Leishmania mexicana

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Leishmania mexicana
Leishmania mexicana.jpg
Leishmania mexicana in a biopsy specimen from a skin lesion stained with H&E. The amastigotes are lining the walls of two vacuoles, a typical arrangement. The species identification was derived from culture followed by isoenzyme analysis.
Scientific classification
Domain: Eukaryota
(unranked): Excavata
Phylum: Euglenozoa
Class: Kinetoplastida
Order: Trypanosomatida
Genus: Leishmania
Species: Leishmania mexicana
Binomial name
Leishmania mexicana
Biagi, 1953, emend. Garnham, 1962
False colour SEM micrograph of Promastigote form Leishmania mexicana as found in the sandfly midgut. The cell body is shown in orange and the flagellum is in red. 119 pixels/μm.
Amastigote form Leishmania mexicana as found in mammalian macrophages, 219 pixels/μm.

Leishmania mexicana is a Leishmania species[1] and is one of the causative species of leishmaniasis.

Leishmania mexicana is an obligate intracellular protozoan parasite that causes the mildest form of leishmaniasis. This species of Leishmania is found in South and Central America. Infection with L. mexicana occurs when an individual is bitten by an infected sand fly that injects the infective promastigotes, which are carried in the proboscis, directly into the skin.

The life cycle of this and other Leishmania species are similar and begin when an infected fly bites and injects it promastigotes in the skin of host and once inside these promastigotes are phagocytosed by macrophages that transform into amastigotes and are able to divide. Upon maximum levels of amastigote divisions, the macrophages burst releasing more amastigotes that are again re-phagocytosed. When an uninfected sand fly bites an infected individual, the fly ingest the amastigotes and these transform into promastigotes and divide in the midgut of the fly, finally these promastigotes migrate to the proboscis and are now able to transmit the disease. There are no blood stages in the life cycle of L. mexicana (unlike Malaria and Trypanosomiasis).

Leishmania LifeCycle.gif

L. mexicana has the ability to cause both a cutaneous and a diffuse cutaneous type of infection. The cutaneous type manifests itself in the form of ulcers at the bite site, here the amastigotes do not spread and the ulcers become visible either a few days or several months after the initial bite, these ulcers heal spontaneously. The diffuse cutaneous type manifests itself when the amastigote spreads cutaneously in those with defective T-cell immunity. This type of infection responds very poorly to drugs and therefore causes sores or ulcers all over the host's body.

In 1994, Robertson et al. noted that the amastigotes of L. mexicana have a higher activity of cystein proteases compared to its promastigote forms. This observation is thought to be an important characteristic that may aid in the survival of the amastigote in the macrophages of its host.

Treatment of Leishmaniasis caused by L. mexicana is generally unnecessary since the infection tends to disappear spontaneously, but in cases where the infection becomes chronic or spreads on the host, the treatment of choice is pentavalent antimony, which works by inhibiting the synthesis of ATP. The drug of choice in the United States is Penstostam.

Prevention of L. mexicana infection can be done by avoiding contact with sandfly-infested areas. Although this can be difficult since these flies have been progressively become more adaptive to urban areas. Research is being done to develop a vaccine against the promastigotes, although the work by Roberts may shed light into developing a vaccine or agent that targets the cystein proteases and other enzymes that are found in abundance in the amastigotes.


  1. ^ Majumdar D, Elsayed GA, Buskas T, Boons GJ (March 2005). "Synthesis of proteophosphoglycans of Leishmania major and Leishmania mexicana". J. Org. Chem. 70 (5): 1691–7. doi:10.1021/jo048443z. PMID 15730289. 

Further Reading[edit]

Rodriguez-Contreras, Dayana; Hamilton, Nicklas (October 2014). "Gluconeogenesis in Leishmania mexicana CONTRIBUTION OF GLYCEROL KINASE, PHOSPHOENOLPYRUVATE CARBOXYKINASE, AND PYRUVATE PHOSPHATE DIKINASE" (PDF). The Journal of Biological Chemistry. VOL 289 (No. 47): 32989–33000. Retrieved 12 February 2015.