Leishmaniasis in dogs in the US: an under-recognized disease that is already here

In 30 seconds

Most US owners assume leishmaniasis is a Mediterranean or Latin American problem that stops at the border. It does not. The parasite is established in American Foxhounds across the country, it rides in with the roughly one million dogs imported each year from endemic regions, and sand flies capable of carrying it live in the southern US. The single most important US difference: there is no USDA or FDA-licensed canine leishmaniasis vaccine here, unlike parts of Europe. Treatment controls the disease for years in many dogs but does not clear the parasite, and the prognosis turns on whether the kidneys are already involved.

What causes it, and what carries it

Canine leishmaniasis is caused by a protozoan parasite, almost always Leishmania infantum in the dog (Merck Veterinary Manual). The same species can infect people, which is why this is treated as a zoonotic disease worldwide (CDC).

In endemic countries the parasite spreads through the bite of female phlebotomine sand flies. In Europe and the Mediterranean the vector is Phlebotomus; in the Americas it is Lutzomyia. Lutzomyia shannoni is present in the southern and southeastern US and is recognized as a potential vector of Leishmania there (Petersen and Barr, 2009). Two other New World species in the South, Lutzomyia diabolica and Lutzomyia anthophora, are also named among the Lutzomyia sand flies considered competent or suspected vectors of Leishmania in the country (Beasley et al., 2022). Their range covers a broad band of the South, so the conditions for local sand fly transmission exist on US soil even though documented vector-borne cases here remain rare.

Why it is in the US at all

Three pathways keep canine leishmaniasis present in the country.

The Foxhound epizootic. The first US outbreak was identified in 1999 in a Foxhound kennel, and within a few years seropositive Foxhounds had been documented across dozens of kennels in more than 20 states and parts of Canada (Petersen and Barr, 2009). What made this striking is how it kept spreading. In this hunting-hound population the parasite passes efficiently from dam to puppies before or around birth, a route called vertical or transplacental transmission (Boggiatto et al., 2011). That mechanism lets the infection persist in a kennel line for generations without any sand fly at all, which is why American Foxhounds are the breed most associated with the disease in the US.

Imported and returning dogs. Around one million dogs enter the US each year, many from countries where leishmaniasis is endemic around the Mediterranean basin, in Latin America, and elsewhere, and there is no mandatory Leishmania screening at import (CAPC). A dog adopted from southern Spain, Italy, Greece, or Brazil, or one that traveled there with its family, can be infected and not show signs for months or years.

A competent vector already here. Because Lutzomyia sand flies live in the southern US, an imported infected dog moving into that range adds the one ingredient local transmission would need. US-acquired vector-borne cases have been hard to confirm, but the parasite recovered from US hounds remains infective to sand flies under study conditions, which is the basis for treating local spread as a real, if low, risk (Schaut et al., 2015).

What it looks like in the dog

Leishmaniasis is a slow, systemic disease, and the signs are easy to mistake for other chronic conditions. Many infected dogs stay subclinical for a long time. When disease appears, common findings include (Merck Veterinary Manual):

Skin changes: scaling and dandruff-like flaking, hair loss especially around the eyes and on the ears and muzzle, thickened crusty skin on the nose and footpads, and slow-healing ulcers over bony points.
Overgrown brittle nails, a classic if inconsistent clue.
Weight loss and muscle wasting despite a normal or reduced appetite, often with lethargy.
Enlarged lymph nodes and sometimes an enlarged spleen.
Eye disease: conjunctivitis and uveitis.
Nosebleeds, lameness, and fever in some dogs.

The finding that drives prognosis is the kidney. Leishmaniasis triggers immune-complex deposition in the kidneys (glomerulonephritis), and progressive protein loss into the urine and chronic kidney disease are the leading causes of death in affected dogs (Merck Veterinary Manual). Any dog being evaluated for this disease needs urine checked for protein, not just bloodwork.

How it is diagnosed

No single test settles every case, so vets combine methods (CAPC; LeishVet guidelines).

Serology measures anti-Leishmania antibodies, usually by quantitative ELISA or IFA. A high antibody level in a dog with compatible signs strongly supports active disease. Quantitative titers also help track response to treatment.
PCR detects parasite DNA. It is most sensitive on tissue such as lymph node, bone marrow, or skin; PCR on peripheral blood alone can miss infections, so a negative blood PCR does not rule the disease out.
Cytology or histopathology can show the organism directly inside macrophages from a node, marrow, or skin sample.

