Treatment of visceral leishmaniasis. Visceral leishmaniasis. Cutaneous form of leishmaniasis

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 invasion foci: 1) natural foci in which Leishmania circulate among wild animals (jackals, foxes, badgers, rodents, including ground squirrels, 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 - sometimes capable of becoming sources of infection; 3) urban foci, in which dogs are the main source of invasion, but the pathogen is also found in synanthropic rats. In general, dogs in rural and urban leishmaniasis foci represent the most significant source of human infection. The leading mechanism of infection is transmissible, through the bite of infested vectors - mosquitoes of the genus Phlebotomus. Infection is possible during blood transfusions from donors with latent invasion and vertical transmission of Leishmania. Mostly children from 1 to 5 years old are sick, but often adults - visitors from non-endemic areas.

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

In the future, leishmania can penetrate into the 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-type hypersensitivity reactions, the invaded cells are destroyed: the invasion acquires a subclinical or latent character. In the latter cases, transmission of pathogens during blood transfusions is possible.

In cases of reduced reactivity or under the influence of immunosuppressive factors (for example, the use of corticosteroids, etc.), intensive reproduction of leishmania in hyperplastic macrophages is noted, specific intoxication occurs, an increase in parenchymal organs occurs with a violation of their function. Hyperplasia of stellate endotheliocytes 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, impaired bone marrow hematopoiesis, anemia and cachexia.

Hyperplasia of SMF elements is accompanied by the production of a large number of immunoglobulins, which, as a rule, do not play a protective role and often cause immunopathological processes. A secondary infection, renal amyloidosis, often develops. In the internal organs, there are changes characteristic of hypochromic anemia.

Specific changes in parenchymal organs undergo regression with adequate treatment. In convalescents, persistent homologous immunity is formed.

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 evaluate 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, loss of appetite, adynamia, slight splenomegaly are noted.

The peak period of the disease begins with a cardinal symptom - fever, which usually has an undulating 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 is also different - from several days to 1-2 months.

Permanent signs of visceral leishmaniasis is an increase and thickening of the liver and mainly the spleen; the latter can occupy most of the abdominal cavity. Liver enlargement is usually less significant. On palpation, both organs are dense and painless; soreness 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 coughing 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 (up to cachexia). The clinical picture of hypersplenism develops, anemia progresses, which is aggravated by damage to the bone marrow. There are granulocytopenia and agranulocytosis, necrosis of the tonsils and mucous membranes of the oral cavity, 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, ascites, and edema. Their occurrence is promoted by hypoalbuminemia. Spleen infarctions are possible.

Due to the enlargement of the spleen and liver, the high standing of the dome of the diaphragm, the heart shifts to the right, its tones become muffled; tachycardia is determined both during the period of fever and at normal temperature; blood pressure is usually low. As anemia and intoxication develop, signs of heart failure increase. There is a lesion of the digestive tract, diarrhea occurs. In women, (oligo) amenorrhea is usually observed, in men, sexual activity decreases.

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

With kala-azar, 5–10% of patients develop cutaneous leishmanoid in the form of nodular and (or) spotty 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 leishmanoid is seen only in India.

In the terminal period of the disease, cachexia, a drop in muscle tone, thinning of the skin develop, and the contours of a huge spleen and enlarged liver appear through a 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.

The acute form, usually detected in young children, is rare, characterized by a rapid course and, if not treated promptly, ends in death.

The subacute form, more frequent, is severe for 5-6 months with the progression of the characteristic symptoms of the disease and complications. Without treatment, death often occurs.

The chronic form, the most frequent and favorable, is characterized by prolonged remissions and usually ends in recovery with timely treatment. Seen in older children and adults.

A significant number of cases of invasion occurs 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 foci, the clinical diagnosis is not difficult to make. Diagnosis is confirmed by microscopic examination. Leishmania is sometimes found 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 cultured to obtain a culture of the pathogen (promastigotes are detected on NNN medium). Sometimes they resort to a biopsy of the lymph nodes, spleen, liver. Apply serological methods of research (RSK, NRIF, ELISA, etc.). A biological test with infection of hamsters can be used.

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

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

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

Antimony preparations 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 every day or every other day, for a course of 10-15 injections.

Apart from specific preparations, pathogenetic therapy and prevention of bacterial deposits are necessary.

