Skin leishmaniasis

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Introduction:

Skinned Leishmaniasis (LC) can be defined as zoonoses resulting from the parasitism of the vertebrate host by a flagellated protozoan of the genus Leishmania, transmitted by the bite of a vector insect: the phlebotoma

Epidemiology:

  • Patheyes: flagellated protozoan of the order of Kinoplastidae and the Trypanosomidae family, comes in two forms:

Amastigote: immobile, intra-cellular of the vertebrate reticulo-histiocytic system, ovoid corpuscle devoid of external flagella

Promastigote: very mobile, encountered in the digestive tract of the phlebotoma and the culture medium, possessing a free anterior flagella that allows it to move actively

  • Taxonomy: Since Laveran and Mesnil described the first species of Leishmania in 1903, the number of taxonomic entities has increased to about thirty, thanks mainly to the methods of electrophoresis of isoenzymes and the breakthrough of biology Molecular

Species normally responsible for visceral theishmaniasis: they can sometimes cause skin leishmaniasis without visceral impairment: L. infanti (Withiterranean, some outbreaks in the Middle East and South Asia), L. donovani

Species responsible for tegumentary leishmaniasis:

  • Ancient world: L. major (widespread in the Maghreb (Algeria, Morocco, Tunisia) and the Middle East), L. tropica, L. aethiopica (Ethiopia, Kenya)
  • New world: L. braziliensis (most widespread in Latin America), L. ginyanensis, L. panamensis, L. Mexican
  • Vector: arthropod: female phlebotoma
  • Tank: wild rodents, sand rats (jirds chaoui), dog, cat…
  • Throughaandte cycle:

When an infected fly eats a blood meal from a mammalian host, it salivates at the bite site and regurgitates the parasite in its promastigote form.

The parasite gains the cells of the reticulo-endothelial system and turns into amastigote, follows a multiplication of the parasite and then lysis of the phagocyte, the parasites released are phagocytized by nive cells

The cycle is completed when a fly takes a blood meal and sucks phagocytes containing Leishmania, into the digestive tract of the arthropod, the parasites differentiate, again, into promastigotes

  • FrequencY: endemic in 88 countries, Algeria: 30,000 cases (2005)
  • Geographical distribution: it is global:

Old world: Mediterranean basin, southern USSR, Turkey, East Asia (India), Africa (Algeria, Morocco, Tunisia, Niger, Chad, Nigeria…)

NWorld: Latin America (Argentina, Mexico)

Algeria: long confined to the historic home of Biskra, the disease has been spreading for the past twenty years to the highlands and the north of the country

Clinical:

  • of thecription type: ulcerro-croutee leishmaniasis (orient button, Biskra nail)

Incubation: 2-3 months (8 days to several months)

Onothingt I thrown:

  • Seat: discovered parts (face, hands, forearms, legs)
  • componentntal injurY:

At the beginning: small,pruriginous papule, dark red, sometimes pustular, single or multiple. In about ten days, an ulceration is formed, it is the ulcerative nodule:

Nodule: 2-3 cm in diameter, poorly limited, mobile compared to deep planes, the center is dug by an ulceration usually hidden by a crust

Ccome inl crust: adhering, brownish yellow, thick, the tearing shows filiform stalactite extensions on the underside

Thelceration: rounded or oval-shaped, 1 to several centimetres in diameter, with steeply trimmed edges, grainy bottom and purulent, it can be superficial and spread or digging

Related Signs: No Pain or Pruritus, No Adenopathy or Lymphangitis Unless Overinfection

  • Clinical forms Of ta danceent button:

Lupoid leishmaniasis: particular shape, frequent, nodule or papule, purple or yellowish pink, smooth or squamo-crusty

  • Vitropression: lupoid hue (yellowish)

Aarisetigoid form: squamo-crustal lesion spread out, resting on a red epidermis, sometimes some very superficial ulcerations

Wartish shape: very limited plate – protruding, papillomatous surface, hyperkeratosic, often dry

Pstudo-tumor form: exuberant lesion

Sporotrichosic form: results from lymphatic spread of leishmanias, giving abscesses on the lymphatic path

Other forms: the new world (Latin America)

  • Diffinsee skin shape (pseudo-lepromatous): nodules, isolated, very numerous
  • the skinishmaniasis

Evolution:

  • In general, persistent and stable, becoming stationary after a few weeks of evolution
  • Spontaneous healing occurs after about a year, at the cost of a depressed scar
  • No cure in 5% of cases – chronic or recurrent skin leishmaniasis

Positive diagnosis:

  • Medical historytic elements: notion of staying in an endemic area, insect bite, resistance to antiseptic and antibiotic treatment
  • clinicl elements: painless character of the lesion despite the red tint, no adenopathy or lymphangitis, seat in the areas discovered
  • The expansionnand Hennts: torpid, persistent and stable evolution in the absence of treatment
  • chapelsnical elements:

ParasitolOgical examinationns: often make it possible to make a diagnosis of certainty

  • Direct examination under an optical microscope: sampling, scraping smear, serouss collected after scarification or biopsy of a lesion border – histological cut

Mare Grunwald-GFor these Cleaderof: Intracellular Leishman Body

wORSHIPre: culture of Biopsic sampling on Navy Mc Neal Nicolle or rabbit serum (IPA) – results in 3-15 days, interesting for pauci-parasitic forms

