Clinical types of cutaneous leishmaniasis. Leishmaniasis: causes, symptoms, diagnosis, treatment and prevention Leishmaniasis causes

Very often, people encounter skin diseases: either a rash appears, or wounds, or it is not yet clear what, it seems like a bite, but it is somehow strange. Very often, a mosquito bite can develop into an infection, one of the forms of which is a disease such as leishmaniasis. It is this disease that we will talk about today. So what is leishmaniasis?

Concept

Leishmaniasis is an infection that occurs not only in humans, but also in animals. It is caused by protozoa of the genus Leishmania and is transmitted through the bites of Lutzomyia mosquitoes.

The simplest leishmania is distributed mainly in hot countries: Asia, Africa, South America.

Most often, the sources of the disease can be already infected people, canine animals (foxes, wolves or jackals) raised at home, and rodents.

With a difficult and long healing process, dangerous not only for humans, but also for animals, is leishmaniasis. bacteria that cause this disease takes a very long time. Mosquitoes are the first to become infected. After which the infection enters the digestive system, where not yet fully mature forms of leishmaniasis mature and turn into a motile flagellated form. Accumulating in the mosquito's larynx, during a new bite they enter the wound and infect the epithelial cells of the animal.

Leishmaniasis: varieties

There are several types of this disease, and each of them is dangerous for the human body in its own way:

• Cutaneous.
• Slimy.
• Visceral leishmaniasis.
• Mucocutaneous.
• Viscerotropic.

Main symptoms of leishmaniasis

The main symptoms of this disease are ulcers on the human body. They can appear several weeks or even months after he is bitten by an insect that carries the infection. Another symptom of the disease may be fever, which can also begin a few days after the bite. Enough time may pass, in some cases about a year. The disease also affects the liver and spleen, which can result in anemia.

In medicine, the first sign of leishmaniasis is an enlarged spleen: it can become larger in size than the liver. Today there are 4 forms of leishmaniasis:

1. Visceral. This is one of the most complex forms of the disease. If treatment is not started as soon as possible, the disease can be fatal.
2. Cutaneous leishmaniasis. It is considered one of the most common forms. Immediately after the bite, pain appears in its place. This form of the disease can be cured only after several months, and even after that a person will remember it by looking at the scar left by the disease.
3. Diffuse cutaneous leishmaniasis - this form of the disease is widespread, its appearance strongly resembles leprosy and is very difficult to treat.
4. Slimy form. It starts with which later leads to tissue damage, especially in the mouth and nose.

Concept and symptoms of visceral leishmaniasis

Visceral leishmaniasis is a form of infectious disease caused by leishmania. The disease occurs when this type of microbe spreads hematogenously from the primary source of infection to any of the human organs: liver, spleen, lymph nodes and even bone marrow. Microorganisms in the organ multiply very quickly, which leads to its damage.

Most often, children are susceptible to this disease. The incubation period is quite long, sometimes lasting up to five months. The disease begins at a slow pace, but in the category of infected people who come to endemic areas, the disease can develop rapidly.

Visceral leishmaniasis symptoms are quite common. In almost all patients they are the same: general malaise, weakness throughout the body, lethargy, complete fever begins very quickly. It passes in waves, and the body temperature can reach 40 degrees. Then there is a slight relief of the condition, which is again replaced by a high temperature, which is also very difficult to bring down.

You can also see signs of a disease such as visceral leishmaniasis on the skin. The symptoms are as follows: pale skin with a grayish tint and often with hemorrhages. It is worth paying attention to the lymphatic system - the lymph nodes will be enlarged.

The main signs of visceral leishmaniasis

The main sign of the disease is the initial defect, which may be isolated and therefore may not be noticed at the first examination. It looks like a small hyperemic papule, covered with scales on top. It occurs in the place where the bite was made by a carrier insect or an animal from the canine family, in whose body there is the causative agent of visceral leishmaniasis.

A constant symptom that you should first pay attention to is an enlarged spleen and liver. It is the spleen that grows at a very rapid pace and, after a couple of months after infection, can occupy the entire left side of the peritoneum. The organs become dense to the touch, but there is no pain. The liver does not enlarge so quickly, but very serious dysfunctions can be observed in it, even ascites.

If the bone marrow is affected by the disease, then symptoms manifest as thrombocytopenia and agranulocytosis, which may be accompanied by a sore throat. The first thing that can be seen on the human body is the rapid appearance of colored pigment spots.

Cutaneous form of leishmaniasis

It is very common and has several forms, one of them is cutaneous leishmaniasis. The pathogen reproduces in the tissues of the human body, where Leishmania ripen at a very rapid pace and turn into flagellated larvae. This is called the primary focus of the disease, and a granuloma is formed. It consists of epithelial cells and plasma cells, macrophages and lymphocytes. Decomposition products can cause significant inflammatory changes, which can lead to lymphangitis or lymphadenitis.

Symptoms of the skin form

The incubation period for cutaneous leishmaniasis is about one and a half months. There are several main stages of the disease:

1. The appearance of a tubercle on the skin and its rapid increase. Its dimensions are within 2 cm.
2. The ulcer appears after a few days. At first it is covered with a thin crust, which later falls off, and a soft pink bottom with weeping appears on the surface, and subsequently an abscess forms. The edges of the ulcer are slightly raised and loose.
3. Scar. After a couple of days, the bottom of the ulcer is completely cleared and covered with granulations, which later becomes scarred.

Main signs of the skin form

There is not only a rural form, but also an urban one, and they are not much different from each other, but we must remember that there are several main features that allow us to distinguish them.

The main and very important circumstance is the correct and thorough collection of anamnesis. A long stay in an urban or rural environment will indicate in favor of one of the forms of the disease. The rural type always occurs in its primary form, but the urban type can take all of the existing forms.

Mucocutaneous form of the disease

In addition to the forms of the disease described above, there is another quite common and very dangerous one - mucocutaneous leishmaniasis (espundia). Its causative agents are mosquitoes.

It can take about 3 months from the insect bite to the first signs of the disease. At the place where a mosquito bites a person, a deep ulcer forms. It involves the mucous membrane, lymphatic system and blood vessels. All this leads to very complex and severe complications, and the prognosis is not encouraging.

Human leishmaniasis in any of the existing forms is very dangerous, as it affects internal organs that are difficult to treat, such as the spleen and liver. It is for this reason that doctors recommend going to the hospital at the first discomfort; in the early stages of the disease, you can quickly recover with minimal consequences.

