in these cases were:

  • pica (inappropriate ingestion) in an area where raccoons were observed (n=10)
  • having abundant raccoon activity in the area (n=8)
  • hiking or working in areas with many raccoons (n=4)
  • having raccoon latrines on the property (n=4)
  • having a pet raccoon in the house (n=4)
  • a history of pica but unknown raccoon exposure (n=2)
  • storing raccoon pelts where a child played (n=1)
  • raccoon infestation of a fireplace (n=1)
  • ingestion of food scraps from public garbage cans (n=1)
  • seeing raccoons in the neighbourhood (n=1)
  • possible source not reported (n=23)

If we look at the two most recent reported cases that were not in our scoping review, one was a child with pica whose home had a raccoon latrine on a roof that allowed feces to drop to the ground below. The other was a young child that was known to (as per normal for young kids) put soil and bark mulch into their mouth. There were no known raccoon latrines in the area, but raccoons were active locally. This largely fits with my assumptions that risk is highest in a definable population that is prone to ingesting things they shouldn’t outside, amplified by the presence of a local raccoons and raccoon latrines.

Some cases had no clear route for ingestion of parasite eggs, but there was a high level of environmental contamination locally, particularly in the form of a local raccoon latrine. That makes sense too since the egg burden can be really high around latrines. If people touch the ground in those areas then inadvertently touch their mouths (a very common event), infection would be possible.

Having a pet raccoon… that’s obviously a problem. It’s one of the reasons we emphasize that raccoons should not be pets (aside from it being illegal in Ontario). Wildlife should be left in the wild or transferred to a proper rehabilitation facility. (Though a recent experience of one of my daughter’s friends finding a baby raccoon and not being able to find a rehabilitator to take it for weeks shows some challenges with that too.)

The people who got infected with no clear source beyond knowing there were raccoons in the area are the most challenging part of the puzzle. Millions upon millions of people live in areas where there’s abundant raccoon activity. These data show there may be some risk from being in those environments. At the same time, while published reports are only a subset of true cases, the number of infections in people is still really low. When you have a situation where millions of people are exposed and a handful get sick, it’s tough to find the right message. The risk isn’t zero, but it’s really, really low.

What this tells me is that the general public shouldn’t fear Baylisascaris and freak out if they see a raccoon walking across their yard. They should take it as a reminder that there are lots of diseases out there in nature, and that we should use common sense (e.g. stay away from raccoons, don’t eat poop) and hygiene (wash your hands) to minimize our risk of exposure.

Who’s not on the list of cases in this report? Raccoon rehabilitators.

The case linked to a pet raccoon shows that keeping a raccoon can create risk, which isn’t surprising. However, there are lots of wildlife rehabilitators that have abundant contact with raccoons and raccoon feces. Previous study has reported antibodies against the parasite in 5-7% of raccoon rehabilitators, showing they can be exposed, but the risk of disease is clearly limited. That’s an important thing to keep in perspective – simply encountering the parasite isn’t enough to cause infection. There’s likely a dose component (more eggs ingested mean more larvae that migrate and cause tissue damage) and a chance component (migration is random, and if the larvae don’t happen to end up in the brain or eye, there may be no issues).

What can the average person do to avoid Baylisascaris?

It comes down to don’t eat raccoon poop:

  • Supervise kids and people with developmental delay when outside, especially young kids and anyone prone to inappropriate ingestion.
  • Avoid putting high risk people in areas where contamination with raccoon feces is likely (e.g. near a latrine, or where feces have been observed).
  • Stay away from raccoons.
  • Discourage raccoons from living around people’s properties and public places like parks (e.g. don’t feed them).
  • Identify and properly clean up raccoon latrines.
  • Don’t keep raccoons as pets.
  • Use good hygiene practices if there is any contact with raccoons (e.g. rehabilitators).
  • Use good hygiene practices, especially hand hygiene, after contact with soil (which is a good general practice that protects against other diseases too, like toxoplasmosis)

These data support the need for hedging, unfortunately. That means we usually can’t say a scenario has zero risk. However, near-zero risk is common, and we have to keep things in perspective. I’m still going to have to answer most with “the risk is really, really low and I wouldn’t worry about it” vs “there’s no risk.”

