The first description of Leishmania tropica was done in 1903 by
James Homer Wright, an American
pathologist. In 1914, it was suggested that L. tropica should be divided into two
subspecies, namely L. tropica minor and L. tropica major, based on the size of the parasites found in skin
lesions.[3] Later, these two subspecies turned out to be
epidemiologically different and were correlated to different types of lesions. L. tropica minor causes dry
nodular lesions in urban environments, while L. tropica major causes wet
ulcerating lesions in rural regions.[4] Bray et al. therefore proposed in 1973 that the subspecies should be considered as two separate species, L. tropica major became L. major, and L. tropica minor became L. tropica,[4] which is the naming that is still being used.[3]
Leishmania species alternate between two main life forms: intracellular
amastigotes in the
sandfly – the
vector – and extracellular motile
promastigotes in the
mammal – the
host.[8] In the mammalian host, promastigotes are introduced into the skin by the bite of a sandfly. After being taken up by
phagocytes, they transform into intracellular amastigotes and stay in this form during the remaining life cycle in the mammalian host.[8] Through simple
division, they can multiply and proceed to infect other phagocytotic cells. Later, depending partly on the
immunity of the host, the infection can become symptomatic and result in leishmaniasis.[7] Sand flies become infected by ingesting phagocytes with Leishmania from a mammalian host. Then, in the sandfly stage, the process differs between Leishmania species. In the life cycle of L. tropica, it develops back into the promastigote stage inside the
midgut of the sandfly vector and migrates to the
proboscis of the sandfly, whereafter the life cycle can repeat itself.[7]
L. tropica causes a broad spectrum of leishmaniasis forms in humans. Most common is a variant called dry-type
cutaneous leishmaniasis. After an
incubation period lasting more than 2 months, a small brownish
nodular lesion will appear with a slowly extending plaque reaching a size of 1–2 centimetres (0.39–0.79 in) after 6 months. This will heal after about 1 year but leaves a scar.[11] Other forms of the disease, which occur more rarely in humans, include
visceral leishmaniasis,
post-kala-azar dermal leishmaniasis (a variant of visceral leishmaniasis),
viscerotropic leishmaniasis, and
leishmaniasis recidivans (a variant of cutaneous leishmaniasis).[3]
Dogs are known to rarely suffer from
visceral,
skin, and
mucosal infection with this species.[10] In cats
asymptomatic infection is thought to be common.[10] Skin and/or mucosal infection is the most common form, with or without visceral infection.[10] Feline visceral infection may occur alone.[10]
Leishmaniasis recidivans
This rare variant of cutaneous leishmaniasis is caused solely by L. tropica in the
Old World and by L. braziliensis in the
New World. It causes a slowly progressing
lesion, usually on the face, and is characterized by the development of
papules or
nodules which form mostly around or in the site of primary healed lesions. Lesions of
leishmaniasis recidivans stay many years and rarely respond to treatment, thus causing
disfigurement and becoming destructive with the years.[12]