Other types of leishmaniasis disease

We have already described several main forms of such a disease as leishmaniasis, but there are several more types of it, perhaps not so common, but also dangerous for humans:

1. Sequential leishmanioma - the presence of a primary form with the addition of secondary symptoms in the form of small nodules.
2. Tuberculoid leishmaniasis. Photos of patients prove that signs of the disease appear at the site of the primary form or at the site of the scar. In this case, the primary defect is caused by the presence of a small tubercle of a soft yellow color, no larger than the head of a pin.
3. Diffuse leishmaniasis. This form of the disease most often occurs in people with a low level of immunity and is characterized by extensive ulcerative lesions of the skin and chronicity of the process.

We have figured out what leishmaniasis is, and we will tell you further how to diagnose it correctly.

Types of diagnosis of leishmaniasis

The clinical diagnosis of a patient with leishmaniasis is made on the basis of epidemiological data and clinical picture. Laboratory diagnostics will help to accurately confirm the presence of the disease. Leishmaniasis is detected by the following methods:

• Testing for bacteria: scrapings are taken from the ulcer and tubercle.
• Microscopic examination: a smear or a thick drop is taken from the patient. This method can detect the presence of leishmania stained according to Romanovsky-Giemsa.

• A liver and spleen biopsy is performed, and in the most severe cases, bone marrow aspirate is performed.
• Serological methods such as RSK, ELISA and others.

There are a huge number of accurate determination methods, and each of them will show the most accurate data and indicate the presence of a disease such as leishmaniasis in the human body. Diagnostics in a short time will allow you to determine the severity of the disease.

Treatment

We have already described what leishmaniasis is and how to correctly diagnose it. Now let's talk a little about how its treatment is carried out.

For the visceral form, pentavalent antimony preparations are used:

1. "Pentostam." It is administered to the patient intravenously, having previously been diluted in a 5% glucose solution. The drug can also be used intramuscularly. The course of treatment lasts for a month.
2. "Glucantim". The drug is used in the same way as Pentostam. If the disease is complex, the dose can be increased and the course of treatment extended for another month, but this can only be done with the permission of the attending physician.
3. "Solyusurmin". The drug can be administered intravenously or intramuscularly; treatment should begin with 0.02 g per kg of body weight. Gradually over 20 days the dose is increased to 1.6 g/kg.

Also, in very severe forms of the disease, treatment with Amphotericin B gives excellent results. The initial dose is 0.1 mg/kg. It gradually increases, but not more than 2 g per day. The drug is administered intravenously; it is first dissolved in a glucose solution.

In the most difficult cases, when all drugs have been used and have not brought the desired results, surgical intervention is prescribed - splenectomy. After such an operation, the patient returns to normal very quickly, but there is a risk of developing other infectious diseases.

For the skin form of the disease, you can use all the drugs we described above, and additionally prescribe heating and ultraviolet radiation.

Consequences of leishmaniasis

The prognosis and outcome of treatment after an infectious disease such as leishmaniasis are ambiguous. Despite the fact that the visceral form occurs with great complications, and it is very dangerous for the patient’s life, with timely treatment the disease goes away without a trace and does not cause much harm to the body.

As a result of the cutaneous form, especially its diffuse version, scars may remain on the skin. And in some rather complex cases, changes in the bone skeleton may even occur.

Possible complications

Complications after leishmaniasis are possible (photos of patients with this disease can be seen in our article). The later the disease is detected and the treatment process begins, the higher the risk of severe complications. With leishmaniasis they can take the following form:

• Liver failure, aggravated by ascites and cirrhosis.
• Severe anemia and disseminated intravascular coagulation syndrome.
• Amyloidosis of the kidneys.
• Ulcers on the mucous membrane of the digestive tract.

In the cutaneous form of the disease, complications are associated mainly with the addition of a secondary infection. It manifests itself as phlegmon and local abscesses, but in the absence of properly selected treatment it can develop into a severe septic form.

What is leishmaniasis? This is a very serious infectious disease that has different forms, each of which is quite dangerous for humans. But there are several prevention methods that will help avoid the disease or prevent its severe form.

Disease prevention

The general principle of leishmaniasis prevention is protective measures. We must try to protect ourselves from mosquito bites, which are carriers of the disease. You should carry out regular disinfection and fight against rodents, try to alienate domestic animals of the canine family that were adopted from the forest.

And drug prevention will only help protect against the skin form of the disease. Thus, a person who travels to endemic areas is vaccinated.

Leishmaniasis is a fairly serious disease; about half a million people die from it every year, so you should treat it with full responsibility and run to the doctor at the first sign. Only the early stages of the disease allow recovery without further consequences.

But it’s the way it is in our country that all “neglected diseases” are not funded, so no one will vaccinate the population until the person himself buys the vaccine and asks for it to be administered. This is how it turns out that the disease is very well known, but there is simply not enough money to properly treat it. Therefore, it is better to do everything possible on your own to prevent infection.

Leishmaniasis is a vector-borne disease of humans or animals caused by Leishmania and transmitted by mosquitoes; characterized by damage to internal organs (visceral leishmaniasis) or skin and mucous membranes (cutaneous leishmaniasis).

White mice, dogs, hamsters, ground squirrels and monkeys are susceptible to laboratory infection with leishmania.

Epidemiology. The main sources of pathogens for visceral leishmaniasis are infected dogs, and for cutaneous leishmaniasis - gophers, gerbils and other rodents. The pathogens are transmitted by mosquitoes of the genus Phlebotomus. The mechanism of transmission of pathogens is transmissible, through the bite of mosquitoes.

Pathogenesis and clinical picture. There are two forms of pathogens of cutaneous leishmaniasis: L. tropica minor - the causative agent of anthroponotic cutaneous leishmaniasis (urban type) and L. tropica major - the causative agent of zoonotic cutaneous leishmaniasis (rural type). With anthroponotic cutaneous leishmaniasis, the incubation period is several months. At the site of the mosquito bite, a tubercle appears, which enlarges and ulcerates after 3-4 months. Ulcers are most often located on the face and upper extremities. The sources of the pathogen are sick people and dogs. For zoonotic cutaneous leishmaniasis, the incubation period is 2-4 weeks. The disease is characterized by a more acute course. Ulcers are most often localized on the lower extremities. The reservoirs of Leishmania are gerbils, ground squirrels, and hedgehogs. The disease is common in Central Asia, the Mediterranean and Transcaucasia. L. braziliensis causes mucocutaneous leishmaniasis, characterized by granulomatous and ulcerative lesions of the skin of the nose and mucous membranes of the oral cavity and larynx. This form is found primarily in South America. Visceral leishmaniasis (kala-azar, or black disease) is caused by L. donovani and occurs in tropical and subtropical climates. The incubation period is 6-8 months. In patients, the liver and spleen are enlarged, the bone marrow and digestive tract are affected.

