Leishmaniasis is a protozoan infection with a transmissible mechanism of spread, characterized by damage to the skin or internal organs by intracellular parasites – leishmania. Leishmaniasis is divided into visceral, occurring with damage to the lungs, liver, spleen, heart, and cutaneous, manifested by papules transforming into ulceration foci. Diagnosis of leishmaniasis is carried out by detecting leishmania in the patient’s blood (in the visceral form) or in the separated skin elements (in the cutaneous form).
General information
Leishmaniasis is caused by seventeen of more than twenty species of protozoan parasites of the genus Leishmania. Leishmanias develop inside host cells (mainly in macrophages and elements of the reticuloendothelial system). During their life cycle, they need to change two owners. In the body of vertebrates, leishmanias are in a non-flagellate form, developing into a flagellate form in the body of an arthropod. Leishmanias are resistant to antibiotics, and are sensitive to drugs of pentavalent antimony.
The vast majority of leishmaniasis are zoonoses (animals are the reservoir and source of infection), only two species are anthroponoses. The species of animals involved in the spread of leishmaniasis are quite limited, so the infection is naturally focal, spreading within the habitat of the corresponding fauna: rodents of sandstone species, canids (foxes, dogs, jackals), as well as mosquito vectors. Mainly foci of leishmaniasis are located in the countries of Africa and South America. Most of them are developing countries, among 69 countries where leishmaniasis is common, 13 are the poorest countries in the world.
A person is a source of infection in the case of a lesion with a cutaneous form of leishmania, while mosquitoes receive a pathogen with detachable skin ulcers. Visceral leishmania in the vast majority of cases is zoonotic, mosquitoes are infected from sick animals. The infectivity of mosquitoes is counted from the fifth day when leishmania enters the insect’s stomach and persists for life. Humans and animals are contagious throughout the duration of the pathogen’s stay in the body.
Leishmaniasis is transmitted exclusively by a transmissible mechanism, the vectors are mosquitoes, get infected by feeding on the blood of sick animals, and are transferred to healthy individuals and people. A person has a high susceptibility to infection, after undergoing cutaneous leishmaniasis, a long-lasting persistent immunity persists, the visceral form does not form such.
Pathogenesis
The pathogen penetrates into the thickness of human skin when bitten by a mosquito, forming a leishmaniasis granuloma in the area of the entrance gate. Subsequently, in the visceral form of infection, the granuloma resolves, and in the cutaneous form, it progresses into an ulcer. Leishmanias spread through the body with a lymph current, affecting regional lymph nodes. Along the lymphatic vessel, parasites can form leishmaniomas – a series of sequentially located specific ulcers.
In South America, there are forms of leishmania occurring with lesions of the mucous membranes of the oral cavity, nasopharynx and upper respiratory tract with severe deformation of deep tissues and the development of polypous formations. The visceral form of leishmaniasis develops as a result of the pathogen scattering through the body and entering the liver, spleen, bone marrow. Less often – in the intestinal wall, lungs, kidneys and adrenal glands.
The resulting immune response suppresses the infection, while the disease proceeds latently, or with poorly expressed symptoms. With immunodeficiency, reduced protective properties, leishmaniasis progresses, proceeds with a pronounced clinic of intoxication syndrome, fever. The reproduction of parasites in the liver contributes to the replacement of hepatocytes with fibrous tissue, pulp atrophy with areas of infarction and necrotization is noted in the spleen. Anemia develops as a result of bone marrow damage. In general, visceral leishmaniasis, progressing, causes general cachexia.
Classification
Leishmaniasis is divided into visceral and cutaneous forms, each form, in turn, is divided into anthroponoses and zoonoses (depending on the reservoir of infection). Visceral zoonotic leishmaniasis: children’s kala-azar (Mediterranean-Central Asian), dum-dum fever (common in East Africa), nasopharyngeal leishmaniasis (skin-mucous, New World leishmaniasis).
Indian kala-azar is a visceral anthroponosis. Cutaneous forms of leishmaniasis are represented by Borovsky’s disease (urban anthroponotic type and rural zoonosis), Pendinsky, Ashgabat ulcers, Baghdad boil, Ethiopian cutaneous leishmaniasis.
Leishmaniasis symptoms
Visceral Mediterranean-Asian leishmaniasis
The incubation period of this form of leishmaniasis ranges from 20 days to several (3-5) months. Sometimes (quite rarely) it takes up to a year. In young children during this period, there may be a primary papule at the site of the introduction of the pathogen (in adults it occurs in rare cases). The infection occurs in acute, subacute and chronic forms. The acute form is usually noted in children, characterized by a rapid course and ends fatally without proper medical care.
The most common subacute form of the disease. In the initial period, there is a gradual increase in general weakness, weakness, increased fatigue. There is a decrease in appetite, paleness of the skin. During this period, palpation can reveal a slight increase in the size of the spleen. Body temperature can rise to subfebrile numbers.
The rise in temperature to high values indicates the onset of the disease during the peak period. The fever has an irregular or undulating character, lasts for several days. Attacks of fever can be replaced by periods of normalization of temperature or decrease to subfebrile values. This course usually lasts 2-3 months. Lymph nodes are enlarged, hepato- and, in particular, splenomegaly is noted. The liver and spleen are moderately painful during palpation. With the development of bronchoadenitis, cough is noted. With this form, a secondary infection of the respiratory system often joins and pneumonia develops.