For a parasite that rarely causes disease in people, the raccoon roundworm Baylisascaris procyonis gets excessive attention. I get an email every few days from people who are worried because:

  • a raccoon pooped on their deck/garage/yard
  • they found a raccoon latrine on their property
  • they found unidentified feces floating in their pool
  • they ran over a raccoon with their car
  • just saw a raccoon walking across their yard

These scenarios all come with different degrees of risk, from zero to low. That said, the reason it gets so much attention is because in the rare instances it does cause infection, the disease can be severe and have long-lasting consequences. Like a lot of zoonotic infections, kids bear the greatest burden of disease; with B. procyonis, that’s because they are more likely to put things in their mouth that may be contaminated with parasite eggs from raccoon feces.

Here are a few quick facts about B. procyonis to keep in mind:

  • It’s a roundworm that lives in the intestinal tract of raccoons.
  • It’s very common in raccoons in North America and is expanding in Europe since the introduction of raccoons (along with the parasite). If you have raccoons in your area, you almost certainly have B. procyonis too.
  • It’s generally harmless to adult raccoons. It probably mainly causes disease in young raccoons with large worm burdens.
  • Raccoons poop out large numbers of B. procyonis eggs all the time. Once these eggs have matured in the environment for a few days, if a person ingests them, the eggs can hatch and the larvae then migrate through the body. Since we’re not raccoons, the larvae don’t know where they’re going, so they can migrate just about anywhere and can cause tissue damage in the process. The damage can be particularly devastating if the reach the eye (ocular larva migrans) or brain (neural larva migrans).
  • Dogs can be infected with B. procyonis too. It’s rare, but sometimes they can develop the intestinal infection with mature roundworms after eating raccoon eggs. In that event, they pass eggs in their feces, just like raccoons do. Fortunately, routine dewormers easily eliminate these roundworms in dogs.

Now onto the real story (Moe will complain that I’m already writing too long of a post and I haven’t even gotten to the main event, but some background is good).

A couple of weeks ago (yes, I’m behind, it’s been a busy month), there was a report of B. procyonis infection in two (unrelated) children in Los Angeles County, California. The cases are pretty typical, but still worth highlighting.

Case 1 was an adolescent with autism spectrum disorder who had a history of pica (eating non-food items). He was hospitalized because of progressive behavioural changes, sleepiness, decreased activity, confusion and abnormal gait. As part of what I assume was a very extensive workup, eosinophilia (an increase in a certain type of white blood cell) was noted in a blood sample, which suggests some type of parasitic infection. Eosinophilia was also noted in a sample of spinal fluid, which essentially screams “neurological parasitic infection.”  An ocular exam also identified a parasite larvae in the back of the eye. The image below (not from this patient) shows what this looks like.

These findings, plus the changes noted on MRI, lead to a very solid presumptive diagnosis of B. procyonis infection. This was confirmed later through detection of antibodies against the parasite in the patient’s blood.

Laser treatment was used to kill the parasite in the eye, and a combination of albendazole (an antiparasitic) and a corticosteroid (to reduce inflammation) was used to treat the neurological component. Very fortunately (since this is often a devastating disease that causes irreversible damage), the child made a full recovery.

The family’s property was investigated to look for a source of infection, and a raccoon latrine was identified on a rooftop, which allowed feces to fall to the ground. Since the child had a history of pica, it’s assumed that he ingested feces or contaminated soil from that area.

Case 2 was an otherwise healthy 15-month-old child who was hospitalized because of acute onset of neurological disease, with weakness, altered gait and changes in muscle tome. Profound eosinophilia was noted in the blood and spinal fluid, but it doesn’t seem like parasitic disease was flagged at that time. A wide range of treatments for different possible causes was implemented initially, none of which included anti-parasitics.