Prevention. It is based on measures for the destruction of mosquitoes, sanitation of sick dogs.

There are Indian kala-azar, Mediterranean visceral leishmaniasis (children), East African and South American visceral leishmaniasis.

What causes visceral leishmaniasis:

Visceral leishmaniasis occurs in countries with subtropical and tropical climates. In the CIS countries (Central Asia, Transcaucasia and South Kazakhstan), sporadic cases of Mediterranean visceral leishmaniasis are recorded.

Mediterranean visceral leishmaniasis is a zoonosis. The reservoir and source of it in cities are dogs, in rural areas - dogs, jackals, foxes, rodents. Leishmania carriers are mosquitoes, the females of which feed on blood, attacking a person at dusk and at night and infecting him when they bite. Mostly children aged 1 to 5 years are ill. The infection season is summer, and the incidence season is autumn of the same year or spring of the following year.

Pathogenesis (what happens?) during Visceral leishmaniasis:

Leishmania penetrate into the cells of the bone marrow and the reticuloendothelial system.

Symptoms of visceral leishmaniasis:

The clinical picture of Indian and Mediterranean visceral leishmaniasis is similar. The incubation period ranges from 20 days to 10 - 12 months. In children, the primary affect (papule) occurs long before the general manifestations of the disease. In the initial period of the disease, weakness, loss of appetite, adynamia, and a slight enlargement of the spleen are noted. The peak period of the disease begins / with a fever, the duration of which ranges from several days to several months. Temperature rises up to 39 - 40 0С are replaced by remissions.

Constant signs of visceral leishmaniasis are enlargement and thickening of the liver and spleen, lymph nodes. In the first 3-6 months of the disease, the spleen enlargement occurs at a rapid pace, then more slowly. Palpation of the liver, spleen, lymph nodes is painless. Bone marrow damage and hypersplenism lead to severe anemia, as evidenced by the pallor of the skin, which sometimes acquires a “porcelain”, waxy or earthy hue. Patients lose weight dramatically, they develop ascites, peripheral edema, and diarrhea. Characterized by hemorrhagic syndrome with hemorrhages in the skin and mucous membranes, bleeding from the nose, gastrointestinal tract, necrosis of the tonsils, mucous membranes of the mouth, gums.

Due to an increase in the liver, spleen and high standing of the diaphragm, the heart shifts to the right, constant tachycardia is determined, and blood pressure decreases. Pneumonia caused by secondary flora often develops. In the terminal period of the disease, cachexia develops, muscle tone decreases sharply, the skin becomes thinner, and the contours of a huge spleen and large liver often appear through the abdominal wall. In the hemogram - characteristic features: a sharp decrease in the number of erythrocytes, leukocytes (especially neutrophils), eosinophils, platelets. ESR is sharply increased (90 mm/h).

Complications of visceral leishmaniasis- pneumonia, enterocolitis, nephritis, thrombo-hemorrhagic syndrome, laryngeal edema, ulcerative stomatitis, noma.

Treatment of visceral leishmaniasis:

Etiotropic agents for the treatment of visceral leishmaniasis are antimony preparations that are administered parenterally (intravenously, intramuscularly). A 20% solution of solyusurmine (Russia), glucanthine (France), neostibasan (Germany), pentostam (England) is used. Convalescents are under observation for 4 months (possibility of relapse!). With bacterial complications, antibiotics are indicated, with pronounced changes in the blood - blood transfusion, leukocyte and erythrocyte mass.

Prevention of visceral leishmaniasis:

Sanitation of dogs with leishmaniasis, mosquito control, protection against mosquito attacks, application of repellents.

Etiology. Life cycle.

Visceral leishmaniasis . Pathogenesis.Clinical features. Complications. Diagnostics.Cutaneous leishmaniasis . Pathogenesis.clinical features.Complications. Diagnostics.Epidemiology and Prevention

Additional questions: What clinical signs make one suspect visceral leishmaniasis (cutaneous leishmaniasis) in a patient? What details of the history indicate the possibility of leishmaniasis in this patient?

Leishmaniasis- protozoan invasions, the causative agents of which are leishmania. L eischmaniasis is widespread in countries with a tropical and subtropical climate on all continents where mosquitoes live. These are typical natural focal diseases. Natural reservoirs are rodents, wild and domestic predators. Human infection occurs when bitten by infested mosquitoes.

