Q&A on leptospirosis: Urban risk, missed vaccines, and diagnostic mistakes

Once thought to affect only dogs with specific, identifiable risk factors, leptospirosis is increasingly being diagnosed in a broader range of patients. In this Q&A adapted from a 2026 Veterinary Meeting & Expo lecture, Jane Sykes, BVSc, DACVIM (SAIM), PhD, MPH, MBA, FNAP, traces the convergence of urban wildlife, social factors, and missed vaccinations driving the disease’s spread. She also explains why diagnosis can be deceptively difficult, outlining how veterinarians can avoid common pitfalls, and discusses what researchers still don’t fully understand.

Sykes is the lead author of the 2023 American College of Veterinary Internal Medicine consensus statement on leptospirosis in dogs. Currently, she is a professor of medicine and epidemiology at the University of California, Davis, School of Veterinary Medicine.

dvm360: Cases of leptospirosis are appearing in otherwise healthy dogs, including puppies. What factors are contributing to these cases in the US?

Sykes: That's a really great question and something that we're actively involved in researching. It does seem like it’s multifactorial. In big cities, it’s likely associated with population growth and rodent proliferation. New evidence suggests rodents might be an important source of infection for dogs.

We also studied an outbreak in West Los Angeles (LA) which was driven, in part, by overcrowding at boarding facilities. We don't know for sure whether dog-to-dog transmission occurred in those doggy daycare-type environments, but we do know that the boarding itself was a risk factor. It might have been due to rodent problems in those facilities, or it might have just been the result of overcrowding, with many dogs in close contact with one another.

We’re also studying an outbreak associated with homelessness and dogs of the homeless. We know that dogs that are in homeless encampments are also at risk for leptospirosis.

Most importantly, however, not being vaccinated is the biggest risk factor. In the LA outbreak, affected dogs were either completely unvaccinated or they had only received one dose without the follow-up booster 3 to 4 weeks later. Many vets didn't even carry leptospirosis vaccines.

Some dogs began getting vaccinated when they started developing leptospirosis. Owners rushed their dogs in for vaccines after hearing about outbreaks in the region, but it was too late. Other dogs acquired the infection before the second dose was administered—before they were able to get protection from a second vaccine.

Again, the disease in puppies is related to the fact that it's difficult to vaccinate a dog by the time they’re 3 months of age. You can start vaccination at around 8 to 9 weeks of age, depending on the vaccine label, with a second dose 3 to 4 weeks later, plus an additional week needed for adequate immunity. It's difficult to get puppies vaccinated in time, and it probably explains some of the cases in this group.

Geriatric and small-breed dogs are also at risk because owners often assume older or small dogs don’t need vaccination.

There’s good, new evidence that the current leptospirosis vaccines are very safe. Studies show adverse reaction rates in small breeds are comparable to those for distemper, hepatitis, and parvovirus vaccines. While we don’t know all circulating serovars nationwide, in the LA outbreak, we identified Canicola through culture. The available four-serovar vaccines do seem to be preventing leptospirosis because we’re pretty much only seeing it in dogs that were not properly vaccinated.

dvm360: What are some common pitfalls you see in leptospirosis diagnosis in clinical practice?

Sykes: This is a great question and is one of the reasons why lepto is such a good disease to talk about to vets: it's really about understanding infectious disease diagnostic testing.

The traditional gold standard is the microscopic agglutination test (MAT), which measures antibodies to various serovars. But because leptospirosis is an acute disease, dogs often haven’t had time to mount an antibody response when they first present. Early serologic tests, including MAT, are often negative or show very low titers. A common mistake is to rule out leptospirosis based on a single early test. You should follow up with a convalescent titer 1 to 2 weeks later to document seroconversion. In practice, many vets wait too long, or owners don’t return once the dog improves, which can complicate diagnosis.

Another challenge is subclinical exposure. Many dogs are exposed but never get sick, yet they develop positive antibody titers. For example, a dog with acute kidney injury from ibuprofen toxicity might have a positive lepto titer from prior exposure, and you might be inclined to say that the dog has leptospirosis, when, in fact, it just was previously exposed subclinically and now it has ibuprofen toxicity. Point-of-care tests can make this more complicated. A rapid test might be negative early in illness or positive due to previous exposure, leading to over- or under-diagnosis.

Regarding commercial rapid tests: the Zoetis Witness detects immunoglobulin M (IgM), indicating recent exposure, while the IDEXX SNAP Lepto test detects IgG, which can reflect past exposure. Dogs can test negative early on with the Witness test and then convert to positive a week later, so timing is critical.

The other group of tests is the PCR-based assays, which a number of different laboratories offer. It’s recommended to test both blood and urine, because early in infection, organisms are present in the blood, and later they are shed in urine. When a dog presents, it’s often unclear which stage of illness it’s in, so both samples should be submitted.

Urine PCR is generally more sensitive than blood, but antibiotics can quickly produce false negatives. Some healthy dogs may shed leptospira DNA without clinical disease. There was a study looking at healthy shelter dogs in Tennessee, Virginia and Kentucky, and over 10% of those healthy shelter dogs were shedding lepto DNA in their urine.

So, dogs can act as carriers, and we've seen some dogs come in that probably had other causes of kidney disease because the pattern of their abnormalities did not align with lepto but we detected lepto DNA in their urine. So, on blood, you can trust it, but on urine, you need to be cautious in interpreting it and make sure that the clinical signs are consistent with lepto.

PCR in general, is often not that sensitive, so if you get a negative urine PCR, it certainly does not rule out leptospirosis.

dvm360: Are there any gaps in leptospirosis research that you believe still need to be addressed, and are there any developments that you anticipate in the next few years?

Sykes: Yes— still don’t fully understand transmission cycles in dogs, which is the focus of our current research. We’re trying to figure out which serovars are circulating among different animal species and in the environment, and what the risks are to humans. Studying this is tricky — the best approach is whole genome sequencing on isolates from urine. In the West Los Angeles outbreak, we found that post-peak, organisms from different dogs were slightly different, suggesting little dog-to-dog transmission during that period, though it could have occurred at the peak.

We need more studies like this to clarify the role of rodents and urban wildlife in transmitting infection to dogs and to map what’s circulating in the environment. It’s really a One Health problem.

We also need broader vaccines that aren’t serovar-specific. Right now, understanding serovars is essential because vaccines are serovar-specific. But once we have non-serovar-specific vaccines, knowing the exact serovars won’t be as critical.