Immunity. Those who have recovered from the disease have lasting, lifelong immunity.

Microbiological diagnostics. In the studied material (smears from tubercles, contents of ulcers, stained according to Romanovsky-Giemsa), small oval-shaped leishmania are detected. Inoculations are also done on appropriate nutrient media to isolate a pure culture of the pathogen.

Treatment and prevention. For the treatment of visceral leishmaniasis, antimony preparations (solusurmin, neostibosan, etc.) and aromatic diamidines (stilbamidine, pentamidine) are used. In the case of cutaneous leishmaniasis, akriquin, sublimate preparations, amphotericin B, monomycin, etc. are used. In order to prevent leishmaniasis, sick dogs are destroyed and rodents and mosquitoes are controlled. Vaccinations are carried out with a live culture of L. tropica major.

Characteristics of the pathogen

The vast majority of leishmaniases are zoonoses (animals are the reservoir and source of infection), only two types are anthroponoses. The species of animals involved in the spread of leishmaniasis are quite limited, so the infection is a natural focal one, spreading within the habitat of the corresponding fauna: rodents of sandstone species, canines (foxes, dogs, jackals), as well as carriers - mosquitoes. Mostly foci of leishmaniasis are located in Africa and South America. Most of them are developing countries, and among the 69 countries where leishmaniasis is common, 13 are the poorest countries in the world.

Humans are the source of infection when affected by the cutaneous form of leishmania, while mosquitoes receive the pathogen from the discharge of skin ulcers. Visceral leishmania in the vast majority of cases is zoonotic; mosquitoes become infected from sick animals. The infectivity of mosquitoes begins on the fifth day that Leishmania enters the insect's stomach and persists for life. Humans and animals are contagious throughout the entire period of stay of the pathogen in the body.

Leishmaniasis is transmitted exclusively through a transmissible mechanism; the carriers are mosquitoes, which acquire the infection by feeding on the blood of sick animals and are transmitted to healthy individuals and people. A person has a high susceptibility to infection; after suffering from cutaneous leishmaniasis, a long-lasting, stable immunity is maintained; the visceral form does not form such.

Pathogenesis

In South America, forms of leishmania are observed that occur with damage to the mucous membranes of the oral cavity, nasopharynx and upper respiratory tract with gross deformation of deep tissues and the development of polypous formations. The visceral form of leishmaniasis develops as a result of the pathogen dispersing throughout the body and entering the liver, spleen, and bone marrow. Less commonly - into the intestinal wall, lungs, kidneys and adrenal glands.

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: childhood kala-azar (Mediterranean-Central Asian), dum-dum fever (common in eastern Africa), nasopharyngeal leishmaniasis (mucocutaneous, 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.

Symptoms of leishmaniasis

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 drags on for up to a year. In young children during this period, a primary papule may be observed at the site of 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 observed in children, is characterized by a rapid course and, without proper medical care, ends in death.

The most common subacute form of the disease occurs. In the initial period, there is a gradual increase in general weakness, weakness, and increased fatigue. There is a decrease in appetite and pale skin. During this period, palpation can reveal a slight increase in the size of the spleen. Body temperature can rise to low-grade levels.

A rise in temperature to high values ​​indicates the entry of the disease into its peak period. The fever is irregular or wave-like and continues for several days. Attacks of fever may be followed by periods of temperature normalization or reduction to subfebrile levels. This course usually lasts 2-3 months. Lymph nodes are enlarged, hepato- and, in particular, splenomegaly are noted. The liver and spleen are moderately painful on palpation. With the development of bronchoadenitis, a cough is noted. With this form, a secondary infection of the respiratory system often occurs and pneumonia develops.

As the disease progresses, the severity of the patient's condition worsens, cachexia, anemia, and hemorrhagic syndrome develop. Necrotic areas appear on the mucous membranes of the oral cavity. Due to a significant enlargement of the spleen, the heart shifts to the right, its sounds are muffled, and the rhythm of contractions is accelerated. There is a tendency to fall in peripheral blood pressure. As the infection progresses, heart failure develops. In the terminal period, patients are cachectic, the skin is pale and thinned, swelling is noted, and anemia is pronounced.

Chronic leishmaniasis occurs latently or with minor symptoms. Anthroponotic visceral leishmaniasis can be accompanied (in 10% of cases) by the appearance on the skin of leishmanoids - small papillomas, nodules or spots (sometimes just areas with reduced pigmentation) containing the pathogen. Leishmanoids can exist for years and decades.

Cutaneous zoonotic leishmaniasis (Borowsky's disease)

Distributed in tropical and subtropical climates. Its incubation period is 10-20 days, can be shortened to a week and extended to one and a half months. In the area of ​​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, which further progresses 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 undermined edges is formed, surrounded by a roll of infiltrated skin with copious discharge of a serous-purulent or hemorrhagic nature.

Around the primary leishmanioma, secondary “tubercles of seeding” develop, progressing into new ulcers and merging into a single ulcerated field (sequential leishmanioma). Typically, leishmaniomas appear on open areas of the skin; their number can vary from a single ulcer to dozens. Leishmaniomas are often accompanied by enlarged 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 significant widespread skin infiltration. Over time, the infiltrate regresses without leaving any consequences. In exceptional cases, small ulcers are observed that heal without noticeable scars. This form of leishmaniasis is quite rare and is usually observed in elderly people.

Tuberculoid cutaneous leishmaniasis

It is observed mainly in children and young people. With this form, small tubercles appear around or on post-ulcer scars, which can increase in size and merge with each other. Such tubercles rarely ulcerate. Ulcers with this form of infection leave significant scars.

Anthroponotic 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 of leishmaniasis

Diagnosis of leishmaniasis

A complete blood count for leishmaniasis shows signs of hypochromic anemia, neutropenia and aneosinophilia with relative lymphocytosis, as well as a reduced platelet concentration. ESR is increased. A biochemical blood test may show hypergammaglobulinemia. Isolation of the causative agent of cutaneous leishmaniasis is possible from tubercles and ulcers; in visceral leishmaniasis, leishmaniasis is detected in blood cultures for sterility. If necessary, to isolate the pathogen, a biopsy of the lymph nodes, spleen, and liver is performed.

As a specific diagnosis, microscopic examination, bacterial culture on NNN nutrient medium, and bioassays on laboratory animals are carried out. Serological diagnosis of leishmaniasis is carried out using RSK, ELISA, RNIF, RLA. During the convalescence period, a positive Montenegro reaction (skin test with leishmanin) is noted. Produced during epidemiological studies.