A complete workup also includes a CBC, a chemistry panel, total protein with serum protein electrophoresis, and crucially a urinalysis with a urine protein-to-creatinine ratio to stage kidney involvement. LeishVet stages dogs from I to IV based on clinical signs, antibody level, and kidney status, and that stage drives both treatment and prognosis (LeishVet guidelines).

Treatment: control, not cure

Owners need to hear this plainly at diagnosis: current drugs reduce parasite burden and clinical signs, but no protocol reliably eliminates the parasite, so relapses occur and most dogs need lifelong management (Merck Veterinary Manual; CAPC).

The two drugs most used in US practice are:

Allopurinol, given orally and typically for many months at minimum, often long term. It is the backbone of maintenance therapy and is widely available in the US. A documented side effect is xanthine crystal and stone formation in the urinary tract, so dogs on it need monitoring (Merck Veterinary Manual).
Miltefosine, an oral antileishmanial. The human formulation is FDA-approved; the veterinary liquid product used abroad is not US-approved, so access in the US is constrained. It is commonly paired with allopurinol.

Meglumine antimoniate, a mainstay in Europe, is not readily available in the US and requires special importation, which is one more reason US management leans on allopurinol-based protocols. Throughout treatment, vets recheck antibody titers, kidney values, and urine protein to decide whether to continue, adjust, or, rarely, attempt to taper.

Prognosis tracks kidney status at the start of therapy. Dogs without renal involvement that are treated and monitored adequately often live for years; a canine leishmaniasis working-group report cites roughly 75 percent of such dogs surviving longer than four years (Roura et al., 2013). Dogs that already have significant proteinuria or chronic kidney disease at diagnosis carry a guarded to poor prognosis, because kidney function can keep declining even when the skin and general condition improve (Merck Veterinary Manual).

Prevention and breeding

Without a licensed US vaccine, prevention rests on cutting exposure and stopping the routes that keep the parasite circulating here.

Reduce sand fly contact if you live in or travel to the southern US or an endemic country. Sand flies are most active from dusk to dawn and in warmer months. Keep dogs indoors overnight during sand fly season and use fine mesh screening.
Use vet-recommended topical repellents. Long-acting synthetic pyrethroid products applied to the dog, available as spot-ons and impregnated collars, are the evidence-based tool for repelling sand flies and are a standard recommendation for dogs in or traveling to endemic areas (CAPC). Choose a product through your veterinarian and follow label intervals.
Do not breed infected dogs. Because vertical transmission sustains the disease in US hound lines, neutering and not breeding seropositive dogs is a primary control measure (Boggiatto et al., 2011).
Do not use infected dogs as blood donors. Transfusion has transmitted the parasite, so a leishmaniasis-positive dog must be excluded from donation (CAPC).
Screen at-risk dogs. Imported dogs, returning travelers, and Foxhounds with vague chronic signs are worth testing, since early diagnosis before kidney damage gives the best outcome.

The public-health note

Leishmania infantum is zoonotic, and dogs are the main domestic reservoir worldwide (CDC). Direct dog-to-human spread does not happen through casual contact; people are infected through sand fly bites, not by petting an infected dog. In a CDC investigation that screened people associated with infected US Foxhound kennels alongside the dogs, no human infections were found, so the practical human risk in the US appears low at present (Duprey et al., 2006). Even so, an infected dog plus a competent local sand fly is the situation public-health authorities watch, which is the real reason vets treat, monitor, and prevent leishmaniasis rather than ignore a disease most US owners have never heard of. People who are immunocompromised should discuss any leishmaniasis-positive household dog with both their physician and veterinarian.

What to check

Whether your dog came from, or has traveled to, a leishmaniasis-endemic country, which is reason to ask your vet about testing.
Whether an American Foxhound or hunting-hound line in your care has been screened, given the breed's known US risk.
Whether any chronic skin, weight-loss, or kidney problem in your dog has had leishmaniasis ruled in or out by serology and, if needed, PCR.
Whether dogs living in or traveling to the southern US are on a vet-recommended sand fly repellent during the warm months.
Whether a diagnosed dog has had a full urine protein workup, since the kidneys decide the prognosis.