LIFE CYCLE
Transmitted by the bite of female phlebotomine sandflies.
The sandflies inject the infective stage, metacyclic promastigotes, during blood meals (1).
Metacyclic promastigotes that reach the puncture wound are phagocytized by macrophages (2)
and transform into amastigotes (3).
Amastigotes multiply in infected cells and affect different tissues, depending in part on which Leishmania species is involved (4).
These differing tissue specificities cause the differing clinical manifestations of the various forms.
Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes (5,6).
In the sandfly's midgut, the parasites differentiate into promastigotes (7), which multiply, differentiate into metacyclic promastigotes and migrate to the proboscis (8)
SIGNS AND SYMPTOMS
Skin sores which erupt weeks to months after the person affected is bitten by sand flies.
Other manifestations anywhere from a few months to years after infection, include fever, damage to the spleen and liver, and anaemia.
In the medical field, leishmaniasis is one of the famous causes of a markedly enlarged spleen, which may become larger even than the liver.
,MAIN FORMS OF LEISHMANIASIS
Visceral leishmaniasis - the most serious form and potentially fatal if untreated.
Cutaneous leishmaniasis - the most common form which causes numerous sores on the body, which heal within a few months leaving unpleasant looking scars.
Diffuse cutaneous leishmaniasis - this form produces widespread skin lesions which resemble leprosy and is particularly difficult to treat.
Mucocutaneous leishmaniasis - commences with skin ulcers which spread causing tissue damage to (particularly) nose and mouth
TREATMENT
There are two common therapies
Sodium stibogluconate SSG (Pentostam) first developed in the 1930s, using derivatives of antimony.
SSG is taken as an I.M over 30 or more days.
Another antimonial drug is meglumine antimoniate (brand name Glucantime).
It is not completely understood how these drugs act against the parasite; they may disrupt its energy production or trypanothione metabolism.
Unfortunately, in many parts of the world, the parasite has become resistant to antimony and for visceral or mucocutaneous leishmaniasis.
AMPHOTERICIN is now the treatment of choice.
Miltefosine (Impavido®), is a new drug for visceral and cutaneous leishmaniasis.
The cure rate of miltefosine in phase III clinical trials is 95%;
Studies in Ethiopia show that is also effective in Africa.
In HIV immunosuppressed people which are coinfected with leishmaniasis it has shown that even in resistant cases 2/3 of the people responded to this new treatment.
Clinical trials in Colombia showed a high efficacy for cutaneous leishmaniasis.
In mucocutaneous cases caused by L.brasiliensis it has shown to be much better effective than other drugs.
VACCINE?
Several potential vaccines are being developed, under pressure from the WHO, but as of 2006 none is available.
Drug-resistant leishmaniasis may respond to immunotherapy (inoculation with parasite antigens plus an adjuvant) which aims to stimulate the body's own immune system to kill the parasite
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