Three months later, the child was taken to a follow-up appointment where he happened to be examined by the same doctor that treated Case 1. An ocular exam was performed and a parasite larva was seen. He was then finally treated with albendazole and corticosteroids. He also had antibodies against B. procyonis in his blood, rounding out the diagnosis. Unfortunately, this patient had serious neurological sequelae, possibly due to the delay in diagnosis and treatment. The eosinophilia should have been a trigger to think about parasitic disease, but it’s not clear why that wasn’t explored. Even with prompt treatment, the prognosis can be poor, but with late treatment, it’s worse.

No source of infection was found at the home of case 2, but raccoons were known to be present in the area. The child had been noted to put soil and bark mulch into his mouth, so presumably this is a really rare and really bad luck situation where a raccoon had defecated in the same area or where the mulch was obtained.

Take-home messages

  • Raccoons should be discouraged from hanging around homes. Not feeding them and preventing them from accessing any food source are key steps (and also helps avoid other diseases raccoons may carry, like rabies!).
  • People with a tendency to stick things in their mouths outside (including soil and feces) are at higher risk of infection. Proper supervision is important. If someone like that lives on or visits the property, there should be extra efforts to prevent raccoons from entering in the yard, and the yard should be inspected regularly for animal feces.
  • Physicians need to have better awareness of zoonotic diseases in general. It’s hard to improve education about oddball diseases like this, but an obvious flag for potential parasitic disease seems to have been missed.

Jason Stull and I recently did a scoping review of human B. procyonis infections. It’s not open access until October, but I’ll write a follow-up post soon highlighting the main findings.

Image from eyerounds.org (University of Iowa)

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Pathogen contamination of raw pet diets isn’t surprising. We know it’s a risk. So a new issue with Darwin’s Natural Pet Products isn’t really surprising either, since they’ve had multiple issues in the past, including ignoring an FDA recall request. They’re back in the news again, but this time it’s because of human illness (with a side of another ignored request). Maybe serious illness in a person will prompt more action, but I don’t see anything about this situation or a recall on their website, so that’s not encouraging.

The latest FDA advisory follows detection of E. coli O157 from a beef-based raw dog food and Salmonella from one duck-based and one chicken-based dog food marketed by Darwin’s. But the really concerning part of the story is how the problem was identified:

  • In August 2024, a four-year-old child was hospitalized with hemolytic-uremic syndrome, a severe and life-threatening consequence of E. coli O157 infection.
  • The investigation led to testing of raw pet food samples from the child’s household, and the E. coli O157 from the pet food was a genetic match to the one from the child.
  • A dog in the household had been sick the day before the child fell ill. The dog’s disease was minor and so it wasn’t taken to a veterinarian. It could have been related to E. coli or Salmonella from the diet, or it may have been unrelated. A link to the diet makes sense though, particularly since the child had direct contact with the dog but not the dog food. There are lots of ways for contaminants from the raw pet to make it into the child, such as cross-contamination in the kitchen, or contact with used food bowls, but the dog is a logical high-risk source.

The time frame is a bit unusual though. The child got since in August 2024, but the pet food wasn’t tested until May/June 2025. The reason for that is not explained, but maybe the family found the old pet food in the freezer and decided to see if it was a potential source, or didn’t think about the pet food until later, and then were able to find some left in the freezer. It seems like the parents directed the testing through a private (but accredited) lab, with info then being reported to the FDA. However, with the genetic match between the bacterium in the diet and the child, and the time frame of when that food would have been purchased (and fed at least in part to the dog) and the child’s illness, it’s a pretty solid story.

Another concerning aspect of this case is detailed in the FDA notice:

The FDA recommended that Arrow Reliance, Inc [the company that manufactured the diet for Darwins] recall the product lots that tested positive for E. coli O157:H7 and Salmonella. To date, the firm has not recalled the affected products. These products, which were manufactured in May or June 2024, were sold frozen, have no expiration date on the label, and could still be in consumers’ freezers. Therefore, the FDA advises consumers to check their freezers for the affected lots of Darwin’s Natural Pet Products prior to feeding to pets.