According to the World Health Organization and the Center for Disease Control in 2004, 1/10 of the world's population is at risk of infection with Leishmania. Only a few imported cases are registered in the Russian Federation.

According to the pathogenic action of Leishmania, the diseases they cause are divided into three main forms: skin;mucocutaneous; visceral.

Human diseases are caused by several types and subspecies of parasites, which are combined into 4 complexes:

L. donovani - the causative agent of visceral leishmaniasis;

L. tropica - causative agent of cutaneous leishmaniasis;

L. brasiliensis - causative agent of brazilian leishmaniasis

L. mexicana - causative agent of leishmaniasis in Central America.

Leishmaniadonovani affects the internal organs, so the disease is called visceral(internal) leishmaniasis.

Leishmania tropica - causes cutaneous leishmaniasis (Borovsky's disease) in humans.

There are two forms of cutaneous leishmaniasis - anthroponotic (cityskuyu) and zoonotic (desert).

Leismania brasiliensis found in South America, and causes mucocutaneous (American) Leishmaniasis. There are many geographic forms of this disease. There are two main geographic forms: visceral leishmaniasis mediterraneanth type found in the Russian Federation, and Indian kala azar.

Morphology. All species are morphologically similar and have the same cycles of development. Leishmania go through two stages in its development:

In the non-flagellated, or leishmanial (amostigous); - in the flagellated, or promastigous.

Leishmanial the form is very small - 3-5 microns in diameter. Its characteristic feature is a round nucleus, which occupies about 1/4 of the cytoplasm; there is no flagellum; a rod-shaped kinetoplast is located perpendicular to the cell surface. These forms live intracellularly (in the cells of the reticuloendothelial system) in macrophages, cells of the bone marrow, spleen, liver of humans and a number of mammals (rodents, dogs, foxes). One affected cell may contain several dozen Leishmania. They reproduce by simple division.

The flagellate-free form, sown on a nutrient medium, turns into a flagellated one. When stained according to Romanovsky, the cytoplasm is blue or bluish-lilac, the nucleus is red-violet, the kinetoplast is stained more intensely than the nucleus (Fig. I).

When a person is bitten by an infected mosquito, mobile forms of Leishmania from his pharynx penetrate into the wound and then penetrate into the cells of the skin or internal organs, depending on the type of Leishmania. Here they are transformed into flagellate-free forms.

Sources of infection in leishmaniasis. The possible role of dogs as a source of infection in visceral leishmaniasis of the Mediterranean type was first pointed out by the French scientist C. Nicole, and this was confirmed by Soviet scientists H.II. Khodukin and M.S. Sofiev. In addition to dogs, some wild animals (jackals, porcupines) can also be the source of the disease. With Indian leishmaniasis (kala-azar), sick people are the source of infection.

A dog affected by leishmaniasis (Fig. 2) develops malnutrition, ulcers appear on the head and skin of the body, and peeling of the skin, especially around the eyes. It is important to take into account that if in young dogs the disease can be acute and even lead to their death, then in adult animals the course of the disease is often more blurred or even asymptomatic (carriage).

Visceral leishmaniasis occurs sporadically in Central Asia, in the south of Kazakhstan, Kyrgyzstan and the Transcaucasus.

In cutaneous leishmaniasis, the source of infection is sick people or wild rodents. The main keepers of Leishmania are the great gerbil and the red-tailed gerbil.

Cutaneous leishmaniasis occurs in many oases in the southern part of Turkmenistan and Uzbekistan. In some places, the transmission of this type of leishmaniasis is so intense that local residents manage to get sick with it even at preschool age.

Visceral leishmaniasis(children, kala-azar, kara-azar) - pathogen - L . donovani . Visceral leishmaniasis is more common in children. After the incubation period, the patient's temperature rises, reaching 39-40 ° C at the height of the disease, lethargy, anemia appear. , pallor, loss of appetite. Incubation period- from 10 days to 3 years, usually - 2-4 months. Symptoms- slowly developing fever and general malaise. Progressive wasting of an anemic patient. Other classic symptoms are protrusion of the abdomen due to enlargement of the liver and spleen. Without treatment - death in 2-3 years.

More acute form - 6-12 months. Clinical symptoms - pulmonary edema, face, bleeding of mucous membranes, breathing complications, diarrhea.

