Cyclospora has been in the news a lot lately because of a large, ongoing outbreak in the US. Total case counts aren’t clear (and official numbers are always an under-estimate) but well in excess of 10,000 people have been infected.

A quick primer on Cyclospora. It’s a genus of protozoal parasites that can cause gastrointestinal disease. Cyclospora cayetanensis is an important cause of disease in people, and is the species we’re dealing with. It’s a human parasite and foodborne infections are  typically associated with fruits and produce. Infected people shed the parasite in feces. The parasite oocysts are not immediately infective after they are shed. It takes 1-2 weeks in the environment for them to sporulate and become infectious. So, direct human-human transmission is not the concern. Transmission occurs from fecal contamination of food or water. Fruits and vegetables are the most commonly implicated food sources, since human hands are involved in picking them, they are often eaten raw and not always washed well.  

It’s a well known cause of foodborne disease, and in normal years ~3000 cases are reported in the US and ~300 in Canada.

As attention gets paid to this human outbreak, questions about risks to, and from, animals arise. I think we can break those down into a couple relevant areas.

Are dogs and cats being exposed to Cyclospora in this outbreak?

It’s likely that dogs and cats are being exposed, but uncommonly and probably at low levels when it occurs. This outbreak seems to be focused on contaminated iceberg lettuce that was produced in central Mexico. While iceberg lettuce may not be the only risk, it’s the main one at this point and presumably few dogs (and even fewer cats) get fed lettuce, so that greatly limits the concerns. Indirect exposure through contaminated hands or surfaces, or cross-contamination of other foods that the animal might eat is always a potential issue, but the overall risk of exposure is presumably very low.

What would happen if a dog or cat ingests Cyclospora?

After exposure, a few different scenarios can occur.

  1. The animal gets sick.
  2. The animal doesn’t get sick but has a subclinical infection and sheds the parasite
  3. The animal doesn’t get infected but the parasite passes intact through the animal’s intestinal tract
  4. The animal doesn’t get infected.

Some foodborne pathogens can cause disease in a wide range of species (e.g. Salmonella). Some are much more limited in who they can infect. Cyclospora cayetanensis is one of the latter. It’s a human parasite. It’s been investigated in many other species, both looking for natural infection and through experimental infection, and the conclusion is that it’s predominantly or exclusively a human parasite. Cyclospora cayetanensis DNA or Cyclospora-like oocysts have occasionally been detected in dog feces, but these findings have not been associated with clinical disease and most likely reflect passive passage after ingestion rather than true intestinal infection. Experimental infection has been attempted in dogs, without successful infection or disease. That’s not a guarantee since artificial infection models are never perfect but it’s one more data point supporting the notion that this parasite isn’t clinically relevant in dogs. Very limited information is available for cats, but there is currently no evidence that cats develop clinical infection or serve as an important reservoir. So, while I don’t think we can say with 100% certainty that does and cats can’t get sick, odds of it being a relevant risk are very low.

Can dogs and cats infect people even if they don’t get sick? 

Living with a dog was a statistically significant risk factor for disease in one outbreak investigation but there are lots of potential confounders there and that doesn’t provide any real evidence of risk. Theoretically, I guess we can’t rule out a dog ingesting the parasite, passing it in feces, then a person getting infected through fecal-oral exposure. That’s a stretch and much lower risk than exposure through contaminated produce. Even if viable oocysts were passed unchanged, they would still require time in the environment to sporulate before becoming infectious, so basic fecal handling practices (picking up feces and hand washing) would reduce the risk even further. I don’t think we can say the risk is zero, but it’s really low and Cyclospora is very low on the list of things I’d be concerned about in any random fecal sample from a dog.

If there’s active Cyclospora in people in the household, I’d pay good attention to avoiding fecal-oral exposure with dog feces. However, I’d say that in a Cyclospora-negative household too.

Take home message: There is currently no evidence that dogs or cats play a meaningful role in the epidemiology of human cyclosporiasis. If there is Cyclospora in your household, focus on preventing fecal contamination and foodborne exposure. Standard hygiene and feces-handling practices are appropriate, but there is no reason to be concerned about pets becoming ill or serving as important sources of infection.

Here’s a screenshot of a quick but useful New World Screwworm (NWS) resource for animal shelters that was developed by University of Wisconsin-Madison Shelter Medicine Program in collaboration with a number of shelter organizations and shelter medicine experts. With the continued re-emergence and spread of NWS from Central America back into the southern US, it’s an issue of importance for animal owners and veterinarians in those areas, and for those who take care of animals that are moved from those areas. Domestic animal cases in the US (including cattle sheep, goats and three dogs) have been limited so far, but will no doubt continue to increase, at least in the short term. Basic awareness is a critical control tool to stop further spread.

For the original post (and larger print) use this link: Humane Prevention and Management of New World Screwworm (NWS) in Shelter and Rescue Dogs and Cats

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Last year around this time, were were talking a lot about a cluster of cases of Rocky Mountain Spotted Fever (RMSF) in dogs (and people) associated with Long Point, Ontario. Prior to 2025, we didn’t consider this tickborne disease to be established in the province, but then we detected multiple confirmed cases in dogs, two confirmed cases in humans, and ticks carrying the causative organism (Rickettsia rickettsii) all in (or linked to) Long Point. We assumed we’d see more in 2026 again, but the only way to know was to wait and see.