How companies can get away with ignoring an FDA request to recall a product that has likely infected someone and caused severe illness is beyond me.

The FDA’s recommendations to consumers are straightforward and are copied below:

  • If consumers have any pet food on the list below, they are advised to throw it away in a secure container. Do not feed it to pets. Do not donate the food.
  • Clean and disinfect all pet supplies and surfaces that the food or pet had contact with.
  • E. coli O157:H7 and Salmonella can affect both people and animals. People with symptoms of E. coli O157:H7 or Salmonella infection should consult their health care providers. Consult a veterinarian if your pet has symptoms of E. coli O157:H7 or Salmonella  infection. See information about human and animal symptoms below.

Here is the product information on the affected lots, also from the FDA notice:

The affected lots of pet food were sold in frozen 2-pound white and clear plastic packages with four separate units. The beef and chicken BioLogics dog food have orange labeling, and the duck Natural Selections dog food has blue labeling. Product lot codes are printed on the front of the lower left unit of the package. The affected varieties and lot codes are:

  • Darwin’s Natural Pet Products, BioLogics All-Natural and Grain Free, Beef Recipe for Dogs
    • Lot 10662, MFG Date: May 30, 2024
  • Darwin’s Natural Pet Products, BioLogics All-Natural and Grain Free, Chicken Recipe for Dogs
    • Lot 10683, MFG date: June 05, 2024
  • Darwin’s Natural Pet Products, Natural Selections Duck Recipe for Dogs
    • Lot 10638, MFG date: May 22, 2024

As someone who works a lot with infectious urinary tract disease in animals and has led urinary treatment guidelines, I guess it’s fitting that my dog got an infection.

To start, I’ll slap myself on the wrist for saying it was a urinary tract infection (UTI). We’ve been trying to improve the terminology in this field by using more precise terms. His specific issue was bacterial cystitis. I’ll use that for the rest of the post, but since UTI is commonly understood, I still use it for some audiences, for now at least.

Ozzie’s peeing predicament

Regular followers of the W&G blog have read about Ozzie more than once in the past. He’s a now almost-3-year-old (and definitely obnoxious) neutered male Labrador retriever.

The male part is relevant. As in people, bacterial cystitis in dogs is most common in females. However, that doesn’t mean that males can’t get bacterial cystitis, or that something particularly unusual is going on if they do. It’s just less common.

Oz also has a risk factor for infectious diseases: He has atopy (environmental allergies) and is therefore on oclacitinib (Apoquel), a drug that’s meant to modulate his immune system to reduce the allergic response, but also causes some degree of immunosuppression. Dogs on this drug aren’t severely immunosuppressed, but there is some increased risk of infection. It’s hard to say if that played a role here, but I suspect it did.

Back to Ozzie’s predicament

Oz went out in the morning and had a big pee. He then urinated small amounts a few more times. Then, throughout the morning, he kept going out to urinate small amounts. He’s a “grass is greener on the other side of the door” dog, who constantly wants in or out, but this was extreme, even for him, and the urination was abnormal. Since he was peeing a lot, it was easy to get a sample – it was turbid with a reddish tinge and some blood clots. That’s clearly not normal.

Stranguria (straining to urinate), pollakiuria (frequent urination) and abnormal-appearing urine scream “bacterial cystitis” but that’s not the only possible cause of these signs. We also always need to bear in mind that there can be other underlying issues (e.g. bladder stone, tumour) that may need to be addressed. That said, common things occur commonly. The fact that he’s male brings in some concern, but run-of-the-mill infections happen in males too, and his oclacitinib treatment provided a potentially straightforward explanation for an uncommon situation.

I looked at the urine under a microscope and there were lots of red blood cells, white blood cells and cocci bacteria within the white blood cells, all of which are supportive of bacterial cystitis involving a Staphylococcus sp.

