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Our emerging concerns about Rocky Mountain Spotted Fever (RMSF) in Long Point, Ontario, have led to a variety of questions from veterinarians and dog owners. (It’s also led to a lot of rumours, and sorting out what’s real illness vs internet chatter and hype is tough – but that’s another story.)

We’re still trying to figure out what’s really going on, but in the meantime we also need to increase awareness about the disease itself and our tracking efforts. Better awareness can lead to earlier testing and treatment, which can save lives (of both dogs and people). So here’s a quick rundown of what you need to know about RMSF.

What causes RMSF, and what signs does it cause?

RMSF is caused by the bacterium Rickettsia rickettsii, which is transmitted by a few different types of ticks. Here in Ontario, the most common tick vector for this bacterium is the American dog tick, Dermacentor variabilis. In other areas, the brown dog tick (Rhipicephalus sanguineus) and the Rocky Mountain wood tick (Dermacentor andersoni) are the main vectors. Historically, the American dog tick has largely been considered a nuisance but not a disease threat in Ontario, with most of the attention focused on the black legged tick (Ixodes scapularis) which transmits the causative agents of Lyme disease and anaplasmosis. That thinking needs to change a bit now, at least around Long Point.

The signs of RMSF are quite variable and often vague. Mild cases are probably missed regularly as they’re easily overlooked or dismissed, with vague signs such as lethargy, decreased appetite or non-specific pain or stiffness. Fever is probably pretty common at some point in disease but is not often detected by owners. More severe cases can involve a wide range of signs, including neurological disease, ocular disease, rash or other skin issues, enlarged spleen or liver, enlarged lymph nodes and increased bleeding tendencies. The latter is related to one of the more consistent findings on bloodwork in affected dogs: thrombocytopenia (decreased platelet count). Severe thrombocytopenia can lead to bleeding in any tissue, but may first be noticed due to petechia or ecchymoses (small dots of patches of bruising) on the gums or on the belly.

How long does it take an infected dog to get sick with RMSF?

The incubation period is the time from exposure to the development of the first signs of disease. That’s particularly relevant in dogs that may have transient exposure to high risk areas (like Long Point), but may not get sick or be tested until they’ve returned to a lower risk area. For RMSF, the incubation period is about 2-14 days. The cases we’ve seen so far in dogs that visited Long Point all developed disease within that window.

How is RMSF diagnosed in dogs?

Most often, PCR is used to detect the DNA of the R. rickettsii in the blood of infected dogs. This test is commonly included in some of the “vector borne” or “fever of unknown origin” PCR panels offered by commercial veterinary diagnostic labs.

We can also test blood samples for antibodies against the bacterium, but detecting antibodies alone is not enough to confirm infection. To do that, we need to test two blood samples, one at the start of disease and one a few weeks later, and show at least a 4-fold increase in antibodies (which is what we’d expect soon after and active infection). This is less less commonly used compared to PCR, and there are fewer labs that offer this kind of serology, because it can only provide a retrospective diagnosis several weeks after the dog gets sick.

It’s important to consider running a PCR for RMSF in any dog that has recently visited Long Point or adjacent areas (or anywhere else RMSF might be present) that also has compatible clinical signs such as fever, decreased platelet count and/or pretty much any non-specific disease of unknown cause. Since signs of RMSF can be so variable, querying exposure history and knowing where the disease is present are important to help know when to test.

Is it easy to miss RMSF in a dog?

Yes, and that’s the big concern because RMSF is very treatable IF it is caught early, but it can be very serious if it’s not.

One of the big diagnostic challenges right now is making sure it’s on the radar for veterinarians and dog owner. In areas where RMSF is endemic, it’s pretty high on the list for sick dogs, so dogs get tested and will even start empirical treatment before test results are available in highly suspect cases. In areas where it’s not a currently known issue (like most of Ontario), it’s easy to miss, which is why it’s so important to spread the word about the current situation. Dogs (and people) may visit areas that are high risk but live in areas that are low risk, where their local veterinarian (or physician) may not have RMSF on the radar at all.

Another major challenge is the often vague clinical signs in dogs, especially early in disease. Most often, RMSF is but one of many potential causes, and the signs of RMSF often overlap with those of immune-mediated diseases, particularly immune-mediated thrombocytopenia (IMTP), a disease caused by the immune system attacking the body’s own platelets. The main treatment for IMTP is immunosuppressive drugs, which are the last thing we want to give a dog with a serious infectious disease. So it’s critical to figure out which disease may be the cause of thrombocytopenia is a dog has potentially been exposed to RMSF before starting treatment.

Does being on a tick preventive rule out RMSF in a dog?

Wouldn’t that be nice… but no it doesn’t, for a few reasons:

  • Compliance. Sometimes people forget to give their dog its preventative, or they get off schedule. Even when they think the dog is up-to-date, a close review sometimes finds lapses.
  • Efficacy. Tick preventives are very good, but they are not 100%. We definitely want dogs on them, but they are not a guarantee that tickborne disease cannot occur, especially diseases where it takes less attachment time for the tick to infect the dog (see below).
  • Speed of kill. How long it takes for a tick to transmit the bacterium and how quickly tick preventives work to kill a tick once it bites has to be considered. The transmission time is very well described for dogs; the Companion Animal Parasite Council says a tick must attach for 5-20 hours to transmit R. rickettsii, although some data from other species suggests the transmission time could be even shorter. Some tick preventives for dogs work very quickly and should kill ticks within minutes to a couple hours, but others can take 12 hours. That’s fine for preventing Lyme disease, since it takes 24-48 hours for Borrelia burgdorferi to be transmitted after a tick attaches, but it may not be quick enough to prevent transmission of RMSF.
    • Even shorter acting tick preventives should still only be be considered a very important aid in the prevention on RMSF. Regardless of the product, it’s still important to avoid ticks, do regular tick checks, and consider RMSF if the dog is sick and has visited a potentially high risk area.

Can RMSF be treated?

RMSF can be effectively treated, but catching it early is very important. The sicker the dog is when treatment is started, the poorer the prognosis. Doxycycline is the treatment of choice, but other things might be needed depending on the type and severity of disease. Usually, the response to doxycycline is quick and obvious, and the prognosis is good if treatment is given early enough.

Spread the word!

We’re continuing to investigate this situation, in both dogs and ticks in the Long Point area, and we have a great team of colleagues working together nationally, provincially and locally, in human and animal health, to maximize the response and communication.