Because RMSF is not a reportable or notifiable disease in Ontario, we only find out about cases through people, physicians, veterinarians and others who let us know about them, or who ask for advice about suspicious cases. Even if we knew about all the diagnosed cases in the province, we’d still only be getting a partial picture, because for an infected dog to get diagnosed and for us to hear about it, a bunch of things need to happen:

  • the dog has to get sick (not all of them do)
  • the dog has to be taken to a veterinarian
  • the veterinarian needs to consider RMSF (which could be easily missed, since this is an emerging disease in our area)
  • the owner needs to agree to (and pay for) testing
  • the test has to be positive
  • someone needs to pick up the phone or send an email to let us know

There are lots of places along that cascade where we can lose a case, so the ones we hear about are no doubt only a subset of the cases that actually occur.

This year (2026), as part of an Ontario Animal Health Network (OAHN) project, we are testing blood samples from dogs in the Long Point area to see if any/some/many have antibodies against R. rickettsii, to help give us an idea of how much this pathogen may be circulating under the radar. Stay tuned for more updates later in the summer!

We’re also focusing on passive surveillance, i.e. encouraging people to let us know about any confirmed or suspicious cases of RMSF in dogs, and collecting as much information about each case as we can. I’m a bit surprised I haven’t heard about more cases so far, but there has been at least one positive dog that visited Long Point regularly. Long Point is a vacation home area, which complicates surveillance because many dogs may visit the area and potentially get infected, but they get sick back at home and go to their local veterinarian, who may not be aware of the risk for RMSF, especially if they don’t ask about travel history. I’ve also heard that there were other sick dogs in the area, but that’s getting into anecdotes (which can be useful but may also be questionable).

What we can say is: RMSF is back again (or more accurately, it hasn’t gone away, so we’re seeing seasonal cases again, as would be expected). I think we can confidently say there’s ongoing risk to dogs and people that live at or visit Long Point. We can also confidently say that the risk should extend to adjacent areas, but we don’t know how far that risk extends. Had all the dogs around Long Point been seronegative (no antibodies against R. rickettsii), then testing dogs from farther away would have been pretty low yield. But as we learn more about what’s going on at Long Point, we can better design our next surveillance steps.

In the interim, tick avoidance remains paramount, particularly in Long Point, including avoiding high-risk tick environments (e.g. long grass), doing diligent tick checks (daily – for dogs and people), and keeping dogs on a good tick preventive medication (which is helpful but does not guarantee full protection from RMSF).

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This post is going to be long a long one, as treatment of Brucella canis infection in dogs is a complicated, and there are a lot of important associated issues to mention. TL;DR – I’m not a fan of the hard line “thou shalt euthanize or lock away a dog with B. canis.” I want to prevent disease spread, but we also need to consider the bigger picture and keep things in perspective and the proper context.

To treat or not to treat? That is the question. In some areas, it’s recommended to euthanize dogs that test positive for B. canis, or to strictly isolate them from other dogs and people. This approach is based mostly on what’s been recommended historically out of an abundance of caution (because a long time ago “someone” said we should do it this way) and unsubstantiated fear, rather than hard evidence of risk. Nonetheless, there are some valid issues to discuss.

Personally, I have no problem treating infected dogs if the owner is aware of the potential risks and all the unknowns. Apart from outbreaks and surveillance testing, I get involved with probably about ten new B. canis cases a year. Considering I deal mainly with weird infectious disease situations, that indicates it’s a fairly uncommon occurrence (or at least uncommonly diagnosed), but it’s common enough that we need to have a plan for handling these cases.

It’s hard to know how common B. canis infection really is in the general dog population. Studies of specific populations like dogs in shelters have reported highly variable results, with some reporting over 50% of dogs affected. I suspect that the prevalence in in the general dog population is probably less than 1%, but 1% of millions of dogs is still a lot of infected dogs.

  • Dogs from shelters, imported dogs and dogs from questionable breeding facilities tend to be higher risk. We did a study of B. canis in commercial dog breeding kennels in Ontario in 2019 and 127/1080 (11.8%) of dogs were infected. That was a biased population, as it included some kennels where there were known reproductive issues or potential for exposure to other infected kennels, but it’s still relevant. We found over 100 infected breeding dogs, having tested only a subset of the breeding dogs in that area.

So, we have to assume there were (and probably still are) hundreds of infected dogs out there being bred. That means there’s presumably lots of human exposure, among breeding kennel owners and staff, and among those who adopt dogs from them. Yet, human infections are very rare and most infectious disease physicians I have talked to have not seen one.

Infection in dogs can cause diseases such as diskospondylitis (which causes back and neck pain) but most infected dogs have no signs of disease and probably never will. That’s good for the dog, but it means we can’t tell who’s likely infected just by looking for signs of illness.

The actual risk to people from exposure to a dog with B. canis is low. There’s presumably a fraction of human infections that go undiagnosed or get misdiagnosed, but even so the number of human infections is likely really low. It’s also treatable in people.  Based on a recent scoping review of B. canis cases in humans (Weese & Weese 2025), the literature is quite sparse. We found reports of infections in only 68 people, and 20% of cases with a known origin were lab-acquired, not from dogs. Signs of disease in these cases were variable; while illness can be severe, fever, malaise, fatigue and chills were most common, and no mortalities were reported. Contact with breeding dogs, especially contact with fetuses or fluids after a dog had aborted from B. canis infection, was an important source of exposure. Since then, there was a case report about an infection in a veterinarian in the UK, presented at the 2026 ESCMID Global conference. The likely source in that case was contact with imported breeding dogs. The veterinarian developed forearm blisters, severe back pain, joint pain, and then fever, headache, chest pain, rash and conjunctivitis, but was eventually diagnosed and successfully treated.