Then the question becomes “to culture, or not to culture?” In a perfect world, we’d always do a culture. However, culture is expensive (very expensive in some places) and the value of the culture has to be considered. I want to do a culture when I’m not confident in what’s going on, when the odds of empirical treatment failure are high and/or when the implications of treatment failure are high. Let’s break those down.

What’s going on?

At that point, I was pretty confident Ozzie just had bacterial cystitis. While he could have something going on at the same time, odds are he didn’t, and culture wouldn’t really help me figure anything out at this stage.

Treatment failure potential

Since we have good guidelines for treatment of infectious urinary tract disease in pets from ISCAID (Weese et al. Vet J 2019) to help us pick approrpiate initial (empirical) antimicrobial therapy, the issue with treatment failure revolves around antimicrobial resistance. Resistance can occur in any infection, but in a young dog with no previous antimicrobial use history, no raw meat or raw treats in his diet, no hospitalization (apart from when he was neutered 2 years ago) and no contact with people that are likely to be shedding a antimicrobial resistant bugs, the odds of him having a resistant infection are really low. So once again, not much value in doing a culture for that reason.

Treatment failure implications

The question I ask regularly is “what will the status of this patient be over the next few days if I guess wrong with my antimcrobial?” If the answer is “likely dead,” I really want a culture and I really want to be confident in my initial drug selection. For Ozzie, the answer is simply “still uncomfortable and peeing a lot.” I’d rather not have that, but the in the grand scheme of things the implications of treatment failure are low. If the initial drug doesn’t work, we have lots of runway to figure out what will work before Ozzie’s in any serious trouble.

Generally I’d like to get a culture done routinely in cystitis cases, but for understandable infections that seem pretty run-of-the-mill in patients at low risk of a resistant infection, I’m fine with empirical treatment (as is common practice in people too).

That said, I did a culture anyway (more out of curiosity than anything else).

Next, I did exactly what we do NOT want people to do: I found some leftover antibiotics in the house and gave that to Ozzie. (Merlin, our previous Lab, had a root canal at one point and was sent home with 14 days (!!!) of antibiotics that we used for a total of 0 days… ignoring instructions from their veterinarian is another thing we do NOT want dog owners doing, but I’m pretty well versed in this area so I changed the treatment).

So Ozzie got amoxicillin-clavulanic acid for 5 days. If I’d had to get a new prescription for him I would have just used amoxicillin, but it was Sunday and I’m lazy, and amox/clav is also a recommended first line drug.

The next day, Ozzie was already looking better. He was peeing less frequently and his urine looked pretty good. There was still a bit of blood, as you can see by the little pellet of red at the bottom of the tube in the picture below. I checked the culture and could already see heavy growth of bacteria. The picture second picture below is the culture plate after 48 hours, which shows a nice, heavy, pure culture of Staphylococcus pseudintermedius.

Ozzie finished his antibiotics and… that was it. He responded well and there wasn’t a need to do anything more. If he relapses, then we need to do more investigation to see what else may be going on, especially since he had a staph infection, which can be associated with development of struvite bladder stones. But, our treatment goal was a healthy dog and since I got that, that was the end. So far, so good since then too. It’s been a couple weeks and he’s had no further issues. Hopefully it was a one-off infection, but we’ll see what happens.

The other thing we want to consider in any infection is whether there’s a risk factor we can mitigate to prevent it from happening again. Here, it’s tough. We could stop his Apoquel, but then he’ll be itchier (uncomfortable) and prone to secondary skin infections from scratching himself. His atopy is fairly seasonal though, so we can get him off treatment for a good part of the year, which helps.

Ozzie was a pretty straightforward case, which is actually a reason to talk about it. We tend to focus writing and and reporting and talking on the weird and wonderful, but routine disease causes most of the problems. Thinking about how we handle those cases is really important, but easy to overlook because they’re so routine.