Introduction

Leishmaniasis is caused by parasites of the genus Leishmania and is endemic in many parts of Africa, Asia and South America.  It is transmitted by the sand fly or the Phlebotimus species.  Leishmaniasis can be causes 3 types of disease i.e. visceral leishmaniasis, cutaneous leishmaniasis and muco-cutaneous leishmaniasis.

	Causative organism	Location
Visceral leishmaniasis	L.d.donovani   L.d.infantum L.d chagasi	China, India, Iran Sudan, Kenya, Ethiopia Mediterranean basin Brazil, Colombia, Venezuela, Argentina
Cutaineous leishmaniasis	L. tropica L. major L. aethiopica L. mexicana	Mediterranean basin, Afghanistan Middle East, W. and N. Africa, Kenya Ethiopia Central America and Amazon basin
Mucocutaineous leishmaniasis	L. braziliensis complex	Brazil, Peru, Ecuador, Columbia, Venezuela

Morphology

Leishmania exist as flagellated extracellular promastigotes in the sandfly vector and as aflagellar obligate intracellular amastigotes within mononuclear phagocytes of their vertebrate hosts.  The various species are not distinguishable morphologically from one another.  When stained with Romanowsky stains such as Giemsa, amastigotes appear as round or oval bodies ranging from 2 - 3 in diameter with a well defined nucleus and kinetoplast, a rod shaped specialised mitochondrial structure that contains extranuclear DNA. The flagellated promastigote form is spindle shaped, measuring 10 - 20 in length, not including the length of the flagellum.  As in the amastigote form a nucleus and kinetoplast are clearly visible. 

Life cycle

Infection starts when a sandfly (Phlebotimus species) takes a blood meal from an infected host.  Small amounts of blood, lymph and macrophages infected with Leishmania amastigotes are ingested. Once ingested the amastigotes transform to promastigotes in the sandfly,  The non infective promastigotes divide and develop into  infective metacyclic promastigotes. These are formed in the midgut of the sandfly and migrate to the proboscis.  When the sandfly bites the extracellular inoculated promastigotes at the site of the bite is phagocytosed by macrophages.  After phagocytosis, transformation to dividing amastigotes occurs within 24 hours.  Reproduction at all stages of the lifecycle is believed to occur by binary fission.  No sexual stage has been identified.

Promastigotes of Leishmania sp.

Amastigotes of Leishmania sp. which have burst out of a macrophage.  They show the characteristic nucleus and kinetoplast.

 Visceral leishmaniasis

The incubation period of VL may vary between 2 weeks and 18 months.  The onset of VL is usually insidious with fever, sweating, weakness and weight loss.  The most prominent findings are fever, hepatosplenomegaly and anaemia.  The sites mainly affected are the liver, spleen and bone marrow.  Enlargement of the liver is due to hyperplasia of Kupffer cells which are packed with amastigotes.  The bone marrow is infiltrated with parasitised macrophages.  Some organs, notably the kidneys, may show pathological changes secondary to deposition of immune complexes. In advanced cases, ascites and oedema can develop.  Deaths are usually due to secondary bacterial infections such as pneumonia, tuberculosis or dysentery.

Laboratory Diagnosis

Cutaineous Leishmaniasis

Following a bite from an infected sandfly, a small red papule appears at the site of the bite about 2 – 8 weeks later.  The papule increases in size radially.  The patient then mounts either a hypersensitive response or an anergic response.

• In a hypersensitive response, the papule eventually ulcerates, becomes depressed and then eventually heals through scarring.  The patient is now immune from subsequent bites. 
• In an anergic response, the nodule grows and spreads over large areas of skin.  This resembles leprosy.

Laboratory Diagnosis

Mucocutaineous Leishmaniasis

Mucocutaneous leishmaniasis or espundia initially develops like cutaneous leishmaniasis but develops into lesions in the mucocutaneous junction of the pharynx resulting in the break down of the palate of the mouth and nose or more rarely the genitalia or anus.  This occurs from a few weeks to several years after the cutaneous lesion has healed.  These lesions result in disfiguring deformities of the nose and mouth.

Laboratory Diagnosis