Features of the course of visceral leishmaniasis depend on the age of the patient. In sick children under the age of 1 year, the disease is characterized by a short incubation period and an acute course. For older children and adults, the disease is characterized by a chronic course. The clinical course also largely depends on the intensity of the invasion of the macroorganism and on the duration of the disease.

If left untreated, it usually ends in death, the immediate cause of which is often complications such as pneumonia, dyspepsia, purulent infection, etc.

Mucocutaneous leishmaniasis– pathogens L . braziliensis , L . Mexicana , common in South America.

The primary lesion is the bite site. Secondarily - damage to the mucous membranes of the nose and pharynx. As a result - a strong disfiguring lesion of the lips, nose, vocal cords. Death is due to secondary infection.

Diagnosis is difficult - cultivation of affected tissues is required for accurate diagnosis. Long-term treatment (several years), preservation of dormant stages in the mucous membranes.

L . mexicana - causes skin forms, sometimes - in the mucous membranes. More often - spontaneous recovery after a few months, with the exception of strange ear lesions. In the latter case - severe disfigurement and the course of the disease up to 40 years.

Cutaneous leishmaniasis(Borovsky's disease, oriental ulcer, Penda ulcer) - L . tropica , L . major . They have similar life cycles and similar disease symptoms, but different distributions.

Complex L . major - Sev. America, Middle East, Western India, Sudan.

Complex L . tropica - Ethiopia, India, European Mediterranean region, Middle East, Kenya, North. Africa.

Cutaneous leishmaniasis occurs in the form anthroponotic and zoonotic types.

Anthroponotic type(late ulcerative cutaneous leishmaniasis of urban type, Ashgabat).

zoonotic type false leishmaniasis (rural type, penda ulcer, acute necrotizing cutaneous leishmaniasis)

When a person is infected with a causative agent of cutaneous leishmaniasis, after an incubation period of 1-2 weeks to several months (with a zoonotic type, this period is usually short), small tubercles appear at the sites of mosquito bites. They are brownish-reddish in color, of medium density, usually not painful. The tubercles gradually increase in size and then begin to ulcerate - after 3-6 months with the anthroponotic type and after 1-3 weeks with the zoonotic. Ulcers occur with swelling of the surrounding tissue, inflammation, and swollen lymph nodes.

The process lasts for several months (with an anthroponotic form - more than a year), ending with recovery. In place of ulcers, scars remain, sometimes disfiguring the patient. After the illness, a strong immunity is formed.

Diagnostics. The main symptoms of the anamnesis are basic in making a clinical diagnosis. Epidemiological data should be taken into account (living in places unfavorable for leishmaniasis, etc.).

The final and reliable diagnosis of visceral leishmaniasis is based on the detection of the pathogen. For this, smears of bone marrow stained according to Romanovsky are microscoped under immersion. Material for research is obtained by puncture of the sternum (with a special needle Arinkin-Kassirsky) or the iliac crest.

Leishmania preparations can be found in groups or singly, intracellularly or freely due to the destruction of cells during the preparation of smears.

In cutaneous leishmaniasis, smears from undissolved tubercles or from an infiltrate near are examined. In some cases, the method of sowing the patient's blood (or material from skin lesions or bone marrow) is used. In a positive case, flagellate forms of leishmania appear in culture on days 2-10.

Prevention of leishmaniasis. Preventive measures are selected in relation to the type of leishmaniasis. With visceral leishmaniasis, household rounds are carried out for early detection of patients. They destroy natural reservoirs (rodents, foxes, jackals, etc.), organize the systematic destruction of stray and neglected dogs, as well as inspections of valuable dogs (hunting chain, watchdogs, etc.). In urban cutaneous leishmaniasis, the main thing is the identification and treatment of sick people. With the zoonotic type, wild rodents are exterminated. A reliable means of individual prevention are vaccinations of a live culture of flagellated forms. A special section of the fight against all types of Leishmania is the destruction of mosquitoes and the protection of people from their bites.

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LeishmaniasisSkin leishmaniasis

Leishmaniasis visceral

Leishmaniasis visceral ( Leishmaniasisvisceralis) is a transmissible protozoal disease characterized predominantly by a chronic course, undulating fever, splenomegaly 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 children's kala-azar; East African visceral leishmaniasis; New World visceral leishmaniasis). Imported sporadic cases of the disease, mainly Mediterranean-Central Asian visceral leishmaniasis, are registered in Russia.