Treatment of leishmaniasis

The etiological treatment of leishmaniasis involves the use of pentavalent antimony preparations. In the visceral form, they are prescribed intravenously with increasing dosage over 7-10 days. In case of insufficient effectiveness, therapy is supplemented with amphotericin B, administered slowly intravenously with a 5% glucose solution. In the early stages of cutaneous leishmaniasis, the tubercles are injected with monomycin, berberine sulfate or methenamine, and these drugs are also prescribed in the form of ointments and lotions.

Formed ulcers are an indication for the administration of miramistin intramuscularly. Laser therapy is effective to speed up the healing of ulcers. Reserve drugs for leishmaniasis are amphotericin B and pentamidine; they are prescribed in cases of recurrent infection and when leishmania is resistant to traditional drugs. To increase the effectiveness of therapy, human recombinant interferon gamma can be added. In some cases, surgical removal of the spleen may be necessary.

Forecast and prevention of leishmaniasis

With mild leishmaniasis, spontaneous recovery is possible. The prognosis is favorable with timely detection and proper medical measures. Severe forms, infection of persons with weakened protective properties, and lack of treatment significantly worsen the prognosis. Cutaneous manifestations of leishmaniasis leave cosmetic defects.

Prevention of leishmaniasis includes measures for the improvement of populated areas, the elimination of mosquito breeding sites (landfills and vacant lots, flooded basements), and disinfestation of residential premises. Individual prevention involves the use of repellents and other means of protection against mosquito bites. If a patient is detected, chemoprophylaxis with pyrimethamine is performed in a team setting. Specific immune prophylaxis (vaccination) is carried out for persons planning to visit epidemically dangerous areas, as well as for the non-immune population of foci of infection.

• What is Leishmaniasis
• What causes Leishmaniasis
• Symptoms of Leishmaniasis
• Diagnosis of Leishmaniasis
• Treatment of Leishmaniasis
• Prevention of Leishmaniasis
• Which doctors should you contact if you have Leishmaniasis?

What is Leishmaniasis

Leishmaniasis(lat. Leishmaniasis) - a group of parasitic natural focal, mainly zoonotic, vector-borne diseases common in tropical and subtropical countries; caused by parasitic protozoa of the genus Leishmania, which are transmitted to humans through mosquito bites.

According to the World Health Organization, leishmaniasis occurs in 88 countries of the Old and New Worlds. Of these, 72 are developing countries, and among these, thirteen are the poorest countries in the world. Visceral leishmaniasis occurs in 65 countries.

Leishmaniasis is one of the neglected diseases.

What causes Leishmaniasis

Reservoir and sources of invasion- humans and various animals. Among the latter, the most important are jackals, foxes, dogs and rodents (gerbils - large, red-tailed, midday, thin-toed ground squirrel, etc.). Infectiousness lasts for an indefinitely long time and is equal to the period of residence of the pathogen in the blood and ulceration of the host’s skin. The duration of cutaneous leishmaniasis in gerbils is usually about 3 months, but can reach 7 months or more.

Main epidemiological signs of leishmaniasis. Indian visceral leishmaniasis (kala-azar), caused by L. donovani, is an anthroponosis. Distributed in a number of areas of Pakistan, Bangladesh, Nepal, China, etc. It is distinguished by outbreaks of the disease that occur from time to time. Mostly teenagers and young people, mainly living in rural areas, are affected.

South American visceral leishmaniasis(visceral leishmaniasis of the New World), caused by L. chagasi, is close in its manifestations to Mediterranean-Central Asian leishmaniasis. The incidence is mainly sporadic in a number of countries in Central and South America.

Anthroponotic cutaneous leishmaniasis of the Old World(Borovsky's disease), caused by L. minor, is common in the Mediterranean, the countries of the Near and Middle East, in the western part of the Hindustan Peninsula, Central Asia and Transcaucasia. The disease occurs mainly in cities and towns where mosquitoes live. Among the local population, children are more likely to get sick; among visitors, people of all ages are more likely to get sick. Summer-autumn seasonality is typical, which is associated with the activity of vectors.

Zoonotic cutaneous leishmaniasis of the Old World(Pendin's ulcer) is caused by L. major. The main reservoir of invasion is rodents (great and red gerbils, etc.). Distributed in the countries of the Middle East, North and West Africa, Asia, Turkmenistan and Uzbekistan. Endemic foci are found mainly in deserts and semi-deserts, in rural areas and on the outskirts of cities. The summer seasonality of infections is determined by the period of mosquito activity. Mostly children are affected; outbreaks of diseases among people of different ages are possible among visitors.

Zoonotic cutaneous leishmaniasis of the New World(Mexican, Brazilian and Peruvian cutaneous leishmaniasis), caused by L. mexicana, L. braziliensis, L. peruviana, L. uta, L. amazoniensis, L. pifanoi, L. venezuelensis, L. garnhami, L. panamensis, are registered in Central and South America, as well as in the southern regions of the USA. The natural reservoir of pathogens is rodents, numerous wild and domestic animals. The disease occurs in rural areas, mainly during the rainy season. People of all ages get sick. Usually infection occurs while working in the forest, hunting, etc.

Pathogenesis (what happens?) during Leishmaniasis

When mosquito bites, Leishmania in the form of promastigotes enters the human body. Their primary reproduction in macrophages is accompanied by the transformation of pathogens into amastigotes (flagellate-free form). In this case, productive inflammation develops, and a specific granuloma is formed at the site of penetration. It consists of macrophages containing pathogens, reticular, epithelioid and giant cells. A primary affect is formed in the form of a papule; later, with visceral leishmaniasis, it resolves without a trace or becomes scarred.

With cutaneous leishmaniasis, destruction of the skin develops at the site of the former tubercle, ulceration and then healing of the ulcer with the formation of a scar. Spreading by the lymphogenous route to regional lymph nodes, leishmania provokes the development of lymphangitis and lymphadenitis, the formation of limited skin lesions in the form of successive leishmaniomas. The development of tuberculoid or diffusely infiltrating cutaneous leishmaniasis is largely due to the state of reactivity of the body (hyperergy or hypoergy, respectively).

Along with cutaneous forms of the disease, so-called mucocutaneous forms can be observed with ulceration of the mucous membranes of the nasopharynx, larynx, trachea and subsequent formation of polyps or deep destruction of soft tissues and cartilage. These forms are registered in South American countries.

Convalescents develop persistent homologous immunity.

Symptoms of Leishmaniasis

In accordance with the clinical features, etiology and epidemiology, leishmaniasis is divided into the following types.