As ever, we’re trying to walk the line between increasing awareness and causing paranoia. We want people (dog owners, veterinarians, general public, physicians) to have RMSF on the radar, and take tick avoidance seriously as always. At the same time, we don’t want to cause panic, feed internet rumour mills, or make people afraid of going outside. It’s always a tricky balance with emerging infectious diseases.

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Lately, there have been quite a few news reports about canine parvovirus in London, Ontario. Overall the report have been pretty balanced, highlighting the fact that parvo is causing problems but not overplaying the issue (which happens all too often). Some reports have said there’s an “outbreak” of parvo in an area.

Sometimes a situation like this may be a true outbreak, but most often, it’s a small cluster among the baseline of endemic disease, or it’s just an “outbreak of discussion,” not disease. My guess is that the issue here is the typical small cluster of cases in a group of inadequately vaccinated dogs that’s gotten some extra attention and media chatter, but that the overall parvo rate and risk in the city is pretty much unchanged. Unfortunately (and as usual), we don’t really know for sure, since data are sparse, anecdotes can be misleading, and we don’t have any formal surveillance for parvo in dogs.

Canine parvovirus is an endemic virus pretty much everywhere on the planet where there are dogs. When it first emerged, it was devastating, causing widespread illness and death. Now, it’s largely controlled in areas where there’s good vaccine coverage in the canine population, but cases still occur because of incomplete vaccine coverage and infection of puppies before they can develop protection from their vaccines.

Vaccination is undeniably the cornerstone of parvovirus control where it’s available. We have really effective and safe vaccines for this very serious disease, that’s caused by a virus that’s highly transmissible and hard to avoid. In one article, a veterinarian was quoted as saying parvo vaccination for dogs is “non-negotiable” in her practice, and that’s a fair position to take.

Our parvo vaccines are incredibly effective. It’s exceedingly rare to see parvovirus in a properly vaccinated dog. Almost invariably, if a “vaccinated” dog gets parvo, it’s a dog that didn’t get a full/proper vaccine course.

Most of the parovirus vaccines currently available on the market are modified live virus (MLV) vaccines which are very effective, and can produce robust immunity with a single dose. However, vaccine response in puppies can be unpredictable. If their mother was vaccinated against (or previously infected with) parvo, she will pass antibodies on to her puppies. Those antibodies hang around for a while, providing some protection but also interfering with vaccine response. That’s why we typically vaccinate puppies at 8, 12 and 16 weeks of age – not because they need multiple doses or a specifically timed series, but rather because we want to start young to try to get the puppy protected ASAP in case those maternal antibodies are starting to disappear, and continue to an age where we’re pretty confident that the puppy will produce its own active immune response to the vaccine.

I want to get at least one dose of parvo vaccine into any puppy at 16 weeks of age or more. An extra booster at 20 weeks of age is a bit of an insurance policy – it’s probably not needed if the puppy got a dose at 16 weeks, but it provides an extra buffer in case the puppy is one of those rare cases that didn’t response to the previous dose because of lingering maternal antibodies.

After that 16 or 20 week dose, we give the dogs another dose in 6-12 months of age. With that, we have given 2 doses that we are quite confident will stimulate an active response and provide immunity, and given over a relatively long time frame (which typically produces a better immune response than a condensed series of vaccines). That should give the dog very solid immunity for at least 3 years (and probably more, but we don’t know how much more in any given dog).

If an adult dog hasn’t been vaccinated before (or it’s vaccine status is unknown), it should respond nicely to a single dose of parvo vaccine. A second can be given a month later, but it’s probably unnecessary. An additional dose 6-12 month later will then establish nice long-lasting immunity.

So, if you have a puppy:

  • Make sure you talk to your veterinarian about vaccinations ASAP. Sadly we see cases of parvo in young puppies where the owner just didn’t get around to getting the dog vaccinated as early as possible (life’s busy and it’s easy to forget…). Parvo can then be fatal, and/or can be very expensive to treat (particularly relative to the cost of a vaccine appointment…).
  • If your puppy has gotten a parvo vaccine, and it’s less than 16 weeks of age, one is NOT enough. We need to makes sure the dog gets that dose at 16 weeks or more. Most “of ‘”vaccine failures” I see are dogs that got their last dose at 12 weeks. That’s not a vaccine failure in my mind, that’s a dog that didn’t get vaccinated properly. Since rabies vaccination can be done (and is ideally done) at 12 weeks of age, some people forget or are less motivated to get the 16 week parvo vaccine, but critical to ensure that gets done. It can be a life-or-death decision for some dogs.

As with most of these “outbreaks,” things will likely die down in London ON, likely from a combination of improved vaccination, the infection burning through the high risk group, and waning attention and discussion. That’s the usual routine. However, we will see similar incidents elsewhere. Parvo will always be a risk wherever there are dogs, so we need to maintain vigilance and vaccine coverage.

Vaccine hesitancy is a challenge in veterinary medicine, just like human medicine. So is complacency. When vaccines work, people don’t see the devastating disease, and they forget why those routine vaccines are so important.

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I recently wrote about a couple cases of Rocky Mountain Spotted Fever (RMSF) in dogs in Ontario. It’s not a disease we expect to find here, but we’re concerned about this tick-borne disease because it can be very nasty, and we do have the ticks for it. Ticks and the diseases they transmit are a evolving issue, especially with the impacts of climate change. We’re seeing more ticks and more disease, both in terms of numbers and ranges.

At the time, I pointed out the possible considerations for a situation where we’d found a small number (2) of unexpected cases in dogs. To recap:

It’s possible this current situation is:

  • A single unusual but precedented case, plus online chatter
  • A cluster of cases from a point source of exposure that will die out
  • One or a cluster of cases from exposure to infected adventitial ticks (i.e. ticks from high risk areas that dropped off traveling birds)
  • An indication that RMSF is emerging in some areas in Ontario

BUT now we’re up to 5 affected dogs. Four had a history of being at Long Point, Ontario, an area that has long been at the forefront of ticks and tickborne disease in Ontario. The other dog had more of a vague history, but may have been in that area too.

Whether it’s 4 or 5, that’s enough of a trend to suggest there might be a local focus in Long Point of ticks carrying Rickettsia rickettsii (the bacterium that causes RMSF, which is transmitted by certain ticks).

Obviously we need to investigate this more. It also means we need to be more aware of this disease and pay even more attention to the ticks. In Ontario, RMSF can be transmitted by the American dog tick, Dermacentor variabilis, which is well established here, but a different species from the tick that typically get the most attention, the black legged tick Ixodes scapularis, which is associated with transmission of Lyme disease.

