Canine leishmaniosis

What it is

Canine leishmaniosis is caused by Leishmania infantum, a protozoan transmitted by female sand flies (Phlebotomus in the Old World, Lutzomyia in the Americas) that bite at dusk and at night. There is also non-vectorial transmission, through blood transfusions, transplacentally and venereally. In the dog, the parasite lives as an amastigote inside macrophages of the skin, bone marrow, spleen, liver and lymph nodes.

Infection does not equal disease: many infected dogs remain subclinical for years or for life. The course depends on the immune response: an effective cell-mediated (Th1-type) response controls the parasite, while a predominantly humoral (Th2-type) response, with abundant non-protective antibodies, allows it to multiply. Much of the damage is caused by circulating immune complexes, which deposit in glomeruli, vessels, joints and the uvea.

It is endemic in the Mediterranean basin and in Latin America, especially Brazil, and also in the Middle East and Asia; it has spread to areas further north and is diagnosed in dogs that travel to or are imported from endemic areas.

It is a zoonosis: L. infantum causes human visceral leishmaniasis, which is severe especially in children and immunocompromised people, and the dog is the main domestic reservoir. The One Health approach relies on protecting dogs from sand fly bites, controlling vectors and diagnosing and treating sick dogs. Human leishmaniasis is notifiable in many countries, and in some the canine disease is too; control follows each country's official programmes.

Who it affects

Dogs in endemic areas or that have travelled to them, especially those that spend the night outdoors. Disease is more common in young adult dogs and in older dogs. Some breeds, such as the Boxer, Cocker Spaniel, Rottweiler and German Shepherd, appear more predisposed, while the Ibizan Hound usually mounts an effective immune response. Cats are also infected but become ill much less often.

Anatomy involved

• Skin: the most frequently affected organ. The typical form is exfoliative dermatitis with silvery-white scales, mainly on the head, around the eyes ("spectacles") and on the ears, often with alopecia. There are also ulcerative forms over bony prominences, ear margins and mucocutaneous junctions, nodular forms and a mild papular dermatitis at bite sites, typical of dogs with a good immune response. There may be hyperkeratosis of the nasal planum and footpads.
• Kidneys: immune-complex deposition causes glomerulonephritis with proteinuria, which can progress to nephrotic syndrome and chronic kidney disease; there is also interstitial nephritis. Kidney disease is the main cause of death in dogs with leishmaniosis.
• Spleen: splenomegaly from proliferation of parasitised macrophages; the spleen, bone marrow and lymph nodes, which are often enlarged generally, are good sites to look for the parasite by cytology or PCR.
• Eyes: blepharitis, conjunctivitis, keratoconjunctivitis (including keratoconjunctivitis sicca) and anterior uveitis, which can be complicated by glaucoma.
• Claws: onychogryphosis, an excessive, curved growth of the claws that is very characteristic, together with brittle claws and paronychia.

Clinical signs

Signs are highly variable and develop gradually: weight loss with preserved or reduced appetite, muscle atrophy (especially of the temporal muscles), lethargy, generalised lymphadenomegaly, splenomegaly, skin lesions, onychogryphosis, epistaxis, ocular lesions, lameness from polyarthritis and, when the kidney is affected, polyuria, polydipsia and vomiting. Laboratory findings include non-regenerative anaemia, hyperglobulinaemia with hypoalbuminaemia and proteinuria, with or without azotaemia.

Diagnosis

• Quantitative serology (indirect immunofluorescence or ELISA): the basis of diagnosis. High titres in a dog with compatible signs confirm the disease; low titres are not enough and require further tests. In-clinic rapid tests are qualitative.
• Cytology of lymph node, bone marrow or spleen aspirates, or of skin lesions: shows the amastigotes but is insensitive.
• PCR (preferably quantitative) on bone marrow, lymph node, spleen, skin or conjunctival swabs: detects infection, although a positive result in a healthy dog does not mean disease.
• Histopathology with immunohistochemistry of skin or other organ lesions.
• Renal assessment: biochemistry, urinalysis and urine protein-to-creatinine ratio, and IRIS staging.
• LeishVet staging: classifies the dog into four stages (mild, moderate, severe and very severe disease) according to serology, signs, laboratory abnormalities and renal function. It guides treatment and prognosis, which worsens with proteinuria and kidney disease.

