Feline Leishmaniasis
Leishmaniasis, caused by the protozoan parasite Leishmania infantum, is an endemic zoonosis in the Mediterranean basin. Dogs are considered the major host for these parasites, as well as the main reservoir for human visceral infection. In recent years, asymptomatic infection or clinical disease caused by L. infantum in cats has been reported in several countries where zoonotic leishmaniasis is present.
Visceral leishmaniasis, the common clinical manifestation of this disease in dogs, is a chronic, severe, protozoal disease of humans, dogs, and certain rodents characterized by cutaneous or mucocutaneous lesions, lymphadenopathy, weight loss, anaemia, lameness, renal failure, and occasionally epistaxis or ocular lesions.
Infection in dogs is prevalent in Central and South America, the Middle East, Asia, and in the Mediterranean region. The disease is endemic in Foxhounds in North America. Isolated cases are diagnosed around the world in animals that have visited endemic areas. Cats and other domestic animals are rarely infected and usually only develop cutaneous ulcers, without showing signs of visceral disease.
Canine leishmaniasis is a zoonosis, and dogs act as a reservoir of the parasite for humans where there is a competent vector.
Aetiology
Leishmania infantum and L donovani are the causative agents in the Mediterranean area and Middle East, whereas L chagasi , L braziliensis , and L mexicana are the major species in Central and South America. The parasites are transmitted as flagellated forms (promastigotes) by the bite of several species of phlebotomine sandflies, which are found worldwide. The flies do not fly long distances and complete their life cycles in an area with a diameter of <1 km. The females take blood only from vertebrates and move at dawn and dusk in search of food. Once inoculated in the skin of the mammalian host, the promastigotes are engulfed by macrophages, in which they transform to amastigotes, an aflagellated form. Inside the macrophages, the amastigotes divide and spread to different organs, especially the bone marrow, lymph nodes, skin, spleen, liver, and kidneys. At least two different pathogenic mechanisms are responsible for the signs and lesions of the disease - the production of granulomatous inflammatory reactions and the formation of circulating immune complexes that deposit in the renal glomeruli, blood vessels, and joints.
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Clinical signs
The incubation period is quite variable, ranging from 3 mo to several years. The clinical features vary widely; main clinical presentations are skin lesions, loss of weight or poor appetite, local or generalized lymphadenopathy, ocular lesions, renal failure, epistaxis, lameness, and anaemia. Occasionally, some dogs have chronic diarrhoea or liver failure. The most common cutaneous lesions are alopecia with severe dry desquamation, usually beginning on the head and extending to the rest of the body. Other animals develop chronic ulceration, located particularly on the head and limbs. The signs invariably show a slow, progressive evolution.
Diagnosis
The results of blood and urine tests also vary greatly. Most animals have a polyclonal hyperproteinemia. Nonregenerative anaemia is present in 50% of dogs. Some animals show leukopenia, whereas others have leukocytosis. In animals with renal lesions, it is also usual to find increased plasma urea and creatinine, proteinuria, and hematuria.
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| Leishmania spp, Giemsa stain, equine skin. Courtesy of Dr. Robert Dunstan |
The most reliable diagnostic test for canine leishmaniasis is direct observation of the parasite in bone marrow or lymph node smears. The amastigotes appear as oval basophilic bodies (4 µm) in the cytoplasm of macrophages. However, it is sometimes impossible to detect the parasite in infected animals, especially in lymph node smears. Serologic methods are useful in diagnosis; indirect immunofluorescence and ELISA are widely used. The results of a serologic test should be interpreted in conjunction with the clinical picture. Although these tests are reliable, a few infected dogs remain seronegative, and there are also seropositive dogs that never develop the disease.
Treatment
For treatment, the drugs of choice are the pentavalent antimony derivatives, particularly N-methylglucamine antimoniate (80-100 mg/kg/day, IM or SC [not approved for use in dogs in the USA]) and sodium stibogluconate (75 mg/kg, SC, bid [available only from the CDC in the USA]). During the first month, the dog is treated with either drug and allopurinol (20 mg/kg, PO, sid; during the next 5 mo, the dog is treated with only allopurinol, which is less expensive and less toxic.
Amphotericin B given IV (0.5-0.8 mg/kg, diluted in 10-60 mL of 5% dextrose given over 45 sec every 48 hr for a total cumulative dose of 8-15 mg/kg is reached) or SC 2-3 times/wk (0.5-0.8 mg/kg added to 500 mL of 0.45% saline and 2.5% dextrose for a total cumulative dosage of 8-26 mg/kg) has also been effective. Relapses after treatment are common with either protocol.
In endemic areas, rapid treatment of infected dogs, control of stray and homeless dogs, and action against the insect vectors are recommended methods of control. Treatment of dogs in non-endemic areas is questionable and probably unwise if a competent vector is present. At present, there is no effective vaccine against canine leishmaniasis.