Etiology and epidemiology .

The causative agent of Mediterranean-Central Asian visceral leishmaniasis - L. infantum. It is a zoonotic disease with a tendency to spread locally. There are three types of foci of invasion:

Natural foci in which Leishmania circulate among wild animals (jackals, foxes, badgers, rodents, including ground squirrels, etc.), which are a reservoir of pathogens;

Rural foci, in which the circulation of pathogens occurs mainly among dogs - the main sources of pathogens, as well as among wild animals that can sometimes become a source of infection;

Urban foci in which dogs are the main source of infection, but the pathogen is also found in synanthropic rats.

Dogs in rural and urban areas are the most significant source of human infection. The leading mechanism of infection transmission is transmissible, through the bite of infested carriers - mosquitoes of the genus Phlebotomus. Infection during blood transfusions from donors with latent invasion and vertical transmission of Leishmania are possible. Mostly children from 1 to 5 years old and adults who come from non-endemic areas get sick.

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

Pathogenesis and pathological anatomy .

In the future, Leishmania can penetrate into the regional lymph nodes, then disseminate to the spleen, bone marrow, liver and other organs, but in most cases, as a result of the immune response, the invaded cells are destroyed, and the invasion becomes subclinical or latent. In these cases, it becomes possible to transmit the infection through blood transfusions. In cases of reduced reactivity or under the influence of immunosuppressive factors, intensive reproduction of Leishmania in macrophages is noted, specific intoxication occurs with an increase in parenchymal organs and a violation of their function. Atrophy of hepatocytes occurs with the development of fibrosis of the liver tissue, atrophy of the spleen pulp and impaired bone marrow hematopoiesis are noted, anemia and cachexia occur. The production of a large number of immunoglobulins as a result of hyperplasia of the elements of the system of mononuclear phagocytes causes various immunopathological processes. A secondary infection, renal amyloidosis, often develops. In the internal organs, there are changes characteristic of hypochromic anemia. In convalescents, persistent homologous immunity is formed.

Clinical picture .

In the initial period, weakness, loss of appetite, adynamia, slight splenomegaly are noted. The period of the peak of the disease begins with a leading symptom - fever, which usually has an undulating character with rises in body temperature to 39-4 ° C, followed by remissions. The duration of febrile periods ranges from several days to several months, the duration of remissions is also different - from several days to 1-2 months. Permanent signs of visceral leishmaniasis are enlargement and hardening of the liver and spleen; the latter can occupy most of the abdominal cavity. Liver enlargement is usually less significant. On palpation, both organs are dense and painless. 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 lymphadenitis, mesadenitis, bronchoadenitis. Pneumonia caused by the attached bacterial flora is often detected.

In the absence of proper treatment, the condition of patients gradually worsens, they lose weight (up to cachexia). The clinic of hypersplenism develops, anemia progresses, aggravated by damage to the bone marrow. There are granulocytopenia and agranulocytosis, often develop necrosis of the tonsils and mucous membranes of the mouth and gums, hemorrhagic syndrome with hemorrhages in the skin, mucous membranes, nasal and gastrointestinal bleeding. Severe hepatosplenomegaly and liver fibrosis lead to portal hypertension, ascites, and edema. Spleen infarctions are possible. Due to the enlargement of the spleen and liver and the high standing of the dome of the diaphragm, the heart shifts to the right, its tones become deaf, tachycardia occurs both during fever and at normal temperature. Arterial pressure is lowered. Diarrhea occurs, in women oligo- or amenorrhea is usually observed, in men sexual activity decreases.

In the hemogram, a pronounced decrease in the number of erythrocytes and a decrease in hemoglobin (up to 40-50 g / l) and a color index (0.6-0.8) are determined. Characterized by anisocytosis, poikilocytosis, anisochromia. Leukopenia and neutropenia are noted with relative lymphocytosis. Thrombocytopenia is also usually detected, a constant sign is aneosinophilia. Characterized by a sharp increase in ESR (up to 90 mm/h). Reduced blood clotting and erythrocyte resistance.

With kala-azar, 5-10% of patients develop cutaneous leishmanoid in the form of nodular and (or) patchy rashes that appear 1-2 years after successful treatment and contain leishmania, which can persist for years and even decades. Currently, cutaneous leishmanoid is seen only in India.