For dog owners:

  • Be aware of the risk of tickborne diseases. For RMSF, be particularly aware if you spend time at Long Point.
  • Talk to your veterinarian about tick prevention medication.
  • Try to avoid high risk areas (e.g. lots of leaf litter, long grass).
  • Perform regular tick checks on your dog after being outside.
  • If your dog has been around Long Point and is sick, don’t be afraid to ask your veterinarian about the possibility of RMSF.

Also for dog owners:

  • Realize that if your dog is exposed to ticks, so you are (but you’re not on tick preventative medications). People can get RMSF too, and it can be serious.
  • If you are exposed to ticks and are sick, make sure your physician knows about your tick exposure and where you’ve been.
  • Perform regular tick checks on yourself after being outside.

For veterinarians:

  • Realize that we may have to consider RMSF in dogs that have not travelled outside Ontario.
  • Be prepared to test dogs that could have RMSF (PCR is the usual approach).

For physicians:

I’ve heard of a few possible cases of Rocky Mountain Spotted Fever (RMSF) in dogs in Ontario in the past week. It’s pretty preliminary information, but it’s relevant to both dog and human health so it’s worth getting some information out about it now. At least one case was a pretty solid diagnosis: Rickettsia rickettsii was identified on PCR, and the dog had clinical signs that fit with RMSF. I’ve also heard rumours of a couple of others from the same general area; in these situations it’s always tough to know how much stock to put into online comments about other cases, but I’m still trying to chase down more information to confirm.

RMSF isn’t considered an endemic disease in Ontario.  We do have one of the main tick vectors (Dermacentor variabilis, the American dog tick, see image) in the province, and locally acquired cases have occasionally been found in dogs and people, but it’s not a disease that’s generally considered much of a risk locally. That’s probably because, despite having a competent tick vector, the causative bacterium (R. rickettsii) wasn’t really prevalent in our wildlife reservoirs (e.g. rodents, rabbits). However, when ticks move they can bring pathogens with them, so it’s possible for new pathogens to gradually work their way into an area and start building up in the reservoir hosts before we recognize the problem.

It’s possible this current situation is:

  • A single unusual but precedented case, plus online chatter
  • A cluster of cases from a point source of exposure that will die out
  • One or a cluster of cases from exposure to infected adventitial ticks (i.e. ticks from high risk areas that dropped off traveling birds)
  • An indication that RMSF is emerging in some areas in Ontario

It’s hard to say which of those is most likely. Strange disease events occur all the time, and most often aren’t the harbinger of a new ongoing problem, but tickborne diseases are changing and we have to be concerned about the last possibility.

Sorting out dog origin and travel history in these cases can be challenging too. At least one of the affected dogs most likely acquired the infection in the Long Point area, a location in Ontario that was one of our first high risk regions for ticks and tickborne disease, and one that would be a logical place to find something new or evolving. More time is needed to sort out how many cases there actually are, and where the dogs might have been exposed.

RMSF is a concern because it can cause severe disease. At least one of these recently affected dogs died. RMSF can also kill people. The prognosis is worse when diagnosis and treatment are delayed, so it’s important for veterinarians and physicians to be aware of any changing regional potential for this disease to occur.

In dogs, RMSF infection can result in a wide range of clinical signs, from no apparent disease to rapid death. Classical signs include fever, weakness, petechia/ecchymoses (dots or blotches from bleeding under the skin), other signs of bleeding (e.g. in the eyes), a rash, joint pain/swelling, swelling of the spleen, and a range of other, often non-specific signs.

Decreased platelet counts are the most common abnormality on a complete blood cell count (CBC), but there may be changes in white blood cell numbers too. Sometimes, other tickborne diseases (e.g. Lyme disease, anaplasmosis) are considered first. Sometimes, it looks like an immune mediated disease, which is more common around here, and which is treated with immunosuppressant drugs – something we don’t want to give a patient with RMSF.

Diagnosis of RMSF is usually based on detection of bacterial DNA in blood by PCR. Serology (antibody testing) is nice to have too, but isn’t as readily available. Antibiotic therapy can be effective, and the prognosis is very good if antibiotics are started before disease is very severe, so early recognition is key.

People don’t get infected with RMSF from dogs, but a diagnosis of RMSF in dogs is relevant to human health since both people and dogs get infected the same way – from an infected tick. If a dog gets infected, it means there are infected ticks in the area that could also infect people. A case report from 2003 about presumptive cases of RMSF in two dogs and their owner highlights this.

  • The report is from the southern US, where a person’s two dogs died. The first had signs that fit with RMSF and was taken to a veterinarian, but because the dog died overnight, samples weren’t submitted for testing. Another dog in the family died 8 days later. A couple of weeks after that, the owner went to the ER with vague signs, then went to her doctor a few days later with progressive disease (that included a fever and rash, which are signs of RMSF). She then was admitted to hospital and shortly thereafter was started on antibiotics, including doxycycline (the drug of choice for treating RMSF). Unfortunately, she deteriorated quickly and died. She was ultimately diagnosed with RMSF. She had two other dogs that also got sick, and one was confirmed to have RMSF.
  • So, this person and their dogs had abundant exposure to infected ticks, and developed RMSF. The dogs got sick in advance of the owner, but that early warning sign was missed. If the person had known to think about RMSF (and mention it to her physicians), it’s possible she would have received earlier treatment and survived. But, the owner didn’t think about it, the veterinarian didn’t raise the issue when the dog was seen, and the physicians presumably didn’t query anything about pets. Multiple opportunities were missed to raise the question of “could this be RMSF?”

That’s why we need to pay attention to animal and human diseases in parallel. There’s lots of talk about One Health, but the talk:action ratio is really high. That’s my ongoing frustration with it: while the One Health concept is great, there’s very little actually being done to improve animal/human/environmental health as a whole. This situation is an area where we can act to spread awareness to maybe help both human and animal health.

American dog tick image from: https://wcvm.usask.ca/learnaboutparasites/parasites/dermacentor-variabilis-american-dog-tick.php

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In areas where ticks and fleas are a concern (which is much of the world), dogs (and to a lesser degree cats) may receive regular tick prevention medications. Some people would rather not use them, whether it’s because of cost, concern about adverse effects, a desire to use more “natural” products or internet misinformation. This, along with far fewer regulations for any compounds not marketed as “drugs,” opens the door for a lot of untested, unproven or downright ineffective products and devices.

Consider ultrasonic insect repellants. These devices are based on the theory that the high frequency sounds they emit are beyond our hearing (and therefore don’t bother us, or our pets) but are discernible to pests, and help drive them away. Various such devices are available commercially, and since they are not drugs and are not marketed as medical devices, the receive very little scrutiny.

Do ultrasonic insect repellants actually work?