HistopathologY:

  • In the usual form: the derma is the seat of polymorphic inflammatory granuloma, in which epithelioid cells coexist – plasma cells that is evocative. Coloring at MGG Leishman's body
  • In the wolfid or rewithrrent form: appearance of tuberuloid granuloma, major lymphocytic infiltrat with the presence of giant cells and rare epithelioid cells and histiocytes. Parasites are rare

Immunological assayns:

  • Montenegro's intradermroaction: its positivity persists for many years allowing a retrospective diagnosis
  • Serology (indirect immunofluorescence by ELISA technique): detects circulating antibodies, often negative in skin leishmaniasis, it has an interest especially in Kala Azar

PCR reviews: raise awareness of research and identification of the species

Lyonhes typing: from cultured parasites – epidemiothegical and scientific interest; electrophoresis of isoenzymes allows the diagnosis of species

Differential diagnosis:

  • in frOnt of its usual shaon of the oriental button: skin infections (boil, ecthyma, anthrax, atypical mycobacteria, etc.) are eliminated, rarely: carcinomas, lymphomas, granuloma in the foreign body.
  • In front Of the lupoid form: sarcoidosis in its angio-lupooid form, myxomatous tubertic lupus, tuberculoid leprosy, lupooid rosacea

Thirdtment:

  • Therapeutic weapons:

Classic general treatments:

  • Antimoniate Of N-methyl-glucamine (Glucantime®):

Presentation: 1 5 ml bulb containing 1.5 g of total product, 1 bulb contains 1/3 of the active product (425 mg)

PosologY:

Adult: 60 mg/kg/d of total product or 20 mg/kg/d of active product

Chferrets: 30 mg/kg/d of total product or 10 mg/kg/d of active product

Therapeintic Regimen: J1 – 1/4 of the total dose in IM, J2 – 1/2 of the total dose in IM, J3 3/4 of the total dose in IM, J4 the total dose in IM. Make a first 15-day treatment followed by a 15-day therapeutic window, a second treatment may be necessary

Shere effects:

Signs of stibio-intolerantthis (anaphylactic type): rash, chills, hyperthermia, myalgia, arthralgia, diarrhea, vomiting, bulbar syndrome, coughy stumble, tachycardia, lipothymia, haemorrhage. They can occur as soon as the first injection – frombenitive cessation of treatment

Signs of stibio-intoxication: cardiac disease (myocarditis, rhythm disorders), liver and pancreatic damage, kidney disease (tubular and glomerular), hematological accident (pancytopenia), polyneuritis. These signs appear during or even at the end of treatment (overdose)

Pre-therapeutic balancethis: kidney function (urea, creatinine, urine chemistry), liver function (TGO, TGP, alkaline phosphatases), NFS, blood spat, ECG, chest x-ray

Contraindications: heart problems (rhythm disorders, FATHER), severe kidney or liver disease, hemorrhagic syndrome, progressive pulmonary tuberculosis

Treatment monitoring: ECG (extended TQ, T-wave reversal), NFS, liver function, kidney function

  • Other:

Pentamidine (Lomidine®): 300 mg injectable bulb, 3-4 mg/kg/d IM, 1 day/2, risk of collapse, neurotic toxicity and diabetes induction (5%)

Amphoterin B (Finngizone®): 50 mg/ml vial for hospital use, adult: 1 mg/kg/d, child: 0.5 mg/kg/d, in IV infusion, dilute in 500 cc of glucated serum 5%, one starts at the initial dose of 0.1 mg/kg/d to increase per weekly level of 0.1 mg/kg/d until the dose of 1 mg/kg/d. Its high toxicity limits its use

General Altorant Trshetments: Fluconazole, Trimethoprim – Sulfamethoxazole

(Bactrim®), Metronidazole (Flagyl®), Ketoconazole (Nizoral®), Chloroquine (Nivaquine®)

Local treatment:

  • Glucantime intrainjury infthetration®: if single lesion or 2 lesions, 1-2 ml (depending on the size of the lesions) at the 4 cardinal points of the lesion at 1 cm from the edges, 1 to 2 times a week for several weeks, do not use near the eye , peri-orificial, periarticular or on a lymphatic path
  • Physical treatment: electrocoagulation, isolated cryotherapy or chemotherapy
  • Surgery: curative (if a single lesion) or restorative (if unsightly scarring)
  • Other: formulation of topical aminosides (Paromomycin and Gentamycin), applied under occlusive dressing
  • Indications:

Localized skin hershmaniasis:

  • Therapeintic abstention: simple L.mandOr forms of an arm or leg
  • Local trshetment (infiltration): if single lesion or two lesions, without lymphatic spread, sits away from peri-orifical or periarticular regions. Other local means: cryotherapy, thermotherapy, surgical exeresis
  • General treatment: recurrent skin leishmaniasis, contraindication to local treatment, immunosuppressed subject

Disseminated skin leishmanThird: Glucantime® generally as a first-line. If failure: Pentamidine, Fluconazole, Flagyl®, Ketoconazole, Fungizone®

  • Preventivee thirdtment:

Vector withtrol: insecticides, mosquito nets, clothing covering the maximum body surface area

Churtsol of the reservoir: very difficult, their destruction by deep ploughing, poisoning, deforestation of periurban areas have not yielded expected results

Vaccination: no vaccine is available