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

Mediterranean-Central Asian visceral leishmaniasis can occur in acute, subacute and chronic forms. The acute form, usually detected in young children, is rare, has a rapid course and, if not treated in time, ends in death. The subacute form occurs more often, is severe, within 5-6 months, with an increase in symptoms and complications. Without treatment, patients often die. The most common form of chronic visceral leishmaniasis. It is the most favorable, characterized by long remissions and usually ends in recovery with timely treatment. Seen in older children and adults. A significant number of cases of invasion occurs in subclinical and latent forms.

The prognosis is serious, with severe and complicated forms and untimely treatment - unfavorable, but mild forms can end in spontaneous recovery.

Diagnosis and differential diagnosis .

Treatment and prevention .

The most effective preparations are pentavalent antimony and pentamidine isothionate. Antimony preparations are administered intravenously for 7-16 days in an increasing dose. If they are ineffective, pentamidine is prescribed at a dose of 0.004 g / kg daily or every other day, 10-15 injections per course. In addition to specific drugs, pathogenetic therapy and prevention of bacterial deposits are necessary.

Prevention of visceral leishmaniasis is based on measures to destroy mosquitoes and sanitize sick dogs.

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

What is Leishmaniasis

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

Leishmaniasis are neglected diseases.

What causes Leishmaniasis

Reservoir and sources of invasion- man and various animals. Among the latter, jackals, foxes, dogs and rodents (gerbils - large, red-tailed, midday, fine-toed ground squirrel, etc.) are of the greatest importance. Infectivity lasts an indefinitely long time and is equal to the period of stay 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 be up to 7 months or more.

The main epidemiological signs of leishmaniasis. Indian visceral leishmaniasis (kala-azar) caused by L. donovani is an anthroponosis. It is distributed in a number of regions of Pakistan, Bangladesh, Nepal, China, etc. It is distinguished by outbreaks of the disease that occur from time to time. Predominantly adolescents and young people, mainly living in rural areas, are ill.

South American visceral leishmaniasis(visceral leishmaniasis of the New World), caused by L. chagasi, is close in its manifestations to the Mediterranean-Central Asian leishmaniasis. Note mainly sporadic incidence 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 urban-type settlements where mosquitoes live. Among the local population, children are more likely to get sick, among visitors - people of all ages. Summer-autumn seasonality is characteristic, which is associated with the activity of carriers.

Zoonotic cutaneous leishmaniasis of the Old World(pendinskaya ulcer) is caused by L. major. The main reservoir of invasion is rodents (large and red gerbil, etc.). Distributed in the countries of the Middle East, North and West Africa, Asia, Turkmenistan and Uzbekistan. Endemic foci are found mainly in the desert and semi-desert, in rural areas and on the outskirts of cities. Summer seasonality of infections is determined by the period of activity of mosquitoes. Children are predominantly ill; among visitors, outbreaks of diseases among people of different ages are possible.

New World zoonotic cutaneous leishmaniasis(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 the Central and South America, as well as in the southern regions of the United States. The natural reservoir of pathogens is rodents, numerous wild and domestic animals. Diseases are found in rural areas, mainly during the rainy season. People of all ages get sick. Usually infection occurs at the time of work in the forest, hunting, etc.

Pathogenesis (what happens?) during Leishmaniasis

When bitten by mosquitoes, Leishmania in the form of promastigotes penetrate the human body. Their primary reproduction in macrophages is accompanied by the transformation of pathogens into amastigotes (a non-flagellated form). At the same time, productive inflammation develops, and a specific granuloma is formed at the site of implementation. It consists of macrophages containing pathogens, reticular, epithelioid and giant cells. The primary affect is formed in the form of a papule; in the future, with visceral leishmaniasis, it resolves without a trace or scars.

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

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

Convalescents develop persistent homologous immunity.

Symptoms of Leishmaniasis

In accordance with the characteristics of the clinic, 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. Anthroponous (Indian kala-azar).

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

Visceral Mediterranean-Asian leishmaniasis.
incubation period. It 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.

The initial period of the disease. Characterized by the gradual development of weakness, loss of appetite, weakness, pallor of the skin, a slight increase in the spleen. The body temperature rises slightly.