The short answer seems to be no. Studies have shown no effect; for example, a study comparing two ultrasonic flea collars in cats found neither was effective (Dryden et al. JAVMA 1989).

In 2016, the New York Attorney General’s Office sent cease and desist letters to companies that were marketing ultrasonic mosquito repellents with claims of efficacy, further supporting that there seems to be no compelling evidence that they work.

Yet, there are still lots of these products around making lots of claims about what they can do.

To me, not having any data for a product related to healthcare is bad (and protection from fleas, ticks and other disease vectors is an important part of healthcare for people and animals, whether drugs, pesiticides or other means are use). Unfortunately there are lots of products on the market for all kinds of things that have absolutely no evidence of effectiveness, just someone who can spin a good story about them.

What’s perhaps even worse is using crap-tastic data to market a product and over-stating its efficacy. (Worse yet is when there is testing that shows something doesn’t work, and the company buries the unfavorable results.)

Overstating efficacy is not just a problem because it misleads consumers to spend money on something that doesn’t work, but also because it can steer people away from effective approaches (tick preventive medications) and ultimately result in increased disease risk.

I got a recent question about a product called Tickless, which is being marketed with claims that it works as a tick repellant for dogs. (Full disclosure: the question came from a pharma company employee. It was a question, not a request for a post. I don’t get any funding from them and got nothing for writing this. I’m writing it because I hate to see animals get preventable diseases because well-meaning owners were misled.) My comments below are focused on this product, but would apply to any similar product.

The company claims “TICKLESS technology underwent rigorous testing and was proven effective by a clinical study at the School of Veterinary Medical Microbiology and Infectious Diseases Laboratory at the University of Camerino, Italy.”

Let’s look at what’s available to support that.

The claim seems to be based on an unrefereed study from 2012 that looked at reduction in fleas and ticks on 30 dogs at each of 2 different shelters. There’s no mention of ethics approval for the study. Dogs had to have not recently received flea/tick medication (good) and had to have at least 4 fleas or ticks on them. A standard method to evaluate them for ticks was used (also good). The each group of 30 dogs was subdivided into 3 groups:

  1. Activated device (n=20)
  2. Treatment with fipronil and lufenuron (n=5), unactivated device
  3. Unactivated device (n=5)

“The subjects included in the experimentation were kept in separate enclosures for the entire duration of the study, ideally in individual enclosures or with a number of other similar dogs”

  • This is a bit hard to follow and potential variation in housing is really important for fleas, since dog-to-dog spread would be the big risk.
  • Tick exposure risk would likely be very low in a shelter. Most ticks are acquired from outdoor environments, so for them, it would be expected that ticks would finish feeding and drop off over time, and new ones would not likely be encountered. That’s a huge factor when assessing a tick preventive.

Their results claim to “…show the effectiveness of Tickles Pet in not permitting an increase in the number of ticks and fleas in all subjects studied and experimentation and to reduce the number of parasites in some subjects.” Specific data are limited:

  • Drugs and inactivated device: “drastic reduction in the number parasites” (expected since drugs work really well, but really vague. We need numbers.)
  • Inactivated device and no drugs: “number of parasites remained stable in so subjects but increased considerably in others” (again… need numbers.)
  • Active device: “number of parasites remained stable, and in some subjects a considerable reduction was observed” (yep… we still need numbers, and analysis!)

They concluded that the study confirmed “the effectiveness of the product in not permitting an increase of the parasites and in reducing the number of parasite (sic) in some subjects, which can therefore be used, without side effects of any kind, on subjects for which an infestation of ticks/fleas has been confirmed, so as to avoid the worsening of the situations, and in healthy subjects so as to prevent infestation.”

That’s a stretch, and it’s not hard to see why this was never published.

They also report a study done using this device at the University of Milan from 1993. It’s a hot mess. They put the device on:

  • 5 parasite-free dogs
    • They were still parasite free (I’m guessing after a week but it’s not clear).
  • 5 “weakly infested” (not sure with fleas or ticks) dogs
    • 4/5 had no parasites after a week. How many of those would have naturally eliminated the parasite, since they don’t inhabit the dog forever? It’s hard to say.
    • No parasites were seen on day 35. There’s also no info about whether these dogs were treated with anything for their parasite infestation.
  • 15 “severely infested” (again, not sure with what) dogs
    • 76% reduction… but there were 15 dogs in the group so the numbers don’t fit. 11/15 would be 73%. 12/15 would be 80%. That’s another red flag.
    • There was 97% reduction by day 35. Again, how many would have eliminated parasites themselves? Plus, 14/15 is 93%, not 97%, and 15/15 is obviously 100%. Where does 97% come from? Are these numbers real? What’s the outcome measure if it’s not dogs that had their infestation eliminated?

They also say “The control at day 15th put in evidence a 80-90% reduction in parasites”

  • What control? How many dogs? What kind of infestation?
  • Also, if there was an actual control group, why report results for it at day 15, and results for the test group at days 7, 9 and 35?

More red flags.

They also claim efficacy based on a 2018 study that was done by VCA, to see “whether or not the European-manufactured, ultrasonic pest-repellent technology of TICKLESS is as effective on pets in the United States as it is on the European counterparts.” But, there’s nothing published about this study, VCA personnel are not quoted in any of the study materials and I can’t see any reports by VCA about the results. That raises a few more red flags.

The content of this study also raises lots of concerns. It reportedly involved giving out collars to 100 dogs. Owners filled out a questionnaire before and after the study period. They said: “The outcome of the test gave a clear picture on the efficacy of the ultrasonic tick and flea repellent since 94% of all pets involved stayed totally free of ticks and 88% stayed totally free of fleas thru out the whole test period.” But…

  • What percentage of dogs without a collar would have been tick-free in these areas anyway?
  • Were any of these dogs also on tick prevention medication?

Without answering those two questions, we can’t interpret anything from this “study.” These results could mean the product worked, it did nothing, or that it was a tick magnet.

They also said that 6% of owners reported finding fewer ticks than normal and 12% reported finding fewer fleas. That’s not actually an encouraging number since there’s likely a placebo effect with subjective assessments like that.

A proper study would have had a control group of dogs with an inactive collar, randomization to provide dogs with either the active or inactive collar, specific criteria for whether or not the dog could be on tick preventive medications, and more detailed information on infestations. That’s a really basic study design, and as cheap and as easy as doing what they did. So why didn’t they do it properly? It’s hard to say… lack of understanding of the basics of study design? Not wanting to actually know whether it works? Not having confidence that it works? Just looking for something that can go on advertising materials (e.g. “scientifically tested”)? Who knows. All I can say is that this study had no hope from the start, and tells us nothing apart from the company can’t or doesn’t want to design a proper trial.