I’m definitely not dismissing the risk of disease from B. canis. I don’t want it and don’t want anyone else to get it either. I want to prevent infections in people and dogs. But using an extremely strict approach might not be all that helpful, and could potentially be detrimental if it discourages testing (more on this below).

Risk of disease and transmission varies depending on the type of dog. Consideration of the type of dog involved is important, but often gets overlooked. The highest risk is contact with female dogs that have recently aborted, fetuses and fluids from an abortion, and newborns and maternal fluids/tissues from infected dogs after giving birth to live puppies. This situation doesn’t apply to most households. The risks from most other dogs are likely low, but they aren’t zero; transmission from a sexually immature dog has been reported (once, from a puppy). Contact with urine is probably next on the list of risky fluids, but it’s still probably low risk overall. Theoretically blood and saliva could pose a transmission risk, but those are likely even lower risk.

Another way we can try to assess the dog-to-human transmission risk is to look at the dog-to-dog transmission risk. I’ve been involved in quite a few cases where someone who already owned one or more dogs adopted a new dog that was subsequently found to be infected with B. canis. Almost always, the new dog was already spayed/neutered, or this was done shortly after adoption before the infection was identified. We have often tested the other dogs in the household in these situations and I don’t think we’ve ever found a positive housemate dog, even after the animals have lived together for years in some cases. That doesn’t mean there’s no risk of transmission, but it provides further support for the limited risk in normal household situations.

When in comes to treatment of B. canis in dogs, there are actually two components to consider: treatment of disease versus elimination of the bacterium.

In dogs that actually get sick from the infection, we usually get a good clinical response to antimicrobial therapy. Certain infections, like diskospondylitis, may take a long time to respond, but they usually do eventually.

Because B. canis is adapted to live in dogs, total eradication of the bacterium is tougher; it requires even longer term antimicrobial therapy, and it’s hard to know if/when the B. canis has been eliminated. Typically, I recommend monitoring dogs on treatment serologically, which measures the amount of antibodies against B. canis in the bloodstream. I aim to treat until the dog has no detectable antibodies anymore (seronegative), realizing that that’s likely over-treating, because the antibodies take a while to disappear even after the infection is gone, but unfortunately it’s the only readily available monitoring tool we have. I anticipate at least 3 months of antimicrobial therapy to start, but it usually takes longer than this. Most of the recurrences that I have seen have been in dogs treated with only a month or two of antimicrobials without any serological monitoring. Unfortunately we don’t have great data on overall response to this treatment regimen, since not many dogs are treated and treatment and monitoring are variable. In my anecdotal experience, most dogs will eventually become seronegative and stay seronegative (assuming they don’t get re-exposed), but I still can’t guarantee complete eradication of the bacterium, so the infection could still recrudesce.

So B. canis is widely distributed in dogs and uncommonly causes disease. It probably doesn’t crack the top 10 list of zoonotic disease risks from dogs. So is it really that big a deal? I still wouldn’t dismiss the risk, because even though B. canis infection in people is rare and treatable, it’s still something we want to prevent. The other issue, though, and the one that prompted this post, is the variability in response to an infected dog, which is sometimes euthanasia – and that’s a very big deal.

  • The question shouldn’t be “does a B. canis infected dog pose a risk of B. canis transmission to people?” because the answer to that is obviously “yes, but a very low risk.”
  • The better questions are “Does a dog with B. canis pose a significantly greater overall health risk to people than any random dog?” or perhaps even more importantly “Does a dog with B. canis that has been diagnosed and is being properly managed pose a significantly greater overall health risk to people than any random dog?” I would argue that the overall health risk to people from a well-managed infected dog is almost identical to that of any other random dog that may or may not be infected, but is not being managed for it. The risk may even be lower in a managed dog because we know the dog is getting regular veterinary care, so other potential problems can be flagged.

We often get tunnel vision on one risk, while ignoring other greater risks. Every dog is harbouring multiple bacteria that can cause serious disease in people under the right circumstances. We don’t have any “zero risk” dogs, we have higher and lower risk dogs, people and situations, but anyone can get a zoonotic infection from any dog. More people die every year from Capnocytophaga canimorsus infection from dogs (a bacterium that’s present in the mouth of pretty much every dog) than have probably ever died from B. canis infection Pasteurella (which is also present in the mouth of most dogs and cats) causes many more infections than B. canis ever will. I could write a few pages on pathogen threats that are much more common than B. canis. That doesn’t mean B. canis isn’t important, but we should think about the big picture and the logic (or lack thereof) of an approach as drastic as euthanasia or long term isolation.

More testing of dogs for B. canis would be useful. Ideally, we’d test all dogs that came from a kennel of unknown B. canis status, so we could understand and mitigate the risk of spread. However, harsh draconian consequences disincentivize testing:

  • “Cute puppy. Since we’re not sure about where he came from, we should test him for Brucella canis. But if he’s positive, we’ll have to euthanize him.” How many vets want to make that offer? How many owners would actually agree to testing knowing that?