Treatment and prevention

First-line treatment combines an antimonial (meglumine antimoniate) or miltefosine with allopurinol, which is continued for months and sometimes for life; aminosidine with allopurinol is a second-line alternative. The availability and legal status of these drugs for dogs vary between countries. Allopurinol can cause xanthine urolithiasis, and antimonials can be nephrotoxic. Proteinuria and kidney disease are managed according to IRIS guidelines. Treatment usually achieves clinical improvement but rarely eliminates the parasite, and relapses are possible; regular clinical, laboratory and serological follow-up is therefore needed. Treating infected dogs without signs or abnormalities with anti-Leishmania drugs is not recommended.

Prevention in endemic areas combines several measures:

• Pyrethroid repellents and insecticides, as collars (deltamethrin, or flumethrin with imidacloprid) or spot-ons (permethrin with imidacloprid), maintained throughout the sand fly season. Permethrin spot-ons are toxic to cats.
• Reducing exposure to the vector, for example by keeping dogs indoors from dusk to dawn.
• Vaccines for seronegative dogs, as a complement to repellents and never instead of them.
• Domperidone, an immunomodulator, in seronegative dogs.
• Not using blood from infected dogs for transfusion and not breeding from infected bitches.

Key studies

• LeishVet guidelines (Solano-Gallego et al., 2011): the reference consensus for clinical management of canine leishmaniosis. It combines review of the evidence, clinical experience and expert consensus, and proposes the four-stage system used to choose treatment, estimate prognosis and plan follow-up.
• World Association for Veterinary Dermatology consensus (Saridomichelakis et al., 2025): a guideline based on a search for randomised trials, systematic reviews and meta-analyses. It recommends meglumine antimoniate or miltefosine with allopurinol as first line and aminosidine with allopurinol as second line; it advises against euthanasia as a public health measure and against anti-Leishmania drugs in subclinically infected dogs. For prevention it recommends deltamethrin or flumethrin-imidacloprid collars, the permethrin-imidacloprid spot-on and domperidone in seronegative dogs; it considers the excreted-secreted protein (LiESP) vaccine optional and recommends the protein Q vaccine in areas with very high seroconversion. All authors declare ties with industry.
• Wylie et al. (2014), systematic review of topical repellents and drug prophylaxis against natural infection. It included 11 studies; all but one were at high risk of methodological shortcomings, and heterogeneity prevented a meta-analysis. Deltamethrin collars, permethrin spot-ons alone or with imidacloprid, and domperidone tended to significantly reduce the proportion of infected dogs.
• Oliva et al. (2014), randomised, double-blind trial of the LiESP/QA-21 vaccine in 90 dogs exposed for two transmission seasons in two highly endemic Mediterranean areas. The vaccine reduced the risk of progressing to active infection or disease, with an efficacy of 68.4%, but the probability of becoming PCR positive was similar in both groups: it does not prevent infection. It was funded by the manufacturer and several authors were its employees.
• Sabaté et al. (2014), randomised, open-label, single-centre trial in 90 seronegative dogs in Valencia (Spain), with periodic courses of domperidone or no treatment. At 12 months 7% of treated dogs had developed disease versus 35% of controls, and at 21 months 11% versus 48%, with a prevention rate of 77% over the whole follow-up. Being open-label and single-centre, the result needs confirmation.
• Gavgani et al. (2002), cluster-randomised trial in 18 villages in Iran, in which all dogs in the intervention villages were fitted with deltamethrin collars. Seroconversion in children was 1.49% versus 2.41% in control villages (OR 0.57), and seroconversion in dogs was also reduced (OR 0.46). It supports that protecting dogs also reduces human infection, although it lasted a single transmission season in one region.