Height period. Usually begins with a rise in body temperature to 39-40 ° C. The fever takes on an undulating or irregular character and lasts from several days to several months, with episodes of high fever and remissions. In some cases, body temperature during the first 2-3 months is subfebrile or even normal.

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

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

Due to hypersplenism and high standing of the diaphragm, the heart shifts somewhat to the right, its tones become muffled, tachycardia and arterial hypotension develop. These changes, along with anemia and intoxication, lead to the appearance and growth of signs of heart failure. Diarrhea, menstrual disorders, impotence are possible.

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

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

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

Cutaneous zoonotic leishmaniasis(pendinskaya ulcer, Borovsky's disease). Found in tropical and subtropical countries. The incubation period varies from 1 week to 1.5 months, averaging 10-20 days. Primary leishmanioma appears at the site of the entrance gate, initially representing a smooth pink papule with a diameter of 2-3 mm. The size of the tubercle increases rapidly, while it sometimes resembles a boil, but 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 is formed up to 1-1.5 cm in diameter, with undermined edges, a powerful infiltrate rim and abundant serous-purulent or sanious exudate; Small secondary tubercles often form around it, the so-called "tubercles of seeding", which also ulcerate and, when merged, form ulcerative fields. This is how a sequential leishmanioma is formed. Leishmaniomas are more often localized on open parts of the body, their number varies from units to tens. The formation of ulcers in many cases accompanies the development of painless lymphangitis and lymphadenitis. After 2-6 months, epithelialization of 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 distribution area. Gradually, the infiltrate resolves without a trace. Small 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 the elderly.

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

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

Complications and prognosis
Running leishmaniasis can be complicated by pneumonia, purulent-necrotic processes, nephritis, agranulocytosis, 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, sepsis. When establishing a diagnosis, epidemiological anamnesis data are used, indicating the patient's stay 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 increase in 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 - an ulcer with undermined edges, a rim of infiltrate and serous-purulent exudate - scar formation).

Laboratory diagnosis of leishmaniasis
In the hemogram, signs of hypochromic anemia, leukopenia, neutropenia and relative lymphocytosis, aneosinophilia, thrombocytopenia, and a significant increase in ESR are determined. 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 - in smears and thick drops of blood stained according to Romanovsky-Giemsa, much more often (95% of positive results) - in smears of bone marrow punctates. The culture of the pathogen (promastigotes) can be obtained by inoculation of punctate on NNN medium. Sometimes, to detect Leishmania, a biopsy of the lymph nodes and even the liver and spleen is performed. 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), which is used only in epidemiological studies, becomes positive.

Leishmaniasis treatment

In visceral leishmaniasis, pentavalent antimony preparations (solusurmin, 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. With insufficient clinical efficacy of drugs, 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 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 an early stage of the disease, tubercles are chipped with solutions of mepacrine, monomycin, urotropine, berberine sulfate; apply ointments and lotions using these funds. With ulcers formed, 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, per course - 11-12 g of the drug). Apply laser irradiation of ulcers. Pentavalent antimony drugs and amphotericin B are prescribed only in severe cases of the disease.

Drugs of choice: antimonil sodium gluconate 20 mg/kg intravenously or intramuscularly once a day for 20-30 days; meglumine antimoniate (glucantim) 20-60 mg/kg deep intramuscularly once a day for 20-30 days. In case of recurrence of the disease or insufficient effectiveness of treatment, a second course of injections should be carried out within 40-60 days. An additional appointment of allopurinol at 20-30 mg/kg/day in 3 oral doses is effective.

Alternative drugs for relapses of the disease and resistance of the pathogen: amphotericin B at 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. In the absence of the effect of chemotherapy, human recombinant y-interferon is additionally prescribed.

Surgery. According to the indications, a splenectomy is performed.

Prevention of Leishmaniasis

The fight against animal carriers of leishmania is carried out in an organized and large-scale manner only with zoonotic cutaneous and visceral leishmaniasis. They carry out deratization measures, landscaping of populated areas, elimination of wastelands and dumps in them, drainage of basements, treatment of residential, household and livestock buildings with insecticides. The use of repellents, mechanical means of protection against mosquito bites is recommended.

After identifying and treating sick people, the source of invasion 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 L. major during the inter-epidemic period among persons traveling to endemic foci, or non-immune persons living in these foci. 04/25/2019

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