Skin leishmaniasis

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Leishmaniasis is a condition caused by protozoans of the trypanosomid class. Three varieties are isolated:

  • Skin leishmaniasis (classic orient button and its semeiological varieties) due to tropical leishmania and leishmania major.
  • American leishmaniasis called leishmaniasis of the new world due to leishmania mexicana and leishmania braziliensis.
  • Visceral leishmaniasis (Kala Azar) due to leishmania Donovani, leishmania Infantum…. These may include skin lesions (post Kala Azar) or only skin lesions (leishmania Infantum).

We will limit ourselves to the study of skin leishmaniasis. These are classically referred to as the Oriental Button: Aleppo Button, Gafsa button, Biskra button …

I- THE ORIENT BUTTON:

Endemic throughout the Mediterranean basin, Central Asia, West and Central Africa. Transmitted by an insect Vector the Phlebotoma whose female stings at night. The virus reservoir is made up of wild rodents (jerboas, meron …) for leishmania major, it is rather human for tropical leishmania.

The average incubation period is 4 weeks but may be longer 2 to 3 months longer. The lesion begins with a small pruriginous papule that turns into a dark red nodity, covered by a sticky crust. The single or multiple element is located on the discovered regions (face, limbs…) where the phlebotoma is pricked. The lesion is painless, does not accompany adenopathies except in cases of overinfection and the general condition is well preserved. Untreated the lesion eventually heals after several months or years of evolution at the cost of an unsightly vicious scar. The immunity conferred is not final.

II- CLINICAL FORMS:

Several forms have been described:

  • The wet form is manifested by a pure-bottomed ulceration, infiltrated.
  • The impetigooid form presents itself as an erosive, crusty, little infiltrated tablecloth.
  • The wartish form simulates warring tuberculosis or tuberculosis lupus.
  • The lupoide form simulates sarcoidosis, tubercular lupus, leprosy.
  • Post Kala Azar skin leishmaniasis occurs at the control of visceral leishmaniasis. The rash is a discrete micropulous that can heal spontaneously or pass to chronicity.
  • Finally, immunodepression (AIDS) promotes the spread of lesions, leishmania varieties deemed to give only skin manifestations may be of interest to the viscera.

III- DIAGNOSIS:

Suspected by the geographical context and clinical appearance of the lesions, the diagnosis is confirmed by the presence of leishmanias in the smears of the lesion colored at MGG and on skin biopsies. Cultivation on NNN medium is possible and allows, if in doubt, diagnostic confirmation.

IV-TREATMENT:

Antimony derivatives (Glucantime) remain the best therapeutic weapon. When the lesion is unique and in localized forms, intralesional injections (1 ml to 2 per lesion once to 2 times/week for a month to one and a half months) are the rule. In multi-element forms and extensive forms glucantime is administered intra-muscularly at a dose of 50 mg/kg/d for 15 days. Fifteen days after the end of the treatment, a second treatment may be necessary. Glucantime is a nephrotoxic product so it is suitable to look for proteinuria before injections. Monitoring of liver and cardiac function is also recommended.

Prevention:

  1. Eradicate the vector
  2. Eradicate the animal virus tank
  3. Protect yourself from the bite of the phlebotoma by using mosquito nets and topical mosquito repellents.