Disincentivizing testing means we get fewer dogs tested, so we treat fewer infected dogs, and we know less about the infection itself and response to treatment.

At the same time, differential application of severe measures is illogical and ineffective. I have a hard time buying into really strict responses to a known infection, while there’s a much larger number of unknown infections that are simply ignored. It doesn’t make sense to euthanized the dog that responsibly gets tested, while all the other infected dogs and their owners are allowed to simply remain blissfully unaware. If the risk from the known-infected dog can be manged (spay/neuter and treatment), it’s going to be much less than the risk from all those other unknown positives.

So, what’s a veterinarian to do when a dog tests positive for B. canis?

The first step is talking to the dog owner. They need to understand the situation and the options. If they decide to treat, that will involve months of medication and periodic repeated testing. That can get expensive, so they have to be willing to commit. They can’t just give a few days or a few weeks of antibiotics and hope for the best.

If not already done, the dog needs to be spayed or neutered. That will greatly drop the transmission risk to people, and prevents breeding-associated infections, which is the main dog-to-dog route of transmission.

The owner needs to realize the limitations of treatment. We can never guarantee that B. canis has been eradicated from the dog, because the bacterium is notorious for laying dormant in tissues and sometimes infection will recrudesce after treatment. With spaying/neutering, the right antimicrobials, adequate treatment duration and recheck monitoring, the risk of recurrence is probably low, and the transmission risk from a spayed/neutered dog with an early recurrence that is detected through routine testing is probably very low. Yes, there are a lot of probablys here, but that’s the nature of a lot of understudied infectious disease issues.

Treatment is not the right thing to do in every situation. If the owner can’t commit to proper management or has particular concerns about B. canis, rehoming the dog may be a better option. Some rescues will take infected dogs, treat them, and find homes for them with people who understand the situation and risks, which is great. Those are niche rescues and niche adopters, but I think it’s perfectly appropriate, for all the reasons above.

If I suddenly found out that my dog Ozzie was B. canis-positive, I wouldn’t consider euthanizing him. He’s neutered, he’d be treated and he’d be monitored. The risk to my family from B. canis would be exceptionally low, we’d be willing to accept that risk (just like we accept many other risks from owning a dog and cats).  Not everyone does risk math the same, and if someone didn’t want to keep a positive dog, I wouldn’t consider that inappropriate at all. You have to do what works best for your scenario.

What I don’t want to see is unnecessary broad draconian measures and loss of family pets for limited benefit in terms of disease prevention. There’s no right or wrong, but a blanket “you have to get rid of the dog” is the wrong approach to me.

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UPDATE: June 11, 2026. Nitenpyram has also been given emergency use approval (EUA) for dogs and cats over 2 pounds and 4 weeks of age.

While completely expected given the steady march of New World screwworm (NWS) through Central America and Mexico over the last several years, this horrific parasite finally crossed the US border back into Texas in the last week, and has thus far been found in several beef calves, a goat and one dog from New Mexico. There’s an overview of NWS for companion animal veterinarians recently published in Clinician’s Brief, or check out our previous post NWS: Primer for Canadian Veterinarians for the basics on this nasty bug. This post is about what drugs we have available to help with prevention and treatment of NWS. Remember that the core component of treatment is removal of the maggots as quickly as possible (and ensuring that they do not reach the ground if they are removed or drop out of a wound), but antiparasitic drugs can be helpful as well, especially for the larvae that may be missed or hard to reach, and they can also help prevent infestation before the damage is done.

Compared to other emerging/re-emerging diseases, we actually have quite few options for treating NWS. Data supporting different drugs is variable, and come from a combination of field studies and basic drug information. In the US, the FDA has given conditional approval or Emergency Use Authorization (EUA) to quite a few products for use against NWS in various species. Beyond that, there are also some other products that should work… lack of conditional authorization or EUA in these cases may be more a reflection of some companies not bothering to pursue the process, rather than the product not being efficacious against this parasite.

Among the effective products for dogs and cats, the main drug class is the isoxazolines. This includes lotilaner, afoxalaner, fluralaner and sarolaner. This class has proven efficacy against NWS, and some products now have approval in the US (more on that below).  Lotilaner’s approval is probably based largely on one small study that showed 100% efficacy (i.e. all larvae died) within 24 hours of a single dose in naturally infested dogs after a single dose (Lopes do Vale et al. 2023). Similarly, afoxolaner (Cutolo et al. 2021) and sarolaner (Oliviera et al. 2019) have shown 100% efficacy in their own small field studies.

Here is a list of some of the products that can potentially be used against NWS in dogs and cats, as well as their current approval / authorization status in the US (if applicable):

Conditional FDA Approval for treatment

  • Credelio Quattro CA-1 (lotilaner, moxidectin, praziquantel): dogs

Emergency Use Authorization for treatment

  • Credelio (lotilaner): dogs and cats
  • NexGard (afoxolaner): dogs
  • NexGard COMBO (esafoxolaner, eprinomectin, praziquantel): cats

Other

  • Nitenpyram also had 100% efficacy within 24 hours of a standard dose in a small study of naturally infested dogs (Correia et al. 2010).
  • Spinosad might be useful, but might be less effective, based on one small study that reported 80% efficacy in treating dogs (Oliveira et al. 2018). I’m wary of comparing all these studies since they are all quite small and heterogenous, but at the same time I wouldn’t reach for spinosad first if there’s no advantage to this product over other available options that might be more effective.
  • Fluralaner (the active ingredient in Bravecto) has Conditional Approval in the US for prevention and treatment of NWS in cattle, but it’s reasonable to assume it would be similarly effective in dogs and cats, in which it’s used at a similar dosage.

