Leishmania

Leishmania spp.
Kingdom	Eukaryota
Phylum	Euglenozoa
Class	Kinetoplastea
Order	Trypanosomatida
Family	Trypanosomatidae
Genus	Leishmania
Species	L. infantum, L. donovani, L.chagasi

Leishmania Life Cycle - Wikimedia Commons

Leishmania donovani in bone marrow cell - Dr. L.L. Moore, Jr.

L. tropica

Yutaka TsutsumiWikiMedia Commons

Overview

Leishmania spp. are intracellular parasites of macrophages from the same family as Trypanosoma spp.. These organisms parasitise human, dogs and wild animals throughout southern Europe, Africa, Asia and South America. The infection is transmitted by sandflies. Infection can cause both cutaneous and visceral disease. Clinical disease cause by Leishmania is termed Leishmaniosis. Three types of Leishmania spp. are described;

1. Hypopylaria - found in lizards that ingest the sandfly intermediate host. Development occurs in the hindgut of the fly.
2. Peripylaria - found in mammals and lizards, development occurs in the fore- and hindgut of the fly.
3. Suprapylaria - found only in mammals transmitted by the bite of a sandfly, development occurs in the fore- and midgut of the fly.

Recognition

Leishmania spp. are ovoid shaped parasites containing a rod shaped 'kinetoplast'. The kinetoplast is associated with a rudimentary flagellum that does not extened beyond the cell margin. The position of the kinetoplast changes as the parasite changes between life stages. Once ingested by a sand fly the parasite takes the promastigote form and the kinetoplast moves the the posterior of the cell.

Life Cycle

The life cycle of Leishamania spp. requires transmission between mammalian (and occasionally reptile) hosts by a blood sucking fly. The sand flies is the intermediate host, in the Old World the flies are of the genus Phlebotomus and in the New World they are of the genus Lutzomyia.

The promastigote form which lacks a flagella is found in he vertebrate hosts macrophages. The amistgote is ingested by the sand fly whilst it feeds on the host, once ingested the Leishamnia will transform into the flagellated promastigote form in the insect gut. Replication by binary fission occurs in the insects gut followed by migration to the proboscis of the insect. The presence of Leishamnia in the insects proboscis allows innoculation of the next host on which the fly feeds with the Leishmania parasite. Crushing the sand fly on the skin of a mammal can allow percutaneous transmission.

Once inside the vertebrate host the Leishmania will invade the hosts macrophages and having done this revert to the amastigote form.

Pathogenesis

Infection with Leishmania can produce either cutaneous or viscreal disease as the infected macrophages proliferate in foci. There is a very long incubation period from infection to pathology, which can take years and therefore many infected dogs either never become symptomatic or remain so for a long period of time. Even once an animal has been treated for leishmaniasis it is not uncommon for clinical symptoms to recur after a lengthy period of remission. Information on the clinical signs and treatment for disease caused by leishmania can be found on the Leishmaniosis page.

Epidemiology

The spread of the disease relies on the presence of the sand fly as a vector. Therfore the regions in which it is found commonly are those in which conditions are suitable for the flies such as the Mediteranean coast, southern Europe as well as in central America and northern Africa. As these flies are very common in these regions controlling there numbers has limited success, however due to control of mosquitos to prevent the spread of malaria the number of sand flies has also been reduced and a reduction in the number of cases of leishmania has been noted. Although this parasite is of primary veterinary importance in dogs, large reservoirs exist in wild animals and stray dogs. This reservoir is easily accessed by the sand fly vector and compounds the issue of controlling the spread of the disease.

Although the UK is not home to any species of sand fly, leishmaniasis is being observed more frequently in the domestic dog population. This has largely been attributed to the increase in the number of animals that travel to areas of Europe and north Africa where the disease is endemic. These animals often acquire the disease whilst abroad but may not show clinical signs until they have been back in the UK for a considerable length of time. There has however been some evidence to show that clost contact between dogs can spread the disease, though this method of transmission is much less common.

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