Are there concerns about overuse of anti-parasitics in pets?

  • Yes, absolutely. These products are quite safe overall but no drug is 100% safe. Some animals experience adverse effects.
  • There are also poorly understood but increasing concerns about the environmental impacts of these drugs (since they are excreted in urine and feces).

I’d love to have a non-pharmaceutical, safe, effective and affordable tick repellant. (I’d love one for me and my pets, especially if it kept mosquitoes away too!) But as much as l’d like this product or similar products to work, we don’t have any evidence that they do. Ticks, mosquitoes and fleas account for massive impacts on human as well as animal health. If we had a safe, effective non-pharma approach, we’d use it. That’s a multi-billion dollar market just waiting for the right product. The fact that we don’t have an effective product on the market even for people shows that we don’t have one that works.

These products themselves are likely relatively harmless, but there’s a potential harm component when people try to use them and therefore forego effective treatments.

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Regulatory bodies sometimes issue “Dear Veterinarian” (or similar) notices about important issues pertaining to drugs and rug use, like the recent FDA’s letter to veterinarians about extralabel use of fenbendazole in dogs.  These notices are used to get important information out to veterinarians, to try to head of future problems.

My topic du jour doesn’t deal with a drug per se, but it’s an important issue that’s outside of any regulatory control. So I’m issuing my own “Dear Veterinarian” letter about the antibiotic nitrofurantoin. It’s not about risks from the drug itself, but rather the risks from how veterinarians use it – largely because of poor information received from diagnostic laboratories.

FOR IMMEDIATE RELEASE (from the desk of JS Weese)

June 17, 2025

Dear Veterinarian:

Nitrofurantoin is an antibiotic that can be very effective for treatment of lower urinary tract infections (e.g. bacterial cystitis) in dogs and cats. However, it only achieves useful drug levels in urine. Therefore, it is not useful for treatment of infections outside of the bladder.

Standard practice is for diagnostic laboratories to not report nitrofurantoin susceptibility for non-urine samples. Unfortunately, they often do anyway. This can lead to inappropriate use of this drug, with potentially serious consequences for the animal.

Sometimes, this occurs because veterinarians fail to indicate what specimen they’ve submitted for culture (e.g. urine vs wound swab). This highlights the importance of veterinarians providing  laboratories with basic specimen information and patient history so the lab can 1) determine whether to report nitrofurantoin susceptibility and 2) determine which breakpoints to use for reporting susceptibility to other antimicrobials (since breakpoints for a few drugs vary between urine and non-urine).

However, all too often laboratories still report nitrofurantoin susceptibility in specimens that are clearly non-urine. This can lead to use of nitrofurantoin by veterinarians for conditions where there is no potential for the drug to be effective, such as wound infections. This can lead to a delay in providing appropriate treatment, progression of disease, and in some situations, death.

While is it the responsibility of veterinarians to understand the drugs that they use, inappropriate reporting of nitrofurantoin susceptibility for specimens not associated with lower urinary tract disease is a major contributing factor to the inappropriate use of this drug that needs to be avoided. Veterinarians need to be aware of this issue to avoid unnecessary animal disease and death.

Sincerely,

Signed: Someone with no regulatory power but who’s tired of dealing with patients that have been harmed by misuse of this drug.

PS: Diagnostic laboratories, if you can’t figure out how to selectively report nitrofurantoin susceptibility only for lower urinary tract specimens, can you please at least put a ‘*’ with the “S” to note that this only applies to treating cystitis?

I’d love to see labs come out with a policy that “if we report something wrong, the test is free.” That seems reasonable to me, and it would provide an impetus for labs to do better at reporting and motivate veterinarians to better understand testing and results, and encourage reporting of issues to labs.

Laboratories aren’t perfect, and neither are their tests. While we’d like them to be perfect, that’s a very high bar. That said, there is some low hanging fruit that would certainly get us closer: things like better nitrofurantoin susceptibility reporting are straightforward and would save some lives.

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Veterinarians sometimes ask me, “Can I give a half dose of a vaccine to small breed dogs?” But more often they say, “An owner wants me to give their small dog a half dose of a vaccine because they are worried about adverse effects. Should I do that?”

The short answer is there is no evidence that decreasing the vaccine dose will have any impact on adverse events, and no data to know what impact it will have on the desired immune response.

Here’s a bit on the longer answer. The key issues are:

  • We don’t know if lower doses of vaccine work in dogs and cats.
  • We don’t know if lower doses of vaccine reduce the risk of adverse events.

It’s possible that lower doses would work and be could carry a lower risk of adverse effects. It’s also possible that lower doses would not provide good protection against the disease for which the vaccine is being given, and would still carry a similar risk of adverse effects, meaning we’d be getting little benefit from the vaccine while maintaining risk. That’s not good.

Why are vaccines dosed per dog (or cat, or person), rather than based on size like other medications?

Vaccines are not like drugs that are dosed to try to reach a certain concentration in blood or tissue, which requires higher doses for larger individuals. Vaccines predominantly work locally in the body, at or near the vaccination site. It doesn’t matter if the individual is big or small, the vaccine still does its work in a small location. We get similar immune responses to the same dose in large or small individuals.

That said, there are some data on the impacts of different vaccine doses on vaccine response and adverse effects. There’s no consistent association, as the vaccine type, target disease and age of the vaccinated individuals all play important roles in response. While we often focus on animal size, age may be a bigger factor and one that’s not usually on the radar.

  • In humans, the approach to vaccination sometimes varies based on age (so indirectly on size, but age is the focus). Vaccines designed for older individuals sometimes have higher antigen loads because the immune response weakens with age. For example, there’s a high dose flu vaccine for seniors, and an older shingles vaccine had 14 times the antigen load of the version used to vaccinate kids against chickenpox (both caused by the same virus). Those products were designed based on concerns that older individuals need more antigen to properly stimulate the immune response, not that we want to use lower doses in smaller individuals.
  • In contrast, the Tdap (tetanus, diphtheria, pertussis) vaccine for young kids actually has more antigen compared to that for older kids and adults. Lower doses for older individuals are meant to reduce adverse reactions, but that’s based on age, not size.

Do lower vaccine doses work, and do they reduce adverse events in pets?

We don’t know, since it hasn’t been studied properly in dogs and cats. While we have to remember that dogs are not people, and that vaccines used in different species also differ, as do the approaches to vaccination (especially frequency of vaccination), we can gain some insight on this from human studies.