Macrocyclic lactones are another class of antiparasitic drugs used as preventatives in dogs and cats. Examples include doramectin, which has conditional approval in the US for prevention and treatment of NWS in cattle, and ivermectin which has EUA for prevention in cattle. It is critical to note that the doses of these drugs used for heartworm prevention in dogs and cats are very low (e.g.4-6 ug/kg) compared to what is used for prevention and treatment of NWS in cattle (200 ug/kg). So while ivermectin, moxidectin, selamectin and milbemycin might be useful at high doses, we cannot assume that dogs/cats getting products like Heartgard, Inteceptor, Sentinel, Milbemax, Proheart and Advantage Multi for routine parasite prevention have any protection against NWS.

Imidacloprid, which is found in products including Advantage II, Advantage Multi, Seresto collars and K9 Advantix II, is also unlikely to have any significant effect on NWS based on its mechanism of action and the low drug levels found in tissue (where the maggots are found) versus in the skin (where this drug is most effective).

None of these products have approval for prevention of NWS in dogs and cats. That’s likely more of a labelling/regulatory issue rather than a true issue with efficacy. Treatment data are simply easier to get: You find some infested animals, treat them, and see what happens. Demonstrating a preventative effect is tougher, especially in the field: You need to put a bunch of animals on the preventive, and then compare the infestation rate in those animals compared to untreated control animals. For a relatively rare disease (at least in this part of the world), you’d need a massive number of dogs or cats to show a preventative effect. Alternatively, an experimental model could be used whereby animals are given preventives or placebo and then deliberately exposed to the NWS flies, but a study like that is a lot more work, a lot more money, and there’s far less appetite for unnecessary use of animal infection models (especially for a nasty parasite like this). Given what we know about the parasite, the drugs and the disease, I think it’s fair to assume that a drug that works for treatment will be useful for prevention. Although I’d never guarantee complete protection, I’d be quite confident in this group of drugs.

The bad news for the southern US is that NWS has returned and will probably be around for a while, as eradication efforts will take time.

The good news is that, unlike for many other emerging or re-emerging diseases, we have effective treatments already available.

We don’t have any approved products in Canada for treatment or prevention of NWS, and I suspect there won’t be much push from drug companies to get any such approval or authorization, since there’s no threat of NWS becoming an endemic issue here. However, we can approach the management of travelling or imported infected dogs in the same way as it’s done in other countries. The treatments in Canada would be extra-label, but that is not uncommon for many conditions we treat, especially when they are rare in Canada.

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As for a lot (or most) conditions we treat with antimicrobials in dogs and cats, data on how best to use antimicrobials before, during and after dental procedures are sparse. We know that antimicrobials are used a lot for canine and feline dental procedures (Weese et al. 2023), and that a large percentage of said use is probably unnecessary. The same is true in human dentistry; even though they have more data and more guidelines, they still struggle with overuse and poor compliance with best practices.

Part of guideline development is assessing the available evidence. Even when we know evidence is lacking, we still want to assess the issue carefully to makes sure there isn’t more evidence than we thought, and to critically assess what little data may be present to help highlight knowledge gaps.

We recently completed a systematic review of infectious complications of dental procedures in dogs and cats, and the impact of antimicrobial prophylaxis (Weese et al. 2026). Specifically, we addressed a series of questions about use of antimicrobials for routine dental procedures, looking at both peri-procedural (i.e. shortly before and up to 24 hours after the procedure) and post-procedural (i.e. more than 24h after the procedure) antimicrobial administration.

  • Unsurprisingly, we found that data were really limited. That’s important itself.  It’s a gap that needs to be filled.
  • We also found that studies rarely looked at (and were rarely well designed to look at) the key outcomes we care about, i.e. clinical disease. We settled on looking at sepsis, infective endocarditis, local tissue infection and adverse events as the critical outcomes.
  • After some debate, we also included bacteremia (bacteria in the bloodstream) as an outcome of interest, even though it’s not a clinical outcome. Bacteremia is a state that may or may not be associated with disease. People and animals are regularly bacteremic and typically have no consequences from it at all. However, bacteremia can progress to infection in rare circumstances. We wouldn’t normally use a non-clinical outcome like that (especially one that is as common as bacteremia), but most of the comparative studies in dogs and cats focused on bacteremia. So we included it, recognizing the limitations.

The systematic review highlighted the commonness of bacteremia associated with dental procedures, as shown in the figure below of the meta-analysis. The proportion column is the prevalence of bacteremia associated with dental procedures in each study, and the pooled prevalence across studies was 47%.  

These studies didn’t report clinical consequences of bacteremia, but when you consider how many dogs and cats undergo dental procedures, the really high bacteremia rates and the really low apparent incidence of dogs and cats getting sick after their procedures, you can understand how bacteremia (seemingly not a big deal) is not a good proxy for clinical disease (which is a big deal).