Visceral leishmaniasis (kala-azar)
1. Zoonotic: Mediterranean-Central Asian (children's kala-azar), East African (dum-dum fever), mucocutaneous leishmaniasis (New World leishmaniasis, nasopharyngeal leishmaniasis).
2. Anthroponotic (Indian kala-azar).

Cutaneous leishmaniasis
1. Zoonotic (rural type of Borovsky's disease, Pendensky ulcer).
2. Anthroponotic (urban type of Borovsky's disease, Ashgabat ulcer, Baghdad boil).
3. Cutaneous and mucocutaneous leishmaniasis of the New World (espundia, Breda disease).
4. Ethiopian cutaneous leishmaniasis.

Visceral Mediterranean-Asian leishmaniasis.
Incubation period. Varies from 20 days to 3-5 months, in rare cases up to 1 year or more. In young children and rarely in adults, long before the general manifestations of the disease, a primary affect occurs in the form of a papule.

Initial period of the disease. Characterized by the gradual development of weakness, loss of appetite, adynamia, pallor of the skin, and a slight enlargement of the spleen. Body temperature rises slightly.

High period. It usually begins with a rise in body temperature to 39-40 °C. The fever takes on a wave-like or irregular pattern and lasts from several days to several months with alternating episodes of high fever and remissions. In some cases, body temperature during the first 2-3 months can be low-grade or even normal.

When examining patients, polylymphadenopathy (peripheral, peribronchial, mesenteric and other lymph nodes), enlargement and hardening of the liver and even to a greater extent of the spleen, painless on palpation, are determined. In cases of development of bronhadenitis, a cough is possible, and pneumonia of a secondary bacterial nature is not uncommon.

As the disease progresses, the condition of patients progressively worsens. Weight loss (even cachexia) and hypersplenism develop. Bone marrow lesions lead to progressive anemia, granulocytopenia and agranulocytosis, sometimes with necrosis of the oral mucosa. Manifestations of hemorrhagic syndrome often occur: hemorrhages in the skin and mucous membranes, bleeding from the nose, and gastrointestinal tract. Fibrous changes in the liver lead to portal hypertension with edema and ascites, which is facilitated by progressive hypoalbuminemia.

Due to hypersplenism and the high position of the diaphragm, the heart shifts somewhat to the right, its sounds become muffled, tachycardia and arterial hypotension develop. These changes, along with anemia and intoxication, lead to the appearance and worsening of signs of heart failure. Possible diarrhea, menstrual irregularities, impotence.

Terminal period. Cachexia, a drop in muscle tone, thinning of the skin, the development of protein-free edema, and severe anemia are observed.

The disease can manifest itself in acute, subacute and chronic forms.
Acute form. Occasionally found in young children. It develops rapidly and without treatment quickly ends in death.
Subacute form. Seen more often. Severe clinical manifestations are characteristic, lasting 5-6 months.
Chronic form. It develops most often, often occurring subclinically and latently.

With visceral anthroponotic leishmaniasis (Indian kala-azar), in 10% of patients, several months (up to 1 year) after therapeutic remission, so-called leishmanoids appear on the skin. They are small nodules, papillomas, erythematous spots or areas of skin with reduced pigmentation, which contain Leishmania for a long time (years and decades).

Cutaneous zoonotic leishmaniasis(Pendin's ulcer, Borovsky's disease). Found in tropical and subtropical countries. The incubation period varies from 1 week to 1.5 months, on average 10-20 days. At the site of the entrance gate, primary leishmanioma appears, initially representing a smooth pink papule with a diameter of 2-3 mm. The size of the tubercle quickly increases, and it sometimes resembles a boil, but is painless or slightly painful on palpation. After 1-2 weeks, necrosis begins in the center of the leishmanioma, resembling the head of an abscess, and then a painful ulcer up to 1-1.5 cm in diameter is formed, with undermined edges, a thick rim of infiltrate and abundant serous-purulent or sanguineous exudate; Small secondary tubercles often form around it, the so-called “tubercles of seeding”, which also ulcerate and, when fused, form ulcerative fields. This is how sequential leishmanioma is formed. Leishmaniomas are most often localized on exposed parts of the body, their number varies from a few to dozens. The formation of ulcers in many cases accompanies the development of painless lymphangitis and lymphadenitis. After 2-6 months, epithelization of the ulcers and their scarring begin. The total duration of the disease does not exceed 6-7 months.

Diffuse infiltrating leishmaniasis. It is characterized by pronounced infiltration and thickening of the skin with a large area of ​​distribution. Gradually the infiltrate resolves without a trace. Minor ulcerations are observed only in exceptional cases; they heal with the formation of barely noticeable scars. This variant of cutaneous leishmaniasis is very rare in older people.

Tuberculoid cutaneous leishmaniasis. Sometimes observed in children and young people. It is characterized by the formation of small tubercles around scars or on them. The latter can increase and merge with each other. As the disease progresses, they occasionally ulcerate; subsequently the ulcers heal with scarring.

Cutaneous antroponotic leishmaniasis. It is characterized by a long incubation period of several months or even years and two main features: slow development and less severe skin lesions.

Complications and prognosis
Advanced leishmaniasis can be complicated by pneumonia, purulent-necrotic processes, nephritis, agranulocytosis, and hemorrhagic diathesis. The prognosis of severe and complicated forms of visceral leishmaniasis with untimely treatment is often unfavorable. In mild forms, spontaneous recovery is possible. In cases of cutaneous leishmaniasis, the prognosis for life is favorable, but cosmetic defects are possible.

Diagnosis of Leishmaniasis

Visceral leishmaniasis should be distinguished from malaria, typhoid-paratyphoid diseases, brucellosis, lymphogranulomatosis, leukemia, and sepsis. When establishing a diagnosis, epidemiological history data are used, indicating that the patient has been in endemic foci of the disease. When examining a patient, it is necessary to pay attention to prolonged fever, polylymphadenopathy, anemia, weight loss, hepatolienal syndrome with a significant enlargement of the spleen.

Manifestations of cutaneous zoonotic leishmaniasis are differentiated from similar local changes in leprosy, skin tuberculosis, syphilis, tropical ulcers, and epithelioma. In this case, it is necessary to take into account the phase nature of the formation of leishmanioma (painless papule - necrotic changes - ulcer with undermined edges, a rim of infiltrate and serous-purulent exudate - scar formation).

Laboratory diagnosis of leishmaniasis
The hemogram reveals signs of hypochromic anemia, leukopenia, neutropenia and relative lymphocytosis, aneosinophilia, thrombocytopenia, and a significant increase in ESR. Poikilocytosis, anisocytosis, anisochromia are characteristic, agranulocytosis is possible. Hypergammaglobulinemia is noted.