A small study of pre-term infants looked at the effects of some physicians using half-dose vaccines (Bernbaum et al. 1989). They showed that 96% of pre-term infants that got the full dose of diphtheria/tetanus/pertussis vaccine responded adequately, while only 45% that got a half dose responded adequately (even after 3 doses), and an extra full dose was required to generate an adequate response.

In contrast, there are a few studies looking at half doses of COVID-19 vaccines, but it’s important to bear in mind that these use different vaccine technology to what is currently used for animal vaccines. COVID-19 vaccine developers also may have erred on the side of extra antigen because of the need to get these vaccines to market ASAP during the pandemic. So it’s a bit of an apples-to-oranges comparison, but shows that it’s fair to look at what happens with lower doses. A few studies showed that lower doses are likely protective, but that there’s no clear evidence that there’s an impact on adverse events.

  • One study (Valim et al. 2022) was a non-inferiority trial that aimed to see if a half dose of the ChAdOx1 COVID-19 vaccine was no worse than a full dose. (That’s the Astra Zenica vaccine that was rolled out initially but was largely phased out when RNA vaccines became available). They showed that the half dose was non-inferior (23.7 vs 25.7 cases of illness per 1000 people/year). The frequency of adverse events was also similar. So, this the lower dose of the vaccine was similarly effective as the full dose, with no difference in safety profile.
  • Another study of the same vaccine (Galvao-Lima 2023) showed that two half doses were similarly protective as two full doses, in terms of prevention of moderate to severe COVID-19 disease. There was no reporting of adverse event rates, so we can’t really interpret much from this.
  • A small study of the Pfizer COVID-19 vaccine (Batmunkh et al 2024) looked at antibody response and adverse effects to full or half doses in people who had already received an initial COVID-19 vaccine series (any type). They found that the half dose was non-inferior to the full dose in terms of the antibody response for most individuals, but it was not as good for those who had received the Gam-COVID-Vac (Sputnik vaccine) for the initial series. Safety data were pretty limited, and the analysis was weak, so I don’t think we can conclude anything about that particular aspect, but it’s more evidence that COVID-19 vaccines can be effective at lower doses.

The first take-home message is that lower doses of vaccines probably work quite well – at least for some vaccines in some populations (I wouldn’t be as confident about the effectiveness of lower doses in seniors or other individuals who might have a harder time responding to a vaccine).

  • That makes sense, since manufacturers don’t aim to find the absolute lowest antigen load that will work in the average person. They want their vaccines to work for the vast majority of the population, across the gamut of immune responses. Many or most individuals would response to less antigen than what is in the vaccine, but some probably do require the full dose – we just can’t easily tell who needs what.

The second take-home message is that there’s not really any clear evidence that reducing the vaccines dose reduces adverse effects. It seems logical that it would, if adverse effects are linked to the magnitude of the immune response and if the magnitude of the immune response varies with dose. However, since vaccines largely work locally, there’s nothing indicating that size is a component of this, and age probably plays more of a role. In dogs, breed does too. While we know that certain things may increase the risk of an adverse event after vaccination, we don’t have much supporting data that dropping the vaccine dose by a half helps to decrease the risk.

Do we have any data regarding using lower vaccine doses in dogs and cats?

No. Some people point to a 2015 study by a controversial veterinarian (who has been cited for practicing without a license on multiple occasions, markets unvalidated tests and pushes various narratives that are well away from the mainstream) (Dodds, AHVMA 2015).  It looked at half dose distemper/parvo vaccination vs full dose in 13 adult dogs (with only 8 dogs tested at some points because they somehow “inadvertently discarded” many samples). The study is small, very weak, doesn’t mention any ethics approval, and it’s unclear if validated tests were used – so it really can’t tell us anything. Even if the data are valid, we have to remember that this involves older (3-9 year-old dogs) that had been previously vaccinated with vaccines that are really effective, so they have a very well primed immune response.  But even then the data aren’t convincing. They showed that some (not all) dogs had increased titres after half dose vaccination, but there’s no control group that received the full dose vaccination, no group that was unvaccinated, and no statistical analysis. They also didn’t look at adverse events. So, I don’t think we can say anything at all from this study, which leaves us with no real data about half vs full dose vaccine administration in dogs and cats.

Is there liability for veterinarians if they don’t administer a full vaccine dose?

Veterinarians are expected to act professionally and reasonably, which includes communicating with owners and discussing options about their animals’ care. However, veterinarians are not expected (and in fact are expected NOT) to simply do what owners request if it’s medically (or ethically) inappropriate. Regulations and legalities vary by region but in general, owners cannot consent to malpractice, so client consent is not an automatic “get out of jail free card” if a veterinarian does something wrong. Even if the client thinks it’s a good idea and specifically requests it, the veterinarian is the professional and must use their expertise to assess the situation and what is or is not appropriate for the patient, so there is a professional risk to the veterinarian as well. Is giving half-dose vaccines malpractice? I’m not a lawyer so I can’t say, but I can think of some important considerations:

  • If a veterinarian gives a half dose of rabies vaccine and issues a rabies certificate or indicates the pet is “properly” vaccinated against rabies (according to the manufacturer’s instructions, which is part of the regulation in Ontario), I’d consider that fraud and malpractice.
  • If a veterinarian gives a half dose of another vaccine and implies that it will work equally well as a full dose, that’s a big concern. It’s using a vaccine off-label without consent.
  • If a veterinarian gives a half dose of another vaccine and tells the owner it may or may not work, that’s probably defensible, but it would be a grey area. If the dog later had a problem (e.g. got sick) and the owner complained, the question might be how well the veterinarian really discussed the issues and risks. Owners can’t give informed consent if they are not adequately informed. If the veterinarian made the recommendation (versus giving into the owner’s request), then I suspect the liability increases, since a veterinarian’s recommendation/suggestion would reasonably be taken by an owner as an indication that the approach is safe and effective.

What should veterinarians do when pet owners are concerned about adverse events after vaccination?

The first and most important step is communication – that’s where things often fall apart. We have to acknowledge that vaccine adverse events are real and can happen to any dog, but are more common in certain breeds (especially small breeds). However, these event are still uncommon, and serious adverse events are quite rare.

A very large study of dogs reported an adverse event rate of 0.19% (19.4 adverse events per 10,000 visits) within 3 days of vaccination (Moore et al. 2023). The serious adverse event rate was even lower, around 2.9/10,000. Rare isn’t zero so we still have to be aware of the risk, but we also have to keep it in perspective. If reducing the dose of vaccines reduced adverse events by let’s say 15% (just to pick a number), that would drop the serious adverse event rate to 2.5/10,000. That’s an absolute risk reduction of 0.4/10,000 visits. We’d need to give 25,000 dogs a half-dose vaccine to prevent one severe reaction, but it’s possible we’d be trading that for an equal or greater increase in risk from the disease we’re trying to prevent with the vaccine. We just don’t know.

