New Research Shows Sires Play a Bigger Role in Leishmania Transmission Than We Thought
When it comes to vertical transmission of Leishmania infantum in dogs, the dam has always been the focus. Makes sense, she carries the puppies, she nurses them, she's the obvious vector of concern. But a new study published in PLOS Neglected Tropical Diseases is asking us to look at the other parent, and the findings should change how breeders and clinicians approach canine leishmaniosis screening.
Some Background
Leishmania infantum causes visceral leishmaniasis (VL) in humans and is a zoonotic disease with dogs as the primary domestic reservoir. Classically, transmission happens through sandfly vectors, Phlebotomus in the Mediterranean basin, Lutzomyia in Central and South America. But in non-endemic regions like the United States, sandfly transmission isn't the story. Here, the disease spreads predominantly through vertical, sexual, and bloodborne routes.
In U.S. hunting hound populations specifically, L. infantum is enzootic — meaning it's consistently present — with no evidence of vector-borne spread. The dam's infection status has long been established as a major risk factor for puppy infection. The sire's? Much less studied. Until now.
What the Study Did
Researchers conducted a retrospective cohort study tracking 24 U.S. hunting hound sires and their L. infantum diagnostic status between 2013 and 2022, then followed 183 of their offspring to assess infection outcomes over time. Pups were evaluated via serology and molecular detection.
The Numbers That Matter
Pups born to sires who tested serologically positive for L. infantum in the year of birth had 1.59 times the risk of becoming diagnostically positive during their lifetime compared to pups from negative sires (RR: 1.59, 95% CI: 1.15–2.20, p = 0.0046).
Then there's the R0 — the basic reproductive number, a metric borrowed from epidemiology that estimates how many new cases one infected individual generates. For the sire's indirect contribution to transmission in this cohort, R0 was 3.71. That's not a trivial number. An R0 above 1 means the disease is spreading; 3.71 means each positive sire is associated with nearly four new infections in the next generation.
Why "Indirect" Matters
The researchers describe the sire's contribution as indirect transmission — the sire isn't carrying the puppies, but his positive status significantly predicts infection in offspring. The mechanism likely involves sexual transmission to the dam, who then transmits vertically, or potentially direct transmission to pups via contact. Either way, the sire is not a passive bystander in this disease cycle.
What This Means Clinically
If you work with hunting hounds, work in a state with enzootic L. infantum populations (think the Northeast and mid-Atlantic), or advise breeders of foxhounds and similar breeds, this study has direct implications:
Screening the dam before breeding is not enough. A negative dam bred to a positive sire produces pups at meaningfully elevated risk. Comprehensive pre-breeding screening needs to include both parents — serology at minimum, ideally in the year of planned breeding.
The study also reinforces the broader point that non-vectorial transmission routes deserve more attention in control strategies, not just in the U.S. but globally. Vector control programs are critical in endemic countries, but they won't address the sexual and vertical transmission cycles driving spread in non-endemic regions.
The Bottom Line
A sire who tests positive for L. infantum in the year of breeding is associated with a 59% increase in lifetime infection risk for his offspring — with an R0 of 3.71 in this cohort. This is a significant finding that expands our understanding of disease transmission dynamics and makes a strong case for bilateral parental screening before breeding in at-risk populations.
The dam still matters. The sire matters too.
Duxbury KR, Richer LM, Petersen CA. Sire risk factors for vertical transmission of Leishmania infantum by the dam. PLOS Neglected Tropical Diseases. 2026. doi: 10.1371/journal.pntd.0014303
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