© 2002 Vetstream Limited. Leishmania infantum

Leishmania infantum
(Leishmania chagasi)

Classification

Taxonomy

Kingdom: Protista
Phylum: Sarcomastigophora.
Subphylum: Mastigophora.
Class: Zoomastigophora.
Order: Kinetoplastida.
Family: Trypanosomatidae.
Genus: Leishmania .
Species: Infantum.

Etymology

Leishmania infantum is in the Leishmania donovani complex. Occasionally incorrectly referred to as L donovani.
Name, L chagasi used for the parasite causing visceral leishmaniasis in dogs in South America.
Name L infantum used because, in the Mediterranean area, visceral disease develops predominantly in infants and young children after exposure to infected sand flies.
Recent evidence suggests that L infantum and L chagasi are identical. The name L infantum should replace the name L chagasi.

Distribution

Endemic in countries of the Mediterranean basin, the Middle East, parts of Africa and Asia and South America.
Recently found to be endemic in Foxhounds in the United States.
Found in dogs that have travelled to an endemic area and then returned to an area free of Leishmania.

Significance

L infantum causes severe systematic disease in dogs .
Dogs are the reservoir host for human infection.
L infantum causes visceral disease particularly in young children and immunosuppressed individuals.

Active Forms

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Active Form 1
Promastigotes
Morphology

Slender, elongate form with a single nucleus, kinetoplast and anterior flagellum .
Develops by longitudinal binary fission.
Motile form.

Color

Dark staining nucleus and rod-shaped kinetoplast in blood stains.

Tolerances

Other

Function

Flagellated promastigotes multiply asexually by longitudinal binary fission in the sand fly midgut and are inoculated into the vertebrate host while feeding.

Development

Reproduction

Asexually by longitudinal binary fission.

Active Form 2
Amastigotes
Morphology

Round intracellular form with rudimentary flagella, 2-3mm .
Found in macrophages of mammalian host.
Develops by longitudinal binary fission.

Color

Dark staining nucleus and rod-shaped kinetoplast in blood stains.

Clinical Effects

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Epidemiology

Habitat

Sand flies found mainly in tropics and subtropics, some species in temperate regions.
Habitats range from desert to savanna to rainforest with each species possessing specific ecological requirements.
Peridomestic species of sand flies vector Leishmania infections to man.

Lifecycle

Promastigotes inoculated into mammalian host while sand fly takes blood meal.
Promastigotes enter macrophages and transform into amastigotes .
Amastigotes divide by binary fission until the host cell ruptures and the parasites are released.
Amastigotes infect nearby macrophages or move through vasculature to infect other organs eg spleen and liver.
Lifecycle completed when sand fly ingests amastigotes while blood feeding.

Transmission

Transmitted by sand flies in the genera Phlebotomus and Lutzomyia.
Transmission of Leishmania spp may also occur via exchange of blood or other body secretions.
Congenital transmission of L infantum also reported in dogs.

Pathological effects

Immunological

Cell-mediated immune responses (Th1 type) required for resistance.
Antibodies produced but are not protective.
Serological examinations by indirect fluorescent antibody (IFA) test done at initial serum dilutions of 1:16. Cut off titer of 1:64 considered positive.
Leishmania parasites have been isolated from dogs with titers of 1:16.
Dogs that develop clinical leishmaniasis thought to have a genetic disposition to mount a humoral rather than cell-mediated immune response.
Cell-mediated immune response to Leishmania antigen and other antigens is decreased in dogs with leishmaniasis.
Dogs with clinical leishmaniasis have higher levels of IgG1 antibodies. Asymptomatic dogs have highter levels of IgG2 antibodies.

Pathological

Cutaneous lesions.
Wasting.
Lymphadenopathy.
Ocular lesions.
Epistaxis .
Anemia .
Renal failure .
Diarrhea .
Lameness.

Other Host Effects

Body temperature is usually normal or below normal.

Clinical signs of canine leishmaniasis are many and variable.
Visceral leishmaniasis is a progressive wasting disease.
Many dogs are naturally resistant and appear clinically normal despite being infected. Show only localized nodular reaction at site of sand fly bite.
In endemic areas, only 10% of infected dogs develop overt clinical disease.
Clinical signs include local or generalized lymphadenopathy, alopecia , cutaneous lesions, anemia , splenomegaly , epistaxis , emaciation, ocular lesions, renal failure , lameness, diarrhea and long deformed claws.

Control

Control via chemotherapies

Meglumine antimonate : 100 mg/kg SC daily for 3 - 4 weeks.
Allopurinol : 20 mg/kg PO daily continuously or 15 mg/kg PO daily in combination with 100 mg/kg SC daily of meglumine antimonate.
Amphotericin B : 0.5-0.8 mg/kg IV or SC 2-3 times/week until reach accumulated dose of 15 mg/kg.
Liposomalized amphotericin B: 3 mg/kg IV daily until reach accumulated dose of 15 mg/kg.
Dogs may relapse after treatment.

Control via environment

Destruction of sand fly habitat.

Vaccination

No approved vaccine against canine leishmaniasis.

Other countermeasures

Insecticide (deltamethrin) inpregnated dog collars provide a possible control measure in endemic areas .

Diagnosis

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Useful samples

Sera for immunological diagnostic studies.
Bone marrow is most likely to contain amastigotes; used for PCR and culture.
Enlarged lymph nodes also good source of parasites; used for PCR and isolation.

Isolation

L infantum can be isolated in a number of liquid or semi-liquid media from lymph node aspirates, bone marrow aspirates or infected tissues taken by biopsy or at necropsy.

Laboratory diagnosis

Serology:
- IFA (gold standard).
- ELISA.
- Immunoblot.
- Agglutination.
PCR on:
- Lymph node aspirates.
- Bone marrow aspirates.
Cytology (for identification of amastigotes) of:
- Lymph node aspirates.
- Bone marrow aspirates.
Culture (for recovery of promastigotes ) of:
- Lymph node aspirates.
- Bone marrow aspirates.

Sources

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Publications

Refereed papers

Baneth G & Shaw S E (2002) Chemotherapy of canine leishmaniasis. Vet Parasitol 106, 315-324.
Lindsay D S, Zajac A M & Barr S C (2002) Canine leishmaniasis in the American Foxhounds: an emerging zoonosis? Comp Cont Ed Pract Vet 24, 304-312.
Mauricio I L, Howard M K, Stothard J R & Miles M A (1999) Genomic diversity in the Leishmania donovani complex. Parasitol 119 237-246.

Other sources of information

Canine Leishmaniasis: an update. (1999) Ed R Killick-Kendrick. Proc Int Canine Leishmania Forum. Barcelona, Spain.
Molyneux D H & Ashford R W (1983) The biology of Trypanosoma and Leishmania, parasites of man and domestic animals. International Publications Service, pp 185-225.

Vetstream contributor(s)

Professor David S Lindsay PhD, Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Center for Molecular Medicine and Infectious Diseases, 1410 Prices Fork Road, Blacksburg, Virginia 24061-0342, USA.
Dr Gad Baneth DVM PhD, School of Veterinary Medicine, Hebrew University of Jerusalem, PO Box 12, Rehovot 76100, ISRAEL.