To investigate this further, we asked whether dental-associated bacteremia is associated with sepsis, endocarditis or other infectious consequences. Only two studies looked at this. Both were small (total of 22 dogs with bacteremia and 11 without) and no infectious consequences or disease were noted in these animals. The data were so limited we couldn’t evaluate them further or draw any conclusions.

We then asked “In dogs and cats undergoing dental procedures, does peri-­procedural administration of antimicrobials reduce the incidence of endocarditis, sepsis, bacteremia or other infectious complications?” But no studies looked at these clinical outcomes. Only two small studies looked at the effects on the incidence of bacteremia, and the meta-analysis (see below) didn’t suggest there was any beneficial effect. The certainty of evidence was really low of course, based on a variety of factors.

That doesn’t mean we can say antimicrobials for dental procedures don’t have any effect, it just means we have nothing suggesting they do. If we look at human dentistry where there are stronger data, antimicrobials are not indicated for these procedures, apart from in certain high risk patients. Our lack of identified effect has to be tempered because the data are weak, but there’s also nothing suggesting antimicrobials are needed (or useful) for routine veterinary dental procedures in most patients.

If there’s no evidence that peri-procedural antimicrobials are useful, there’s even less reason to think that post-procedural antimicrobials are useful, yet this is commonly done in veterinary and human dentistry. We aimed to address the question “In dogs and cats undergoing dental procedures, does post-­procedural administration of antimicrobials reduce the incidence of endocarditis, sepsis, bacteraemia or other infectious complications?” There were no data for this at all. If we look at data and guidelines from human dentistry, routine post-procedural antimicrobials are not typically recommended, or useful.

Did this review actually tell us anything? Yes and no. I think we ended up with the conclusions we were expecting, i.e. bacteremia is commonly associated with dental procedures, there’s no evidence that antimicrobials are useful for routine dental procedures, and the data are really limited.

The fact that we have no supporting evidence for routine use of antimicorbials for dental procedures was an important finding in this case. When we have an intervention (i.e. antimicrobial use) that has potential harms (e.g. cost, adverse events like diarrhea, selection for antimicrobial resistance, administration challenges, pain from administering a pill to an animal with a sore mouth), the default ought to be not to use it unless we have compelling data or a plausible reason to think that the benefits outweigh the harms. For the routine veterinary dental procedures, we have no such data or reason to justify routine antimicrobial use.

Google’s parent company Alphabet has attracted some attention recently base on its request to release up to 32 million mosquitoes in Florida and California. No, it’s not part of a master plan to annoy people or spread disease. Believe it or not, it’s actually an effective method to reduce mosquitoes and the risk of mosquito borne disease.

The reason this seemingly counterintuitive action works comes down to the biology of the relationship between mosquitoes and a bacterium called Wolbachia, which infects many types of insects and parasites. In veterinary medicine, its most significant role is in heartworm disease in dogs, in which Wolbachia are beneficial to the heartworms themselves, so part of the treatment for heartworm is using antibiotics to kill the Wolbachia.

But in mosquitoes, Wolbachia are harmful, not helpful, so we can use this to our advantage. The plan is to release male Aedes aegypti mosquitoes that are infected with Wolbachia. Remember that male mosquitoes don’t bite, so since they don’t feed on blood they don’t spread disease, but they are important for making future generations of mosquitoes.

  • If an infected male mosquito mates with an uninfected female, no viable mosquito larvae are produced, leading to fewer mosquitoes overall.
  • If an infected male mosquito mates with an infected female, viable offspring are produced, but they are also infected with Wolbachia. This is still helpful though, because infected females have shorter lifespans, and the Wolbachia infection also reduces the survival and transmission of various important pathogens in the females, including dengue virus, zika virus, chikungunya virus and yellow fever virus.  

This is in fact a well proven approach to mosquito control. It’s similar to the release of sterile male flies for eradication of New World screwworm, which is being ramped up even more since the first two cases of the current outbreak were detected in Texas earlier this week. (Check out our previous post on NWS for Canadian veterinarians, and the CFIA announcement on new control measures at the Canadian border.)

This is one of those plans that at first glance may make some people wonder what’s going on. It feeds the conspiracy theory crowd that doesn’t like when anyone does anything, but it’s actually a safe and proven process. Mosquitoes have been called the world’s deadliest animal for good reason, because mosquito borne diseases are leading killers internationally. Using biology to counter biology is both a crude and elegant way to address this problem.

Mosquito image source: https://en.wikipedia.org/wiki/File:Aedes_aegypti.jpg

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I wasn’t very quick to write about this because while some incidents of contamination of raw pet food prompt recalls, such contamination is a largely expected event that occurs every day under the radar.

This was also another example of a company ignoring an FDA request to recall raw pet foods in response to contamination, but that too is unfortunately a well known phenomenon when it comes to raw pet food companies.

Listeria contamination adds another dimension, though. Listeria is notorious for contaminating production facilities, particularly those that have suboptimal cleaning, disinfection and maintenance. This can result in widespread and prolonged contamination, with corresponding disease risks. The large number of diets (and over 180 lots) involved in this recall shows the potential scope of Listeria contamination. The company ignoring the problem for some time also likely contributed to unnecessary infections (both detected and undetected).

