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:
- Pathogen: 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 leishmaniasis: they can sometimes cause skin leishmaniasis without visceral impairment: L. infantum (Mediterranean, 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. guyanensis, L. panamensis, L. mexicana
- Vector: arthropod: female phlebotoma
- Tank: wild rodents, sand rats (mériones chaoui), dog, cat…
- Parasite 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…)
New World: 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:
- Description type: ulcerro-croutee leishmaniasis (orient button, Biskra nail)
Incubation: 2-3 months (8 days to several months)
Orient button:
- Seat: discovered parts (face, hands, forearms, legs)
- Elemental 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
Central crust: adhering, brownish yellow, thick, the tearing shows filiform stalactite extensions on the underside
Ulceration: 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 the orient button:
Lupoid leishmaniasis: particular shape, frequent, nodule or papule, purple or yellowish pink, smooth or squamo-crusty
- Vitropression: lupoid hue (yellowish)
Anousetigoid 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
Pseudo-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)
- Diffuse skin shape (pseudo-lepromatous): nodules, isolated, very numerous
- Skin leishmaniasis
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:
- Anamnestic elements: notion of staying in an endemic area, insect bite, resistance to antiseptic and antibiotic treatment
- Clinical elements: painless character of the lesion despite the red tint, no adenopathy or lymphangitis, seat in the areas discovered
- Evolutionary elements: torpid, persistent and stable evolution in the absence of treatment
- Paraclinical elements:
Parasitological examinations: 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
May-Grunwald-Giemsa Coloring: Intracellular Leishman Body
▪ Culture: 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 lupoid or recurrent form: appearance of tuberuloid granuloma, major lymphocytic infiltrat with the presence of giant cells and rare epithelioid cells and histiocytes. Parasites are rare
Immunological examinations:
- 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
Leishmanias typing: from cultured parasites – epidemiological and scientific interest; electrophoresis of isoenzymes allows the diagnosis of species
Differential diagnosis:
- In front of its usual shape 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
Treatment:
- 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
Children: 30 mg/kg/d of total product or 10 mg/kg/d of active product
Therapeutic 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
Side effects:
Signs of stibio-intolerance (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 – definitive 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 balance: kidney function (urea, creatinine, urine chemistry), liver function (TGO, TGP, alkaline phosphatases), NFS, blood spat, ECG, chest x-ray
Contraindications: heart problems (rhythm disorders, BAV), 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 (Fungizone®): 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 Alterant Treatments: Fluconazole, Trimethoprim – Sulfamethoxazole
(Bactrim®), Metronidazole (Flagyl®), Ketoconazole (Nizoral®), Chloroquine (Nivaquine®)
Local treatment:
- Glucantime intra–injury infiltration®: 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 leishmaniasis:
- Therapeutic abstention: simple L.major forms of an arm or leg
- Local treatment (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 leishmaniasis: Glucantime® generally as a first-line. If failure: Pentamidine, Fluconazole, Flagyl®, Ketoconazole, Fungizone®
- Preventive treatment:
Vector control: insecticides, mosquito nets, clothing covering the maximum body surface area
Control 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