Leishmania is a vector-borne protozoan parasite transmitted by phlebotomine sand flies. The most important species in domestic animals is L. infantum (known as L. chagasi in South America), and whilst dogs are the main reservoir hosts of the disease, it is zoonotic and potentially fatal in both dogs and humans.
Canine leishmaniasis (or viscerocutaneous leishmaniasis, as it affects both the skin and internal organs) is endemic in over 90 countries and remains a veterinary and public health concern through importation in non-endemic countries.
Pathogenesis
Leishmania is an intracellular protozoan parasite that has two stages of lifecycle, which requires two hosts: a sand fly and a mammal.
Transmission is confirmed in two principal routes; vector-borne through the bites of sandflies, and vertically from dam to pup. Transmission is confirmed in two principal routes; vector-borne through the bites of sandflies, and vertically from dam to pup. There have been other reported less common routes of transmission that include blood transfusions of infected products and cases of close contact/fighting between infected dogs.
It is important to note that not all species of sandflies are competent vectors, and not all Leishmania species are transmissible via sandflies. In canines, the most common is L. infantum.
L. infantum promastigotes are deposited into the skin via bites of infected sandflies, and invade macrophages whereby they replicate as intracellular amastigotes. Depending on the immune response mounted, the infection could persist from subclinical to clinical disease.
The incubation period may last months to sometimes years, in which the parasite disseminates throughout the host's body, primarily to the hemolymphatic systems organs.
Clinical presentation
Canine leishmaniosis is a multisystemic disease with variable clinical manifestations. The clinical pathology of the disease is most often attributed to inappropriate immune-mediated mechanisms rather than direct activity of the virus itself. The most common presentations include:
- Cutaneous skin lesions: generalised or localised to the face, muzzles, ears, and limbs
- Exfoliative dermatitis
- Erosive-ulcerative dermatitis
- Nodular/papular/pustular dermatitis
- Mucocutaneous dermatitis
- Hyperkeratosis
- Lymphadenomegaly
- Ocular abnormalities
- Uveitis
- Keratoconjunctivitis
- Manifestations of renal disease (PU/PD)
- Splenomegaly/hepatomegaly
- Vomiting
- Epistaxis
- Colitis/melena
- Anorexia/lethargy
Diagnosis
With canine leishmaniasis, a high antibody titre combined with clinical signs is often considered conclusive. The following are methods to utilise in diagnosing Leishmania in your patient.
- Clinical signs (as described above)
- Haematology
- Mild to moderate nonregenerative anaemia
- Thrombocytopenia (seen more commonly in advanced cases)
- Biochemistry
- Serum hypoproteinemia, hyperglobulinemia, and hypoalbuminemia (decreased albumin:globulin ratio). Marked hyperglobulinemia in dogs with no clinical disease but from an endemic area should suggest canine leishmaniosis.
- Raised urea/creatinine (azotemia) – renal pathology is common. Immune-complex glomerulonephritis may eventually develop and is a hallmark of this disease. It is believed to be the main natural cause of death.
- Grossly increased liver enzymes – ALT, ALKP, GGT
- Urinalysis
- Urea Protein:Creatinine ratio (UPC) – proteinuria present due to renal pathology
- Cytology
- Samples taken from lymph nodes, spleen, skin impressions or joint fluids stained with a Giemsa stain or a quick commercial stain. Amastigotes can be seen present in macrophages, but often there are a low number of detectable parasites, even in clinical advanced cases.
- Elisa (serology) – high antibody titres
- PCR – most sensitive
- Histopathology
- Granulomatous inflammation associated with a variable number of Leishmania amastigotes within macrophages
- High levels of antinuclear bodies and circulating immune complexes that deposit in the kidneys, blood vessels and joints as the disease progresses
Treatment
Treated dogs can remain carriers of infection and may relapse and/or remain infectious to sandflies. Treatment options include:
- Allopurinol as a solo agent: 10mg/kg PO BID for 6-12 months or longer
- Allopurinol (same dose as above) + Miltefosine (2mg/kg/day PO for 4 weeks)
- Allopurinol (same dose as above) + Meglumine antimoniate (50-100 mg/kg SC for 4-6 weeks). This is not approved in the USA, yet considered most effective.
It is important to monitor closely for adverse side effects and repeat haematology and biochemistry regularly. Stopping treatment with allopurinol is only recommended when clinical signs disappear, when the haematology/biochemistry abnormalities return to normal, or the animal becomes seronegative. In some cases this may mean a lifetime treatment.
Other treatment is symptomatic to the clinical manifestations and may include antibiotics, fluid support, anti-emetics, gastroprotectants.
Prevention
Topical insecticides that contain permethrin, imidacloprid, or deltamethrin to reduce the likelihood of bites from sandflies.