This recall finally happened months after the US FDA issued a recall request in January 23, 2026 following an owner complaint about their sick dog, and after more reports of dogs on the diets getting sick. The initial recall request was for just 8 lots of various diets, all of which had tested positive for Listeria and other bugs. It’s hard to say how many animals got sick as a result of this incident; Listeria could easily be missed in a dog or cat since it’s not something for which veterinarians typically test.

The company finally responded with a recall on May 22, 2026. The recall affects Raaw Energy diets produced between July 17, 2025 and Dec 23, 2025, as well as “Beef and Turkey Medley” lots produced on March 31, 2026. The notice also states “Some products produced during this timeframe were not tested, and bacterial presence was identified during the same period. As a result, products manufactured within these dates could possibly be affected.” Based on this, combination with the wide date range, I would assume that any diet from this company could be involved at this point. Lack of a positive test for a particular diet doesn’t mean much unless you know how much testing was done.

Ignoring FDA recall requests is an unfortunate pattern with some raw pet food companies. It took months for this company to take action, creating more disease risk for animals and people. I can’t understand why companies are allowed to do this, nor why consumers would continue to purchase from a company that ignores an FDA recall request. If nothing else, you’d think the company would be worried about legal liability if there are further illnesses (especially in people handling the food, or those living with / looking after the dogs), but apparently the short term benefit of ignoring the FDA and continuing to sell contaminated food took precedent.

I’m not going to get into the raw pet food debate (again) here. There’s lots of information in our blog archives, and more information about risk reduction with regard to raw diets can be found on the Worms & Germs Resources – Pets page. Regardless of differences in opinion about the pros and cons of raw diets, I hope we can at least agree on not feeding pets food from companies that ignore food safety problems and contribute to unnecessary disease spread.

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I’ve seen quite a bit of “can your dog or cat get hantavirus?” discussion in media lately, in follow up to the recent cluster of human hantavirus cases associated with a South Atlantic cruise ship. Fortunately, unlike past articles about many other emerging infectious diseases, these have mainly been pretty low key. They’ve highlighted the minimal concern about dogs and cats getting infected and even lower concern that they could infect someone else. Yay.

It is nonetheless important to note is that research on hantavirus in dogs and cats is very limited, so we need to consider “absence of evidence” vs “evidence of absence”. We don’t even know all we need to know about this hantavirus strain (Andes virus) in people; the unique nature of the cruise ship cluster shows this. Animals are much lower down the research priority pecking order.

A few studies have looked at antibodies against hantaviruses in healthy dogs and cats. Finding antibodies means the animal was likely infected at some point and fought off the infection. It doesn’t tell us whether or not they got sick, or whether they could have spread it, but it gives us a basic indication of susceptibility.

These studies tell that a small but appreciable percentage of dogs and cats in areas where hantaviruses are present have evidence of past infection. That’s not overly surprising. They don’t tell us if they got sick or not. If illness caused by hantavirus was really common, we might figure it out based on the clinical cases popping up, but we don’t do a good job identifying rare, sporadic problems, especially in pets, because they’re not routinely tested. I’ve dealt with lots of cases of severe respiratory disease in dogs and cats, and have never tested for hantavirus (maybe we should in some regions, but finding a lab that offers a PCR test for the virus would be the first step). So I’d be wary of dismissing the possibility too quickly, but at the same time it’s not something I’m worried about.

The risk to people posed by infected animals is presumably even lower. We know that people are susceptible to hantaviruses and can get severe disease. Infected people should be more likely to transmit hantaviruses, yet that seems to be really rare, and only a concern with one type of hantavirus (the Andes virus, which was identified in the cruise ship cluster). If dogs and cats are less susceptible to infection in the first place, they likely pose even less risk of transmitting the virus.

Furthermore, we need to remember that not all hantaviruses are the same. There are actually numerous hantaviruses, each with different reservoir hosts and potential issues. We don’t have good data for all the different combinations of hantavirus types and animal species.

While lack of evidence of a problem doesn’t mean there’s no potential problem, it’s encouraging. We have known about hantaviruses for years, and domestic animals have had lots of exposure. Dogs and cats may be at higher risk of exposure than people because they are more likely to catch reservoir hosts (rodents) or root around areas contaminated with rodent urine and feces. Since we’re not seeing suspicious hantavirus cases in dogs and cats, that’s a good sign that the risks are at least low.

BUT we can’t ignore the potential risk altogether. A little common sense is useful to mitigate risks, especially when we don’t know what they are or if they exist. A lot of it is just applying the prevention messaging that is going out to people to other animals.

  • Limit contact with rodents. That is easier said than done for free-roaming dogs and cats, but efforts to keep animals under control and reduce rodent exposure are useful for a bunch of reasons.
  • Reduce rodent access and infestations in households.
  • Take care in areas potentially contaminated with rodent feces and urine. If you’re cleaning out your contaminated shed, maximize ventilation, wear gloves, mask, and eye protection, and wet down surfaces before disturbing them (e.g. sweeping). Also don’t let your dog “help” by shoving his nose in every contaminated corner (or as the case would be with my dog Ozzie, eating everything he can find).

Those are the main things I’d recommend for dogs and cats in areas where hantaviruses are present. Realistically, I’d say the same thing for any other area too, since it’s possible there is unknown hantavirus activity, and hantavirus isn’t the only infectious disease concern when it comes to rodent contact.

