Page 522 - ONLINE PROCEEDING BOOK WSAVA 2017
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An Urban Experience
WSVA7-0332
INFECTIOUS DISEASES I
TREATMENT OF CANINE LEISHMANIASIS AND DRUG RESISTANCE
G. Baneth1
1Hebrew University, Koret School of Veterinary Medicine, Rehovot, Israel
TREATMENT OF CANINE LEISHMANIASIS AND DRUG RESISTANCE
Gad Baneth, DVM, PhD. Dipl. ECVCP
Koret School of Veterinary Medicine, Hebrew University, Rehovot 76100, Israel
Email: gad.baneth@mail.huji.ac.il
Canine leishmaniosis (CanL) is a major zoonotic disease endemic in more than 70 countries in the world. It
is enzootic in regions of southern Europe, Northern Africa, the Middle East, Central Asia, China, South
and Central America and has emerged also in dogs in the USA. CanL is also an important concern in non- endemic countries where imported disease constitutes a veterinary and public health problem. Dogs are the main animal reservoir for human visceral leishmaniosis and the disease is usually fatal if not treated in people (1, 2).
CanL is a good example of a disease in which infection does not equal clinical illness due to the high prevalence of subclinical infection. This makes CanL a diagnostic challenge for the veterinary practitioner, clinical pathologist and public health of cial in endemic countries as well as non-endemic regions where imported infection is a concern. The typical history reported by owners
of dogs with CanL includes the appearance of skin lesions, ocular abnormalities, or epistaxis (1-4). These
are commonly accompanied by weight loss, exercise intolerance and lethargy. Dogs from all breeds can be infected with leishmaniosis. The age distribution of the disease is bimodal with a peak of prevalence at 2-4 years and a secondary peak from the age of 7 years.
The incubation period prior to the appearance of clinical signs may last 3 months up to several years. On physical examination, the main clinical signs associated with CanL are dermal lesions, lymphadenomegaly, splenomegaly, abnormal nails growth (onychogryposis) and poor body condition. Additional  ndings include: epistaxis, renal failure, decreased appetite, polyuria and polydypsia, vomiting, melena and lameness (1-4).
The main drugs used for treatment of CanL include:
• The pentavalent antimony meglumine antimoniate (Glucantime®) which selectively inhibits leishmanial glycolysis and fatty acid oxidation,.
• Miltefosine (Milteforan®) which is an alkylphosphocholine drug whose antileishmanial mode of action is not entirely understood.
• Allopurinol which acts by inhibiting protein translation through interfering with RNA synthesis.
Despite the World Health Organization’s (WHO) recommendation to reserve anti-leishmanial drugs used for treatment of humans for use in human leishmaniosis and not for veterinary purposes due to potential of drug resistance development (5), pentavalent antimonials and miltefosine are often used for treatment of dogs with CanL. Treatment of CanL usually includes a combined regimen with meglumine antimoniate or miltefosine administered for 4 weeks and allopurinol administered simultaneously and then continuously used for long term therapy (2-4).
Amphothericin B which acts by binding to ergosterol in the parasite’s cell membrane and altering its permeability is also effective against L. infantum but it is highly nephrotoxic. Some other drugs such as marbo oxacin and aminosidine are sometimes used as second line agents (2).
Anti-leishmanial treatment often achieves clinical improvement in dogs with leishmaniosis but it is frequently not associated with the elimination of the parasite (1-4). Treated dogs may remain carriers of the disease, experience clinical relapses and be infectious
to sand  ies. The successful treatment of CanL is particularly dif cult due to the fact that it is lengthy and often does not result in complete elimination of infection, allowing potential relapse of clinical disease and further transmission of infection from treated animals. A clinical staging system for CanL divides the disease into 4 clinical stages based on clinical signs, clinicopathological abnormalities and level of anti-leishmanial antibodies (3, 4). This system is helpful for decisions on the therapy most suitable for each patient and for consideration of
a prognosis. The clinical stage may change if the dog deteriorates or improves.
Drug resistance has been widely described in human cutaneous and visceral leishmaiasis. Reports on drug resistance in the canine disease are more scarce. Disease relapse in dogs with CanL during allopurinol treatment has recently been described and associated with allopurinol resistance of L. infantum isolated from relapsed animals. Leishmania infantum strains isolated in culture from relapsed dogs were signi cantly less susceptible to allopurinol in comparison to isolates
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42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS


































































































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