With cutaneous leishmaniasis, pathogens can be detected in material obtained from tubercles or ulcers, with visceral leishmaniasis - in smears and thick drops of blood stained according to Romanovsky-Giemsa, much more often (95% of positive results) - in smears of bone marrow punctures. A culture of the pathogen (promastigote) can be obtained by inoculating the punctate on NNN medium. Sometimes a biopsy of the lymph nodes and even the liver and spleen is performed to detect leishmania. Serological reactions are widely used - RSK, ELISA, RNIF, RLA, etc., biological tests on hamsters or white mice. During the period of convalescence, a skin test with leishmanin (Montenegro reaction), used only in epidemiological studies, becomes positive.

Treatment of Leishmaniasis

For visceral leishmaniasis, pentavalent antimony preparations (solyusurmin, neostibosan, glucantim, etc.) are used in the form of daily intravenous infusions in increasing doses starting from 0.05 g/kg. The course of treatment is 7-10 days. If the clinical effectiveness of the drugs is insufficient, amphotericin B is prescribed at 0.25-1 mg/kg slowly intravenously in a 5% glucose solution; The drug is administered every other day for a course of up to 8 weeks. Pathogenetic therapy and prevention of bacterial complications are carried out according to well-known schemes.

In cases of cutaneous leishmaniasis, at the early stage of the disease, the tubercles are injected with solutions of mepacrine, monomycin, hexamine, berberine sulfate; ointments and lotions are used using these products. For formed ulcers, intramuscular injections of monomycin are prescribed at 250 thousand units (for children 4-5 thousand units/kg) 3 times a day, the course dose of the drug is 10 million units. You can treat with aminoquinol (0.2 g 3 times a day, 11-12 g of the drug per course). Laser irradiation of ulcers is used. Pentavalent antimony drugs and amphotericin B are prescribed only in severe cases of the disease.

Drugs of choice: sodium antimonyl gluconate 20 mg/kg IV or IM once a day for 20-30 days; meglumine antimoniate (glucantim) 20-60 mg/kg deep IM once a day for 20-30 days. If the disease relapses or treatment is insufficiently effective, a second course of injections should be administered within 40-60 days. Additional administration of allopurinol 20-30 mg/kg/day in 3 doses orally is effective.

Alternative drugs for relapses of the disease and resistance of the pathogen: amphotericin B 0.5-1.0 mg/kg IV every other day or pentamidine IM 3-4 mg/kg 3 times a week for 5-25 weeks. If chemotherapy has no effect, human recombinant interferon γ is additionally prescribed.

Surgery. Splenectomy is performed according to indications.

Prevention of Leishmaniasis

Control of animal carriers of leishmania is carried out in an organized manner and on a large scale only for zoonotic cutaneous and visceral leishmaniasis. They carry out deratization measures, improvement of populated areas, elimination of vacant lots and landfills, drainage of basements, treatment of residential, household and livestock premises with insecticides. The use of repellents and mechanical means of protection against mosquito bites is recommended.

After identifying and treating sick people, the source of the infection is neutralized. In small groups, chemoprophylaxis is carried out by prescribing chloridine (pyrimethamine) during the epidemic season. Immunoprophylaxis of zoonotic cutaneous leishmaniasis is carried out with a live culture of promastigotes of the virulent strain of L. major during the inter-epidemic period among persons traveling to endemic foci or non-immune individuals living in these foci. 04/05/2019

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Leishmaniasis

Leishmaniasis (leishmanioses) is a group of protozoal vector-borne diseases of humans and animals, characterized by predominant damage to internal organs (visceral leishmaniasis) or skin and mucous membranes (cutaneous leishmaniasis). There are geographical types of the disease - leishmaniasis of the Old and New Worlds.

Historical information. The first description of cutaneous leishmaniasis belongs to the English physician Pocock (1745). The clinical picture of the disease was described in the works of the Russell brothers (1756) and domestic researchers and doctors N. Arendt (1862) and L.L. Heidenreich (1888).

The causative agent of cutaneous leishmaniasis was discovered by P.F. Borovsky in 1898, described by the American researcher J. Wright in 1903. In 1900-1903. V. Leishman and S. Donovan discovered in the spleen of patients with kala-azar the causative agent of visceral leishmaniasis, identical to the microorganism described by P.F. Borovsky.

The assumption of a connection between leishmaniasis and mosquitoes was made in 1905 by Press and the Sergent brothers and proven in an experiment by A. Donatier and L. Parrot in 1921. In 1908 by S. Nicole and in 1927-1929. N.I. Khodukin and M.S. Sofiev established the role of dogs as one of the main reservoirs of pathogens of visceral leishmaniasis. The studies of V.L. Yakimov (1931) and N.N. Latyshev (1937-1947), who established the presence of natural foci of visceral leishmaniasis in Turkmenistan, were of great importance for understanding the epidemiology of the disease. As a result of efforts undertaken in 1950-1970. In the fight against leishmaniasis, the incidence of some forms of leishmaniasis in our country has been practically eliminated (cutaneous anthroponotic and urban form of visceral leishmaniasis).

The causative agents of leishmaniasis belong to the genus Leishmania, family Trypanosomatidae, class Zoomastigophorea, phylum Protozoa.

The life cycle of Leishmania occurs with a change of hosts and consists of two stages: amastigote (flagellateless) - in the body of vertebrates and humans, and promastigote (flagellate) - in the body of the arthropod mosquito.

Leishmania in the amastigote stage have an oval shape and size (3-5) x (1-3) microns; when stained according to Leishman or Romanovsky-Giemsa, homogeneous or vacuolated blue cytoplasm, a centrally located nucleus and ruby-red kinetoplast are differentiated; usually found in cells of the mononuclear phagocyte system.

Leishmania is transmitted by blood-sucking insects - mosquitoes of the genera Phlebotomus, Lutzomyia, and the family Phlebotomidae.

Leishmaniasis visceral

Leishmaniasis visceral (leishmaniosis visceralis) is a transmissible protozoal disease characterized by a predominantly chronic course, undulating fever, splenoid and hepatomegaly, progressive anemia, leukopenia, thrombocytopenia and cachexia.

There are anthroponotic (Indian visceral leishmaniasis, or kala-azar) and zoonotic visceral leishmaniasis (Mediterranean-Central Asian visceral leishmaniasis, or childhood kala-azar; East African visceral leishmaniasis; New World visceral leishmaniasis). Sporadic imported cases of the disease, predominantly Mediterranean-Central Asian visceral leishmaniasis, are recorded in Russia.

Leishmaniasis visceral Mediterranean-Central Asian

Etiology. The causative agent is L. infantum.