If an owner is concerned but their pet has never had a vaccine reaction before, talking about the overall low risk and the measures that can be taken to detect and address vaccine reactions is a good start.

If the individual animal has had a vaccine reaction in the past, then we should do a risk assessment and tailor the vaccination program for that pet to help decrease the risk. That could entail no longer vaccinating against all diseases, no longer vaccinating against some diseases (e.g. stop distemper/parvo vaccination but continue for rabies and lepto), changing vaccination regimens (e.g. splitting vaccines over multiple visits), vaccinating after pre-medication, or continuing to vaccinate as per usual, but being ready to respond if there’s a problem.

Is the issue of vaccine reactions in small breed dog actually related to size or breed?

That’s an important question, since I think many people often think “the dog is smaller, so the dog should get a lower dose,” like we do for drugs. It’s a logical inference, but if we look at the Moore study, breed played a big role. The table below shows the differences in adverse event rates between breeds. Small breeds dominated the highest risk breeds, but whether that’s because of their size or genetic factors is far from certain. Since some larger dogs cracked the top 10 list as well, we have to consider that genetics play an important role, and that size may just be along for the ride.

We can say that small breeds are higher risk for adverse events, but that’s not necessarily because they are small, it might be because of their genetics. Disentangling those is tough. If anything, we probably should explore safety and efficacy of lower doses in higher risk breeds (not just “small dogs”), and look at the impact of age on vaccine response too.

Key points:

  • Half dose vaccines likely work in some, if not most, animals, but we don’t have any data to provide any confidence in that hypothesis.
  • We have nothing to suggest that lower vaccine doses reduce adverse events.
  • Higher adverse event rates in small breed dogs might be in part due to their size, but genetic factors likely play a big role.

Ultimately, I think using half doses of vaccines is bad medicine, since we are creating risk (potential for a poorer response, albeit low, which creates higher risk of disease) in the absence of any reasonable evidence that there’s a corresponding benefit (of any sort, let alone one that results in a net benefit).

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If I’m talking to veterinarians or veterinary students about infectious diseases and I mention Capnocytophaga canimorsus, I usually get a blank stare (or “capno-what?”). If I’m talking to physicians, it’s usually the same response, unless they’re infectious disease physicians or trainees (but I still get “capno-what?” from some of them on occasion).

Capnocytophaga canimorsus is a bit of a niche zoonotic bacterium, but it’s an important one. It can be found in the mouths of most dogs, so people are really commonly exposed, but human infections are rare. However, when infection does happen, it tends to be very severe or even fatal. Not having a spleen (e.g. if a person had to have their spleen removed at some point) is a huge risk factor for infection. Other types of immunocompromising disorders and alcohol abuse are other known risk factors.  For more details on Capnocytophaga, check out the infosheet in Worms & Germs Resources – Pets page.

A recent case report (Sorensen et al, 2025) reminds us that the risk of infection with this bacterium is no solely from dogs; the report describes a severe Capnocytophaga infection in a person linked to a cat bite.   Cats can also carry Capnocytophaga in their mouths, but it’s much less common than it is in dogs.

The affected patient was a 53-year-old man who (unsurprisingly) didn’t have a spleen and was heavy alcohol user (two big risk factors for infection). He had a two-day history of fever, chills, diarrhea and lethargy, with progressive weakness and decreased mental acuity. He then developed a purplish discolouration on his face, back, arms, legs and abdomen. He was taken to the emergency room, where a small cat bite was noticed. He then deteriorated quickly.

It’s not clear whether seeing the bite wound changed their initial approach, but he got the infectious disease kitchen sink treatment: ceftriaxone, vancomycin, azithromycin and atovaquone.  Despite this, his disease progressed to severe septic shock, DIC, purpura fulminans and multiorgan failure. Blood cultures were negative, so antibiotics were changed to meropenem, vancomycin, doxycycline and penicillin, and molecular testing was done to look for a fastidious bacterium. That’s how they detected C. canimorsus.

Although the patient gradually improved, the severity of infection resulted (as is common with this disease) in the need for multiple amputations. Both his legs were amputated below the knee, along with multiple fingers. (There are photos included in the case report.)

The authors concluded “Although C. canimorsus is typically associated with dog bites and scratches, it can show up after exposure to cats, as seen in this case, and should be considered along with more common pathogens such as Pasteurella multicoda and Bartonella henselae.”

A common issue with C. canimorsus infections is not considering it until it’s too late. I’ve talked to many family members of people who had this infection, and a common theme is that there was no querying of animal contact or animal bites until after the diagnosis was eventually made, and the family didn’t think to report any animal bites (when they knew about them).

Animal contact and bite history can be really important when someone gets sick, and is takes seconds to ask, but too often the question is never asked. That’s a healthcare gap. At the same time, we need better education of the public so that people can advocate for themselves and know to tell healthcare providers about animal contacts, especially animal bites.

I’ve written a lot in general about the risks of rabies and other infectious diseases from imported dogs. However, we have to remember that borders are political, not biological, and that rabies (like certain US presidents) doesn’t respect such borders, whether they’re between countries or between provinces. 

Whenever we move animals or people, we risk moving diseases with them. In 2021 and 2022, we detected two rabid dogs in Ontario that were both imported from Iran. However, there are also risks with movement of people or animals from different risk areas within the same country, particularly very large countries like Canada. Arctic fox-variant rabies is present right across the north in Canada (see map below), and there is always a risk of it spilling over into dogs in northern communities. Then sometimes, those dogs get moved south and bring rabies with them. It’s happened before, and it’s just happened again, this time involving a dog from Nunavut that was moved to Winnipeg MB, where is subsequently developed rabies. Here are some of the highlights of the case:

  • A 1.5-year old dog in a community in Nunavut was seen chasing a fox, along with some other dogs (which is not an unusual occurrence in the north) on February 27. It wasn’t clear (or at least not reported) whether there was any direct contact with the fox. If a dog has contact with an unusual fox and/or there is a chance the dog was exposed to saliva from such a fox (which is how rabies is transmitted), the typical recommendation would be to keep the dog under observation or confined for up to 6 months depending on its vaccination status and whether it’s able to receive a rabies vaccine within 7 days of the exposure. However, this isn’t always feasible in northern communities where dogs are often allowed to roam extensively and access to veterinary services and vaccines is very limited. It’s also important to remember that there is always a risk that dogs allowed outside unsupervised (even in the south) can have unobserved contact with wildlife, which puts them at risk for rabies exposure.
  • The dog was then moved by a dog rescue group from Nunavut to Winnipeg on March 31 where it was quarantined for 2 weeks. This kind of quarantine after transport is a good general infection control practice for other disease that may come to light after the stress of travel, but it’s not long enough to rule out the risk of rabies. After arrival in Winnipeg, the dog was vaccinated against rabies and then spayed a couple of weeks later.
  • The dog began showing signs of rabies on April 18, two days after the spay. Signs included hypersalivation, stargazing and aggression. It died two days later, and tested positive for rabies. Typing of the virus will presumably confirm the Arctic fox variant.