With the progression of the disease, there is an aggravation of the severity of the patient’s condition, cachexia, anemia, hemorrhagic syndrome develops. Necrotic areas appear on the mucous membranes of the oral cavity. Due to a significant increase in the spleen, the heart shifts to the right, its tones are deaf, the rhythm of contractions is accelerated. There is a tendency to a drop in peripheral blood pressure. With the progression of infection, heart failure is formed. In the terminal period, patients are cachexic, the skin is pale and thinned, edema is noted, anemia is expressed.
Chronic leishmaniasis occurs latently, or with minor symptoms. Anthroponous visceral leishmaniasis can be accompanied (in 10% of cases) by the appearance of leishmanoids on the skin – small papillomas, nodules or spots (sometimes just areas with reduced pigmentation) containing the pathogen. Leishmanoids can exist for years and decades.
Cutaneous zoonotic leishmaniasis
It is common in tropical and subtropical climates. Its incubation period is 10-20 days, can be reduced to a week and lengthened to one and a half months. In the area of the introduction of the pathogen in this form of infection, a primary leishmanioma is usually formed, initially having the appearance of a pink smooth papule about 2-3 cm in diameter, later progressing into a painless or slightly painful boil when pressed. After 1-2 weeks, a necrotic focus forms in leishmanioma, and soon a painless ulceration with undercut edges is formed, surrounded by a roller of infiltrated skin with abundant discharge of serous-purulent or hemorrhagic nature.
Secondary “tubercles of insemination” develop around the primary leishmanioma, progressing into new ulcers and merging into a single ulcerated field (sequential leishmanioma). Usually leishmaniomas appear in open areas of the skin, their number can range from a single ulcer to dozens. Often, leishmaniomas are accompanied by an increase in regional lymph nodes and lymphangitis (usually painless). After 2-6 months, the ulcers heal, leaving scars. In general, the disease usually lasts about six months.
Diffuse infiltrating leishmaniasis
It is characterized by a significant widespread infiltration of the skin. Over time, the infiltration regresses, leaving no consequences. In exceptional cases, small ulcers are noted, healing without noticeable scars. This form of leishmaniasis is quite rare, usually observed in the elderly.
Tuberculoid cutaneous leishmaniasis
It is observed mainly in children and young people. In this form, small bumps appear around post-ulcer scars or on them, which can increase in size and merge with each other. Such tubercles rarely ulcerate. Ulcers in this form of infection leave significant scars.
Anthroponous form of cutaneous leishmaniasis
It is characterized by a long incubation period, which can reach several months and years, as well as slow development and moderate intensity of skin lesions.
Complications
Long-term leishmaniasis progresses with the development of pneumonia, nephritis, agranulocytosis, hemorrhagic diathesis, and can also be complicated by purulent-necrotic inflammation.
Diagnostics
A general blood test for leishmaniasis shows signs of hypochromic anemia, neutropenia and aneosinophilia with relative lymphocytosis, as well as a reduced concentration of platelets. ESR is increased. A biochemical blood test may show hypergammaglobulinemia. Isolation of the causative agent of cutaneous leishmaniasis is possible from tubercles and ulcers, with visceral leishmania, they are found in blood culture for sterility. If necessary, a biopsy of lymph nodes, spleen, liver is performed to isolate the pathogen.
As a specific diagnosis, microscopic examination, back-sowing on the nutrient medium NNN, bioassays on laboratory animals are carried out. Serological diagnosis of leishmaniasis is carried out using RSC, ELISA, RNIF, RLA. In the period of reconvalescence, a positive reaction of Montenegro is noted (a skin test with leishmanin). It is produced during epidemiological studies.
Leishmaniasis treatment
Etiological treatment of leishmaniasis consists in the use of preparations of pentavalent antimony. In the visceral form, they are prescribed intravenously with an increase in dosage for 7-10 days. In case of insufficient efficacy, therapy is supplemented with amphotericin B, administered with 5% glucose solution intravenously slowly. In the early stages of cutaneous leishmaniasis, the tubercles are pricked with monomycin, berberine sulfate or urotropin, and these drugs are also prescribed in the form of ointments and lotions.
Formed ulcers are an indication for the appointment of miramistin intramuscularly. Laser therapy is effective to accelerate the healing of ulcers. The reserve drugs for leishmaniasis are amphotericin B and pentamidine, they are prescribed in cases of recurrent infection and resistance of leishmaniasis to traditional remedies. To increase the effectiveness of therapy, human recombinant gamma interferon can be added. In some cases, surgical removal of the spleen may be necessary.
Prognosis and prevention
With easily flowing leishmaniasis, independent recovery is possible. The prognosis is favorable with timely detection and proper medical measures. Severe forms, infection of persons with weakened protective properties, lack of treatment significantly worsen the prognosis. Skin manifestations of leishmaniasis leave cosmetic defects.
Prevention of leishmaniasis includes measures for the improvement of settlements, the elimination of places of settlement of mosquitoes (landfills and wastelands, flooded basements), disinsection of residential premises. Individual prevention consists in the use of repellents and other means of protection against mosquito bites. When a patient is detected, pyrimethamine chemoprophylaxis is performed in a team. Specific immune prophylaxis (vaccination) is carried out to persons planning to visit epidemiologically dangerous areas, as well as to the non-immune population of foci of infection.