Don’t panic over hantavirus, especially when it comes to pets. However, we shouldn’t ignore the potential for animal and interspecies concerns. More surveillance would help determine what the issues really are.

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I got a lot of media questions about hantavirus after the recent cluster of human cases was identified associated with a cruise ship, but those questions were primarily focused on basic facts about virus itself and its general epidemiology. As things have dragged on, there are now more questions about hantavirus and companion animals – not because there are any major issues with pets and this virus, but more likely just because people are getting bored with the usual talking points and are looking for other content.

That said, there are some interesting aspects to consider when it comes to hantavirus and dogs and cats. Pets can be exposed to hantavirus just like people, through contact with reservoir species (i.e. rodents), or their feces, urine or saliva. Cats and dogs are technically at higher risk of exposure in many ways, since they are more likely to have close contact with rodents and to be sniffing around contaminated areas.

I want to start with the key point that the issues with hantavirus in pets are near negligible. I’m going to talk about some areas we should think about with emerging or unusual disease events out of an abundance of caution, not because there’s a major concern with this specific event. So please don’t freak out. Finding that sweet spot between awareness and panic is tough with infectious diseases.

This post will focus on issues to consider specific to the cruise ship cluster. I’ll try to cover some of the more general considerations with hantavirus and pets in another post.

Key point: Despite evidence of human-to-human transmission of this particular hantavirus strain (Andes virus) on the ship, such transmission is still rare. If human-to-human transmission is rare, human-to-pet transmission should be at least as rare, if not even rarer.

Issues with pets and emerging diseases in general revolve around three main concerns:

  1. Pets getting sick (concern for pet health and potential for them to be sources of infection)
  2. Pets getting infected but not sick (no concern for pet health, but bigger to other animals and people to have infectious but apparently healthy animals around us)
  3. Pets acting as vectors of a pathogen whereby they are not infected but can move the virus from place to place (e.g. virus contamination of their haircoats)

We don’t know that any of these are an issue, and they are probably of no concern with this cluster. Infections in dogs and cats are already very rare, and even if infected, the transmission risk from a pet would be very low. But this is also an opportunity to take some basic and practical prevention measures when the risk isn’t well known.

I haven’t seen any reports of dogs being on the ship (e.g. service animals). That removes the highest risk situation with regard to transmission. That leaves us with pets owned by people who have left the ship. Those who have been released from the cruise ship are being monitored, and in some situations tested. Different countries are taking different approaches, but it seems like voluntary quarantine is being used in many places. That focuses primarily on keeping potentially exposed people away from other people. The question I always have with household quarantine is “what about the pets?” This question seems pretty simple, and has come up in the context of various diseases, but rarely do we get an answer.

  • If someone is quarantining in a household, we need to know if they have pets, and if there is a risk to/from the pet for the disease in question. If there is, or if we can’t say there’s no risk, we should treat the animal like a person, i.e. try to keep the quarantined person away from the pet as well. That helps ensure they don’t infect or contaminate the animal, both for the animal’s health and to avoid the risk the pet might then pose to other animals or people.

With other infectious diseases (not likely applicable here), there can also be concerns about the animal acting as a mechanical vector that can lead to indirect transmission, similar to a contaminated surface or object. As I’m writing this, Alice (my cat) is perched next to me. If I have a respiratory virus and touch my face, and then her, I may contaminate her haircoat. If she then visits someone else in the house they pet her a short time later, that could transfer virus to them, even though Alice wasn’t infected. The worst case scenario is I contaminate or infect Alice, and then she goes outside and infects another animal. Then maybe I’ve released the virus into the broader community, or the wildlife population. This was something we were trying to get across when voluntary isolation was used when SARS-CoV-1 emerged in the early 2000s, and then again with SARS-CoV-2 during the COVID-19 pandemic (rarely with any success).

Again, the issues with this hantavirus cluster specifically are very limited and there’s probably no concern:

  • The odds of a person that is quarantining being infected are really low.
  • The odds of an infected person infecting an animal are even lower.
  • The odds of a person being infected, infecting their animal and that animal getting sick or transmitting the virus to someone else approach zero.

So, why are we even talking about it? Good question. We probably know enough about Andes virus to just say “don’t worry.” However, our knowledge of the potential role of pets in a lot of diseases is pretty low, and we can take simple steps to reduce that risk.

My emphasis here is we should default to assuming there could be cross-species transmission issues and apply basic control measures accordingly, unless/until we determine that there’s no need, rather than waiting until we see a problem and then reacting. With Andes virus, a rapid risk assessment could be done to determine the likely risk and the relative certainty of risk, to determine whether or not it is necessary to tell people to isolate from animals too. Despite all our past experiences and recognition of the scope of susceptible species for many emerging diseases, we are still reactionary when it comes to risks to and from animals.

  • Do I want people to worry about their pets if they’ve been exposed? No.
  • Do I want exposed persons to isolate from their pets? Maybe. If they are isolating from people, it makes sense to isolate from their pets. However, if that’s not practical or if the pet is the person’s key emotional support through quarantine, I’d have them quarantine together.
  • Do I want people to fear animals that might have been in contact with an exposed person? No. We’ve seen over-reactions like this in the past.

The issues with hantavirus and most pets are near negligible, but it’s another reminder that the difference between “humans” and “animals” is in our brains. To a virus, we are all just animals of different species, and we all have the potential to be a nice susceptible host.