Epidemiology. Mediterranean-Central Asian visceral leishmaniasis is a zoonosis prone to focal spread. There are 3 types of foci of invasion: 1) natural foci, in which leishmania circulates among wild animals (jackals, foxes, badgers, rodents, including gophers, etc.), which are a reservoir of pathogens; 2) rural foci in which the circulation of pathogens occurs mainly among dogs - the main sources of pathogens, as well as among wild animals - which can sometimes become sources of infection; 3) urban foci in which dogs are the main source of infection, but the pathogen is also found in synanthropic rats. In general, dogs in rural and urban foci of leishmaniasis represent the most significant source of infection in humans. The leading mechanism of infection is transmissible, through the bite of infested carriers - mosquitoes of the genus Phlebotomus. Infection through blood transfusions from donors with latent invasion and vertical transmission of leishmania are possible. Mostly children from 1 to 5 years old are affected, but often adults - visitors from non-endemic areas - are also affected.

The incidence is sporadic; local epidemic outbreaks are possible in cities. The infection season is summer, and the morbidity season is autumn of the same or spring of the next year. The foci of the disease are located between 45°N. and 15° S in the Mediterranean countries, in the northwestern regions of China, in the Middle East, Central Asia, Kazakhstan (Kzyl-Orda region), Azerbaijan, Georgia.

Subsequently, leishmania can penetrate regional lymph nodes, then disseminate to the spleen, bone marrow, liver and other organs. In most cases, as a result of the immune response, primarily delayed hypersensitivity reactions, the destruction of invaded cells occurs: the invasion becomes subclinical or latent. In the latter cases, transmission of pathogens through blood transfusions is possible.

In cases of reduced reactivity or when exposed to immunosuppressive factors (for example, the use of corticosteroids, etc.), intensive reproduction of leishmania in hyperplastic macrophages is observed, specific intoxication occurs, and an increase in parenchymal organs occurs with disruption of their function. Hyperplasia of stellate endothelial cells in the liver leads to compression and atrophy of hepatocytes, followed by interlobular fibrosis of the liver tissue. There is atrophy of the spleen pulp and germinal centers in the lymph nodes, a violation of bone marrow hematopoiesis, anemia and cachexia occur.

Hyperplasia of the SMF elements is accompanied by the production of a large amount of immunoglobulins, which, as a rule, do not play a protective role and often cause immunopathological processes. Secondary infection and renal amyloidosis often develop. Changes characteristic of hypochromic anemia are noted in the internal organs.

Specific changes in parenchymal organs undergo reverse development with adequate treatment. Convalescents develop stable homologous immunity.

Clinical picture. The incubation period ranges from 20 days to 3-5 months, sometimes 1 year or more. At the site of leishmania inoculation in children 1-1.5 years old, less often in older children and adults, a primary affect occurs in the form of a papule, sometimes covered with scales. It is important to correctly assess this symptom, since it appears long before the general manifestations of the disease. During visceral leishmaniasis, 3 periods are distinguished: initial, peak of the disease and terminal.

In the initial period, weakness, decreased appetite, adynamia, and slight splenomegaly are noted.

The period of the height of the disease begins with a cardinal symptom - fever, which usually has a wave-like character with rises in body temperature to 39-40 ° C, followed by remissions. The duration of fever ranges from several days to several months. The duration of remission also varies - from several days to 1-2 months.

Constant signs of visceral leishmaniasis are enlargement and hardening of the liver and mainly the spleen; the latter may occupy most of the abdominal cavity. Liver enlargement is usually less significant. On palpation, both organs are dense and painless; pain is usually observed with the development of periosplenitis or perihepatitis. Under the influence of treatment, the size of the organs decreases and can return to normal.

Mediterranean-Central Asian visceral leishmaniasis is characterized by involvement in the pathological process of peripheral, mesenteric, peribronchial and other groups of lymph nodes with the development of polylymphadenitis, mesadenitis, bronchoadenitis; in the latter cases, paroxysmal cough may occur. Pneumonia caused by bacterial flora is often detected.

In the absence of proper treatment, the condition of patients gradually worsens, they lose weight (to the point of cachexia). The clinical picture of hypersplenism develops, anemia progresses, which is aggravated by bone marrow damage. Granulocytopenia and agranulocytosis occur, and necrosis of the tonsils and mucous membranes of the oral cavity and gums (noma) often develops. Hemorrhagic syndrome often develops with hemorrhages in the skin, mucous membranes, nasal and gastrointestinal bleeding. Severe splenohepatomegaly and liver fibrosis lead to portal hypertension, the appearance of ascites and edema. Their occurrence is promoted by hypoalbuminemia. Splenic infarction is possible.

Due to the enlargement of the spleen and liver, the high position of the dome of the diaphragm, the heart shifts to the right, its sounds become dull; tachycardia is determined both during fever and at normal temperature; blood pressure is usually low. As anemia and intoxication develop, signs of heart failure increase. Damage to the digestive tract is noted, and diarrhea occurs. Women usually experience (oligo)amenorrhea, and men have decreased sexual activity.

The hemogram determines a decrease in the number of red blood cells (up to 1-2 * 10^12 / l or less) and hemoglobin (up to 40-50 g / l or less), color index (0.6-0.8). Poikilocytosis, anisocytosis, and anisochromia are characteristic. Leukopenia (up to 2-2.5 * 10^9 /l or less), neutropenia (sometimes up to 10%) with relative lymphocytosis are noted, agranulocytosis is possible. A constant symptom is aneosinophilia, and thrombocytopenia is usually detected. Characterized by a sharp increase in ESR (up to 90 mm/h). Blood clotting and erythrocyte resistance are reduced.

During kala-azar, 5-10% of patients develop cutaneous leishmanoids in the form of nodular and/or macular rashes that appear 1-2 years after successful treatment and contain leishmania, which can persist in them for years and even decades. Thus, a patient with cutaneous leishmanoid becomes a source of pathogens for many years. Currently, cutaneous leishmanoids are observed only in India.

In the terminal period of the disease, cachexia, a decrease in muscle tone, thinning of the skin develop, and the contours of a huge spleen and enlarged liver appear through the thin abdominal wall. The skin takes on a porcelain appearance, sometimes with an earthy or waxy tint, especially in cases of severe anemia.

Mediterranean-Central Asian visceral leishmaniasis can manifest itself in acute, subacute and chronic forms.

Acute form, usually detected in young children, it is rare, characterized by a rapid course and, if not treated in a timely manner, ends in death.

Subacute form, more frequent, progresses severely over 5-6 months with progression of the characteristic symptoms of the disease and complications. Without treatment, death often occurs.

Chronic form, the most common and favorable, characterized by long-term remissions and usually ends in recovery with timely treatment. It is observed in older children and adults.