As is normal, there was an investigation to identify people and animals that might have been exposed to the dog during the short period when it would have been infectious (up to 10 days prior to starting to show clinical signs). “Several” people are receiving rabies post-exposure prophylaxis (PEP), including three who handled the dog when it was sick. Most likely, many of these people had little or no true risk of exposure, but understandably public health tends to very much err on the side of caution when it comes to rabies exposure in people. 

It was reported that “One dog in the foster home received post-exposure vaccination but does not require a quarantine as it was fully vaccinated prior to its exposure.” That’s because if the dog was vaccinated and received a booster within 7 days of the potential exposure, it would typically only be subject to an observation period, which is much less strict than a quarantine or confinement period which is used for higher-risk dogs.

Two other related dogs were moved from the community over a six-week period, but they were transported at different times and had no contact with the affected dog since February. So while those dogs would have the same risk of exposure to an infected fox as any dog in the community, there was no increased risk due to exposure to the dog that developed rabies, because there was no contact during the dog’s potential infectious period (starting from approximately April 8).

We can’t eradicate rabies from wildlife across Canada, particularly in areas like the north where populations are so widely dispersed and often inaccessible. Wildlife-to-domestic animal contacts always carry some degree of disease transmission risk, and the risk of rabies is particularly high in endemic areas when reservoir species like foxes are involved. When we move at-risk dogs, we then create additional risks for others. 

That isn’t to say we shouldn’t move dogs at all, as there are sometimes compelling and compassionate reasons to do so. But we need to take some basic precautions and always be aware of those risks. Ideally, we’d start by improving rabies vaccination of dogs in northern communities, which not only helps keep the dogs safe, but also protects community members who live in close contact with free-roaming community dogs. However, there are a lot of barriers to providing vaccination and other basic veterinary care in the North. Cases like this, and like the recent cases of confirmed rabid foxes in northern Ontario, highlight the importance of working together as a society to help overcome these long-standing barriers.

Distribution of rabies virus variants in Canada, 2016 to 2020 (Public Health Agency of Canada)

Last week I wrote about the recently updated ISCAID antimicrobial use guidelines for canine pyoderma, specifically regarding surface pyoderma. The full guidelines are freely available online (Loeffler et al. Vet Derm 2025). Today I’m going to cover the highlights about the “big one”: superficial folliculitis. I call it the big one because it’s so common in dogs, and it’s the one where we can have a big impact by convincing more people to using topical treatment as the first option, instead of reaching for systemic antimicrobials.

The three most important points to remember about superficial folliculitis in this context are:

  • It’s a staph-driven disease.
  • It basically always has an underlying cause, particularly allergies (e.g. food, flea, atopy). If we don’t address the underlying cause, the infection will inevitably come back. Too often, the underlying cause doesn’t get addressed, or doesn’t get addressed until multiple rounds of infection have occurred.
  • It’s a superficial infection, so we can approach it from the surface (topically). 

Here are the main treatment recommendations from the new guidelines. For full details, as well as information about diagnosis and other issues, check out the complete document.

  • Diagnosis is based on clinical signs and cytological analysis (cocci and neutrophils)
  • Topical antimicrobial therapy as the sole antibacterial treatment is the treatment-­of-­choice. The best evaluated treatment is 2-4% chlorhexidine.
  • Response to topical therapy should be re-­assessed by a veterinarian after 2–3 weeks of treatment.
  • Topical treatment should be continued until the lesions have resolved and underlying problem has been addressed (when possible).

When are systemic antimicrobials indicated for superficial folliculitis?

This choice is mainly based on owner and patient factors, not the disease. There are no clinical reasons to use systemic over topical antimicrobial therapy alone. However, if the owner cannot or will not treat the dog topically, then systemic antimicrobials are indicated. Systemic antimicrobials can also be considered if there has been no response to 2 weeks of topical treatment, but other causes (e.g. uncontrolled underlying disease, or a different disease) are more likely if compliance with the topical treatment was actually good and there was no response.

Culture and susceptibility testing is recommended if systemic antimicrobials are used. It’s particularly important if there are risk factors for resistance, such as previous rounds of antimicrobial treatment. 

  • The authors of these guidelines had a lot of debate about this. Ideally, we culture every time we’re thinking about using a systemic antibiotic. If the animal is not at high risk of having a resistant infection, culture is less valuable, and cost becomes an issue, so it’s fair to not culture cases where the risk if resistance is likely low. However, it’s best practice to culture whenever we can.

Additional treatment recommendations from the new guidelines include:

Clindamycin, cefalexin, cefadroxil and amoxicillin-­clavulanate are the recommended first line options for superficial follicultis if systemic antimicrobials are warranted. 

  • If there’s a suspicion (based on cytology) that the infection is not caused by staph, then a culture would be indicated because these drugs focus on staph.
  • Adjunctive topical treatment should be used in addition to systemic antimicrobials whenever possible. 

How long should systemic antimicrobials be given?

  • “An initial 2-­ week course may be dispensed, and an appointment for re-­examination by a veterinarian should be scheduled before the end of the course to determine whether systemic treatment can be stopped or whether longer treatment is required.”
  • “Clinical resolution of superficial pyoderma can be assumed, and systemic antimicrobials stopped when primary lesions of pyoderma (papules, pustules and erythematous epidermal collarettes) are no longer found.”

Long-term management of superficial folliculitis

  • Addressing the underlying disease is critical. It can take time and money, but will reduce disease (and also ultimately save time and money).
  • Regardless of whether systemic or topical treatment is used, “topical treatment can be continued longer than systemic therapy, and is potentially life-­long, where the primary causes cannot be resolved and the risk of recurrence remains.”
  • “There is no evidence to support extending systemic antimicrobial therapy beyond the resolution of clinical signs associated with infection; instead, underlying primary causes must be identified and addressed.”

Up next: recommendations on the nastier and more complicated condition, deep pyoderma.