A significant number of cases of invasion occur in subclinical and latent forms.

Forecast. Serious, with severe and complicated forms and untimely treatment - unfavorable; mild forms may result in spontaneous recovery.

Diagnostics. In endemic areas, clinical diagnosis is not difficult to make. Confirmation of the diagnosis is carried out using microscopic examination. Leishmania is sometimes detected in a smear and a thick drop of blood. The most informative is the detection of leishmania in bone marrow preparations: up to 95-100% positive results. Bone marrow punctate is inoculated to obtain a culture of the pathogen (promastigotes are detected on NNN medium). Sometimes they resort to a biopsy of the lymph nodes, spleen, and liver. Serological research methods are used (RSK, NRIF, ELISA, etc.). A biological test can be used to infect hamsters.

In convalescents, an intradermal test with leishmanin (Montenegro reaction) becomes positive.

Differential diagnosis is carried out with malaria, typhus, influenza, brucellosis, sepsis, leukemia, lymphogranulomatosis.

Treatment. The most effective drugs are 5-valent antimony, pentamidine isothionate.

Antimony drugs are administered intravenously for 7-16 days in a gradually increasing dose. If these drugs are ineffective, pentamidine is prescribed at 0.004 g per 1 kg per day daily or every other day, for a course of 10-15 injections.

Besides specific drugs, pathogenetic therapy and prevention of bacterial deposits are necessary.

Prevention. Based on measures to exterminate mosquitoes and sanitize sick dogs.

Leishmaniasis cutaneous

Leishmaniasis cutaneous (leishmaniosis cutanea) is a vector-borne protozoan, endemic to tropical and subtropical climates, clinically characterized by limited skin lesions followed by ulceration and scarring. Clinical forms, severity and outcomes are determined by the immunobiological reactivity of the body.

There are cutaneous leishmaniasis of the Old World (anthroponotic and zoonotic subtypes) and cutaneous leishmaniasis of the New World. In Russia, predominantly imported cases of the disease are recorded.

Leishmaniasis cutaneous zoonotic

Synonym: desert-rural, wet, acute necrotizing cutaneous leishmaniasis, Pendinsky ulcer

Etiology. Pathogen – l. major, which differs in antigenic and biological properties from the causative agent of anthroponotic (urban) cutaneous leishmaniasis – L. minor.

Epidemiology. The main reservoir and source of infection is the greater gerbil; natural contamination of other rodent species and some predators (weasels) has been established. The pathogens are transmitted by mosquitoes of the genus Phlebotomus, mainly Ph. pappayasii, which become infectious 6-8 days after bloodsucking on rodents. Infection occurs through the bite of an infected mosquito. There is a clear summer seasonality of incidence, coinciding with the flight of mosquitoes. Found in rural areas. Receptivity is universal. In endemic areas, the incidence is detected mainly in children and visitors, since most of the local population develops active immunity, and recurrent diseases are rare. Epidemic outbreaks of the disease are possible.

The invasion is common in African and Asian countries (India, Pakistan, Iran, Saudi Arabia, Yemen, the Middle East, Turkmenistan, Uzbekistan).

Pathogenesis and pathological picture. At the site of inoculation, Leishmania multiply in macrophages and cause focal productive inflammation with the formation of a specific granuloma (leishmanioma), consisting of macrophages, epithelial, plasma cells, lymphocytes and fibroblasts. Macrophages contain a large number of amastigotes. After 1-2 weeks, destruction develops in the granuloma, an ulcer forms, which then scars. Lymphogenous dissemination of leishmania with the formation of successive leishmaniomas, lymphangitis, and lymphadenitis is often observed. With hyperergic reactivity, a tuberculoid type of lesion is observed; leishmania is rarely found in the lesions. The hypoergic type of reactivity causes diffuse-infiltrating forms of the disease with a large number of pathogens in the lesions.

Clinical picture. The incubation period lasts from 1 week to 1-1.5 months, usually 10-20 days.

The following forms of cutaneous leishmaniasis are distinguished: 1 – primary leishmanioma – a) tubercle stage, b) ulceration stage, c) scarring stage; 2 – sequential leishmanioma; 3 – diffuse infiltrating leishmaniasis; 4 – tuberculoid cutaneous leishmaniasis.

At the site of introduction of leishmania into the skin, a primary smooth pink papule, 2-3 mm in size, appears, which quickly becomes large in size, sometimes resembling a boil with lymphangitis and an inflammatory reaction of surrounding tissues, but is not painful on palpation (primary leishmanioma). After 1-2 weeks, central necrosis of leishmanioma begins, followed by the formation of ulcers of various shapes and sizes up to 1.0-1.5 cm or more, with undermined edges, copious serous-purulent, often sanguineous discharge, moderately painful on palpation.

Around the primary leishmanioma, multiple (from 5-10 to 100-150) small nodules (“tubercles of infestation”) often form, which ulcerate and, merging, form ulcerative fields. Leishmaniomas are usually localized on open areas of the skin of the upper and lower extremities and on the face.

After 2-4, sometimes 5-6 months, epithelization and scarring of the ulcer begins.

From the moment the papule appears until the scar forms, no more than 6-7 months pass. Sometimes ulceration and scarring of the area of ​​lymphangitis and lymphadenitis are observed. Tuberculoid and diffuse infiltrating types of lesions are rarely observed. Secondary bacterial infection delays recovery.

Forecast. Favorable, but cosmetic defects may occur.

Differential diagnosis. Cutaneous leishmaniasis must be differentiated from epithelioma, leprosy, skin tuberculosis, syphilis, and tropical ulcers.

Treatment. Treatment tactics and choice of drug depend on the stage and severity of the disease. In the early stages, intradermal injection of leishmania with a solution of mepacrine (acryquin), monomycin, methenamine, berberine sulfate, and the use of ointments and lotions containing these agents can be effective. At the ulcer stage, treatment with monomycin is effective (adults 250,000 units three times a day, 10,000,000 units per course, children - 4000-5000 units per 1 kg of body weight 3 times a day), aminoquinol (0.2 g three times a day, for the course 11-12 years). The use of laser therapy is effective, especially in the tubercle stage (according to B.G. Bardzhadze), after which rough scars do not form.

In severe cases, 5-valent antimony preparations are used.

Prevention. They are carrying out a set of measures to combat mosquitoes and desert rodents. Vaccination with a live culture of b is effective. ta1og – no later than 3 months before entry into the endemic area. The vaccine provides lifelong immunity.

Anthroponotic cutaneous leishmaniasis is characterized by less severe and slower dynamics (“year-old ulcer”) of lesions.